Cognitive impairments in poly-drug ketamine users
H.J. Liang
a
, C.G. Lau
a
, A. Tang
a
, F. Chan
a
, G.S. Ungvari
b,c
, W.K. Tang
a,
⁎
a
Department of Psychiatry, Chinese University of Hong Kong, Hong Kong, China
b
The University of Notre Dame Australia/Marian Centre, Perth, Australia
c
School of Psychiatry & Clinical Neurosciences, University of Western Australia, Perth, Australia
HIGHLIGHTS
• Cognitive domains were compared between poly-drug ketamine users and controls.
• Poly-drug ketamine users were further divided into current and ex-users.
• Both current and ex-users had verbal and visual memory impairments.
abstract article info
Keywords:
Ketamine
Substance abuse
Cognitive function
Memory
Executive function
Rationale: Cognitive impairment has been found to be reversible in people with substance abuse, particularly
those using ketamine. Ketamine users are often poly-substance users. This study compared the cognitive
functions of current and former ketamine users who were also abusing other psychoactive substances with
those of non-users of illicit drugs as controls.
Methods: One hundred ketamine poly-drug users and 100 controls were recruited. Drug users were divided
into current (n = 32) and ex-users (n = 64) according to the duration of abstinence from ketamine
(N 30 days). The Beck Depression Inventory (BDI), the Hospital Anxiety Depression Scale (HADSA) and the
Severity of Dependence Scale (SDS) were used to evaluate depression and anxiety symptoms and the severity
of drug use, respectively. The cognitive test battery comprised verbal memory (Wechsler Memory Scale III:
Logic Memory and Word List), visual memory (Rey–Osterrieth Complex Figure, ROCF), executive function
(Stroop, Wisconsin Card Sorting Test, and Modified Verbal Fluency Test), working memory (Digit Span Backward),
and general intelligence (Information, Arithmetic and Digit-Symbol Coding) tests.
Results: Current users had higher BDI and HADSA scores than ex-users (p b 0.001 for BDI and p = 0.022 for
HADSA) and controls (p b 0.001 for BDI and p = 0.002 for HADSA). Ex-users had higher BDI (p = 0.006) but
equal HADSA scores (p = 1.000) compared to controls. Both current and ex-users had lower scores on Logical
Memory delayed recall (p = 0.038 for current users and p = 0.032 for ex-users) and ROCF delayed recall
(p = 0.033 for current users and p = 0.014 for ex-users) than controls. Current users also performed worse on
ROCF recognition than controls (p = 0.002). No difference was found between the cognitive functions of current
and ex-users.
Conclusions: Ketamine poly-drug users displayed predominantly verbal and visual memory impairments, which
persisted in ex-users. The interactive effect of ketamine and poly-drug use on memory needs further investigation.
© 2013 Elsevier Ltd. All rights reserved.
1. Introduction
Ketamine is a frequently abused drug, particularly among youth.
In 2009, 1.7% of 12th grade high school students reported the use of
ketamine over the past year (Morgan, Muetzelfeldt, & Curran, 2009;
National Institute on Durg Abuse, 2010). An investigation in the United
Kingdom confirmed the rising trend of ketamine use: in club settings,
its life-time prevalence rose from 25.5% in 1999 to 39.8% by 2003
(McCambridge, Winstock, Hunt, & Mitcheson, 2007). Ketamine is
currently the most commonly abused drug by young people in
Hong Kong; approximately 70% of local ketamine abusers are under
the age of 21 (Narcotics Division Security Bureau, 2012).
Pharmacologically, ketamine reacts by non-competitively antago-
nizing the N-Methyl-D-aspartate (NMDA) receptor, thereby interfer-
ing with the transmission of excitatory amino acid glutamate and
aspartate, and also with other monoamines such as dopamine and
serotonin (Olney, Newcomer, & Farber, 1999). These pharmacological
actions mediate the effect of ketamine on cognitive functions and
psychiatric symptoms (Wolff & Winstock, 2006). Repeated ketamine
consumption induces cognitive impairment, manifested as poor
Addictive Behaviors 38 (2013) 2661–2666
⁎ Corresponding author at: Department of Psychiatry, Shatin Hospital, Shatin, N.T.,
Hong Kong, China. Tel.: +852 2636 7760; fax: +852 2648 3394.
E-mail address: tangwk@cuhk.edu.hk (W.K. Tang).
0306-4603/$ – see front matter © 2013 Elsevier Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.addbeh.2013.06.017
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