• Michael C Lewis and Sheila R Barnett.
• Department of Anesthesiology, University of Miami School of Medicine, (R-370), 1611 NW 12th Avenue, Miami 33136, USA. mclewis@med.miami.edu
• Med. Hypotheses. 2004 Jan 1;63(3):402-6.

AbstractA model previously presented by Uchida in this journal [Med. Hypotheses 53 (1997) 103] described a mechanism for postoperative delirium. It described an increased level of melatonin resulting in a central "serotonin shortage". This construct adequately explained only the hypoactive type of delirium. Recently it has been shown that a reduction in urinary metabolites of melatonin is associated with hyperactive delirium, whereas urinary metabolites were increased in the hypoactive variant. These findings suggest that this initial paradigm requires modification. We propose that both the agitation seen in hyperactive delirium, and the somnolence associated with the hypoactive form could be explained by a disturbance of central tryptophan homeostasis. It is postulated that intervention in the form of melatonin administration may restore tryptophan levels, and prevent delirium.Copyright 2004 Elsevier Ltd.

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