The incidence of unpleasant dreams after sub-anaesthetic ketamine.
Mark Blagrove, Celia J. A. Morgan, H Valerie Curran, Leslie Bromley, Brigitte Brandner
Psychopharmacology March 1, 2009 DOI: 10.1007/s00213-008-1377-3 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Randomized controlled trial Peer reviewed |
|---|---|
| Sample size | 30 |
| Population | Healthy volunteers |
| Intervention | Ketamine |
| Dose | sub-anaesthetic dose |
| Duration | Three nights after infusion |
| Topics | Esketamine Ketamine |
| Key findings | Ketamine causes significantly more unpleasant dreams over the three nights after administration compared to placebo. |
Abstract
Ketamine is an N-methyl-D: -aspartate (NMDA) receptor antagonist with psychotogenic effects and for which there are diverse reports of whether pleasant or unpleasant dreams result during anaesthesia, post-operatively or after sub-anaesthetic use. To assess in healthy volunteers the incidence of unpleasant dreams over the three nights after receiving a sub-anaesthetic dose of ketamine, in comparison to placebo, and with retrospective home nightmare frequency as a covariate. Thirty healthy volunteers completed questionnaires about retrospective home dream recall and were then given either ketamine (n = 19, males = 9, mean age = 23.5 years; mean ketamine blood plasma = 175.29 ng/mL) or placebo (n = 11, males = 5, mean age = 25.4 years). Dream recall and pleasantness/unpleasantness of dream content were recorded by questionnaire at home for the three nights after infusion. Ketamine resulted in significantly more mean dream unpleasantness relative to placebo and caused a threefold increase in the odds ratio for the incidence of an unpleasant dream. The number of dreams reported over the three nights did not differ between the groups. The incidence of unpleasant dreams after ketamine use was predicted by retrospectively assessed nightmare frequency at home. Ketamine causes unpleasant dreams over the three post-administration nights. This may be evidence of a residual psychotogenic effect that is not found on standard self-report symptomatology measures or a result of disturbed sleep electrophysiology.