Search

This pilot study explored the feasibility of using ketamine to increase hypnotizability scores. Ketamine, classified as a dissociative hallucinogen, is used clinically as an anesthetic in high doses and as a treatment for chronic pain and depression in lower doses. Low-dose ketamine can contribute to dissociation and heightened perceptions and feelings of detachment, arguably hypnotic-like states. The authors predicted that a low dose of ketamine in healthy volunteers who scored in the low hypnotizable range on the Stanford Clinical Hypnotizability Scale would (a) cause an increase in subjective ratings of dissociation and (b) lead to an increase in hypnotizability. The findings were in the predicted direction, warranting further investigation into the use of this agent to increase hypnotizability.

Rationale: The precise nature of the impact of the N-methyl-D-aspartate antagonist, ketamine, upon human episodic memory, has yet to be elucidated fully., Objectives: This study sought to assess the effects of ketamine on the sub-processes facilitating memory encoding and retrieval., Methods: We evaluated the effects of the drug on a series of memory performance measures depending upon whether it was administered at the encoding or retrieval stage and on the nature of the encoding task used. Twelve healthy volunteers participated in a double-blind, placebo-controlled, randomized, within-subjects study. Intravenous infusions of placebo, 50 ng/ml ketamine or 100 ng/ml ketamine were administered. We investigated the effects of ketamine on three key aspects of episodic memory: encoding vs retrieval processes, source memory, and depth of processing. Data were analysed using both multinomial modelling and standard measures of item discrimination and response bias., Results: Deleterious effects of ketamine on episodic memory were primarily attributable to its effects on encoding, rather than retrieval processes. Recognition memory was impaired for items encoded at an intermediate level of processing, but preserved for shallowly and deeply encoded items. Increased source guessing bias was also observed when encoding took place under ketamine., Conclusions: The effects of ketamine upon episodic memory seem, therefore, to predominate at encoding. Furthermore, our results are also consistent with a specific impairment of encoding processes that result in subsequent recollective, as opposed to familiarity-based, retrieval. The observed effects are compatible with memory deficits seen in schizophrenia and thus provide some support for the ketamine model of the disease.

We investigated the effects of subdissociative dose ketamine on executive processes during a working memory task. A total of 11 healthy volunteers participated in a double-blind, placebo-controlled, randomized, within-subjects study. They attended on three occasions, receiving intravenous infusions of placebo, a lower ketamine dose, and a higher ketamine dose. On each occasion, they underwent a series of tasks engaging working memory function in verbal and visuo-spatial domains. Further tasks explored aspects of long-term memory, planning, attention, and perceptual processing. With respect to working memory/executive function, a highly specific pattern of impairment was observed. Impairments were seen only at the higher dose of ketamine and restricted to a subgroup of the verbal working memory tasks: While visuo-spatial working memory showed no evidence of impairment, and while simple maintenance processes during verbal working memory were also unimpaired, higher dose ketamine produced a significant impairment in the manipulation of information within working memory. This process-specific effect of ketamine was reflected in a drug-by-task interaction. The specificity of this ketamine effect suggests that the earliest effect of NMDA receptor blockade is in higher order control of executive function rather than in more basic maintenance processes.