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Comment & Response |

Ramelteon and the Prevention of Delirium

Robert H. Howland, MD1
[+] Author Affiliations
1Western Psychiatric Institute and Clinic, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
JAMA Psychiatry. 2014;71(10):1195. doi:10.1001/jamapsychiatry.2014.483.
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To the Editor In their article, Hatta et al1 demonstrated that ramelteon may prevent the development of delirium. They suggested that this prophylactic effect might be mediated by the action of ramelteon on melatonin receptors 1 and 2 (MT1 and MT2) directly regulating activity of the suprachiasmatic nucleus. Two other potential mechanisms should be considered.

One hypothesis of delirium pathophysiology is that pathologically sustained high levels of cortisol occurring with acute stress can precipitate and/or sustain delirium.2 The pars tuberalis is the rostral part of the anterior pituitary.3 Most pituitary hormones, including adrenocorticotropic hormone (ACTH) and follicle-stimulating hormone, are produced in the pars distalis of the anterior pituitary. Endocannabinoid signaling molecules have been detected in the human pars tuberalis.3 Cannabinoid receptor 1 has been detected in the human pars distalis, localized mainly on ACTH and follicle-stimulating hormone cells.3 Mammalian pars tuberalis contains high levels of MT1 receptors.3 Endocannabinoid signaling is involved in the regulation of the hypothalamic-pituitary-adrenal axis, and low endocannabinoid levels have been associated with an increased risk for delirium.4 It is conceivable that ramelteon MT1 receptor binding might regulate pituitary endocannabinoid signaling and cannabinoid receptor 1–mediated ACTH release, thereby attenuating an aberrant hypothalamic-pituitary-adrenal axis stress response that could trigger delirium in a group of high-risk patients.2

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