Abstract
Background: Previous studies have examined the effects of long-term ketamine use on gray matter volume. But it is unclear whether chronic ketamine use alters cortical thickness and whether cortical thickness changes in chronic ketamine users are associated with cognitive deficits observed in chronic ketamine users.Methods: Here, 28 chronic ketamine users and 30 healthy controls (HCs) were recruited. Cortical morphometry based on Computational Anatomy Toolbox (CAT12) was used to measure cortical thickness. Cognitive performance was measured by MATRICS Consensus Cognitive Battery (MCCB). Two-sample t-test was used to assess differences in cortical thickness and cognitive performance between the two groups. Partial correlation analysis was used for assessing correlations between cortical thickness changes and clinical characteristics, cognitive performance in chronic ketamine users.Results: Chronic ketamine users exhibited significantly reduced cortical thickness in frontal, parietal, temporal, and occipital lobes compared to HC [false discovery rate (FDR) corrected at p < 0.05]. In chronic ketamine users, the average quantity (g) of ketamine use/day was negatively correlated with cortical thickness in the left superior frontal gyrus (SFG), right caudal middle frontal gyrus (MFG), and right paracentral lobule. The frequency of ketamine use (days per week) was negatively correlated with cortical thickness in the left isthmus cingulate cortex. Duration of ketamine use (month) was negatively correlated with cortical thickness in the left precentral gyrus. The chronic ketamine users showed significantly poorer cognitive performance on the working memory (P = 0.009), visual learning (P = 0.009), speed of processing (P < 0.000), and Matrics composite (P = 0.01). There was no correlation between scores of domains of MCCB and reduced cortical thickness.Conclusion: The present study observed reduced cortical thickness in multiple brain areas, especially in the prefrontal cortex (PFC) in chronic ketamine users. Dose, frequency, and duration of ketamine use was negatively correlated with cortical thickness of some brain areas. Our results suggest that chronic ketamine use may lead to a decrease of cortical thickness. But the present study did not observe any correlation between reduced cortical thickness and decreased cognitive performance in chronic ketamine users.
Highlights
Ketamine, a derivative of phencyclidine, is a non-competitive antagonist of N-methyl-D-aspartate glutamate receptor [1]
We found that cortical thickness was significantly reduced in the frontal, parietal, temporal, and occipital lobes in chronic ketamine users compared to HCs
Consistent with a previous study, the present study found that the frequency, duration, and average quantity of ketamine used were correlated with abnormal cortical thickness changes, which was most prominent in the frontal lobes of chronic ketamine users
Summary
A derivative of phencyclidine, is a non-competitive antagonist of N-methyl-D-aspartate glutamate receptor [1]. Ketamine administration in rodents led to a dose- and timedependent increase in neuronal cell death in the frontal cortex [5], hippocampus, and thalamus [5] It suggested that chronic ketamine use probably results in abnormal brain structure changes. Another study found extensive atrophy in multiple brain regions in patients with 2–4 years of chronic ketamine use, especially in the frontal, parietal, and occipital cortices [7] These findings reflect the deleterious effects of chronic ketamine use on brain regions, such as the PFC [6, 7], which is a key brain region for cognitive functions (e.g., working memory) [8,9,10]. It is unclear whether chronic ketamine use alters cortical thickness and whether cortical thickness changes in chronic ketamine users are associated with cognitive deficits observed in chronic ketamine users
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