21 - Smith2014

G Model
DAD-5271; No. of Pages 33 ARTICLE IN PRESS

Drug and Alcohol Dependence xxx (2014) xxx–xxx
Contents lists available at ScienceDirect
Drug and Alcohol Dependence

journal homepage: www.elsevier.com/locate/drugalcdep
Review
Deficits in behavioural inhibition in substance abuse and addiction:

A meta-analysis
Janette L. Smith a,∗ , Richard P. Mattick a , Sharna D. Jamadar b , Jaimi M. Iredale a
a
National Drug and Alcohol Research Centre, University of New South Wales, Sydney 2052, NSW, Australia
b
Monash Biomedical Imaging & School of Psychological Sciences, Monash University, Melbourne 3800, VIC, Australia
a r t i c l e i n f o a b s t r a c t
Article history: Aims: Deficits in behavioural inhibitory control are attracting increasing attention as a factor behind the
Received 11 April 2014 development and maintenance of substance dependence. However, evidence for such a deficit is varied in
Received in revised form 14 August 2014 the literature. Here, we synthesised published results to determine whether inhibitory ability is reliably
Accepted 14 August 2014
impaired in substance users compared to controls.
Available online xxx
Methods: The meta-analysis used fixed-effects models to integrate results from 97 studies that compared
groups with heavy substance use or addiction-like behaviours with healthy control participants on two
Keywords:
experimental paradigms commonly used to assess response inhibition: the Go/NoGo task, and the Stop-
Inhibition
Behavioural control Signal Task (SST). The primary measures of interest were commission errors to NoGo stimuli and stop-
Substance abuse signal reaction time in the SST. Additionally, we examined omission errors to Go stimuli, and reaction time
Pathological gambling in both tasks. Because inhibition is more difficult when inhibition is required infrequently, we considered
Meta-analysis papers with rare and equiprobable NoGo stimuli separately.
Review Results: Inhibitory deficits were apparent for heavy use/dependence on cocaine, MDMA, metham-
phetamine, tobacco, and alcohol (and, to a lesser extent, non-dependent heavy drinkers), and in
pathological gamblers. On the other hand, no evidence for an inhibitory deficit was observed for opioids
or cannabis, and contradictory evidence was observed for internet addiction.
Conclusions: The results are generally consistent with the view that substance use disorders and addiction-
like behavioural disorders are associated with impairments in inhibitory control. Implications for
treatment of substance use are discussed, along with suggestions for future research arising from the
limitations of the extant literature.
© 2014 Elsevier Ireland Ltd. All rights reserved.
Contents
1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
2. Method . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
2.1. Search strategy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
2.2. Inclusion/exclusion criteria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
2.3. Effect size calculations and pooling strategies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
3. Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
3.1. Characteristics of included studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
3.2. Equiprobable Go/NoGo task . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
3.3. Frequent-Go/rare-NoGo task . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
3.4. Stop signal task . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4. Discussion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.1. Inhibitory deficits . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.2. Attentional/discrimination deficits . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
∗ Corresponding author. Tel.: +61 2 9385 0274; fax: +61 2 9385 0222.
E-mail address: janette.smith@unsw.edu.au (J.L. Smith).
http://dx.doi.org/10.1016/j.drugalcdep.2014.08.009
0376-8716/© 2014 Elsevier Ireland Ltd. All rights reserved.
Please cite this article in press as: Smith, J.L., et al., Deficits in behavioural inhibition in substance abuse and addiction: A meta-analysis.
Drug Alcohol Depend. (2014), http://dx.doi.org/10.1016/j.drugalcdep.2014.08.009
G Model
2 J.L. Smith et al. / Drug and Alcohol Dependence xxx (2014) xxx–xxx
4.3. Heterogeneity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.4. Dependence vs. heavy vs. light/recreational use . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.5. Polydrug use . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.6. Comorbid psychopathologies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.7. Length of abstinence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.8. Proportion of females . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.9. Lack of research . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.10. Clinical implications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.11. Alternative explanation of the effect . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.12. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Author disclosures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Role of funding source . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Conflict of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
1. Introduction The pattern of performance differences is important in deter-

mining the underlying deficit. A high rate of commission errors,
There has been increasing interest in the contribution of impair- with no change in omission errors and (sometimes) a short RT, is
ments in inhibitory control of overt behaviour to the development the clearest evidence of a deficit in inhibition. In contrast, a high rate
and maintenance of addiction (e.g., Fillmore, 2003; Goldstein and of omission errors may reflect problems with sustained attention
Volkow, 2002; Hester et al., 2010; Jentsch and Pennington, 2014; (Trommer et al., 1988), or in conjunction with long RT, slowing of
Jentsch and Taylor, 1999; Leeman et al., 2014a,b; Lubman et al., responses in order to compensate for a deficit in inhibition (Wright
2004; Perry and Carroll, 2008; Yücel and Lubman, 2007). The abil- et al., 2014). Further, increased rates of both commission and
ity to delay, withhold or interrupt a behavioural response is a key omission errors may be interpreted as a failure to adequately dis-
aspect of executive function; the suppression of an inappropriate criminate between stimuli requiring and not requiring a response.
immediate response allows time for other processes (e.g., formulat- When increases are observed in all three measures, a more general
ing predictions of the consequences of possible actions) to facilitate deficit in executive control is suggested (Wright et al., 2014). Thus,
the transition to a more appropriate course of behaviour (Barkley, the pattern of performance as a whole must be taken into account
1997). Effective inhibitory control is required in everyday life, as when interpreting group differences in the Go/NoGo task.
when we must withhold the expression of spiteful, peculiar or oth- The stop-signal task is a second experimental paradigm viewed
erwise socially inappropriate thoughts. In the context of substance as a prototype for measuring inhibitory control (Logan and Cowan,
use, impaired control is implicated in using more of the substance, 1984). In a typical stop-signal task, participants press one button
or using more often, than intended, and in failed attempts to control with the left hand to stimuli of one type (e.g., a leftward arrow),
or reduce use. These impairments are reflected in the DSM-5 crite- and another button with the right hand to stimuli of another type
ria for substance use disorders (American Psychiatric Association, (e.g., a rightward arrow). On some trials, a “stop-signal” (e.g., an
2013). auditory tone) is presented after the primary (Go) stimulus, indi-
The construct of behavioural inhibition is usually measured cating that the participant should withhold their response to the
via self-report or observer-report measures of impaired con- Go stimulus. The stop-signal is presented randomly and at variable
trol/rash impulsiveness as a trait, or via behavioural performance delays on a low percentage of trials, often, but not always, 25%, so
on tasks requiring inhibition. An extensive literature suggests that that participants cannot predict when stop-signals will occur. Note
self-reported impairments in control are reliably associated with that several methods are available for setting stop-signal delays;
greater past and future substance use (e.g., Gullo et al., 2014; these are functionally equivalent (Logan, 1994; Logan et al., 1984).
Leeman et al., 2014a,b, 2009; Lester et al., 2012; Ryan et al., 2013; According to Logan and Cowan’s (1984) seminal model, whether a
Verdejo-García et al., 2008). In this article, we review the evidence response is successfully inhibited on a stop-signal trial depends
for an inhibitory deficit in the two experimental paradigms most on the relative finishing times of response execution processes
commonly used to assess inhibition, the ‘Go/NoGo’ and ‘stop-signal’ (triggered by the Go stimulus) and response inhibition processes
tasks. (triggered by the stop-signal). A unique feature of this task is that
In the Go/NoGo task, participants must make a button press it allows the calculation of the stop-signal reaction time (SSRT), the
response to stimuli of one type (Go stimuli, e.g., a green shape) and time required to stop a response, estimated from the probability
withhold that response to stimuli of another type (NoGo stimuli, of stopping at different stop-signal delays (Logan, 1994). Healthy
e.g., a red shape). The need for inhibition to NoGo stimuli can be control adults usually require 200–250 ms to stop a response (e.g.,
manipulated by requiring button presses to Go stimuli to be fast Band et al., 2003). The ability to estimate the SSRT represents a
(e.g., Benikos et al., 2013; Jodo and Kayama, 1992) or by decreasing strong advantage of the stop-signal task over the Go/NoGo task, as
NoGo stimulus probability, ensuring the Go response is prepotent it is not possible to estimate the time required for inhibition in the
by virtue of its high frequency. Variations on the Go/NoGo task may Go/NoGo task. The stop-signal task holds an additional advantage
include a cue which precedes and predicts the Go or NoGo stimulus; over the Go/NoGo task in that the speed of the Go response and
the urgency of inhibition is increased when the cue incorrectly pre- the speed of the Stop response are considered to be independent
dicts a Go stimulus (e.g., Randall and Smith, 2011). Note that many (Logan and Cowan, 1984; Logan et al., 1984). Thus, a longer SSRT is
continuous performance tasks fall under this umbrella, although reflective of an inhibitory deficit, while a longer Go RT is reflective
they may not be explicitly referred to as Go/NoGo tasks. The main of inattention (e.g., Lijffijt et al., 2005); the meaning of a longer SSRT
variables of interest are the rate of commission errors (failure to is not altered by the pattern of results for Go RT. Disadvantages of
inhibit a response to NoGo targets, or false alarms), the rate of the stop-signal task relative to the Go/NoGo task include that the
omission errors (failure to respond to Go targets, or misses), and stop-signal task is designed to achieve approximately 50% failures
the reaction time (RT) to Go stimuli. of inhibition overall, and participants may thus feel that the task
G Model
J.L. Smith et al. / Drug and Alcohol Dependence xxx (2014) xxx–xxx 3
is too difficult and become discouraged from continuing, and that (Luijten et al., 2014) included only studies using neuroimaging
more trials are required than the Go/NoGo task (and therefore it methods, and ignored many behavioural studies (not using neu-
may take longer to administer). roimaging) which also shed light on this issue.
The Go/NoGo and stop-signal tasks are quite different in their The work presented herein synthesised published results to
methods and assumptions, and are thought to measure similar address two research questions: (a) whether inhibitory ability, as
but distinct aspects of inhibition–namely, withholding a prepared measured by accepted and valid measures of this construct (SSRT in
response that has not yet been initiated (in the Go/NoGo task), and the stop-signal task, and rate of commission errors to NoGo stimuli
cancellation of a response that is already underway (in the stop- in two versions of the Go/NoGo task) is reliably impaired in users
signal task; Wright et al., 2014; Barkley, 1997). There is a modest but of various substances compared to non-using controls; and (b)
significant correlation (r = 0.41) between commission errors and whether performance deficits are specific to inhibitory processing,
SSRT within individuals (e.g., Schachar et al., 2011), and analyses of or are also present for Go RT in both tasks, and omission errors to Go
brain activity show both common and distinct networks of activa- trials in the Go/NoGo task, potentially reflecting a discrimination or
tion being required for the stop-signal and Go/NoGo tasks (McNab attention deficit.
et al., 2008; Rubia et al., 2001; Swick et al., 2011; Zheng et al., 2008).
Thus, there are strong similarities and also differences between the 2. Method
components of inhibition tapped via the stop-signal and Go/NoGo 2.1. Search strategy
tasks. On a related note, some researchers hold that whether a
Go/NoGo task requires inhibition depends on NoGo stimulus prob- A literature search with no date restrictions was conducted in the PubMed,
ability (e.g., Aron et al., 2014): only when Go trials are frequent PsycINFO, Project Cork, DRUG, Medline, Medline in process, Embase and CINAHL
electronic databases by an author and a qualified librarian at the National Drug
and NoGo trials rare is a prepotent tendency to respond built up,
and Alcohol Research Centre, University of New South Wales. The search terms
requiring inhibition when a NoGo stimulus is unexpectedly pre- used were “Go-NoGo”, “NoGo”, “SSRT”, “stop-signal”, “response inhibition”, “inhibit”
sented. Those authors argue that the equiprobable Go/NoGo task with explosion, “disinhibit” with explosion, “neurocognitive function”, “executive
requires only a decision to respond or not respond and does not function”, “executive dysfunction”, “cognitive control”, “cognition disorders” and
“reaction time” in combination with “alcohol”, “nicotine”, “cannabis”, “cocaine”,
require inhibition. While we do not disagree that inhibition is more
“opioids”, “heroin”, “ecstasy”, “MDMA”, “GHB”, “LSD”, “steroids”, “polydrug”, “illicit”,
difficult with frequent-Go/rare-NoGo tasks, we hold that inhibi- “street drugs”, “designer drugs”, “substance”, “gambl” with explosion, and “inter-
tion is nonetheless required in equiprobable Go/NoGo tasks, since net”. The titles, abstracts and texts of the retrieved articles were scanned by two
it produces similar brain electrical activity (e.g., Pfefferbaum and authors to determine eligibility. We also reviewed the reference lists of articles that
Ford, 1988; Bruin and Wijers, 2002; Nieuwenhuis et al., 2003) met inclusion criteria for further relevant articles.
and activates similar areas of the brain (e.g., Garavan et al., 2006;
Mostofsky et al., 2003; Vallesi et al., 2009; Watanabe et al., 2002). 2.2. Inclusion/exclusion criteria
Furthermore, it is likely that the typical instructions given in the
Included papers were required to: (a) be presented in English; (b) be conducted
Go/NoGo task (“respond to Go stimuli as quickly as possible”) create
on human participants; (c) compare a drug-dependent or chronic heavy-user group
an additional bias toward fast responses, which must be overcome to a control (non-using or limited use) group; (d) specify the main drug of abuse;
with inhibition even for equiprobable NoGo stimuli (Nieuwenhuis (e) report at least one measure from the following: SSRT, Go RT in the stop-signal
et al., 2003). Lastly, Wright et al. (2014) have shown that NoGo stim- task, NoGo commission errors, Go omission errors, Go RT in the Go/NoGo task; (f)
provide sufficient information for calculating effect sizes (either in the published
ulus probability is not a moderator of effect size. In this review, we
article, or provided by an author on request). We excluded papers which delivered
consider papers which use the stop-signal, frequent-Go/rare-NoGo, stop-signals at only one delay (Logan, 1994, those for which the stop-signal indi-
and equiprobable Go/NoGo tasks, since they tax inhibitory capabili- cated that participants should change, rather than stop, the initiated response, and
ties at different levels, with the stop-signal being the most pure test those where the probability of NoGo stimuli was more than 50% (inhibition is not
of inhibition, and the equiprobable Go/NoGo being the weakest. required in such circumstances; e.g., Nieuwenhuis et al., 2003; Randall and Smith,
2011). We also excluded studies of the within-subject acute effects of drugs, and
Although there are a substantial number of research papers
those on family members of substance-dependent individuals, including studies of
examining the possibility of an inhibitory deficit in substance abuse, in utero exposure. We did not set an age limit for participants in studies; although
much of this research reports apparently contradictory findings it is possible that inclusion of adolescent samples may bias the results due to devel-
and/or suffers from small sample sizes, raising issues of statisti- opmentally poorer inhibition (e.g., Williams et al., 1999), only five studies explicitly
cal power. The majority of the papers surveyed have fewer than stated that they included adolescent participants (Dinn et al., 2004; Heitzeg et al.,
2010; Huddy et al., 2013; Tapert et al., 2007; Wetherill et al., 2013), and all other
30 participants per group, providing adequate power to detect studies either explicitly stated a minimum age of 18 or had group mean ages well
only large effects. When non-significant results are reported, they into adulthood (see Tables 1–3
may be interpreted to mean a lack of impairment in inhibition, ). The pattern of results for inhibitory measures is not altered by the exclusion
although a lack of power is also a reasonable explanation (Snyder, of these studies. Lastly, we did not consider the achieved probability of successful
inhibition in papers using the staircase/tracking method for setting stop-signal delay
2013). Vote-counting approaches (e.g., “3 papers found a significant
(see Logan, 1994); all such papers achieved close to 50% successful inhibition on
deficit, while 6 did not”) rely solely on statistical significance (itself average, and thus the calculation of SSRT can be considered reliable (see Congdon
a function of both the magnitude and sampling error of an esti- et al., 2012; Band et al., 2003).
mated effect) and do not deal well with situations of low power, Of the 265 papers identified, 28 papers were excluded for being out of scope
but meta-analytic approaches allow small-moderate effects that (measuring inhibition at the neural not motor level, and regarding the role of NoGo-
A, a neurite growth inhibitor, in spinal cord injury and recovery), and a further 140
are non-significant at the study level to contribute to a significant did not meet the inclusion criteria above, resulting in 97 papers being retained for the
effect across studies, due to a reduction in the sampling error via meta-analysis. There were an insufficient number of studies to separately examine
increased sample size (Lipsey and Wilson, 2001; Snyder, 2013). dependent vs. heavy-user groups, with the exception of alcohol dependence/heavy
Hence, a meta-analysis of inhibitory deficits in substance users is drinkers. We also included studies examining pathological gambling and internet
addiction for an indication of problems associated with an addiction-like pathology
required. Previously published reviews and meta-analyses in this
without the neurotoxic effects of drug administration.
area have either reported results for only one substance, limiting
their conclusions (e.g., alcohol: Aragues et al., 2011; Stavro et al., 2.3. Effect size calculations and pooling strategies
2013; stimulants: Li and Sinha, 2008), or have collapsed results
Where performance was reported as accuracy or hit rate, values were trans-
across classes of substance used, potentially mixing results from
formed to error rate before calculation of effect sizes. Where multiple groups or
different drug classes (e.g., Goldstein and Volkow, 2002; Lipszyc measures were reported, we selected the most representative group (e.g., pooling
and Schachar, 2010; Wright et al., 2014). A recent qualitative review across sexes, or using the groups who had been abstinent for the shortest period
of inhibitory control which broke results down by substance used of time), and calculated effect sizes for measures that were most representative
4
DAD-5271; No. of Pages 33

G Model
Table 1
Characteristics of study samples and effect sizes (with correction for small sample sizes) by study, for papers reporting on equiprobable Go/NoGo tasks (except Townshend and Duka, 2005, which had a NoGo probability of 48%).
Criteria refers to the diagnostic criteria used for entry into control and substance user groups. Readers are referred to the original papers for further details; bolded text indicates a significant result within that study; italicised
text indicates the study was an outlier and is not included in the meta-analysis for that measure. Effect sizes with asterisks indicate that the paper was the sole eligible paper reporting that measure, and therefore that a weighted
mean effect size could not be calculated. Dashes indicate that the study did not report data for that measure.
Study Control group User group
N % Female Mean Criteria N % Female Mean age Criteria Length of abstinence Notes e.g., means used, NoGo errors Go errors Go RT
age correlation analysis
Cocaine
Parvaz et al. 23 34.8 40.7 No major psychiatric 14 7.1 43.9 DSM-IV cocaine 7.2 ± 5.6 days Longer abstinent group – – −0.741*
(2012) disorder, no current dependence (mean ± SD), confirmed and no reward
abuse or dependence (n = 11) or cocaine via urinalysis condition used; a
on any substance abuse (n = 3), no group with recent use
J.L. Smith et al. / Drug and Alcohol Dependence xxx (2014) xxx–xxx
except nicotine, other major were intermediate
ARTICLE IN PRESS
negative urine screen psychiatric between controls and
for all substances disorder, no longer abstinence, and
current abuse or not significantly
dependence on any different from either
other substance
except nicotine
MDMA
Gamma et al. 17 41.2 26.0 No past or current use 16 50.0 22.6 40+ uses, no Asked to abstain from No correlation between 0.209 0.563 0.384*
(2005) of ecstasy, no current current Axis-I drugs (except alcohol lifetime use of MDMA
Axis-I diagnosis, not diagnosis, not and nicotine) for at or cannabis and any
excluded for lifetime excluded for least 7 days before performance measure
use of other drugs lifetime use of testing, but no
other drugs confirmatory urinalysis
Quednow et al. 15 0.0 23.4 Illicit drug-naïve, no 18 0.0 24.2 50+ uses over 1+ Mean 17 days, Reward-punishment 0.245 −0.133 –
(2007) present psychiatric years, no present minimum 3 days, condition used;
illness or family history psychiatric illness confirmed via positive correlation
of severe psychiatric or family history of urinalysis between commission
illness severe psychiatric errors and cumulative
illness, not cannabis dose, years of
excluded for use of amphetamine use,
other substances cocaine use per week,
years of cocaine use,
and cumulative cocaine
dose; omission errors
did not correlate with
drug consumption
Tobacco
Dinn et al. 116 73.3 18.6 Did not currently use 23 60.9 18.6 Smoked cigarettes Not specified Block 2 data used 0.148* −0.048* 0.120*
(2004) tobacco products, not within the past
excluded for other month, not
major psychiatric excluded for other
diagnoses or substance major psychiatric
use diagnoses or
substance use
G Model
Table 1 (Continued)
Alcohol
dependence
Bjork et al. 41 34.1 38.5 No serious psychiatric 130 26.2 39.8 DSM-IV alcohol Minimum 1 week in Immediate memory 0.613 0.134 −0.419
(2004) disorders, no parental dependence, no monitored treatment task used
drinking problems, not psychotic unit
excluded for symptoms, other
depression. comorbidities
noted but not
excluded, no
craniofacial
features suggestive
of fetal alcohol
ARTICLE IN PRESS
syndrome
Cohen et al. 30 0.0 25.9 Mean 4 drinking 17 0.0 36.1 Mean 21.3 drinking 28 days in monitored Pooled over left and – – 0.620
(1997) days/month, mean 2 days/month, mean treatment unit right handed
drinks/occasion, no 11 drinks/occasion, responses; AD group
psychiatric disorders, no history of made more
and no psychiatric intravenous drug commission and
disorders or alcohol use, no current omission errors than
dependence in treatment controls, but not
first-degree relatives medications e.g., statistically significant,
Antabuse, not and not enough
excluded for abuse information for
of other drugs calculation of an effect
secondary to size.
alcohol
Goudriaan 49 30.6 35.8 No treatment for a 46 21.7 47.4 DSM-IV alcohol 3–12 months; urine – 0.752 0.245 –
et al. (2005) mental disorder in past dependence, no negative for alcohol,
3 years, no lifetime comorbid lifetime cannabis and
substance abuse or substance abuse or benzodiazepine use
dependence, no history dependence, no
of psychosis, negative history of psychosis
urinalysis
Kamarajan 30 46.7 24.1 No personal or family 30 46.7 34.3 DSM-IV alcohol Breath and urine – 0.409 0.385 0.071
et al. (2005) history of psychiatric dependence, no negative (drugs not
disorders or substance current treatment specified), length of
use disorders medications e.g., abstinence otherwise
Antabuse, not unspecified
excluded for other
substance use,
conduct disorder,
ADHD or
oppositional
defiant disorder
Karch et al. 16 0.0 39.3 No substance abuse, no 16 0.0 41.6 ICD-10 alcohol 12.6 ± 7.5 days – −0.058 −0.145 −0.218
(2008) psychiatric disorders dependence, no (mean ± SD)
except depression polysubstance
abuse, no comorbid
psychiatric
disorders except
depression
5
6

G Model
Table 1 (Continued)
Noël et al. 40 50.0 43.6 No Axis-I Diagnosis, no 40 50.0 44.7 DSM-IV alcohol 15–21 days, (mean 19.7 Neutral RT used; 0.642 0.668 −0.184
(2007) drug-use disorder in dependence, no days), abstinent from commission errors
the year before study, other Axis-I all drugs in monitored significantly related to
abstain from drugs 5 diagnosis treatment unit with severity of alcoholism
days, alcohol for 24 h urinalysis and breath (total number of prior
analysis routine and on detoxifications)
day of testing
Pandey et al. 58 0.0 21.1 No personal or family 78 0.0 40.7 DSM-IV alcohol Completed a 30 day – −0.327 0.371 0.597
ARTICLE IN PRESS
(2012) history of major dependence, no detoxification
psychiatric or first-degree family program, urine and
substance-related history of breath negative on day
disorders, instructed to psychiatric of testing
abstain from alcohol disorders, not
and other drugs for at excluded for
least 5 days before history of other
testing substance use
(except
hallucinogens),
conduct disorder,
ADHD,
oppositional
defiant disorder
Rubio et al. 96 0.0 38.9 No current or past 247 0.0 40.3 DSM-IV alcohol 4–6 weeks Pooled across 0.211 0.423 –
(2007) psychiatric disorder, no dependence, no detoxification personality disorders
parental suspected history of groups
drinking problems psychiatric
disorder related to
neuropsychological
impairment, no
bipolar disorder, no
psychotic
symptoms, no
maternal alcohol
problems
Thoma et al. 20 55.0 40.9 No past or present 20 40.0 44.6 ICD-10 alcohol 12.2 ± 7.1 days – 0.653 – 0.115
(2007) psychiatric illness dependence, no (mean ± SD) in
comorbid monitored treatment
psychiatric unit
disorder (except
depression), not
excluded for
polysubstance use
G Model
Table 1 (Continued)
Heavy drinking
López-Caneda 25 56.0 18.6 Those who drank less 23 43.5 18.8 6+ drinks/episode Asked to abstain from First evaluation data −0.242 −0.120 0.031
et al. (2012) than the requirements at least once/week, drugs and alcohol for used
for the heavy drinker or 6+ 12 h, none reported
group; no family drinks/episode at binge drinking in the 2
history of first-degree least once/month days prior to testing
alcohol dependence or and during these
substance abuse, no episodes drank 3+
ARTICLE IN PRESS
personal or family drinks/hour; for a
history of major period of at least 2
psychological years, no family
disorders, no use of history of
illegal drugs (except first-degree alcohol
cannabis), AUDIT dependence or
score < 20 substance abuse,
no personal or
family history of
major
psychological
disorders, no use of
illegal drugs
(except cannabis),
AUDIT score < 20
Oddy and Barry 13 53.8 26.1 Consume ≤ 10 13 84.6 20.2 Consume 23+ Not specified – – – 0.567
(2009) drinks/month drinks/month
Rubio et al. 149 35.6 36.8 AUDIT ≤ 7, no current 471 37.2 37.7 AUDIT ≥8, no Negative urinalysis for – −0.147 0.149
(2008) or lifetime substance current or lifetime alcohol, cocaine,
abuse or dependence substance abuse or opiates and cannabis
(except nicotine), dependence on the day of and 2
psychotic, mood or (except nicotine), days before testing;
anxiety disorders psychotic, mood or smoking not restricted
anxiety disorders before participation
Townshend 32 62.5 20.9 AUQ binge drinking 37 40.5 20.9 AUQ binge Asked to abstain from 48% NoGo; Pooled 0.330 – –
and Duka score ≤ 16, consume at drinking score ≥24, recreational drugs at across males and
(2005) least 6 drinks per week, consume at least 6 least 1 week, alcohol at females
no current or past drinks per week, least 12 h
mental illness, no no current or past
alcohol or drug mental illness, no
dependence (except alcohol or drug
nicotine) dependence
(except nicotine)
7
8

G Model
Table 1 (Continued)
Opioids
Forman et al. 13 46.2 34.8 No Axis-I diagnosis 13 46.2 35.3 DSM-IV opiate In MMT 0–21 days – – – −0.517
(2004) (except depression), no dependence, in (mean 15.5 days),
substance abuse or methadone saliva testing positive
dependence including maintenance for opiates (10/10
nicotine, negative treatment, no tested), cocaine (4/10)
saliva tests for all Axis-I diagnosis and negative for
substances tested other than alcohol (0/10) at time
substance abuse or of testing
dependence or
depression, not
ARTICLE IN PRESS
excluded for
nicotine
dependence
Fu et al. (2008) 18 0.0 29.6 At most occasional 30 0.0 33.4 DSM-IV heroin Abstinent from heroin – – – 0.618
social use of alcohol dependence, no 4–11 weeks (mean 7.6,
and cigarettes, history of SD 2.16), negative
reported no use of psychiatric illness, urinalysis for morphine
psychoactive self-report at time of test
substances for 3 days abstinent from
before scan, no history drugs except
of psychiatric illness heroin, nicotine
and occasional
diazepam and
tramadol) for 3
months
Liang et al. 48 0.0 39.0 No history of illegal 88 0.0 40.81 History of heroin 9.1 ± 4.7 months Neutral condition used 0.107 0.096 –
(2014) drug use, alcohol use, reported (mean ± SD)
misuse or alcohol heroin as drug of
dependence, no choice, not in
current or past opioid substitution
psychiatric disorder treatment, no
current or past
psychiatric
disorder (except
substance-related
disorders)
Yang et al. 14 0.0 41.0 No psychiatric 14 0.0 41.0 DSM-IV heroin 4.7 ± 6.4 months – −0.170 −0.409 −0.027
(2009) condition abuse or (mean ± SD)
dependence, no
previous
consumption of
other drugs, no
excessive alcohol
intake, no other
psychiatric
conditions
G Model
Table 1 (Continued)
Cannabis
Quednow et al. 15 0.0 23.4 Illicit drug-naïve, no 17 0.0 25.4 3.9 ± 4.7 uses per Mean 7.1 days, Reward-punishment −0.043* 0.099* –
(2007) present psychiatric week (mean ± SD), minimum 3 days, condition used;
illness or family history lifetime uses confirmed via positive correlation
of severe psychiatric 1033.4 ± 1348.6), urinalysis between commission
illness no substantial errors and cumulative
previous use of cannabis dose, years of
amphetamine or amphetamine use,
cocaine, no present cocaine use per week,
psychiatric illness years of cocaine use,
or family history of and cumulative cocaine
severe psychiatric dose; omission errors
illness, not did not correlate with
ARTICLE IN PRESS
excluded for use of drug consumption.
other substances
Gambling
Goudriaan 49 30.6 35.8 No treatment for a 48 16.7 39.0 DSM-IV Urine negative for – 0.504 0.113 –
et al. (2005) mental disorder in past pathological alcohol, cannabis and
3 years, no lifetime gambling, no benzodiazepine use
substance abuse or comorbid lifetime
dependence, no history substance abuse or
of psychosis, negative dependence, no
urinalysis history of psychosis
Rodriguez- 40 0.0 32.0 SOGS < 4 (men 0.32), no 39 0.0 34.6 DSM-IV Not specified Non-ADHD group used −0.083 0.126 –
Jimenez et al. ADHD, psychotic or pathological
(2006) affective disorders, no gambling, no
substance use ADHD, psychotic or
(excluding nicotine and affective disorders,
caffeine) in the no substance use
previous year (excluding nicotine
and caffeine) in the
previous year
Internet
addiction
Liu et al. (2014) 11 0.0 22.5 Do not meet internet 11 0.0 23.5 Internet addiction, Not specified Original task means 0.296 – -
addiction criteria, no no lifetime used
lifetime substance use substance use
disorder (except disorder (except
nicotine), no current nicotine), no
depression, no history current depression,
of bipolar or psychotic no history of
disorder bipolar or
psychotic disorder
Zhou et al. 26 26.9 25.0 Non-smokers, no Axis-I 26 26.9 25.0 YDQ Internet Not specified – 0.643 3.940* 0.063*
(2010) or personality addiction, no Axis-I
disorders, no alcohol or or personality
substance dependence disorders, no
alcohol or
substance
dependence
9
10

G Model
Table 2
Characteristics of study samples and effect sizes (with correction for small sample sizes) by study, for papers reporting on frequent-Go/rare-NoGo tasks. Notes on coding are the same as for Table 1.
N % female Mean Criteria N % female Mean Criteria Length of abstinence % NoGo Notes e.g., means used, NoGo Go Go RT
Age age correlation analysis errors errors
Cocaine
Bell et al. 45 22.2 38.1 No DSM-IV Axis I 27 11.1 37.8 DSM-IV cocaine 0.87–100 weeks, mean 12 No relationship 0.052 – −0.216
(2014) diagnosis dependence, no other 32.3 weeks, confirmed between commission
DSM-IV Axis-I via random urinalysis errors and duration of
diagnosis except abstinence, years of
depression or use, or age
dependence. Not
excluded for
abuse/dependence on
other substances
Connolly et al. 9 22.2 30.5 No psychiatric illness, 9 22.2 36.4 DSM-IV cocaine 1–5.1 weeks, mean 2.4 6 Short-term abstinent −0.423 – 0.420
(2012) no history of substance dependence, no other weeks, confirmed via group used; no
abuse disorders psychiatric illness or random urinalysis difference in
ARTICLE IN PRESS
other substance performance for
dependence, not controls, long-term
excluded for abuse of and short-term
other substances abstinent groups
Hester and 15 53.3 31.0 No current or past 15 40.0 40.0 No current or past Last use 12–72 h (mean 12 – 1.377 – −0.239
Garavan psychiatric disorder, no psychiatric disorder, no 41 h), confirmed via
(2004) dependence on any dependence on any urinalysis
substance other than substance other than
caffeine or nicotine, cocaine, caffeine or
‘non-drug-using’, nicotine. Average use 5
negative urinalysis for times/week (range
all substances 1–7), for past 14 years
(range 5–27). Excluded
if urine positive for any
drug other than
cocaine, nicotine or
cannabis.
Hester et al. 22 27.3 39.9 No current or past 21 28.6 40.3 No current or past Last use 12–60 h (mean 20 Repeat NoGo means 0.763 – 0.727
(2007) psychiatric disorder, no psychiatric disorder or 45 h), confirmed via used; no relationship
dependence on any dependence on urinalysis between commission
substance other than substance other than errors and use
nicotine, cocaine or nicotine. behaviour
‘non-drug-using’, Excluded if urine
negative urinalysis for positive for any drug
all substances other than cocaine,
nicotine or cannabis.
Hester et al. 15 13.3 42.7 No Axis-I disorder or 15 13.3 38.2 DSM-IV cocaine 30–1825 days (mean 20 Neutral condition 0.624 – −0.446
(2013) substance dependence. dependence, no other 335); confirmed via means used; no
Negative urinalysis for Axis-I diagnosis except random urinalysis for relationship between
alcohol and all depression. Not at least the 4 weeks task performance and
substances (apart from excluded for prior to testing either years of use or
nicotine) abuse/dependence on duration of abstinence
other substances.
Excluded if urine
positive for alcohol or
other substances (apart
from nicotine)
Kaufman et al. 14 71.4 30.0 Nondrug users, 13 38.5 37.0 Active cocaine users, Last use 18–72 h; 6 – 1.042 1.542 –
(2003) negative urinalysis for mean years of use 11.2 confirmed via
all substances years (range 1–22) urinalysis
G Model
Table 2 (Continued)
Morie et al. 21 4.8 41.0 No drug use history, no 20 5.0 39.0 Past DSM-IV substance 1–24 months, mean 15 15 Neutral task used 0.099 −0.239* −0.051
(2014) Axis-I diagnosis dependence, no Axis-I months, confirmed via
diagnosis. 13 identified random urinalysis at
cocaine as drug of outpatient treatment
choice, 7 identified centre or inpatient
heroin, but used treatment
cocaine in comparable
amounts
Sokhadze et al. 15 53.3 37.0 No Axis-I diagnosis, 19 36.8 42.1 DSM-IV cocaine abuse 16 subjects use within 20 – – – 0.892
(2008) ‘non-drug using’, no or dependence, no 72 h confirmed via
current or past other Axis-I diagnosis urinalysis; remainder
dependence except except PTSD. Use of negative screen,
caffeine or nicotine cocaine, amphetamine, abstinent less than 60
opiates and cannabis days.
ARTICLE IN PRESS
tested via urinalysis;
excluded if positive for
amphetamine or
opiates. Eight tested
positive for cannabis,
16 regular smokers
Methamphetamine
Leland et al. 19 15.8 40.3 No history of Axis-I 19 10.5 40.4 Current DSM-IV Mean 34 days (range 32 Uncued means used 0.576* 0.000* 0.038*
(2008) disorders methamphetamine 25–50)
dependence,
treatment-seeking
MDMA
Hoshi et al. 27 0.0 32.0 No history of 25 0.0 28.6 Use 1+/month, 25+ Mean 14 days, 25 Current user group 0.547 0.575* −0.793
(2007) recreational drug use lifetime uses, no minimum 3 days, used; Ex-users
except alcohol, no current or history of confirmed via (abstinent mean 1017
current or history of addiction, no current urinalysis before days) showed reduced
addiction, no current depression, not testing commission and
depression excluded for other drug omission errors and
use history longer RT than
current-users; ex-users
were not significantly
different to controls
Roberts and 20 50.0 22.5 Illicit drug naïve, no 20 50.0 22.4 40+ uses over 1 year, Ecstasy: Mean 16 days 10 – 0.562 – 0.372
Garavan current or history of excluded if > 10 (minimum 2 days);
(2010) psychiatric problems, lifetime uses of other Cannabis: range 0.5–12
negative urine screen illicit drugs except days; Other drugs: 10
cannabis, no current or weeks. Confirmed via
history of psychiatric urinalysis
problems, not excluded
for recent cannabis use
Roberts et al. 20 65.0 23.1 No illicit drug use 20 50.0 24.0 Minimum 5 uses (mean Asked to abstain from 25 – −0.099 – 0.022
(2013) history lifetime dose 178 MDMA minimum 7
tablets), not excluded days, other illicit drugs
for other drug use minimum 24 h and
ideally 7 days,
confirmed via
urinalysis
11
12

G Model
Table 2 (Continued)
Tobacco
Buzzell et al. 15 53.3 21.4 No current or previous 15 53.3 21.9 Smoking for at least 1 At least one hour 20 – 0.586 0.730 −0.361
(2014) history of smoking year (13/15 abstained for at
least two hours)
Evans et al. 22 59.1 25.0 Smoked 5–100 lifetime 26 42.3 30.2 15+/day for 1+ years, Ad lib consumption 9 Satiated group used; −0.132 0.516 0.657
(2009) cigarettes not currently before testing deprived group (10.5 h)
attempting to quit showed no differences
to satiated group;
deprived also had
longer RT than controls
Luijten et al. 20 30.0 21.6 <10 lifetime cigarettes, 19 26.3 21.4 10+/day for 2+ years, At least 1 h, confirmed 25 Neutral means used; 0.629 0.366 −0.244
(2011) no current substance no current substance by breath analysis no correlation between
abuse or other abuse (except commission errors and
ARTICLE IN PRESS
psychiatric illness nicotine), no other number cigarettes/day
current psychiatric
illness
Luijten et al. 17 58.8 24.5 <10 lifetime cigarettes, 19 68.4 26.9 15+/day for 2+ years, 1 h, not confirmed by 13 Neutral means used 0.136 −0.285 0.017
(2013a) no current substance no current substance breath analysis
abuse or dependence, abuse or dependence
or other psychological (except nicotine), or
illness other psychological
illness
Luijten et al. 23 39.1 21.7 <10 lifetime cigarettes, 25 28.0 22.6 15+/day for 3+ years, 4 h, confirmed with 12 Placebo means used 0.071 −0.090 0.612
(2013b) no current substance no current substance breath analysis
abuse or dependence abuse or dependence
or other psychiatric (except nicotine), or
illness other psychiatric
illness
Nestor et al. 13 61.5 23.6 Never smoked 10 50.0 23.0 10+ cigarettes/day for Ad lib consumption 10 Current smokers used; 0.957 0.323 −0.272
(2011) cigarettes, no lifetime 2 + years, no lifetime 15 min before testing; no correlation between
major psychiatric major psychiatric urine negative for task performance and
illness, no current or illness, no current or other drugs withdrawal, urge to
past substance past substance smoke, or usage
dependence, no family dependence (except parameters. Ex
history of psychiatric nicotine), no family smokers (abstinent
illness history of psychiatric mean 85 weeks)
illness, no past or showed slower RT than
current use of products controls and current
to facilitate quit smokers, and fewer
attempts commission errors
than current smokers
(equal to controls).
Alcohol
dependence
Easton et al. 7 0.0 40.0 DSM-IV nicotine 18 0.0 40.0 DSM-IV alcohol 14 days according to 20 Pooled over IPV+ and −0.116 −0.165* –
(2008) dependence, no dependence and subject report, urine IPV− groups
schizophrenia, bipolar nicotine dependence, negative for other
disorder, or current no schizophrenia, drugs
suicidal or homicidal bipolar disorder, or
plans current suicidal or
homicidal plans
G Model
Table 2 (Continued)
Fallgatter et al. 20 20.0 40.8 No lifetime or family 20 20.0 44.1 DSM-IV alcohol 10 days in monitored 10 – 0.394 – −0.272*
(1998) history of alcohol dependence treatment unit
dependence or other
psychiatric disorders
Salgado et al. 30 33.3 46.9 No current substance 31 16.1 49.0 DSM-IV alcohol 15–120 days, 20 No correlation between 0.862 – –
(2009) disorder (except dependence, no other determined by daily performance and days
tobacco), no current current substance self-report and weekly abstinent
depression, no history disorder (except family-report
of psychotic disorder, tobacco), no current
OCD, impulse control depression, no history
disorder (e.g., of psychotic disorder,
pathological gambling, OCD, impulse control
borderline personality, disorder (e.g.,
ADHD or eating pathological gambling,
ARTICLE IN PRESS
disorder), not excluded borderline personality,
for benzodiazepine or ADHD or eating
antidepressant use disorder), not excluded
for benzodiazepine or
antidepressant use
Heavy drinking
Heitzeg et al. 20 45.0 19.2 Low (maximum 4, 21 42.9 19.3 At least 5 (mean 11.4) Negative urinalysis for 24 FH-group used −0.260 – 0.198
(2010) mean 0.9) reported drinking-related multi-drug five-panel
alcohol problems, no problems, at least one screen
parental history of parent with an alcohol
alcohol use disorder, no use disorder diagnosis,
chronic mental illness, no chronic mental
no history of psychosis illness, no history of
or schizophrenia in psychosis or
first-degree relatives, schizophrenia in
no evidence of fetal first-degree relatives,
alcohol effects in no evidence of fetal
participant, no Axis-I alcohol effects in
disorder except participant, no Axis-I
conduct disorder, disorder except
ADHD. conduct disorder,
ADHD, prior substance
use disorder
Henges and 69 62.3 19.6 Calculated peak 40 50.0 19.5 Peak BAC ≥.08 g%, Not specified 20 Pooled across males 0.163 – −0.293
Marczinski BAC < 0.08 g%, mean 1 mean 4 heavy drinking and females;
(2012) heavy drinking days in past month commission errors
(5 + drinks) day in past following invalid cues
month and RT following valid
cues used. Positive
relationships between
commission errors and
total number of drinks
consumed, number of
heavy drinking days,
highest number of
drinks consumed;
trend level for number
of drunk days. RT did
not correlate with
these measures
13
14

G Model
Table 2 (Continued)
Kreusch et al. 36 66.7 21.1 AUDIT ≤ 7 (mean 3.3), 35 45.7 21.2 AUDIT ≥11 (mean Not specified 25 Experiment 1 neutral 0.015 – −0.173
(2013) consume at least 1 16.5), no regular use of condition data used,
drink per week (mean other substances collapsed across males
2.4), no regular use of except nicotine, mean and females and across
other substances 23.3 drinks/week logo present and
except nicotine absent
Moreno et al. 26 57.7 20.1 No history of alcohol 22 54.5 19.5 6+ drinks/episode At least 3 days (not 25 – 0.084 – –
(2012) consumption or use of 1+/month, CAGE score confirmed via urine or
illicit drugs, CAGE 1–2, no continuous use breath analysis)
score = 0, no diagnosis of other illegal drugs,
of psychiatric disorders no diagnosis of
or substance-related psychiatric disorders or
ARTICLE IN PRESS
addictive illnesses substance-related
addictive illnesses
Murphy and 41 48.8 20.4 Drink alcohol at least 41 46.3 21.2 Drink alcohol at least Not specified 10 Commission errors did 0.586 0.388 –
Garavan once a week, AUDIT once a week, AUDIT not contribute to
(2011) ≤10 (mean 7.6), no ≥11 (mean 19.9), no discrimination of
regular use of other regular use of other problem and
drugs drugs non-problem drinkers
Petit et al. 18 44.4 21.6 AUDIT ≤ 11 (mean 6.5), 17 52.9 21.0 AUDIT ≥ 12 (mean Not specified 30 Neutral condition 2.570 0.710 −0.317
(2012) no past or current drug 16.9), no past or used; Commission
consumption (other current drug errors correlated with
than alcohol or consumption (other AUDIT items relating to
nicotine), no family than alcohol or impaired control
history of alcoholism, nicotine), no family
abstainers excluded history of alcoholism
Rossiter et al. 55 72.7 26.4 AUDIT ≤ 7 (mean 3.7), 30 36.7 28.4 AUDIT ≥ 16 (mean Not specified 13 Neutral condition used −0.143 – −0.075
(2012) no current or past 19.4), no current or
dependence on past dependence on
nicotine, no abuse of nicotine, no abuse of
alcohol or other drugs, drugs other than
no current or past alcohol, no current or
history of psychiatric past history of
illness psychiatric illness
Wetherill et al. 20 45.0 17.6 Infrequent (less than 20 45.0 18.5 Frequent (more than 4 70 days since last binge 32 Follow-up data used; −4.769 – –
(2013) once a month) times/month) episode (among heavy Inhibitory performance
low-level (up to 4 low-level (1–2 drinkers); mean 127 at baseline
drinks/occasion) drinks/occasion) or any days since last cannabis uncorrelated with
drinking, no parental binge (>4 use, 131 days since last lifetime number of
history of bipolar, drinks/occasion) other drug use drinks at follow-up
psychotic or antisocial drinking, no parental
personality disorder, history of bipolar,
no maternal drug use psychotic or antisocial
while pregnant, no personality disorder,
Axis-I diagnosis, not no maternal drug use
excluded for cannabis while pregnant, no
or other drug use Axis-I diagnosis, not
excluded for cannabis
or other drug use
G Model
Table 2 (Continued)
Opioids
Constantinou 16 56.3 32.7 Never used opiates, no 16 50.0 37.6 Current users in Reported abstinence at 25 Current user group and 0.161* 0.706* 1.065*
et al. (2010) problematic alcohol or methadone least 1 month pre-stress values used;
drug use, no history of maintenance benzodiazepines, at ex-users (abstinent
psychotic disorder treatment (MMT), not least 3 days crack; 19.2 ± 13.1 months)
under acute effects of breathalysed negative were not significantly
alcohol, or alcohol on day of different to current
benzodiazepines or testing. users; compared to
crack cocaine, no controls, ex-users
history of psychotic made more omission
disorder errors (p = 0.096) and
commission errors
ARTICLE IN PRESS
(p = 0.056), and had a
longer RT (p = 0.092)
Cannabis
Hester et al. 16 6.3 25.3 Minimal cannabis use 16 6.3 24.7 Use 5–7 days/week for 38.0 ± 47.7 h 11 Averaged NoGo −0.075 – −0.173
(2009) history (mean lifetime previous 2 years, (mean ± SD), urine accuracy used;
joints 3.0), no past or smoked minimum 500 positive for cannabis, commission errors
current psychiatric joints, no past or urine/breath negative correlated negatively
illness, no past or current psychiatric for all other drugs and with age of onset of
current drug illness, no past or alcohol cannabis use
dependence (including current drug
alcohol and nicotine) dependence (including
alcohol and nicotine)
Moreno et al. 26 57.7 20.1 No history of alcohol 20 45.0 20.4 Use cannabis more At least 3 days (not 25 – 0.790 – –
(2012) consumption or use of than once/month, confirmed via urine or
illicit drugs, CAGE CAGE score 1–2, no breath analysis)
score = 0, no diagnosis diagnosis of psychiatric
of psychiatric disorders disorders or
or substance-related substance-related
addictive illnesses addictive illnesses
Pope et al. 71 85.9 39.5 Used cannabis 1–50 74 25.7 36.0 Use cannabis at least 7 Urine positive for 20 Current heavy user 0.109 −0.109 0.280
(2001) times in lifetime, and times per week, cannabis at testing; group and day 0 data
no more than once in minimum 5000 negative urinalysis for used; Ex users
past year, less than 100 lifetime episodes of all other drugs tested (abstinent minimum 3
lifetime uses of other cannabis use, less than months) not
drugs of abuse, no 100 lifetime uses of significantly different
current Axis-I disorder other drugs of abuse, from current users or
except simple phobia no current Axis-I controls on any
or social phobia disorder except simple measure
phobia or social phobia
Tamm et al. 19 31.6 23.4 Used cannabis less than 19 15.8 23.7 Use cannabis at least 36 h for alcohol and 10 Non-ADHD groups −0.291 – –
(2013) 4 times in previous once/month for the illicit drugs, 1 h for used
year, no regular binge past year, no regular nicotine and caffeine,
drinking (> 4 drinks on binge drinking (> 4 not confirmed via
one occasion once or drinks on one occasion urinalysis
more/week), no regular once or more/week),
(monthly) use of other no regular (monthly)
substances use of other substances
15
16

G Model
Table 2 (Continued)
Tapert et al. 15 26.7 17.9 Maximum 5 lifetime 15 26.7 18.1 Minimum 60 uses 28 days, confirmed 25 – −0.122 −0.150 −0.293
(2007) cannabis uses (mean (mean 475.6), no Axis-I with minimum 9 urine
0.5), no Axis-I psychiatric disorder, no screens
psychiatric disorder, no significant maternal
significant maternal drug or alcohol use
ARTICLE IN PRESS
drug or alcohol use during pregnancy, no
during pregnancy, no family history of
family history of bipolar I or psychotic
bipolar I or psychotic disorders, not excluded
disorders, not excluded for other drug or
for other drug or alcohol use
alcohol use
Gambling
van Holst et al. 15 0.0 36.2 Gambled maximum 15 0.0 34.4 Current treatment for Urine negative for 29 Neutral means used −0.149* 0.550* 0.726*
(2012) twice/year, no lifetime gambling problems, alcohol, amphetamine,
schizophrenia or SOGS ≥5 (mean 11.6), benzodiazepines,
psychotic episodes, no 93% met DSM-IV opioids and cocaine
diagnosis of manic pathological gambling
disorder, OCD, alcohol criteria, no lifetime
use disorders, schizophrenia or
substance dependence, psychotic episodes, no
or PTSD diagnosis of manic
disorder, OCD, alcohol
use disorders,
substance dependence,
or PTSD
Internet
addiction
Dong et al. 12 0.0 20.2 IAT < 4, no psychiatric 12 0.0 20.5 IAT ≥7, no other Not specified 25 – −0.164 – 0.262
(2010) disorders psychiatric disorders
Sun et al. 61 18.0 20.7 IAT < 5, no history of 52 19.2 21.5 IAT ≥5, no history of Not specified 25 – −0.448 0.143* 0.167
(2009) drug abuse or drug abuse or
diagnosed psychiatric diagnosed psychiatric
disorders disorders
G Model
Table 3
Characteristics of study samples and effect sizes (with correction for small sample sizes) by study, for papers reporting on the stop-signal task. Notes on coding are the same as for Table 1.
Study N% female Mean Criteria N% female Mean Criteria Length of abstinence % Stop, Notes e.g., means used, SSRT Go RT
Age Age delay correlation analysis
method
Cocaine
Bednarski et al. 27 55.6 34.9 No current or past 23 52.2 36.2 Current DSM-IV Urine positive for 25, – 0.098 0.087
(2011) dependence on any cocaine dependence, cocaine at admission to staircase
substance (except no past or current monitored treatment
nicotine), no current or dependence on unit; tested after 14
past history of another substance days
psychotic disorders, no (except nicotine)
current depression or
anxiety symptoms
requiring treatment
−0.273
ARTICLE IN PRESS
Colzato et al. 12 16.7 29.0 No past or current 12 16.7 29.0 Use 1–4 g/month for 2+ Asked to refrain from 30, SSRT positively 0.950
(2007) cocaine use, no Axis-I years, no Axis-I drugs for 2 days and staircase correlated with
diagnosis including diagnosis including caffeine for 12 h, saliva lifetime cocaine
substance abuse substance abuse taken during session exposure in grams, but
but not analysed not with peak and
monthly dose
Crunelle et al. 17 0.0 33.0 DSM-IV ADHD, no 11 0.0 36.0 MINI cocaine 677 ± 569 days 25, ADHD group used as 1.077 −0.127
(2013) other MINI diagnosis, dependence, DSM-IV (mean ± SD) staircase control; nicotine
no use of other drugs ADHD, no use of other dependence did not
apart from alcohol, drugs apart from correlate with any
cannabis or nicotine alcohol, cannabis or performance measure
nicotine
Ersche et al. 59 23.3 32.3 No history of drug 58 11.7 32.5 DSM-IV cocaine Urine positive for 25, – 0.553 0.677
(2011) abuse or psychotic dependence, no history cocaine on day of staircase
disorder, negative of psychotic disorder, testing
urinalysis on day of majority met criteria
testing for all illicit for dependence on
substances tested other substances
Fillmore and 22 45.5 40.5 No major Axis-I 22 31.8 40.1 No major Axis-I Urine positive for 27, delays Controls had higher 3.390 −0.482
Rush (2002) disorder, no history of disorder, DAST ≥4, cocaine on day of probability of
chronic cocaine use, no self-reported recent testing inhibition; probability
current cocaine use, cocaine use, of inhibition not
negative urinalysis on self-reported habitual related to weekly
day of testing for cocaine use past 6 alcohol use
cocaine, no other drug months, not treatment
use except alcohol, seeking, no other drug
nicotine and cannabis use except alcohol,
nicotine and cannabis
Li et al. (2006) 41 51.2 34.1 No history of cocaine 18 50.0 39.1 Current DSM-IV Urine positive for 33, – 0.641 0.339
use, no cocaine dependence, cocaine at admission to staircase
abuse/dependence on no abuse/dependence monitored treatment
other substances (apart on other substances unit; tested after
from nicotine), no (apart from nicotine), minimum 14 days
history of psychotic no history of psychotic
disorders, no current disorders, no current
depression or anxiety depression or anxiety
symptoms requiring symptoms requiring
treatment treatment
17
18

G Model
Table 3 (Continued)
method
Li et al. (2008) 15 0.0 36.6 No history of cocaine 15 0.0 37.7 Current DSM-IV Urine positive for 25, – 0.421 −0.378
use, no cocaine dependence, cocaine at admission to staircase
abuse/dependence on no abuse/dependence monitored treatment
other substances (apart on other substances unit; tested after
from nicotine), no (apart from nicotine), minimum 14 days
history of psychotic no history of psychotic
disorders, no current disorders, no current
depression or anxiety depression or anxiety
symptoms requiring symptoms requiring
treatment treatment
van der Plas 34 47.1 28.9 No history of 22 72.7 34.5 DSM-IV substance Minimum 15 days in 25, – 0.831 −0.402
ARTICLE IN PRESS
et al. (2009) psychiatric disorders dependence (primarily monitored treatment staircase
including substance cocaine), not excluded unit, negative
abuse or dependence if other drugs used in urinalysis for opiates,
past 30 days stimulants, cannabis on
(principally cannabis), day before testing and
no current depression randomly in monitored
or psychosis treatment unit
Vonmoos et al. 66 30.3 30.3 Cocaine-naïve, no 28 25.0 32.5 DSM-IV cocaine Minimum 72 h for all 25, Dependent group used; −0.083 −0.162
(2013) Axis-I disorder dependence, no use of illicit substances staircase No difference in task
including ADHD, no opioids, no polydrug (average 21 ± 34 days), performance for
form of addiction or use, no acute major minimum 24 h for recreational vs.
lifetime illicit depression, and no alcohol, confirmed via dependent users; SSRT
substance use > 15 other Axis-I disorder urinalysis; did not correlate with
occasions, except except cocaine, any use parameters
recreational cannabis cannabis or alcohol
use abuse, other affective
disorders, or ADHD
Zhang et al. 54 46.3 37.7 No dependence on any 54 35.2 39.8 Current DSM-IV Urine positive for 25, – 0.471 −0.215
(2014) substance (apart from cocaine, no cocaine at admission to staircase
nicotine), no history of dependence on other monitored treatment
psychotic disorders, no substances (apart from unit; tested after 14 ± 9
current depression or nicotine), no history of days
anxiety symptoms psychotic disorders, no
requiring treatment current depression or
anxiety symptoms
requiring treatment
Methamphetamine
Monterosso 29 65.5 27.5 Non-smokers, no 11 36.4 27.5 DSM-IV 5–7 days, confirmed 25, Non-smoker control 1.534 −0.342
et al. (2005) current Axis-I methamphetamine via random urinalysis staircase group used; Positive
diagnosis, negative dependence, no other in monitored correlation between
urinalysis for all drugs current Axis-I treatment unit SSRT and MA use
diagnosis including (ln g/week), but not
dependence on other years of use
illicit substances, 1+
years of using 1+ grams
of MA per week
G Model
Table 3 (Continued)
method
Tabibnia et al. 25 48.0 33.2 No current Axis-I 24 45.8 33.4 DSM-IV 4–15 days, confirmed 25, Positive correlation 0.646 −0.067
(2011) diagnosis, no current methamphetamine via urinalysis on day of staircase between SSRT and MA
psychotropic dependence, no other testing and every 2nd craving in the MD
medication, current Axis-I day in monitored group; no such
non-smokers, negative diagnosis including treatment unit correlation for Go RT
urinalysis for all drugs dependence on other
illicit substances, 1+
years of using 1+ grams
of MA per week
ARTICLE IN PRESS
including substance MA), not excluded if unit, negative
abuse or dependence other drugs used in urinalysis for opiates,
Khat
Colzato et al. 20 10.0 30.7 Occasional use of 20 10.0 31.3 DSM-IV substance Asked to refrain from 30, No correlation between 1.786* 0.623*
(2011) alcohol and cannabis dependence, occasional drugs for 24 h and staircase SSRT and use
but no other drug use use of alcohol and alcohol for 12 h, saliva parameters
reported cannabis but no other taken during session
drug use reported but not analysed
Tobacco
Billieux et al. 25 56.0 25.7 1–10 cigarettes/day, no 25 56.0 25.7 11–20 cigarettes/day, Non-deprived 25, Positive correlation 0.587 –
(2010) other substance use, no no other substance use, staircase between SSRT and
history of psychiatric no history of nicotine dependence
problems psychiatric problems score (FTND)
de Ruiter et al. 17 0.0 34.7 Non-smokers, most 18 0.0 33.8 15+ cigarettes/day, Negative urine screen 13, – 0.021 0.325
(2012) major psychiatric most major psychiatric for alcohol, staircase
disorders excluded, no disorders excluded, no amphetamines,
history of alcohol or history of alcohol or benzodiazepines,
drug abuse, negative drug abuse (except opioids or cocaine;
urine screen tobacco) time since last
cigarette not specified
Galvan et al. 25 44.0 19.0 <5 lifetime cigarettes, 25 40.0 19.3 Daily smoking for 6+ Smoke ad libitum until 25, – −0.204 0.139
(2011) no Axis-I psychiatric months, no Axis-I 30 min before testing, staircase
disorder including psychiatric disorder maximum abstinence
current drug abuse or including current drug 17.5 h); abstinence
dependence abuse or dependence from other drugs
(except nicotine) confirmed by urinalysis
Monterosso 29 65.5 27.5 Non-smokers, no 14 28.6 27.5 15+ cigarettes/day, Not specified 25, – 0.000 0.093
et al. (2005) current Axis-I >15 ppm CO in expired staircase
diagnosis, negative air, no current Axis-I
urinalysis for all drugs disorder except
nicotine dependence
19
20

G Model
Table 3 (Continued)
method
Venugopalan 26 60.6 22.6 Maximum 5 cigarettes 28 48.6 23.2 10+ cigarettes/day for Less than 1 h; 25, not Same pattern of results 0.573 0.117
(2010) per day, not necessarily 5 + years, Fagerstrom abstinence from other specified when participants
every day, for a score 10+, no current drugs confirmed by tested after 18 h
minimum 3 years, Axis-I disorder urinalysis abstinence
Fagerstrom score <9, including substance
no current Axis-I abuse (except nicotine
disorder including and caffeine)
substance abuse
(except nicotine and
caffeine)
Alcohol
dependence
−0.159
ARTICLE IN PRESS
Goudriaan 50 30.0 35.6 No substance abuse or 48 22.9 47.2 DSM-IV alcohol 3–12 months; urine 25, – 0.760
et al. (2006) dependence, no major dependence, minimum negative for alcohol, staircase
psychiatric disorders, MMSE score 25, no cannabis or
no current treatment other substance abuse benzodiazepines
for mental disorders, or dependence (except
no ADHD, OCD or nicotine), no major
antisocial personality psychiatric disorders,
disorder no current treatment
except for alcohol
dependence, not
excluded for manic
episodes, OCD, ADHD,
antisocial personality
disorder
Lawrence et al. 25 0.0 41.5 No psychiatric illness 19 0.0 44.3 DSM-IV alcohol Four in AD group had 25, Go reaction time was 0.570 1.242
(2009) dependence, no consumed alcohol in staircase positively correlated
comorbid psychiatric past 48 h, remainder with duration of
illness were abstinent >1 alcohol abuse but
week uncorrelated with
length of abstinence
Li et al. (2009) 24 25.0 35.5 No substance 24 25.0 38.7 DSM-IV alcohol Recent use of illicit 25, – −0.148 0.679
dependence except dependence, no substances ruled out staircase
nicotine, no other comorbid substance via urinalysis at
Axis-I psychiatric dependence except admission to a
disorder, no current nicotine, no other monitored treatment
depression or anxiety Axis-I psychiatric unit; tested 11–17 days
symptoms requiring disorder, no current later
treatment depression or anxiety
symptoms requiring
treatment
Rubio et al. 96 0.0 38.9 No current or past 247 0.0 40.3 DSM-IV alcohol 4–6 weeks Not Pooled across 0.334 –
(2007) psychiatric disorder, no dependence, no history detoxification specified personality disorders
parental suspected of psychiatric disorder groups
drinking problems related to
neuropsychological
impairment, no bipolar
disorder, no psychotic
symptoms, no
maternal alcohol
problems
G Model
Table 3 (Continued)
method
Schmaal et al. 16 0.0 41.7 No DSM-IV diagnosis 16 0.0 42.9 DSM-IV alcohol Minimum 2 weeks; 20, Placebo means used; −0.588 −0.333
(2013) (except nicotine dependence, no other negative urine test for staircase no relationship
dependence), negative DSM-IV diagnosis alcohol, cocaine, between SSRT and
urine screen (except nicotine amphetamine, ecstasy severity of alcohol
dependence) and opiates; some use problems (AUDIT
of cannabis and score), number of
benzodiazepines 2–4 cigarettes smoked/day,
weeks before the study alcohol consumed in
was allowed. past 6 months,
abstinence period,
craving or physical
ARTICLE IN PRESS
symptoms
Sjoerds et al. 16 37.5 47.1 No lifetime Axis-I 31 45.2 46.5 DSM-IV alcohol 14.7 ± 22.3 days 20, Healthy control group 0.212 0.324
(2013) disorders, no current dependence, no (mean ± SD), breath staircase used; SSRT positively
substance abuse or comorbid lifetime alcohol confirmed at correlated with
dependence (except Axis-I diagnosis except 0.0%, urine negative for severity of alcohol
nicotine), abstinent at depression or anxiety benzodiazepines and problems (AUDIT
least 24 h from alcohol disorders, no other drugs of abuse on day score) and number of
current substance of testing cigarettes smoked/day
abuse or dependence
(except nicotine)
including substance alcohol), not excluded unit, negative
abuse or dependence if other drugs used in urinalysis for opiates,
Heavy drinking
Bednarski et al. 21 76.2 25.0 Females: maximum 9, 20 55.0 23.8 Females: minimum 10, Negative urinalysis for 25, – −0.112 0.219
(2012) mean 3 drinks/month mean 25 drinks/month stimulants, opioids, staircase
Males: maximum 16, Males: minimum 17, cannabis and
mean 6 drinks/month mean 35 drinks/month benzodiazepines on
All: no Axis-I disorders, All: no Axis-I disorders, day of testing
no current or past illicit no current or past illicit
substance use, negative substance use, negative
urine screen, not urine screen, not
excluded for nicotine excluded for nicotine
dependence dependence
Moreno et al. 26 57.7 20.1 No history of alcohol 22 54.5 19.5 6+ drinks/episode At least 3 days (not 25, delays – 0.537 –
(2012) consumption or use of 1+/month, CAGE score confirmed via urine or
illicit drugs, CAGE 1–2, no continuous use breath analysis)
score = 0, no diagnosis of other illegal drugs,
of psychiatric disorders no diagnosis of
or substance-related psychiatric disorders or
addictive illnesses substance-related
addictive illnesses
21
22

G Model
Table 3 (Continued)
method
Nederkoorn 30 50.0 21.1 Consume between 1 31 48.4 21.1 Consume at least 11.5 Not specified 25, delays Pooled across males 0.388 –
et al. (2009) and 11.5 (females) or (females) or 12.5 and females, Session 1
12.5 (males) (males) drinks/week Neutral data used
drinks/week
Papachristou 29 79.3 27.6 AUDIT ≤ 10, no 13 69.2 20.9 AUDIT ≥11, no Not specified 25, – −0.034 –
et al. (2012) psychiatric or psychiatric or staircase
substance abuse substance abuse
disorders except disorders except
nicotine nicotine
Rubio et al. 149 35.6 36.8 AUDIT ≤ 7, no current 471 37.2 37.7 AUDIT ≥8, no current Negative urinalysis for Not SSRT at baseline 0.238
(2008) or lifetime substance or lifetime substance alcohol, cocaine, specified, positively correlated
abuse or dependence abuse or dependence opiates and cannabis staircase with alcohol
ARTICLE IN PRESS
(except nicotine), (except nicotine), on the day of and 2 consumption at 4 year
psychotic, mood or psychotic, mood or days before testing; follow-up, and
anxiety disorders anxiety disorders smoking not restricted negatively correlated
before participation with months elapsed to
meeting criteria for
alcohol dependence;
long SSRT a risk factor
for alcohol dependence
at follow-up
Smith and 17 100.0 20.1 Consumed 4+ 13 100.0 20.0 Consumed 4+ Not specified 25, delays SSRT positively 0.791 0.036
Mattick drinks/episode less drinks/episode at least correlated with
(2013) than once a month, once/month, no regular hazardous and harmful
including never, no use of other drugs, no drinking (AUDIT score)
regular use of other other psychiatric
drugs, no other diagnosis (except
psychiatric diagnosis depression)
(except depression)
Yan and Li 12 41.7 27.8 Consume 0–4 9 33.3 28.3 Consume 5–24 Not specified 25, – −0.094 0.391
(2009) drinks/month, no drinks/month, no staircase
reported use of illicit reported use of illicit
substances substances
Cannabis
Grant et al. 214 28.5 21.2 No cannabis use over 16 37.5 21.8 Use at least once/week Not asked to alter their 25, – −0.013 0.339
(2012) the past 12 months, no for past 1 year, no usual habits staircase
axis-I disorders, no axis-I disorders (except
history of non-cannabis cannabis dependence),
illicit drug use no history of
non-cannabis illicit
drug use
Huddy et al. 12 41.7 25.3 No history of cannabis 26 42.3 25.3 Use at least once in Not specified 25, Never and continuing −0.149 −0.298
(2013) use, presenting with past 3 months, staircase use groups used,
psychotic illness for presenting with matched for psychotic
the first time, received psychotic illness for illness; both psychotic
no more than 12 weeks the first time, received groups showed longer
of antipsychotic no more than 12 weeks SSRT and Go RT than
medication of antipsychotic non-psychotic controls
medication
G Model
Table 3 (Continued)
method
Jutras-Aswad 50 40.0 22.8 No history of major 50 26.0 22.5 DSM-IV cannabis Asked to abstain from 33, – −0.298 0.091
et al. (2012) psychiatric disorders dependence (74% using alcohol or drugs staircase
(bipolar, ADHD, current, 26% past), no (except nicotine) on
psychosis, pervasive history of major day of testing
developmental psychiatric disorders
disorder, major (bipolar, ADHD,
affective disorder, psychosis, pervasive
motor tics or Tourette’s developmental
syndrome), no disorder, major
excluded for past affective disorder,
cannabis use, other motor tics or Tourette’s
drug use not assessed syndrome), other drug
ARTICLE IN PRESS
use not assessed
Moreno et al. 26 57.7 20.1 No history of alcohol 20 45.0 20.4 Use cannabis more At least 3 days (not 25, delays – 0.757 –
(2012) consumption or use of than once/month, confirmed via urine or
illicit drugs, CAGE CAGE score 1–2, no breath analysis)
score = 0, no diagnosis diagnosis of psychiatric
of psychiatric disorders disorders or
or substance-related substance-related
addictive illnesses addictive illnesses
Ramaekers 12 33.3 22.8 Maximum once/week 12 25.0 23.2 Use more 4 times/week Urine negative for Not Placebo time 0–1 h −0.371 –
et al. (2009) use of cannabis, no for the past year, no morphine, cocaine, and specified, means used
history of drug abuse history of drug abuse meth/amphetamines delays
(except cannabis), no (except cannabis), no and alcohol; controls
more than 25 more than 25 but not heavy users
drinks/week, all drinks/week, all excluded if cannabis
cigarette smokers cigarette smokers detected on day of
testing
Theunissen 12 33.3 22.8 Maximum once/week 12 25.0 23.2 Use more 4 times/week Occasional users: 50, delays Placebo means used; 0.569 –
et al. (2012) use of cannabis, no for the past year, no minimum 5 days, SSRT positively
history of drug abuse history of drug abuse heavy users: continue correlated with THC
(except cannabis), no (except cannabis), no normal use. Alcohol: concentration
more than 20 more than 20 24 h, urine negative for measured before
drinks/week (mean drinks/week (mean opiates, amphetamine, performance of the
8.5), no more than 25 7.4), no more than 25 cocaine, task
cigarettes/day (mean cigarettes/day (mean methamphetamine,
6.2) 6.3) benzodiazepines
Gambling
de Ruiter et al. 17 0.0 34.7 Engaged in gambling 17 0.0 35.3 Current treatment for Negative urine screen 13, – 0.000 0.118
(2012) maximum twice/year, gambling problems for alcohol, staircase
most major psychiatric (82% lifetime DSM-IV amphetamines,
disorders excluded, no pathological gambling), benzodiazepines,
history of alcohol or most major psychiatric opioids or cocaine
drug abuse, negative disorders excluded
urine screen (except anxiety
disorders, depression,
OCd, PTSD and ADHD),
no history of alcohol or
drug abuse (except
tobacco)
23
24

G Model
Table 3 (Continued)
method
Goudriaan et al. 50 30.0 35.6 No substance abuse or 49 18.4 37.3 DSM-IV pathological Urine negative for 25, – 0.637 0.022
(2006) dependence, no major gambling, minimum alcohol, cannabis or staircase
psychiatric disorders, MMSE score 25, no benzodiazepines
no current treatment other substance abuse
for mental disorders, no or dependence (except
ADHD, OCD or nicotine), no major
antisocial personality psychiatric disorders,
disorder no current treatment
except for problem
gambling, not excluded
for manic episodes,
OCD, ADHD, antisocial
personality disorder
Grant et al. 26 61.5 50.4 No history of 29 62.1 50.4 DSM-IV pathological Negative urinalysis, 25, Baseline data used for 0.799 0.341
(2010) psychiatric illness gambling, no lifetime drugs tested staircase gamblers; after 10
ARTICLE IN PRESS
bipolar disorder, unspecified weeks memantine
dementia or any treatment, SSRT for
psychotic disorder, no gamblers shortened
current substance and was marginally
abuse or dependence longer than controls
(except nicotine) (p = 0.068)
Lawrence et al. 25 0.0 41.5 No psychiatric illness, 19 0.0 37.0 SOGS ≥3 (76% scored 5 Not specified 25, – 0.023 0.292
(2009) SOGS ≤ 2 or more, no comorbid staircase
psychiatric illness
Odlaug et al. 135 40.7 23.4 Gambled at least 5 46 50.0 45.4 DSM-IV pathological Not specified 25, Pathological gamblers 0.919 0.615
(2011) times in past year, no gambling, no other staircase group used; at-risk
current Axis-I disorder current Axis-I disorder gamblers (who did not
meet PG criteria)
displayed SSRT and Go
RT not significantly
different to controls
and better than
pathological gamblers
Rodriguez- 40 0.0 32.0 SOGS < 4 (men 0.32), no 39 0.0 34.6 DSM-IV pathological Not specified 25, Non-ADHD group used −0.392 –
Jimenez et al. ADHD, psychotic or gambling, no ADHD, staircase
(2006) affective disorders, no psychotic or affective
substance use disorders, no substance
(excluding nicotine and use (excluding nicotine
caffeine) in the and caffeine) in the
previous year previous year
Internet
addiction
Choi et al. 21 42.9 23.3 Maximum 2 h/day 20 45.0 22.4 IAT ≥70, minimum Not specified 25, – −0.058 –
(2013) internet use, no history 4 h/day and 30 h/week staircase
of psychiatric disorder, using the internet, no
no alcohol or substance past or current
abuse psychiatric illness, not
excluded for depressive
disorder, no alcohol or
substance abuse
Choi et al. 24 45.8 22.4 IAT < 40, maximum 23 47.8 23.2 IAT ≥70, minimum Not specified 25, – −0.019 −0.618*
(2014) 2 h/day using the 4 h/day using the staircase
internet, drug-naïve, no internet, drug-naïve
history of psychiatric
disorder
G Model
(e.g., using control condition or placebo values, rather than various experimental omission errors, and 7 of 30 for Go RT. For stop-signal studies, 21
condition or on-medication values). These details are provided in Tables 1–3. of 47 papers measuring SSRT, and 4 of 36 reporting Go RT reported
For the stop-signal task, we calculated mean effect sizes for the stop-signal
significant differences. Of course, the role of meta-analysis is to
reaction time and for Go reaction time, where available. For the Go/NoGo task,
we considered separately those papers with close to equiprobable NoGo trials, and integrate the effects from all studies to determine the overall effect.
those with rare (<40%) NoGo trials, and calculated mean effect sizes for commis-
sion errors, omission errors and Go RT. For all measures, a positive effect indicates
poorer performance in the substance-using group (i.e., more errors of commission 3.2. Equiprobable Go/NoGo task
or omission, or longer response execution or response inhibition times). Effect sizes
for all papers were coded by one author, with independent calculations confirmed
by two other authors (half each). Initially, agreement was reached on 84% of effect Table 1 presents information on the individual studies using the
sizes. Those coders then met to adjudicate any inconsistencies (the majority of equiprobable Go/NoGo task included in the meta-analyses, while
which were minor and resulted from simple data recording/entry errors), result- Table 4 presents the weighted mean effect sizes and homogeneity
ing in final 100% agreement. For each measure, we calculated Cohen’s d in line with
analyses for each group for commission (NoGo) errors, omission
guidelines from Lipsey and Wilson (2001) and performed with the associated web-
page http://www.campbellcollaboration.org/resources/effect size input.php, using (Go) errors and Go RT. We adhere to Cohen’s (1992) classification
means and standard deviations or standard errors where possible; occasionally, F, of effect sizes as small (0.2), medium (0.5) and large (0.8).
t or p values were used with sample size to estimate the effect size. In order to As can be seen from inspecting the data, the evidence for
correct for overestimation of the effect size associated with small sample sizes, we increased commission errors to NoGo stimuli, indicative of a deficit
applied Hedge’s (1980) correction to each effect size, and calculated inverse variance
in response inhibition, in substance-abusing groups is small-to-
weights for each study using the corrected effect size.
When all coding was completed, outliers (defined as effect sizes ± 3 standard medium on the whole, and differs based on the drug abused
deviations from the mean effect size in each analysis) were excluded. This is an (see emboldened significant results in Table 4). Small but positive
acceptable cut-off (Lipsey and Wilson, 2001) and has been used in recent meta- effect sizes, indicating poorer performance in the abusing group
analyses (e.g., Wright et al., 2014; Snyder, 2013). Studies with outlier effect sizes
compared to controls, were seen almost exclusively. Breaking the
were excluded only from the analysis on which they were an outlier. These outliers
are included for completeness in Tables 1–3, in italicised font. Within each analy- results down by drug, MDMA users, heavy drinkers, opioid users,
sis (e.g., NoGo errors for alcohol dependence), only one effect size was calculated and pathological gamblers displayed no deficit in performance for
from each study, although most studies reported more than one measure (e.g., also any measure. Increased commission errors, indicative of deficits
reporting Go errors for alcohol dependence), and some studies reported results from in inhibition, were displayed only for internet addicts and alco-
more than one group (e.g., also reporting NoGo errors for methamphetamine users).
hol dependent groups. However, alcohol dependent groups also
In the latter case, the control group appears more than once within Tables 1–3, but
not within an individual analysis of mean effect size. displayed significantly increased omission errors, suggesting that
The weighted mean effect size (fixed effects model) was calculated as the sum this group may have problems with stimulus discrimination, rather
of weighted adjusted effect sizes, for each of the k effect sizes, divided by the sum than inhibition per se.
of the weights for all k studies in the analysis. We also calculated the standard error
of the mean as well as 95% confidence intervals, and tested the null hypothesis that
mean effect size = 0 using a z-score transformation, with significance set at p < 0.05,
two-tailed. 3.3. Frequent-Go/rare-NoGo task
Lastly, we also assessed heterogeneity in effect sizes with the Q statistic (Hedges
and Olkin, 1985), assessed for significance against a chi-square distribution with Table 2 presents information on the individual studies using the
k − 1 degrees of freedom. If Q is significant, substantial heterogeneity between effect
frequent-Go/rare-NoGo task included in the meta-analysis, while
sizes is indicated for that analysis. However, no analysis of moderator variables was
possible, since no measure had the required minimum 20 effect sizes recommended Table 5 presents the weighted mean effect sizes and homogeneity
for sufficient power for moderator analysis (Marin-Martinez and Sanchez-Meca, analyses for each group.
1998; Sánchez-Meca and Marín-Martínez, 1998). The weighted mean effect sizes are again generally positive,
indicating poorer performance in the abusing groups, and mostly
3. Results specific to commission errors. Breaking results down by drug,
stimulants produced small but significant effects, with increased
3.1. Characteristics of included studies commission errors in cocaine users, MDMA users, and tobacco
smokers. These groups did not display significant differences in
97 published papers met inclusion criteria, reporting on a total Go reaction time, suggesting that poorer inhibitory performance
of 6524 participants (3119 control and 3405 user). The number of is not the result of a speed-accuracy trade-off. Similarly, the lack of
studies and number of control and user participants included dif- a difference in omission errors for tobacco smokers also suggests
fered between drugs: cocaine: 19 studies, 526 controls, 416 users; that poorer performance in these groups is specific to inhibitory
methamphetamine: 4 studies, 107 controls, 71 users; khat: 1 study, processing. Note that considerable heterogeneity between studies
20 controls, 20 users; MDMA: 5 studies, 99 controls, 99 users; was observed for both measures in cocaine users, and Go RT in
tobacco: 12 studies, 348 controls, 247 users; alcohol dependence: MDMA users, although, as noted above, no analysis of moderator
18 studies, 602 controls, 852 dependent participants; heavy drink- variables in producing this heterogeneity was possible.
ing: 17 studies, 613 controls, 856 heavy drinkers; opioids: 5 studies, Similar to MDMA, alcohol dependent groups displayed highly
109 controls, 161 users; cannabis: 11 studies, 462 controls, 277 significant performance decrements for commission errors to NoGo
users; gambling: 8 studies, 357 controls, 262 gamblers; internet stimuli, but no changes in performance for omission errors or
addiction: 6 studies, 155 controls, 144 internet addicts. Note that Go RT were observed in the single papers that reported these
not every study reported every measure, so the number of partic- measures. For heavy drinkers relative to controls, there was no sig-
ipants included in each effect size calculation is less than this in nificant deficit observed in behavioural inhibition or reaction time,
every case. although a significant deficit was observed for errors of omission.
Results were mixed between measures. For equiprobable For cannabis users, small-to-medium but non-significant effects
Go/NoGo studies, of 21 papers examining commission errors were observed. This would suggest these disorders are not associ-
(i.e., responding to NoGo stimuli), 6 report significant differences ated with deficits in inhibitory control or attention in the Go/NoGo
between user groups and controls; for omission errors (i.e., fail- task. Studies on internet addiction showed that inhibitory perfor-
ing to respond to Go stimuli), 4 of 18 papers reported a significant mance was actually significantly better in heavy internet users
effect, and for Go RT, 5 of 16 papers described a significant dif- compared to controls. In summary, there is evidence for a deficit
ference. For frequent-Go/rare-NoGo tasks, significant results were in Go/NoGo task performance in drugs of abuse generally, but this
reported for 10 of 37 papers for commission errors, 4 of 18 for appears to differ by drug abused, and for some drugs, may be due
G Model
Table 4
Weighted mean effect sizes (g) and heterogeneity analysis by group and outcome measure for the equiprobable Go/NoGo task.
Substance Effect size analysis Heterogeneity analysis
Variable k g SE CI lower CI upper z p Q df p
MDMA NoGo errors 2 0.227 0.248 −0.258 0.712 0.916 0.360 0.005 1 0.944
Go errors 2 0.210 0.249 −0.279 0.699 0.842 0.400 1.952 1 0.162
Go RT – – – – – – – – – –
Alcohol NoGo errors 7 0.427 0.076 0.278 0.577 5.608 <0.001 9.846 6 0.131
dependence Go errors 7 0.345 0.071 0.206 0.485 4.845 <0.001 5.972 6 0.426
Go RT 7 0.075 0.089 −0.100 0.250 0.842 0.400 21.294 6 0.002
Heavy NoGo errors 3 −0.098 0.084 0.262 0.067 −1.166 0.244 3.609 2 0.165
drinking Go errors 2 0.123 0.089 −0.052 0.299 1.376 0.169 0.784 1 0.376
Go RT 2 0.215 0.234 −0.244 0.674 0.918 0.359 1.181 1 0.277
Opioids NoGo errors 2 0.056 0.162 −0.262 0.374 0.344 0.731 0.437 1 0.509
Go errors 2 0.005 0.162 −0.314 0.323 0.029 0.977 1.435 1 0.231
Go RT 3 0.133 0.204 −0.266 0.533 0.654 0.513 5.364 2 0.068
Gambling NoGo errors 2 0.236 0.152 −0.062 0.534 1.554 0.120 3.691 1 0.055
Go errors 2 0.119 0.151 −0.177 0.415 0.788 0.431 0.002 1 0.964
Go RT – – – – – – – – – –
Internet NoGo errors 2 0.537 0.237 0.072 1.001 2.264 0.024 0.455 1 0.500
addiction Go errors – – – – – – – – – –
Go RT – – – – – – – – – –
Note: Bold type indicates a significant result; positive effect sizes (g) indicate poorer performance by the substance abusing group; dashes indicate that an insufficient number
of papers reported data for calculation of a weighted mean; k = number of studies; SE = standard error.
Table 5
Weighted mean effect sizes (g) and heterogeneity analysis by group and outcome measure for the frequent-Go/rare-NoGo task.
Cocaine NoGo errors 7 0.440 0.128 0.188 0.691 3.423 0.001 15.778 6 0.015
Go errors – – – – – – – – – –
Go RT 7 0.106 0.125 −0.139 0.352 0.850 0.395 14.151 6 0.028
MDMA NoGo errors 3 0.351 0.176 0.005 0.696 1.987 0.047 2.934 2 0.231
Go errors – – – – – – – – – –
Go RT 3 −0.178 0.177 −0.525 0.169 −1.004 0.315 7.936 2 0.019
Tobacco NoGo errors 6 0.248 0.136 0.018 0.549 2.091 0.037 6.862 5 0.231
Go errors 6 0.234 0.135 −0.031 0.500 1.731 0.084 6.507 5 0.260
Go RT 6 0.148 0.136 −0.118 0.414 1.091 0.275 9.930 5 0.077
Alcohol NoGo errors 3 0.531 0.186 0.166 0.897 2.851 0.004 3.819 2 0.148
dependence Go errors – – – – – – – – – –
Go RT – – – – – – – – – –
Heavy NoGo errors 6 0.110 0.098 −0.082 0.302 1.126 0.260 7.329 5 0.197
drinking Go errors 2 0.481 0.188 0.113 0.849 2.562 0.010 0.605 1 0.437
Go RT 5 −0.115 0.111 −0.373 0.062 −1.399 0.162 2.103 4 0.717
Cannabis NoGo errors 5 0.112 0.118 −0.120 0.343 0.944 0.345 7.049 4 0.133
Go errors 2 −0.116 0.151 −0.413 0.181 −0.766 0.444 0.010 1 0.920
Go RT 3 0.127 0.140 −0.147 0.400 0.907 0.364 2.865 2 0.239
Internet NoGo errors 2 −0.397 0.173 −0.737 −0.057 −2.296 0.022 0.397 1 0.529
addiction Go errors – – – – – – – – – –
Go RT 2 0.183 0.172 −0.153 0.520 1.068 0.286 0.044 1 0.834
Note: Bold type indicates a significant result; positive effect sizes (g) indicate poorer performance by the substance abusing group; dashes indicate that insufficient data were
reported; k = number of studies; SE = standard error.
to a general problem with inattention and/or discrimination of for each group for SSRT and Go RT. Here, the evidence for inhibitory
stimuli, rather than being specific to inhibitory trials. deficits is clearer, due to the independent nature of the Go and Stop
processes (Logan, 1994). That is, the interpretation of a longer SSRT
3.4. Stop signal task (as reflecting an inhibitory deficit) is not changed by a significantly
longer Go RT.
Table 3 presents information on the individual studies using As shown in Table 6, there were medium-large deficits in
the stop-signal task included in the meta-analysis, while Table 6 SSRT for methamphetamine and gambling, and small-medium
presents the weighted mean effect sizes and homogeneity analyses effects for cocaine, alcohol dependence and heavy drinking.
G Model
Table 6
Weighted mean effect sizes (g) and heterogeneity analysis by group and outcome measure for the stop-signal task.
Cocaine SSRT 9 0.464 0.088 0.291 0.636 5.274 <0.001 13.300 8 0.102
Go RT 10 −0.004 0.084 −0.168 0.160 −0.052 0.959 22.164 9 0.008
Methamphetamine SSRT 3 0.724 0.185 0.362 1.086 3.917 <0.001 5.990 2 0.050
Go RT 3 −0.312 0.179 −0.664 0.040 −1.738 0.082 1.442 2 0.486
Tobacco SSRT 5 0.218 0.134 −0.045 0.481 1.624 0.104 6.277 4 0.179
Go RT 4 0.159 0.151 −0.137 0.454 1.053 0.292 0.308 3 0.959
Alcohol dependence SSRT 6 0.395 0.086 0.227 0.562 4.612 <0.001 7.944 5 0.159
Go RT 5 −0.015 0.122 −0.255 0.224 −0.127 0.899 10.292 4 0.036
Heavy drinking SSRT 7 0.248 0.077 0.098 0.399 3.240 0.001 5.913 6 0.433
Go RT 3 0.198 0.210 −0.215 0.610 0.940 0.347 0.385 2 0.825
Cannabis SSRT 6 0.004 0.119 −0.230 0.239 0.037 0.971 11.101 5 0.049
Go RT 3 0.102 0.144 −0.181 0.385 0.705 0.481 2.135 2 0.344
Gambling SSRT 5 0.625 0.107 0.415 0.835 5.841 <0.001 10.356 4 0.035
Go RT 5 0.327 0.105 0.121 0.533 3.115 0.002 5.437 4 0.245
Internet addiction SSRT 2 −0.040 0.213 −0.458 0.378 −0.185 0.853 0.008 1 0.929
Go RT – – – – – – – – – –
Note: Bold type indicates a significant result; positive effect sizes (g) indicate poorer performance by the substance abusing group; dashes indicate that insufficient data were
reported; k = number of studies; SE = standard error.
Inhibitory deficits were not apparent overall for tobacco smok- 4.1. Inhibitory deficits
ers or cannabis users, although substantial heterogeneity was
apparent in the latter effect. There were no significant effects The primary measures of inhibition in this meta-analysis were
for Go RT for most analyses, with the exception of gambling. the rate of commission errors in the Go/NoGo tasks, and SSRT
Lastly, no evidence for an inhibitory deficit in internet addicts was in the stop-signal task. Overall, larger effect sizes were found in
observed. the frequent-Go/rare-NoGo studies than in the equiprobable tasks,
with the largest effects in the stop-signal task. As mentioned earlier,
the two tasks measure different aspects of inhibition, with cancella-
4. Discussion tion of an initiated response (as in the stop-signal task) being more
difficult than withholding a planned but uninitiated response (as in
Many individual research studies have investigated inhibitory Go/NoGo tasks) (e.g., Wright et al., 2014). It appears here that the
control deficits in substance use disorders and in addiction-like stop-signal task is more sensitive to deficits than the Go/NoGo task,
behavioural disorders such as pathological gambling and inter- since several studies show larger effects for SSRT than commission
net addiction. However, the pattern of results varies considerably errors recorded from the same sample (Moreno et al., 2012; Rubio
between studies, and many studies have small sample sizes, et al., 2008, 2007; but see Rodriguez-Jimenez et al., 2006). For future
limiting their power to detect effects. Here, we present the largest research, authors should carefully assess which aspect of inhibition
and most comprehensive systematic and quantitative review of they wish to measure, and select the task accordingly.
inhibitory control deficits in substance use and addiction-like disor- The strongest results were observed for psychostimulants,
ders to date. In comparison to previous quantitative and qualitative with an inhibitory deficit confirmed in the frequent-Go/rare-
reviews, the current review was based on a larger number of papers NoGo task for cocaine, MDMA and tobacco, and in the stop-signal
(97) than Lipszyc and Schachar (2010; 5 papers), Stavro et al. (2013; task for cocaine and methamphetamine (and khat, see Table 3),
6 papers), Wright et al. (2014; 32 papers) and Luijten et al. (2014; but not tobacco. That the largest inhibitory deficits were
41 papers), and provides a separate effect size estimate for each obtained for cocaine and amphetamines is consistent with their
class of drug instead of collapsing across drug types (Lipszyc and known neuropsychopharmacology, and with the known neu-
Schachar, 2010; Wright et al., 2014), or reporting results from a ropsychopharmacology of the cortical and subcortical networks
single substance (e.g., alcohol dependence: Stavro et al., 2013). that underlie motor control. Successful behavioural inhibition
Consistent with these previous reports, we confirmed a small- relies principally on dopaminergic and serotonergic prefrontal-
medium deficit in inhibition in several, but not all, substance-using subcortical pathways (for a review, see Jentsch and Pennington,
groups. 2014), and behavioural inhibition in the stop-signal task is asso-
In the discussion below, we review (a) whether a performance ciated with dopamine release in the prefrontal inhibitory control
deficit on inhibitory tasks was observed in a range of substance network (Albrecht et al., 2014). Acute administration of stimulant
dependent groups and in groups with addiction-like behavioural drugs is associated with increased availability of dopamine (either
problems, (b) whether this performance deficit was specific to by stimulating their release or inhibiting reuptake; Goldstein and
inhibition or reflected a more general deficit in response speed, Volkow, 2002; Everitt and Robbins, 2005), and chronic adminis-
attention or discrimination, (c) the possible sources of heterogene- tration results in long-term damage (Ricaurte et al., 1984; Volkow
ity between and within studies, and (d) suggestions for future et al., 2001; Wang et al., 2004). Thus, the strong deficits observed
research arising from the limitations of both the extant literature for most stimulants is likely due to the damage caused by chronic
and the current meta-analysis. administration of dopaminergic drugs and the key role that
G Model
dopamine, and dopaminergic areas of brain, play in behavioural Go RT in the stop-signal task was small but significant for patho-
inhibition. logical gamblers, although in the stop-signal task, the stop and go
Significant medium (g = 0.4–0.5) deficits in inhibition were also processes are considered to be independent and thus the interpre-
observed for all tasks for alcohol dependence, consistent with tation of the longer SSRT is not altered by the longer Go RT. For all
Stavro et al.’s (2013) effect size of 0.460. With a lower level of expo- other substances and inhibitory task measures, effect sizes were
sure to alcohol, heavy drinkers did not show any significant deficits small and non-significant, indicating that performance deficits are
in either Go/NoGo task, but did show a small deficit in inhibitory specific to poor inhibition.
capacity in the stop-signal task. Thus, it appears that alcohol likely
has a dose-dependent effect on inhibitory capacity. 4.3. Heterogeneity
For opioids, there were few papers examining inhibitory perfor-
mance in either version of the Go/NoGo task, and none reporting There were several instances where we detected heterogene-
stop-signal performance. However, based on this sparse evidence, ity in effect sizes between studies. The small number of studies
there was no suggestion of an inhibitory deficit overall or in any reporting each measure precludes a thorough investigation of the
individual study, suggesting that inhibition is probably not a core possible sources of such heterogeneity; however, some potential
deficit in opioid dependence. Similarly, there was no evidence of sources are discussed below. These include several aspects con-
any performance deficit in cannabis users, although there were a cerning inclusion and exclusion criteria for studies, namely, the
larger number of papers on which to base this statement. Substan- heaviness of use of the drug of interest, polydrug use, comorbid psy-
tial heterogeneity was detected for the SSRT effect sizes between chopathologies, the length of abstinence from the drug of interest,
studies, with only one study (Moreno et al., 2012) reporting sig- and the proportion of females included in the sample. We discuss
nificant effects for any measure. However, a recent review (Luijten each of these in turn.
et al., 2014) of neuroimaging studies of inhibition in users of vari-
ous substances concluded that brain activation of prefrontal and 4.4. Dependence vs. heavy vs. light/recreational use
parietal areas was greater during inhibitory trials for cannabis
dependent groups compared to controls, suggesting that cannabis Firstly, studies varied considerably in the inclusion criteria for
users had to “work harder” in order to achieve the same behavioural the user groups. Tables 1–3 list the inclusion and exclusion criteria
performance in the Go/NoGo task. The possibility of such a com- for controls and users in every study included in the meta-analysis.
pensatory mechanism requires further investigation, particularly For alcohol, there were sufficient studies to split analyses accord-
in the stop-signal task, where no neuroimaging studies of cannabis ing to dependence vs. heavy drinking, but for all other classes of
have been published, and where the factors contributing to poor drugs, there were too few studies to allow such an approach. As a
inhibitory performance can be separated by the race model (Logan, result, the studies on cocaine, for example, mostly involve cocaine
1994; Logan et al., 1984). dependent participants, but some (e.g., Colzato et al., 2007; Fillmore
Lastly, we also considered the possibility of inhibitory deficits and Rush, 2002; Hester and Garavan, 2004; Kaufman et al., 2003)
in other addiction-like behavioural disorders, namely pathological classify groups according to the amount, frequency and length of
gambling and internet addiction. We found no evidence of per- use. A similar problem is observed for studies on cannabis, MDMA,
formance deficits for pathological gamblers in the equiprobable and heavy drinking, where no universally agreed-upon definition
Go/NoGo task (Table 4) or the frequent-Go/rare-NoGo task (one exists. In the case of alcohol, researchers classify participants based
paper examined this, detailed in Table 2), but on the other hand, on the number of drinks consumed per unit of time, the frequency
we found a medium-large effect for SSRT (g = 0.625). This pattern of of binge drinking (variously defined), the AUDIT score (with various
results suggests that pathological gambling is not associated with a thresholds), the number of alcohol-related problems, or estimated
deficit in withholding, but rather is associated with a deficit in stop- peak blood alcohol concentration. Note that these represent min-
ping an inappropriate response. This is a substantially larger mean imum use required for the entry to the study, and the variability
effect size than that calculated by Lipszyc and Schachar (2010) above this level may be different in each study.
(g = 0.13), based on only two papers, one of which was excluded For this reason it is difficult to assess the possible role that vari-
as an outlier from the current analysis. Internet addiction showed ations in heaviness of use or severity of dependence may play in
contradictory results: internet addicts showed a medium-sized producing heterogeneity. Helpfully, many of the studies included
inhibitory deficit compared to controls in the equiprobable task, a in the meta-analysis reported correlations between behavioural
small-medium advantage in the frequent-Go/rare-NoGo task, and performance and heaviness of use. These are roughly evenly split
no difference in the stop-signal task, although the number of papers between those studies finding significantly poorer performance in
considered was small in all cases. Thus, we consider that more heavier users (Quednow et al., 2007; Noël et al., 2007; Henges and
research into inhibitory deficits in internet addiction is warranted. Marczinski, 2012; Petit et al., 2012; Hester et al., 2009; Colzato et al.,
2007; Monterosso et al., 2005; Tabibnia et al., 2011; Billieux et al.,
4.2. Attentional/discrimination deficits 2010; Lawrence et al., 2009; Sjoerds et al., 2013; Smith and Mattick,
2013; Theunissen et al., 2012) and those finding no significant rela-
In contrast to the inhibitory deficits apparent across a range of tionship (Gamma et al., 2005; Bell et al., 2014; Hester et al., 2007,
drug classes and experimental tasks, there was little evidence of 2013; Luijten et al., 2011; Nestor et al., 2011; Crunelle et al., 2013;
differences in omission errors or reaction time, suggesting that the Fillmore and Rush, 2002; Vonmoos et al., 2013; Colzato et al., 2011;
above mentioned performance differences are specific to inhibi- Schmaal et al., 2013; Odlaug et al., 2011). It is apparent that relation-
tion. Alcohol dependent groups displayed an increase in omission ships between heaviness of use and inhibitory performance may
error rate for the equiprobable Go/NoGo task; in conjunction with alter results obtained, and future research should more carefully
the increase in commission errors and no change in reaction assess and report use behaviour in their participants (both controls
time, this pattern of results suggests problems with discrimina- and user groups).
tion between stimuli, rather than a deficit specific to inhibition or
a slowing of responses in order to compensate for an inhibitory 4.5. Polydrug use
deficit (Wright et al., 2014). Heavy drinkers also displayed an
increase in omission errors for the frequent-Go/rare-NoGo task, On a related note, studies varied in the extent to which they
indicative of failures of attention in this group. Lastly, the effect for assessed for use of other drugs (both licit and illicit), and whether
G Model
such use was allowed and noted, or excluded, for both con- 4.8. Proportion of females
trols and users (see Tables 1–3). We note that in many studies,
participants were not excluded for alcohol and/or tobacco use, The samples on which the studies report were overwhelm-
which themselves are associated with small deficits in inhibi- ingly male-dominated (see Tables 1–3). Although this is reflective
tion. Here, we classified papers based on the primary drug of of the increased lifetime incidence of substance use disorders in
abuse, but recognise that illicit substance users are often poly- males (e.g., Compton et al., 2007), some research has suggested
drug users (e.g., European Monitoring Centre for Drugs and Drug that inhibitory function is more affected in women, at least in heavy
Addiction, 2002; Australian Institute of Health and Welfare, 2011), drinkers (e.g., Nederkoorn et al., 2009; Townshend and Duka, 2005).
and note that such polydrug use may produce larger deficits than It is unclear whether this result generalises to other drugs; but if
use of a single drug alone. In this respect, each researcher must the sex difference is robust, an abundance of males in published
choose whether to recruit a ‘pure’ sample (that is, one which has studies may have resulted in a smaller effect size than if both sexes
exposure only to the drug of interest) or a ‘representative’ sam- were equally represented.
ple (where polydrug use is allowed and perhaps expected). Both
positions are equally valid; we only note that this is a possible 4.9. Lack of research
source of heterogeneity between studies which may affect the
results, and which should be carefully considered in all future There were several areas where only one study had reported
research. results on a particular task or measure, meaning that no weighted
mean effect size could be calculated. Only one study reported
equiprobable Go/NoGo task performance for cocaine, tobacco and
4.6. Comorbid psychopathologies
cannabis, and none reported on methamphetamine or khat users.
For the frequent-Go/rare-NoGo task, only one study reported per-
The studies included in the meta-analysis varied in the extent
formance for methamphetamine, opioids and gambling, and none
to which comorbid psychopathologies were assessed and included
on khat users. Similarly, only one study reported stop-signal task
or excluded (see Tables 1–3). Although substantial inhibitory
performance for khat, and there were no studies of opioid or MDMA
deficits were observed across a number of drugs and in addiction-
users. Furthermore, there were several instances where, despite
like pathological gambling, an inhibitory deficit is by no means
more than one paper reporting performance for a particular group
specific to addiction. Deficits in inhibition are also apparent in
and task, researchers did not report all the measures available for
attention-deficit/hyperactivity disorder (AD/HD), obsessive com-
that task, meaning that again a weighted mean effect size could
pulsive disorder, reading disability and schizophrenia (Lipszyc
not be calculated for every measure. Given the lack of pertinent
and Schachar, 2010; Wright et al., 2014), depression (Snyder,
research in some areas, and the incompleteness of research in oth-
2013) and traumatic brain injury (Dimoska-Di Marco et al.,
ers, future work should seek to determine the extent of inhibitory
2011). These and other psychiatric disorders are often comor-
deficits in these groups, and to report all available measures for the
bid with substance use disorders (e.g., Kaye and Darke, 2004;
chosen tasks.
McKetin et al., 2005), in line with the recent notion that vari-
ous psychological disorders share common genetic, behavioural
4.10. Clinical implications
and cognitive factors (Psychiatric Genomics Consortium, 2013;
Rzhetsky et al., 2007). Thus, it is possible that the effect sizes
The finding of an inhibitory deficit in substance use disorders as
are inflated by comorbidities, and a pure sample with only the
well as pathological gambling suggests the possibility of new treat-
substance use disorder of interest may show smaller effects.
ment avenues aiming to address this deficit. Stimulant medication
Indeed, a study by Rodriguez-Jimenez et al. (2006) showed that
is known to improve inhibitory control in, for example, AD/HD (e.g.,
inhibitory deficits were apparent only in pathological gamblers
Lawrence et al., 2005; Okazaki et al., 2002; Sunohara et al., 1999;
with comorbid AD/HD, with marginally better performance in
Turner et al., 2004), and may improve outcomes among substance
pure pathological gambling compared to controls. Further research
abusing individuals (e.g., Brady et al., 2011; Dean et al., 2011; Hart
should carefully assess the possibility of comorbid disorders and
et al., 2007; Joos et al., 2013; Mereu et al., 2013; Preti, 2007; Schmaal
exclude these participants, or (probably better) report their results
et al., 2013; Sofuoglu et al., 2013) or pathological gamblers seek-
separately.
ing treatment (Grant et al., 2010; Grant and Kim, 2006; Paine et al.,
2013). The results of the current study suggest that, if behavioural
4.7. Length of abstinence inhibition is deficient in users of some but not all drugs, then med-
ication to improve inhibition may be an effective treatment in only
Studies also varied on the length of abstinence of participants some drugs. Secondly, behavioural training of inhibition has been
in the user groups (e.g., for studies examining SSRT in alcohol shown previously to reduce alcohol consumption in the week after
dependence, length of abstinence ranged between 48 hours and 12 training (Bowley et al., 2013; Houben et al., 2011, 2012; Jones et al.,
months), and whether this was by self-report or confirmed objec- 2011a,b, 2013), and it remains to be seen whether this effect gen-
tively (e.g., via urine, breath or hair analysis, or residence in an eralises to other substances, or lasts beyond a one week follow-up.
inpatient monitored treatment unit; see Tables 1–3). The length Future research should focus on further examination of training and
of abstinence is an important contributor of heterogeneity since medication methods of improving behavioural control as it relates
cognitive function is known to worsen in early abstinence (e.g., to substance use.
Dingwall et al., 2011). The time-course of recovery of function
from withdrawal to protracted abstinence is an under-researched 4.11. Alternative explanation of the effect
domain, especially in relation to differential recovery rates for
different drugs and for different aspects of cognitive function. The current study cannot, and was not designed to, address
Therefore, we suggest that future research should consider and whether such inhibitory deficits were caused by chronic substance
report the range of durations in their participant groups more abuse, or whether these deficits were pre-existing and perhaps
carefully, and focus on establishing the time course of recovery of contributory to the development of substance use disorders. We
different aspects of cognitive function with cessation of different think it likely that both factors play a part: there is growing evi-
substances. dence of pre-existing differences in brain and behavioural indices
G Model
of inhibition which predict greater substance use 1.5–6 years later Aron, A.R., Robbins, T.W., Poldrack, R.A., 2014. Inhibition and the right inferior frontal
(e.g., Mahmood et al., 2013; Norman et al., 2011; Tarter et al., 2003; cortex: one decade on. Trends Cogn. Sci. 18, 177–185.
Australian Institute of Health and Welfare, 2011. 2010 National Drug Strategy
Rubio et al., 2008), and there is also evidence that commencement Household Survey Report. Australian Institute of Health and Welfare, Canberra.
of binge drinking alters cognitive function within a 9 months period Band, G.P.H., Van der Molen, M.W., Logan, G.D., 2003. Horse-race model simulations
(Maurage et al., 2009), not to mention the neurotoxic effects of years of the stop-signal procedure. Acta Psychol. 112, 105–142.
Barkley, R.A., 1997. Behavioural inhibition, sustained attention, and executive func-
of abuse in the typically older dependent groups in the studies tions: constructing a unifying theory of ADHD. Psychol. Bull. 121, 65–94.
reviewed here. More research is needed in this area to discrimi- Bednarski, S.R., Erdman, E., Luo, X., Zhang, S., Hu, S., Li, C.-S.R., 2012. Neural pro-
nate between the relative roles of these two processes and their cesses of an indirect analog of risk taking in young nondependent adult alcohol
drinkers—an fMRI study of the stop signal task. Alcohol. Clin. Exp. Res. 36,
importance in understanding substance-related problems.
768–779.
Bednarski, S.R., Zhang, S., Hong, K.-I., Sinha, R., Rounsaville, B.J., Li, C.-s.R., 2011.
4.12. Conclusions Deficits in default mode network activity preceding error in cocaine dependent
individuals. Drug Alcohol Depend 119, e51–e57.
Bell, R.P., Foxe, J.J., Ross, L.A., Garavan, H., 2014. Intact inhibitory control processes in
This review of 97 studies examining inhibition in substance abstinent drug abusers (I): a functional neuroimaging study in former cocaine
using groups, as well as groups with addiction-like pathologies, addicts. Neuropharmacology 82, 143–150.
Benikos, N., Johnstone, S.J., Roodenrys, S.J., 2013. Varying task difficulty in the
improves on previous reviews by including more research papers
Go/Nogo task: the roles of inhibition, arousal and effort. Int. J. Psychophysiol.
and calculating overall effect sizes individually within each drug 87, 262–272.
class. Results support the concept of a behavioural control deficit Billieux, J., Gay, P., Rochat, L., Khazaal, Y., Zullino, D., Van der Linden, M., 2010. Lack
of inhibitory control predicts cigarette smoking dependence: evidence from a
in substance abuse and dependence (Fillmore, 2003; Goldstein and
non-deprived sample of light to moderate smokers. Drug Alcohol Depend. 112,
Volkow, 2002; Hester et al., 2010; Jentsch and Pennington, 2014; 164–167.
Yücel and Lubman, 2007), but importantly, this is apparent only for Bjork, J.M., Hommer, D.W., Grant, S.J., Danube, C., 2004. Impulsivity in abstinent
users of some classes of drug. The review will contribute to a nar- alcohol-dependent patients: relation to control subjects and type 1-/type 2-like
traits. Alcohol 34, 133–150.
rowing of theory concerning the importance of inhibitory control Bowley, C., Faricy, C., Hegarty, B.D., Johnstone, S.J., Smith, J.L., Kelly, P.J., Rushby, J.A.,
to the development and maintenance of substance abuse disorders, 2013. The effects of inhibitory control training on alcohol consumption, implicit
and a significant integration of the extant literature. alcohol-related cognitions and brain electrical activity. Int. J. Psychophysiol. 89,
342–348.
Brady, K.T., Gray, K.M., Tolliver, B.K., 2011. Cognitive enhancers in the treatment
Author disclosures of substance use disorders: clinical evidence. Pharmacol. Biochem. Behav. 99,
285–294.
Bruin, K.J., Wijers, A.A., 2002. Inhibition, response mode, and stimulus probability:
Role of funding source a comparative event-related potential study. Clin. Neuro. 113, 1172–1182.
Buzzell, G.A., Fedota, J.R., Roberts, D.M., McDonald, C.G., 2014. The N2 ERP component
This study was funded by a UNSW Vice-Chancellor’s Postdoc- as an index of impaired cognitive control in smokers. Neurosci. Lett. 563, 61–65.
Choi, J.-S., Park, S.M., Lee, J., Hwang, J.Y., Jung, H.Y., Choi, S.-W., Kim, D.J., Sohee Oh
toral Research Fellowship to JLS. RPM is supported by an Australian Lee, J.-Y., 2013. Resting-state beta and gamma activity in Internet addiction. Int.
Government NHMRC Principal Research Fellowship (2013-2017; J. Psychophysiol. 89, 328–333.
#1045318). The National Drug and Alcohol Research Centre at the Choi, J.-S., Park, S.M., Roh, M.-S., Lee, J.-Y., Park, C.-B., Hwang, J.Y., Gwak, A.R., Jung,
H.Y., 2014. Dysfunctional inhibitory control and impulsivity in Internet addic-
University of New South Wales is supported by funding from the tion. Psychiatry Res. 215, 424–428.
Australian Government under the Substance Misuse Prevention Cohen, H.L., Porjesz, B., Begleiter, H., Wang, W., 1997. Neurophysiological correlates
and Service Improvements Grants Fund. of response production and inhibition in alcoholics. Alcohol. Clin. Exp. Res. 21,
1398–1406.
Cohen, J., 1992. A power primer. Psychol. Bull. 112, 155–159.
Contributors Colzato, L.S., Ruiz, M., Van Den Wildenberg, W.P.M., Bajo, M.T., Hommel, B., 2011.
Long-term effects of chronic khat use: impaired inhibitory control. Front.
Psychol. 1, 219.
JLS and RPM were responsible for the study concept and design. Colzato, L.S., van den Wildenberg, W.P.M., Hommel, B., 2007. Impaired inhibitory
JLS completed literature search; JLS and SDJ reviewed identified control in recreational cocaine users. PLoS One 2, e1143.
papers for inclusion in the study; JLS, RPM and JMI independently Compton, W.M., Thomas, Y.F., Stinson, F.S., Grant, B.F., 2007. Prevalence, correlates,
disability, and comorbidity of DSM-IV drug abuse and dependence in the United
scored effect sizes for each study. JLS performed all statistical States: results from the national epidemiologic survey on alcohol and related
analyses and drafted the manuscript. All authors provided critical conditions. Arch. Gen. Psychiatry 64, 566–576.
revision of the manuscript for intellectual content, and all authors Congdon, E., Mumford, J.A., Cohen, J.R., Galvan, A., Canli, T., Poldrack, R.A., 2012.
Measurement and reliability of response inhibition. Front. Psychol. 3, 37.
approved the final version for publication.
Connolly, C.G., Foxe, J.J., Nierenberg, J., Shpaner, M., Garavan, H., 2012. The neurobio-
logy of cognitive control in successful cocaine abstinence. Drug Alcohol Depend.
Conflict of interest 121, 45–53.
Constantinou, N., Morgan, C.J.A., Battistella, S., O’Ryan, D., Davis, P., Curran, H.V.,
2010. Attentional bias, inhibitory control and acute stress in current and former
No conflict declared. opiate addicts. Drug Alcohol Depend. 109, 220–225.
Crunelle, C.L., Veltman, D.J., van Emmerik-van Oortmerssen, K., Booij, J., van den
Brink, W., 2013. Impulsivity in adult ADHD patients with and without cocaine
Acknowledgements dependence. Drug Alcohol Depend. 129, 18–24.
de Ruiter, M.B., Oosterlaan, J., Veltman, D.J., van den Brink, W., Goudriaan, A.E., 2012.
Thanks are due to Mrs Mary Kumvaj, the NDARC Librarian, for Similar hyporesponsiveness of the dorsomedial prefrontal cortex in problem
gamblers and heavy smokers during an inhibitory control task. Drug Alcohol
assistance with the literature search. Thanks are also due to the Depend. 121, 81–89.
authors of studies in this meta-analysis who provided additional Dean, A.C., Sevak, R.J., Monterosso, J.R., Hellemann, G., Sugar, C.A., London,
data on request. E.D., 2011. Acute modafinil effects on attention and inhibitory con-
trol in methamphetamine-dependent humans. J. Stud. Alcohol Drugs 72,
943–953.
References Dimoska-Di Marco, A., McDonald, S., Kelly, M., Tate, R., Johnstone, S., 2011. A
meta-analysis of response inhibition and Stroop interference control deficits
Albrecht, D.S., Kareken, D.A., Christian, B.T., Dzemidzic, M., Yoder, K.K., 2014. Corti- in adults with traumatic brain injury (TBI). J. Clin. Exp. Neuropsychol. 33,
cal dopamine release during a behavioral response inhibition task. Synapse 68, 471–485.
266–274. Dingwall, K.M., Maruff, P., Fredrickson, A., Cairney, S., 2011. Cognitive recovery dur-
American Psychiatric Association, 2013. DSM-5. Diagnostic and Statistical Manual ing and after treatment for volatile solvent abuse. Drug Alcohol Depend. 118,
of Mental Disorders, fifth ed. American Psychiatric Publishing, Arlington, VA. 180–185.
Aragues, M., Jurado, R., Quinto, R., Rubio, G., 2011. Laboratory paradigms of impuls- Dinn, W.M., Aycicegi, A., Harris, C.L., 2004. Cigarette smoking in a student sample:
ivity and alcohol dependence: a review. Eur. Addict. Res. 17, 64–71. neurocognitive and clinical correlates. Addict. Behav. 29, 107–126.
G Model
Dong, G., Zhou, H., Zhao, X., 2010. Impulse inhibition in people with Internet addic- Hester, R., Simoes-Franklin, C., Garavan, H., 2007. Post-error behavior in active
tion disorder: electrophysiological evidence from a Go/NoGo study. Neurosci. cocaine users: poor awareness of errors in the presence of intact performance
Lett. 485, 138–142. adjustments. Neuropsychopharmacology 32, 1974–1984.
Easton, C.J., Sacco, K.A., Neavins, T.M., Wupperman, P., George, T.P., 2008. Neurocog- Hoshi, R., Mullins, K., Boundy, C., Brignell, C., Piccini, P., Curran, H., 2007. Neurocogni-
nitive performance among alcohol dependent men with and without physical tive function in current and ex-users of ecstasy in comparison to both matched
violence toward their partners: a preliminary report. Am. J. Drug Alcohol Abuse polydrug-using controls and drug-naïve controls. Psychopharmacology 194,
34, 29–37. 371–379.
Ersche, K.D., Barnes, A., Jones, P.S., Morein-Zamir, S., Robbins, T.W., Bullmore, E.T., Houben, K., Havermans, R.C., Nederkoorn, C., Jansen, A., 2012. Beer à no-go: learn-
2011. Abnormal structure of frontostriatal brain systems is associated with ing to stop responding to alcohol cues reduces alcohol intake via reduced
aspects of impulsivity and compulsivity in cocaine dependence. Brain 134, affective associations rather than increased response inhibition. Addiction 107,
2013–2024. 1280–1287.
European Monitoring Centre for Drugs and Drug Addiction, 2002. 2002 Annual Houben, K., Nederkoorn, C., Wiers, R.W., Jansen, A., 2011. Resisting temptation:
Report on the State of the Drugs Problem in the European Union and Norway. decreasing alcohol-related affect and drinking behavior by training response
Office for Official Publications of the European Communities, Luxembourg. inhibition. Drug Alcohol Depend. 116, 132–136.
Evans, D.E., Park, J.Y., Maxfield, N., Drobes, D.J., 2009. Neurocognitive variation in Huddy, V.C., Clark, L., Harrison, I., Ron, M.A., Moutoussis, M., Barnes, T.R.E., Joyce, E.M.,
smoking behavior and withdrawal: genetic and affective moderators. Genes 2013. Reflection impulsivity and response inhibition in first-episode psychosis:
Brain Behav. 8, 86–96. relationship to cannabis use. Psychol. Med. 43, 2097–2107.
Everitt, B.J., Robbins, T.W., 2005. Neural systems of reinforcement for drug addiction: Jentsch, J.D., Pennington, Z.T., 2014. Reward, interrupted: inhibitory control and its
from actions to habits to compulsion. Nat. Neurosci. 8, 1481–1489. relevance to addictions. Neuropharmacology 76, 479–486.
Fallgatter, A.J., Wiesbeck, G.A., Weijers, H.-G., Boening, J., Strik, W.K., 1998. Event- Jentsch, J.D., Taylor, J.R., 1999. Impulsivity resulting from frontostriatal dysfunc-
related correlates of response suppression as indicators of novelty seeking in tion in drug abuse: implications for the control of behaviour by reward-related
alcoholics. Alcohol Alcohol. 33, 475–481. stimuli. Psychopharmacology 146, 373–390.
Fillmore, M.T., 2003. Drug abuse as a problem of impaired control: current Jodo, E., Kayama, Y., 1992. Relation of a negative ERP component to response inhi-
approaches and findings. Behav. Cogn. Neurosci. Rev. 2, 1–19. bition in a Go/No-go task. EEG Clin. Neurophysiol. 82, 477–482.
Fillmore, M.T., Rush, C.R., 2002. Impaired inhibitory control of behavior in chronic Jones, A., Cole, J., Goudie, A., Field, M., 2011a. Priming a restrained mental set reduces
cocaine users. Drug Alcohol Depend. 66, 265–273. alcohol-seeking independently of mood. Psychopharmacology 218, 557–565.
Forman, S.D., Dougherty, G.G., Casey, B.J., Siegle, G.J., Braver, T.S., Barch, D.M., Jones, A., Field, M., Christiansen, P., Stancak, A., 2013. P300 during response inhibition
Stenger, V.A., Wick-Hull, C., Pisarov, L.A., Lorensen, E., 2004. Opiate addicts is associated with ad-lib alcohol consumption in social drinkers. J. Psychophar-
lack error-dependent activation of rostral anterior cingulate. Biol. Psychiatry 55, macol. 27, 507–514.
531–537. Jones, A., Guerrieri, R., Fernie, G., Cole, J., Goudie, A., Field, M., 2011b. The effects of
Fu, L.-p., Bi, G.-h., Zou, Z.-t., Wang, Y., Ye, E.-m., Ma, L., Ming, F., Yang, Z., 2008. priming restrained versus disinhibited behaviour on alcohol-seeking in social
Impaired response inhibition function in abstinent heroin dependents: an fMRI drinkers. Drug Alcohol Depend. 113, 55–61.
study. Neurosci. Lett. 438, 322–326. Joos, L., Goudriaan, A.E., Schmaal, L., Fransen, E., van den Brink, W., Sabbe, B.G.C., Dom,
Galvan, A., Poldrack, R.A., Baker, C.M., McGlennen, K.M., London, E.D., 2011. Neu- G., 2013. Effect of modafinil on impulsivity and relapse in alcohol dependent
ral correlates of response inhibition and cigarette smoking in late adolescence. patients: a randomized, placebo-controlled trial. Eur. Neuropsychopharmacol.
Neuropsychopharmacology 36, 970–978. 23, 948–955.
Gamma, A., Brandeis, D., Brandeis, R., Vollenweider, F.X., 2005. The P3 in ‘ecstasy’ Jutras-Aswad, D., Jacobs, M.M., Yiannoulos, G., Roussos, P., Bitsios, P., Nomura, Y., Liu,
polydrug users during response inhibition and execution. J. Psychopharmacol. X., Hurd, Y.L., 2012. Cannabis-dependence risk relates to synergism between
19, 504–512. neuroticism and proenkephalin SNPs associated with amygdala gene expres-
Garavan, H., Hester, R., Murphy, K., Fassbender, C., Kelly, C., 2006. Individual dif- sion: case-control study. PLoS One 7, e39243.
ferences in the functional neuroanatomy of inhibitory control. Brain Res. 1105, Kamarajan, C., Porjesz, B., Jones, K.A., Choi, K., Chorlian, D.B., Padmanabhapillai, A.,
130–142. Rangaswamy, M., Stimus, A.T., Begleiter, H., 2005. Alcoholism is a disinhibitory
Goldstein, R.Z., Volkow, N.D., 2002. Drug addiction and its underlying neurobiologi- disorder: neurophysiological evidence from a Go/No-Go task. Biol. Psychol. 69,
cal basis: neuroimaging evidence for the involvement of the frontal cortex. Am. 353–373.
J. Psychiatry 159, 1642–1652. Karch, S., Jäger, L., Karamatskos, E., Graz, C., Stammel, A., Flatz, W., Lutz, J.,
Goudriaan, A.E., Oosterlaan, J., de Beurs, E., van den Brink, W., 2005. Decision making Holtschmidt-Täschner, B., Genius, J., Leicht, G., Pogarell, O., Born, C., Möller, H.-J.,
in pathological gambling: a comparison between pathological gamblers, alcohol Hegerl, U., Reiser, M., Soyka, M., Mulert, C., 2008. Influence of trait anxiety on
dependents, persons with Tourette syndrome, and normal controls. Cogn. Brain inhibitory control in alcohol-dependent patients: simultaneous acquisition of
Res. 23, 137–151. ERPs and BOLD responses. J. Psychiatr. Res. 42, 734–745.
Goudriaan, A.E., Oosterlaan, J., De Beurs, E., Van Den Brink, W., 2006. Kaufman, J.N., Ross, T.J., Stein, E.A., Garavan, H., 2003. Cingulate hypoactivity in
Neurocognitive functions in pathological gambling: a comparison with alco- cocaine users during a GO-NOGO task as revealed by event-related functional
hol dependence, Tourette syndrome and normal controls. Addiction 101, magnetic resonance imaging. J. Neurosci. 23, 7839–7843.
534–547. Kaye, S., Darke, S., 2004. Injecting and non-injecting cocaine use in Australia: physical
Grant, J., Chamberlain, S., Odlaug, B., Potenza, M., Kim, S., 2010. Memantine shows and psychological morbidity. Drug Alcohol Rev 23, 391–398.
promise in reducing gambling severity and cognitive inflexibility in pathological Kreusch, F., Vilenne, A. l., Quertemont, E., 2013. Response inhibition toward alcohol-
gambling: a pilot study. Psychopharmacology 212, 603–612. related cues using an alcohol go/no-go task in problem and non-problem
Grant, J.E., Chamberlain, S.R., Schreiber, L., Odlaug, B.L., 2012. Neuropsychological drinkers. Addict. Behav. 38, 2520–2528.
deficits associated with cannabis use in young adults. Drug Alcohol Depend. Lawrence, A., Luty, J., Bogdan, N., Sahakian, B., Clark, L., 2009. Impulsivity and
121, 159–162. response inhibition in alcohol dependence and problem gambling. Psychophar-
Grant, J.E., Kim, S.W., 2006. Medication management of pathological gambling. Minn. macology 207, 163–172.
Med. 89, 44–48. Lawrence, C., Barry, R., Clarke, A., Johnstone, S., McCarthy, R., Selikowitz, M., Broyd,
Gullo, M.J., Loxton, N.J., Dawe, S., 2014. Impulsivity: four ways five factors are not S., 2005. Methylphenidate effects in attention deficit/hyperactivity disorder:
basic to addiction. Addict. Behav. 39, 1547–1556. electrodermal and ERP measures during a continuous performance task. Psy-
Hart, C.L., Haney, M., Vosburg, S.K., Rubin, E., Foltin, R.W., 2007. Smoked cocaine chopharmacology 183, 81–91.
self-administration is decreased by modafinil. Neuropsychopharmacology 33, Leeman, R.F., Beseler, C.L., Helms, C.M., Patock-Peckham, J.A., Wakeling, V.A., Kahler,
761–768. C.W., 2014a. A brief, critical review of research on impaired control over alcohol
Hedges, L.V., 1980. Unbiased estimation of effect size. Eval. Educ. 4, 25–27. use and suggestions for future studies. Alcohol. Clin. Exp. Res. 38, 301–308.
Hedges, L.V., Olkin, I., 1985. Statistical Methods for Meta-Analysis. Academic Press, Leeman, R.F., Hoff, R.A., Krishnan-Sarin, S., Patock-Peckham, J.A., Potenza, M.N.,
Orlando, FL. 2014b. Impulsivity, sensation-seeking, and part-time job status in relation to
Heitzeg, M.M., Nigg, J.T., Yau, W.-Y.W., Zucker, R.A., Zubieta, J.-K., 2010. Striatal dys- substance use and gambling in adolescents. J. Adolesc. Health 54, 460–466.
function marks preexisting risk and medial prefrontal dysfunction is related to Leeman, R.F., Toll, B.A., Taylor, L.A., Volpicelli, J.R., 2009. Alcohol-induced disinhi-
problem drinking in children of alcoholics. Biol. Psychiatry 68, 287–295. bition expectancies and impaired control as prospective predictors of problem
Henges, A.L., Marczinski, C.A., 2012. Impulsivity and alcohol consumption in young drinking in undergraduates. Psychol. Addict. Behav. 23, 553–563.
social drinkers. Addict. Behav. 37, 217–220. Leland, D.S., Arce, E., Miller, D.A., Paulus, M.P., 2008. Anterior cingulate cortex and
Hester, R., Bell, R.P., Foxe, J.J., Garavan, H., 2013. The influence of monetary pun- benefit of predictive cueing on response inhibition in stimulant dependent indi-
ishment on cognitive control in abstinent cocaine-users. Drug Alcohol Depend. viduals. Biol. Psychiatry 63, 184–190.
133, 86–93. Lester, B.M., Lin, H., DeGarmo, D.S., Fisher, P.A., LaGasse, L.L., Levine, T.P., Shankaran,
Hester, R., Garavan, H., 2004. Executive dysfunction in cocaine addiction: evi- S., Bada, H.S., Bauer, C.R., Hammond, J.A., Whitaker, T.M., Higgins, R.D., 2012.
dence for discordant frontal, cingulate, and cerebellar activity. J. Neurosci. 24, Neurobehavioral disinhibition predicts initiation of substance use in children
11017–11022. with prenatal cocaine exposure. Drug Alcohol Depend. 126, 80–86.
Hester, R., Lubman, D.I., Yücel, M., 2010. The role of executive control in human drug Li, C.-s.R., Huang, C., Yan, P., Bhagwagar, Z., Milivojevic, V., Sinha, R., 2008. Neural
addiction. In: Self, D.W., Staley Gottschalk, J.K. (Eds.), Behavioral Neuroscience correlates of impulse control during stop signal inhibition in cocaine-dependent
of Drug Addiction. Springer, Berlin Heidelberg, pp. 301–318. men. Neuropsychopharmacology 33, 1798–1806.
Hester, R., Nestor, L., Garavan, H., 2009. Impaired error awareness and anterior cingu- Li, C.-s.R., Luo, X., Yan, P., Bergquist, K., Sinha, R., 2009. Altered impulse control in
late cortex hypoactivity in chronic cannabis users. Neuropsychopharmacology alcohol dependence: neural measures of stop signal performance. Alcohol. Clin.
34, 2450–2458. Exp. Res. 33, 740–750.
G Model
Li, C.-s.R., Milivojevic, V., Kemp, K., Hong, K., Sinha, R., 2006. Performance monitoring Nederkoorn, C., Baltus, M., Guerrieri, R., Wiers, R.W., 2009. Heavy drinking is asso-
and stop signal inhibition in abstinent patients with cocaine dependence. Drug ciated with deficient response inhibition in women but not in men. Pharmacol.
Alcohol Depend. 85, 205–212. Biochem. Behav. 93, 331–336.
Li, C.-s.R., Sinha, R., 2008. Inhibitory control and emotional stress regulation: Nestor, L., McCabe, E., Jones, J., Clancy, L., Garavan, H., 2011. Differences in bottom-up
neuroimaging evidence for frontal-limbic dysfunction in psycho-stimulant and top-down neural activity in current and former cigarette smokers: evidence
addiction. Neurosci. Biobehav. Rev. 32, 581–597. for neural substrates which may promote nicotine abstinence through increased
Liang, C.-W., Zhong, R.Y.-X., Chung, Y.-C., Pan, C.-H., Yen, M.-Y., Cheng, C.-P., Hsu, W.- cognitive control. NeuroImage 56, 2258–2275.
Y., 2014. Using cognitive modeling to investigate the psychological processes of Nieuwenhuis, S., Yeung, N., van den Wildenberg, W., Ridderinkhof, K.R., 2003. Elec-
the Go/NoGo discrimination task in male abstinent heroin misusers. Addiction trophysiological correlates of anterior cingulate function in a go/no-go task:
109, 1355–1362. effects of response conflict and trial type frequency. Cogn. Affect. Behav. Neu-
Lijffijt, M., Kenemans, J.L., Verbaten, M.N., van Engeland, H., 2005. A meta- rosci. 3, 17–26.
analytic review of stopping performance in attention-deficit/hyperactivity Noël, X., Van der Linden, M., d’Acremont, M., Bechara, A., Dan, B., Hanak, C., Ver-
disorder: deficient inhibitory motor control? J. Abnorm. Psychol. 114, banck, P., 2007. Alcohol cues increase cognitive impulsivity in individuals with
216–222. alcoholism. Psychopharmacology 192, 291–298.
Lipsey, M.W., Wilson, D.B., 2001. Practical Meta-Analysis. Sage Publications, Thou- Norman, A.L., Pulido, C., Squeglia, L.M., Spadoni, A.D., Paulus, M.P., Tapert, S.F., 2011.
sand Oaks, CA. Neural activation during inhibition predicts initiation of substance use in ado-
Lipszyc, J., Schachar, R., 2010. Inhibitory control and psychopathology: a meta- lescence. Drug Alcohol Depend. 119, 216–223.
analysis of studies using the stop signal task. J. Int. Neuropsychol. Soc. 16, Oddy, B.W., Barry, R.J., 2009. The relationship of N2 and P3 to inhibitory processing
1064–1076. of social drinkers in a Go/NoGo task. Int. J. Psychophysiol. 72, 323–330.
Liu, G.-C., Yen, J.-Y., Chen, C.-Y., Yen, C.-F., Chen, C.-S., Lin, W.-C., Ko, C.-H., 2014. Odlaug, B.L., Chamberlain, S.R., Kim, S.W., Schreiber, L.R.N., Grant, J.E., 2011. A
Brain activation for response inhibition under gaming cue distraction in internet neurocognitive comparison of cognitive flexibility and response inhibition in
gaming disorder. Kaohsiung J. Med. Sci. 30, 43–51. gamblers with varying degrees of clinical severity. Psychol. Med. 41, 2111–2119.
Logan, G.D., 1994. On the ability to inhibit thought and action: a users’ guide to the Okazaki, S., Maekawa, H., Ozaki, H., Futakami, S., 2002. Topographic changes of
stop signal paradigm. In: Dagenbach, D., Carr, T.H. (Eds.), Inhibitory Processes in ERP during a CPT-AX task at pre- and post-medication of methylphenidate in
Attention, Memory and Language. Academic Press, San Diego, CA, pp. 189–239. children with ADHD. Int. Congr. Ser. 1232, 705–710.
Logan, G.D., Cowan, W.B., 1984. On the ability to inhibit thought and action: a theory Paine, T.A., Asinof, S.K., Diehl, G.W., Frackman, A., Leffler, J., 2013. Medial prefrontal
of an act of control. Psychol. Rev. 91, 295–327. cortex lesions impair decision-making on a rodent gambling task: reversal by
Logan, G.D., Cowan, W.B., David, K.A., 1984. On the ability to inhibit simple and choice D1 receptor antagonist administration. Behav. Brain Res. 243, 247–254.
reaction time responses: a model and a method. J. Exp. Psychol. Hum. Percept. Pandey, A.K., Kamarajan, C., Tang, Y., Chorlian, D.B., Roopesh, B.N., Manz, N., Stimus,
Perform. 10, 276–291. A., Rangaswamy, M., Porjesz, B., 2012. Neurocognitive deficits in male alcoholics:
López-Caneda, E., Cadaveira, F., Crego, A., Gómez-Suárez, A., Corral, M., Parada, M., an ERP/sLORETA analysis of the N2 component in an equal probability Go/NoGo
Caamaño-Isorna, F., Rodríguez Holguín, S., 2012. Hyperactivation of right inferior task. Biol. Psychol. 89, 170–182.
frontal cortex in young binge drinkers during response inhibition: a follow-up Papachristou, H., Nederkoorn, C., Havermans, R., van der Horst, M., Jansen, A., 2012.
study. Addiction 107, 1796–1808. Can’t stop the craving: the effect of impulsivity on cue-elicited craving for alco-
Lubman, D.I., Yucel, M., Pantelis, C., 2004. Addiction, a condition of compulsive hol in heavy and light social drinkers. Psychopharmacology 219, 511–518.
behaviour? Neuroimaging and neuropsychological evidence of inhibitory dys- Parvaz, M.A., Maloney, T., Moeller, S.J., Woicik, P.A., Alia-Klein, N., Telang, F., Wang,
regulation. Addiction 99, 1491–1502. G.-J., Squires, N.K., Volkow, N.D., Goldstein, R.Z., 2012. Sensitivity to monetary
Luijten, M., Littel, M., Franken, I.H.A., 2011. Deficits in inhibitory control in smokers reward is most severely compromised in recently abstaining cocaine addicted
during a Go/NoGo task: an investigation using event-related brain potentials. individuals: a cross-sectional ERP study. Psychiatry Res. 203, 75–82.
PLoS One 6, e18898. Perry, J., Carroll, M., 2008. The role of impulsive behavior in drug abuse. Psychophar-
Luijten, M., Machielsen, M.W.J., Veltman, D.J., Hester, R., de Haan, L., Franken, I.H.A., macology 200, 1–26.
2014. Systematic review of ERP and fMRI studies investigating inhibitory con- Petit, G., Kornreich, C., Noël, X., Verbanck, P., Campanella, S., 2012. Alcohol-related
trol and error processing in people with substance dependence and behavioural context modulates performance of social drinkers in a visual Go/No-Go task: a
addictions. J. Psychiatry. Neurosci. 39, 149–169. preliminary assessment of event-related potentials. PLoS One 7, e37466.
Luijten, M., O’Connor, D.A., Rossiter, S., Franken, I.H.A., Hester, R., 2013a. Effects of Pfefferbaum, A., Ford, J.M., 1988. ERPs to stimuli requiring response production and
reward and punishment on brain activations associated with inhibitory control inhibition: effects of age, probability and visual noise. EEG Clin. Neurophysiol.
in cigarette smokers. Addiction 108, 1969–1978. 71, 55–63.
Luijten, M., Veltman, D.J., Hester, R., Smits, M., Nijs, I.M.T., Pepplinkhuizen, L., Pope, H.G., Gruber, A.J., Hudson, J.I., Huestis, M.A., Yurgelun-Todd, D., 2001. Neu-
Franken, I.H.A., 2013b. The role of dopamine in inhibitory control in smokers ropsychological performance in long-term cannabis users. Arch. Gen. Psychiatry
and non-smokers: a pharmacological fMRI study. Eur. Neuropsychopharmacol. 58, 909–915.
23, 1247–1256. Preti, A., 2007. New developments in the pharmacotherapy of cocaine abuse. Addict.
Mahmood, O.M., Goldenberg, D., Thayer, R., Migliorini, R., Simmons, A.N., Tapert, S.F., Biol. 12, 133–151.
2013. Adolescents’ fMRI activation to a response inhibition task predicts future Psychiatric Genomics Consortium, 2013. Identification of risk loci with shared
substance use. Addict. Behav. 38, 1435–1441. effects on five major psychiatric disorders: a genome-wide analysis. Lancet 381,
Marin-Martinez, F., Sanchez-Meca, J., 1998. Testing for dichotomous moderators in 1371–1379.
meta-analysis. J. Exp. Educ. 67, 69–81. Quednow, B., Kühn, K.-U., Hoppe, C., Westheide, J., Maier, W., Daum, I., Wagner, M.,
Maurage, P., Pesenti, M., Philippot, P., Joassin, F., Campanella, S., 2009. Latent dele- 2007. Elevated impulsivity and impaired decision-making cognition in heavy
terious effects of binge drinking over a short period of time revealed only by users of MDMA (Ecstasy). Psychopharmacology 189, 517–530.
electrophysiological measures. J. Psychiatry Neurosci. 34, 111–118. Ramaekers, J., Kauert, G., Theunissen, E., Toennes, S., Moeller, M., 2009. Neurocog-
McKetin, R., McLaren, J., Kelly, E., 2005. The Sydney Methamphetamine Market: Pat- nitive performance during acute THC intoxication in heavy and occasional
terns of Supply, Use, Personal Harms and Social Consequences. National Drug cannabis users. J. Psychopharmacol. 23, 266–277.
Law Enforcement Research Fund Monograph No. 13, Australasian Centre for Randall, W.M., Smith, J.L., 2011. Conflict and inhibition in the cued-Go/NoGo task.
Policing Studies, Adelaide. Clin. Neurophysiol. 122, 2400–2407.
McNab, F., Leroux, G., Strand, F., Thorell, L., Bergman, S., Klingberg, T., 2008. Common Ricaurte, G.A., Seiden, L.S., Schuster, C.R., 1984. Further evidence that amphetamines
and unique components of inhibition and working memory: an fMRI, within- produce long-lasting dopamine neurochemical deficits by destroying dopamine
subjects investigation. Neuropsychologia 46, 2668–2682. nerve fibers. Brain Res. 303, 359–364.
Mereu, M., Bonci, A., Newman, A., Tanda, G., 2013. The neurobiology of modafinil as Roberts, C., Fairclough, S., Fisk, J., Tames, F., Montgomery, C., 2013. Electrophysiolog-
an enhancer of cognitive performance and a potential treatment for substance ical indices of response inhibition in human polydrug users. J. Psychopharmacol.
use disorders. Psychopharmacology 229, 415–434. 27, 779–789.
Monterosso, J.R., Aron, A.R., Cordova, X., Xu, J., London, E.D., 2005. Deficits in Roberts, G.M.P., Garavan, H., 2010. Evidence of increased activation underlying cog-
response inhibition associated with chronic methamphetamine abuse. Drug nitive control in ecstasy and cannabis users. NeuroImage 52, 429–435.
Alcohol Depend. 79, 273–277. Rodriguez-Jimenez, R., Avila, C., Jimenez-Arriero, M.A., Ponce, G., Monasor, R.,
Moreno, M., Estevez, A.F., Zaldivar, F., Montes, J.M.G., Gutiérrez-Ferre, V.E., Esteban, Jimenez, M., Aragües, M., Hoenicka, J., Rubio, G., Palomo, T., 2006. Impulsivity
L., Sánchez-Santed, F., Flores, P., 2012. Impulsivity differences in recreational and sustained attention in pathological gamblers: influence of childhood ADHD
cannabis users and binge drinkers in a university population. Drug Alcohol history. J. Gambl. Stud. 22, 451–461.
Depend. 124, 355–362. Rossiter, S., Thompson, J., Hester, R., 2012. Improving control over the impulse
Morie, K.P., Garavan, H., Bell, R.P., De Sanctis, P., Krakowski, M.I., Foxe, J.J., 2014. Intact for reward: sensitivity of harmful alcohol drinkers to delayed reward but not
inhibitory control processes in abstinent drug abusers (II): a high-density elec- immediate punishment. Drug Alcohol Depend. 125, 89–94.
trical mapping study in former cocaine and heroin addicts. Neuropharmacology Rubia, K., Russell, T., Overmeyer, S., Brammer, M.J., Bullmore, E.T., Sharma, T., Sim-
82, 151–160. mons, A., Williams, S.C.R., Giampietro, V., Andrew, C., Taylor, E., 2001. Mapping
Mostofsky, S.H., Schafer, J.G.B., Abrams, M.T., Goldberg, M.C., Flower, A.A., Boyce, A., motor inhibition: conjunctive brain activations across different versions of
Courtney, S.M., Calhoun, V.D., Kraut, M.A., Denckla, M.B., Pekar, J.J., 2003. fMRI Go/No-Go and Stop tasks. NeuroImage 13, 250–261.
evidence that the neural basis of response inhibition is task-dependent. Cogn. Rubio, G., Jiménez, M., Rodríguez-Jiménez, R., Martínez, I., Ávila, C., Ferre, F., Jiménez-
Brain Res. 17, 419–430. Arriero, M.A., Ponce, G., Palomo, T., 2008. The role of behavioral impulsivity in
Murphy, P., Garavan, H., 2011. Cognitive predictors of problem drinking and AUDIT the development of alcohol dependence: a 4-year follow-up study. Alcohol. Clin.
scores among college students. Drug Alcohol Depend. 115, 94–100. Exp. Res. 32, 1681–1687.
G Model
Rubio, G., Jiménez, M., Rodríguez-Jiménez, R., Martínez, I., Iribarren, M.M., Jiménez- Townshend, J.M., Duka, T., 2005. Binge drinking, cognitive performance and
Arriero, M.A., Ponce, G., Ávila, C., 2007. Varieties of impulsivity in males with mood in a population of young social drinkers. Alcohol. Clin. Exp. Res. 29,
alcohol dependence: the role of Cluster-B personality disorder. Alcohol. Clin. 317–325.
Exp. Res. 31, 1826–1832. Trommer, B.L., Hoeppner, J.-A.B., Lorber, R., Armstron, K.J., 1988. The Go-NoGo
Ryan, K.K., MacKillop, J., Carpenter, M.J., 2013. The relationship between impulsi- paradigm in attention deficit disorder. Ann. Neurol. 24, 610–614.
vity, risk-taking propensity and nicotine dependence among older adolescent Turner, D.C., Clark, L., Dowson, J., Robbins, T.W., Sahakian, B.J., 2004.
smokers. Addict. Behav. 38, 1431–1434. Modafinil improves cognition and response inhibition in adult attention-
Rzhetsky, A., Wajngurt, D., Park, N., Zheng, T., 2007. Probing genetic overlap among deficit/hyperactivity disorder. Biol. Psychiatry 55, 1031–1040.
complex human phenotypes. Proc. Natl. Acad. Sci. USA 104, 11694–11699. Vallesi, A., McIntosh, A.R., Alexander, M.P., Stuss, D.T., 2009. FMRI evidence of a
Salgado, J.V., Malloy-Diniz, L.F., Campos, V.R., Abrantes, S.S.C., Fuentes, D., Bechara, functional network setting the criteria for withholding a response. NeuroImage
A., Correa, H., 2009. Neuropsychological assessment of impulsive behavior in 45, 537–548.
abstinent alcohol-dependent subjects. Rev. Bras. Psiquiatr. 31, 4–9. van der Plas, E.A.A., Crone, E.A., van den Wildenberg, W.P.M., Tranel, D., Bechara, A.,
Sánchez-Meca, J., Marín-Martínez, F., 1998. Testing continuous moderators in meta- 2009. Executive control deficits in substance-dependent individuals: a compar-
analysis: a comparison of procedures. Br. J. Math. Stat. Psychol. 51, 311–326. ison of alcohol, cocaine, and methamphetamine and of men and women. J. Clin.
Schachar, R.J., Forget-Dubois, N., Dionne, G., Boivin, M., Robaey, P., 2011. Heritability Exp. Neuropsychol. 31, 706–719.
of response inhibition in children. J. Int. Neuropsychol. Soc. 17, 238–247. van Holst, R.J., van Holstein, M., Van Den Brink, W., Veltman, D.J., Goudriaan, A.E.,
Schmaal, L., Joos, L., Koeleman, M., Veltman, D.J., van den Brink, W., Goudriaan, A.E., 2012. Response inhibition during cue reactivity in problem gamblers: an fMRI
2013. Effects of modafinil on neural correlates of response inhibition in alcohol- study. PLoS One 7, e30909.
dependent patients. Biol. Psychiatry 73, 211–218. Venugopalan, V., 2010. Compulsion and Control: Prefrontal and Mesolimbic Sys-
Sjoerds, Z., van den Brink, W., Beekman, A.T.F., Penninx, B.W.J.H., Veltman, D.J., 2013. tems in Human Addiction. Department of Neurology and Neurosurgery, McGill
Response inhibition in alcohol-dependent patients and patients with depres- University, Montréal, QC, p. 172.
sion/anxiety: a functional magnetic resonance imaging study. Psychol. Med., Verdejo-García, A., Lawrence, A.J., Clark, L., 2008. Impulsivity as a vulnerability
1–13 (FirstView). marker for substance-use disorders: review of findings from high-risk research,
Smith, J.L., Mattick, R.P., 2013. Evidence of deficits in behavioural inhibition and problem gamblers and genetic association studies. Neurosci. Biobehav. Rev. 32,
performance monitoring in young female heavy drinkers. Drug Alcohol Depend. 777–810.
133, 398–404. Volkow, N.D., Chang, L., Wang, G.-J., Fowler, J.S., Franceschi, D., Sedler, M., Gatley,
Snyder, H.R., 2013. Major depressive disorder is associated with broad impairments S.J., Miller, E., Hitzemann, R., Ding, Y.-S., Logan, J., 2001. Loss of dopamine trans-
on neuropsychological measures of executive function: a meta-analysis and porters in methamphetamine abusers recovers with protracted abstinence. J.
review. Psychol. Bull. 139, 81–132. Neurosci. 21, 9414–9418.
Sofuoglu, M., DeVito, E.E., Waters, A.J., Carroll, K.M., 2013. Cognitive enhancement Vonmoos, M., Hulka, L.M., Preller, K.H., Jenni, D., Schulz, C., Baumgartner, M.R.,
as a treatment for drug addictions. Neuropharmacology 64, 452–463. Quednow, B.B., 2013. Differences in self-reported and behavioral measures of
Sokhadze, E., Stewart, C., Hollifield, M., Tasman, A., 2008. Event-related potential impulsivity in recreational and dependent cocaine users. Drug Alcohol Depend.
study of executive dysfunctions in a speeded reaction task in cocaine addiction. 133, 61–70.
J. Neurother. 12, 185–204. Wang, G.-J., Volkow, N., Chang, L., Miller, E., Sedler, M., Hitzemann, R., Zhu, W.,
Stavro, K., Pelletier, J., Potvin, S., 2013. Widespread and sustained cognitive deficits Logan, J., Ma, Y., Fowler, J.S., 2004. Partial recovery of brain metabolism in
in alcoholism: a meta-analysis. Addict. Biol. 18, 203–213. methamphetamine abusers after protracted abstinence. Am. J. Psychiatry 161,
Sun, D.-L., Chen, Z.-J., Ma, N., Zhang X.-c. Fu, X.-M., Zhang, D.-R., 2009. Decision- 242–248.
making and prepotent response inhibition functions in excessive internet users. Watanabe, J., Sugiura, M., Sato, K., Sato, Y., Maeda, Y., Matsue, Y., Fukuda, H.,
CNS Spectr. 14, 75–81. Kawashima, R., 2002. The human prefrontal and parietal association cortices
Sunohara, G.A., Malone, M.A., Rovet, J., Humphries, T., Roberts, W., Taylor, M.J., are involved in No-Go performances: an event-related fMRI study. NeuroImage
1999. Effect of methylphenidate on attention in children with Attention Deficit 17, 1207–1216.
Hyperactivity Disorder (ADHD): ERP evidence. Neuropsychopharmacology 21, Wetherill, R.R., Squeglia, L.M., Yang, T.T., Tapert, S.F., 2013. A longitudinal examina-
218–228. tion of adolescent response inhibition: neural differences before and after the
Swick, D., Ashley, V., Turken, U., 2011. Are the neural correlates of stopping and not initiation of heavy drinking. Psychopharmacology 230, 663–670.
going identical? Quantitative meta-analysis of two response inhibition tasks. Williams, B.R., Ponesse, J.S., Schachar, R.J., Logan, G.D., Tannock, R., 1999. Develop-
NeuroImage 56, 1655–1665. ment of inhibitory control across the life span. Dev. Psychol. 35, 205–213.
Tabibnia, G., Monterosso, J.R., Baicy, K., Aron, A.R., Poldrack, R.A., Chakrapani, S., Lee, Wright, L., Lipszyc, J., Dupuis, A., Thayapararajah, S.W., Schachar, R., 2014. Response
B., London, E.D., 2011. Different forms of self-control share a neurocognitive inhibition and psychopathology: a meta-analysis of Go/No-Go task performance.
substrate. J. Neurosci. 31, 4805–4810. J. Abnorm. Psychol. 123, 429–439.
Tamm, L., Epstein, J.N., Lisdahl, K.M., Molina, B., Tapert, S., Hinshaw, S.P., Arnold, L.E., Yan, P., Li, C.-s.R., 2009. Decreased amygdala activation during risk taking in non-
Velanova, K., Abikoff, H., Swanson, J.M., 2013. Impact of ADHD and cannabis use dependent habitual alcohol users: a preliminary fMRI study of the stop signal
on executive functioning in young adults. Drug Alcohol Depend. 133, 607–614. task. Am. J. Drug Alcohol Abuse 35, 284–289.
Tapert, S.F., Schweinsburg, A.D., Drummong, S.P.A., Paulus, M.P., Brown, S.A., Yang, Yang, B., Yang, S., Zhao, L., Yin, L., Liu, X., An, S., 2009. Event-related potentials in
T.T., Frank, L.R., 2007. Functional MRI of inhibitory processing in abstinent ado- a Go/Nogo task of abnormal response inhibition in heroin addicts. Sci. China C,
lescent marijuana users. Psychopharmacology 194, 173–184. Life Sci. 52, 780–788.
Tarter, R.E., Kirisci, L., Mezzich, A., Cornelius, J.R., Pajer, K., Vanyukov, M., Gardner, Yücel, M., Lubman, D.I., 2007. Neurocognitive and neuroimaging evidence of
W., Blackson, T., Clark, D.B., 2003. Neurobehavioral disinhibition in childhood behavioural dysregulation in human drug addiction: implications for diagnosis,
predicts early age at onset of substance use disorder. Am. J. Psychiatry 160, treatment and prevention. Drug Alcohol Rev. 26, 33–39.
1078–1085. Zhang, S., Hu, S., Bednarski, S.R., Erdman, E., Li, C.-s.R., 2014. Error-related func-
Theunissen, E.L., Kauert, G.F., Toennes, S.W., Moeller, M.R., Sambeth, A., Blan- tional connectivity of the thalamus in cocaine dependence. NeuroImage Clin. 4,
chard, M.M., Ramaekers, J.G., 2012. Neurophysiological functioning of occasional 585–592.
and heavy cannabis users during THC intoxication. Psychopharmacology 220, Zheng, D., Oka, T., Bokura, H., Yamaguchi, S., 2008. The key locus of common response
341–350. inhibition network for No-go and stop signals. J. Cogn. Neurosci. 20, 1434–1442.
Thoma, P., Wiebel, B., Daum, I., 2007. Response inhibition and cognitive flexibility Zhou, Z.-H., Yuan, G.-Z., Yao, J.-J., Li, C., Cheng, Z.-H., 2010. An event-related poten-
in schizophrenia with and without comorbid substance use disorder. Schizophr. tial investigation of deficient inhibitory control in individuals with pathological
Res. 92, 168–180. internet use. Acta Neuropsychiatr. 22, 228–236.

21 - Smith2014

Diunggah oleh

Informasi Dokumen

Judul Asli

Hak Cipta

Format Tersedia

Bagikan dokumen Ini

Bagikan atau Tanam Dokumen

Opsi Berbagi

Apakah menurut Anda dokumen ini bermanfaat?

Apakah konten ini tidak pantas?

Hak Cipta:

Format Tersedia

21 - Smith2014

Diunggah oleh

Hak Cipta:

Format Tersedia

G Model

DAD-5271; No. of Pages 33 ARTICLE IN PRESS

Contents lists available at ScienceDirect

Drug and Alcohol Dependence

Deﬁcits in behavioural inhibition in substance abuse and addiction:

1. Introduction The pattern of performance differences is important in deter-

DAD-5271; No. of Pages 33

Study Control group User group

Study Control group User group

DAD-5271; No. of Pages 33

Study Control group User group

Study Control group User group

DAD-5271; No. of Pages 33

Study Control group User group

Study Control group User group

DAD-5271; No. of Pages 33

Study Control group User group

Study Control group User group

DAD-5271; No. of Pages 33

Study Control group User group

Study Control group User group

DAD-5271; No. of Pages 33

Study Control group User group

Study Control group User group

DAD-5271; No. of Pages 33

Study Control group User group

DAD-5271; No. of Pages 33

DAD-5271; No. of Pages 33

DAD-5271; No. of Pages 33

DAD-5271; No. of Pages 33

Substance Effect size analysis Heterogeneity analysis

Variable k g SE CI lower CI upper z p Q df p

Substance Effect size analysis Heterogeneity analysis

Variable k g SE CI lower CI upper z p Q df p

Substance Effect size analysis Heterogeneity analysis

Variable k g SE CI lower CI upper z p Q df p

Anda mungkin juga menyukai