Drugs with potent central anticholinergic effects, such as tricyclic antidepressants and antihistamines, are particularly likely to cause delirium. Many medications that are commonly used in the ICU yet not generally considered to be anticholinergic, such as H 2 blockers, opiates, furosemide, digoxin, glucocorticoids, and benzodiazepines, were recently shown to have central anticholinergic properties [16, 17] . Volatile anesthetics, such as sevoflurane, and intravenous anesthetics, such as propofol, also have anticholinergic effects and may be responsible not only for postoperative delirium but also for the more complex phenomena of postoperative cognitive dysfunction [18] . Acute illness itself may be associated with production of endogenous anticholinergic substances [19] . In one study, 8 out of 10 elderly medical inpatients had had detectable anticholinergic activity in their serum, even though no medication used by these individuals had anticholinergic activity. Characterization of such substances might improve our understanding of delirium and lead to useful intervention strategies. Considering that activation of specific cholinergic pathways can inhibit proinflammatory cytokine synthesis and protect against endotoxemia and ischemia-reperfusion injury [20] , it is tempting to speculate that inhibition of these pathways, whether exogenous or endogenous, might contribute not only to CD but also to other outcomes of critical illness.