The incidence of unpleasant dreams after sub-anaesthetic ketamine.

Ketamine, an NMDA receptor antagonist, increases the unpleasantness of dreams for three nights after a sub-anaesthetic dose. In a placebo-controlled study with 30 healthy volunteers, those given ketamine reported significantly more unpleasant dreams, with a threefold increase in the odds of having an unpleasant dream. The number of dreams recalled did not differ between groups. People who already had frequent nightmares at home were more likely to have unpleasant dreams after ketamine. This effect may reflect a lingering psychotogenic influence or disrupted sleep physiology not captured by standard symptom questionnaires.

Study at a glance

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.