J Gambl Stud

DOI 10.1007/s10899-017-9683-5

REVIEW PAPER

Pathological Gambling and Motor Impulsivity:

A Systematic Review with Meta-Analysis

Nahian S. Chowdhury1 • Evan J. Livesey1 • Alex Blaszczynski1 •

Justin A. Harris1

Ó Springer Science+Business Media New York 2017

Abstract Motor impulsivity, which is an impairment in withholding and cancelling

inappropriate responses, may account for the inability for pathological gamblers (PGs) to
inhibit their urges to gamble. The aim of this systematic review was to perform a quan-
titative and qualitative synthesis of existing studies in order to assess whether PGs without
comorbid substance use disorder have elevated motor impulsivity, relative to healthy
controls. An exhaustive literature search led to the identification of 20 studies which met
inclusion criteria. A meta-analysis was then conducted on the following measures: stop
signal reaction time from the stop signal task; commission errors, omission errors, and Go
reaction time from the Go/No-Go task; and the motor impulsiveness subscale of the Barratt
Impulsiveness Scale (BIS-Motor). The results revealed a moderate to large mean effect
size of stop signal reaction time, small to moderate mean effect sizes for commission
errors, omission errors and Go reaction time, and a large mean effect size for the BIS-
Motor. Significant heterogeneity in effect sizes was observed on most behavioural mea-
sures, but not for the BIS-Motor or omission errors on the Go/No-Go task. Overall, these
results suggest that motor impulsivity may be one of the features of PG psychopathology,
accounting for their poor inhibitory control over gambling behaviours. Moreover, other
deficits in sustained attention, or more generally in executive/cognitive control, may be
present in PGs. We discuss the implications, limitations of existing research, and suggested
avenues for future studies, particularly the need to acknowledge heterogeneity amongst
PGs and amongst different behavioural measures.

Keywords Gambling
Impulsivity
Inhibitory control
Executive function

& Nahian S. Chowdhury

ncho1135@uni.sydney.edu.au
1
School of Psychology, University of Sydney, Camperdown, NSW 2006, Australia

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Introduction

Although many individuals gamble without experiencing difficulties, it becomes an issue

for some, whereby it gradually impacts an individual’s capacity to achieve their personal,
relational and vocational goals, leading to a pattern of pathological gambling (PG). The
symptoms of PG (or Gambling Disorder, as named in the DSM-V) are much like the
symptoms of tolerance and withdrawal in substance dependence (e.g. gambling with
increasing amounts of money to experience the desired arousal and restlessness/irritability
during attempts to resist gambling), and are characterised by a loss of control over one’s
gambling behaviour (Grant and Chamberlain 2014). Major models have attempted to
explain why PGs find it so difficult to control their urge to gamble, even in the face of
negative life consequences. These models attempt to integrate various interacting factors,
where certain factors are more or less prominent in each individual gambler (Sharpe 2002),
or where each individual gambler can be categorised in one of three pathways representing
a certain combination of factors (Blaszczynski and Nower 1998). These include social
factors such as gambling accessibility and familial/cultural attitudes towards gambling,
biological factors such as genetic predispositions and altered neurotransmitter systems, and
psychological factors such as associative learning, mood disturbances, gambling related
arousal and cognitive biases. However, consensus suggests that the characteristic that can
account for most cases of PG is impulsivity (Grant et al. 2016).
Impulsivity is a complex construct that has been difficult to define. Most definitions
(Caswell et al. 2013; Chamberlain and Sahakian 2007; Evenden 1999; Logan et al. 1997;
Moeller et al. 2001; Stanford et al. 2009) suggest that a behaviour is impulsive if it is
inappropriate in a particular context, is prematurely expressed with little consideration of
the future consequences and leads to undesirable outcomes in the short-term and/or long-
term. Impulsivity is also complex in that it is a multifaceted construct—there are different
types of impulsivity which rely on separate neurological processes and which are measured
in different ways. Researchers have distinguished two primary types of impulsivity: cog-
nitive and motor impulsivity (Brunner and Hen 1997; Caswell et al. 2013; Chamberlain
and Sahakian 2007; Kraplin et al. 2014; Kraplin et al. 2015; Malloy-Diniz et al. 2007;
Olmstead et al. 2009; Vassileva et al. 2007). Cognitive impulsivity refers to impulsivity in
decisions, whereby an individual is biased towards smaller immediate rewards as opposed
to larger delayed rewards, or where an individual makes quick decisions under conditions
of uncertainty. Tasks such as the delay discounting task (e.g. Alessi and Petry 2003) and
the information sampling task (e.g. Lawrence et al. 2009) have been used to measure this
facet of impulsivity. Motor impulsivity on the other hand, refers to impulsivity in action,
characterised by an impaired ability to inhibit (delay, withhold and interrupt) inappropriate
responses. The ability to inhibit inappropriate responses is an important aspect of human
functioning, as it allows individuals to evaluate the consequences of these responses, and to
express more appropriate responses. Therefore, it is possible that this aspect of functioning
is impaired in PG, and can account for the unsuccessful attempts to inhibit the urge to
gamble. Accordingly, the goal of this systematic review will be to evaluate whether this
aspect of impulsivity plays a role in the aetiology of PG.
Motor Impulsivity has been measured in two ways; through self-report and through
laboratory tasks. The most widely used measures are described below.

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Go/No-Go Task

The Go/No-Go (GNG) task (Donders 1969) consists of ‘‘go’’ trials, where the participant is
required to make a speeded response (e.g. pressing a key when a red square appears), as
well as ‘‘no-go’’ trials, where the participant is required to withhold responding (e.g.
withholding a response when a black square appears). The key dependent measure
reflective of motor impulsivity is the number of responses made to no-go stimuli (com-
mission errors), as this represents an individual’s ability to inhibit an inappropriate
response. Other dependent measures include the absence of a response to a go stimulus
(omission errors), which is thought to be a measure of sustained attention (Trommer et al.
1988), as well as the reaction time on go trials (Go RT), where it is thought that impulsivity
leads to faster (or rash) responding on these trials (Rentrop et al. 2008).

Stop Signal Task

The stop-signal task (Logan and Cowan 1984) is similar to the GNG task; however, it
requires cancellation of an already cued response. Along with go trials, there are also a
certain number of ‘‘stop’’ trials, where the go stimulus is followed by a ‘‘stop signal’’ after
a certain interval (the ‘‘Stop Signal Delay’’, SSD), signalling to participants that they must
cancel their initiated response. Researchers usually attempt to identify the SSD at which
there is a 50% probability of inhibiting the response (the critical SSD). A staircasing
method is used, where the SSD will increase or decrease by a certain interval (e.g. 50 ms)
on each trial based on the success or failure to inhibit a response on the previous trial,
which should lead to a 50% success rate in inhibition. Hence, the mean SSD identified
through this staircasing procedure becomes equivalent to the critical SSD. Based on a
horse-race model where ‘‘go’’ and ‘‘stop’’ processes compete, the critical SSD is then
subtracted from the average Go RT to identify the Stop-Signal Reaction Time (SSRT) of
the participant. This is the average amount of time required for a participant to successfully
cancel their response after the onset of the stop signal. Hence, longer SSRTs are reflective
of impaired inhibitory control over behaviour. Refer to Fig. 1 for a schematic represen-
tation of the stop-signal task.

Fig. 1 A schematic representation of the stop-signal task, where the go stimulus is a left arrow and the stop
signal is an auditory beep. The critical SSD (the SSD at which there is a 50% chance of successful
inhibition) is identified through a staircasing method, and is then subtracted from the Mean Go RT to
identify the SSRT. According to a horse race model, the go process will be executed if the SSD on any trial
is higher than the critical SSD, whilst the stop process will be executed if the SSD is lower than the critical
SSD. Individuals who are high in motor impulsivity have longer SSRTs, such that they require longer to
execute their stop response

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Barratt-Impulsiveness Scale

The Barratt Impulsiveness Scale (BIS-11) (Patton et al. 1995) is a self-report questionnaire
which contains three subscales: non-planning, attentional, and motor impulsiveness sub-
scales. The Non-planning subscale measures an individual’s orientation towards the pre-
sent and relates to delay discounting tasks. The Attentional subscale measures an
individual’s ability to stay focused on daily activities. The Motor subscale measures an
individual’s tendency to respond without prior thought, containing items such as ‘‘I do
things without thinking’’ and ‘‘I act on the spur of the moment’’. Researchers have com-
plemented the Stop-Signal Task and GNG task using the motor-impulsiveness subscale the
BIS-11, as this subscale has been thought to reflect a similar concept of inhibitory control
(Kraplin et al. 2015; Leppink et al. 2016; Meule 2013). However, weak or inconsistent
correlations between self-report and laboratory-task measures of impulsivity have been
found (e.g. Enticott et al. 2006). One explanation for this is that self-report questionnaires
are reflective of trait impulsivity (a stable personality feature) whilst laboratory tasks are
reflective of state impulsivity (a transitory or momentary feature specific to a situation)
(Meule 2013), suggesting that even the attribute of motor impulsivity itself requires a
multi-dimensional conceptualisation.
In the following systematic review, we will perform a qualitative and quantitative
synthesis of empirical studies that compare pathological gamblers with healthy controls on
measures obtained from the stop-signal task (SSRT), the GNG task (commission errors,
omission errors and Go RT) and the BIS-11 (Motor Impulsiveness Subscale). This will
allow us to address the question of whether motor impulsivity represents a major com-
ponent of PG psychopathology and what areas of further research are required. To our
knowledge, two meta-analyses have previously been conducted (Lipszyc and Schachar
2010; Smith et al. 2014) comparing PGs (and other addictions) with healthy controls on
Stop-Signal and/or GNG task performance, however both analyses had low power and did
not account for the possible confounds of comorbid substance use disorder, restricting
conclusions made about the isolated effects of PG. Furthermore, these meta-analyses only
assessed laboratory-task measures of impulsivity, with no analysis of self-report measures.
We aim to build on these analyses by including studies with PG samples without comorbid
substance use disorder, and to investigate both laboratory-task and self-reported measures
of impulsivity to allow for more multi-faceted conclusions.

Methods

Literature Search

An exhaustive search was conducted by the primary author in the PsycINFO, PubMed,
Medline, Embase and CINAHLelectronic databases with no date restrictions, on the 22nd
of November 2016. The search terms used were ‘‘gambling’’, ‘‘pathological gambling’’ and
‘‘problem gambling’’, in combination with ‘‘impulsivity’’, ‘‘impulsive behaviour’’, ‘‘ex-
ecutive function’’, ‘‘inhibition’’, ‘‘response inhibition’’, ‘‘cognitive control’’ and ‘‘in-
hibitory control’’. Once all duplicates were removed, the primary author partially screened
the titles, abstracts and texts of the received articles, identifying studies which compare
gamblers and a control group on a behavioural and/or self-reported measure of motor
impulsivity. Once identified studies were partially screened, two of the authors

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independently reviewed the remaining papers for full-text screening. Initially, an agree-
ment of 86% was reached on the exclusion and inclusion of papers. The authors then made
contact to discuss any inconsistencies, reaching a final agreement of 100%.

Exclusion/Inclusion Criteria

Studies were required to fulfil nine criteria. They had to (a) be presented in English
(although we acknowledge that this may be a source of bias in our analysis) b) be con-
ducted on human participants (c) compare a control group to a gambling group (d) contain
a gambling group who met criteria for DSM-IV pathological gambling or DSM-V gam-
bling disorder as assessed by diagnostic instruments such as the South Oaks Gambling
screen (SOGs), (e) contain a group of gamblers who did not meet criteria for comorbid
substance use disorder (aside from caffeine or nicotine dependence) (f) contain a control
group which differs significantly in gambling severity (g) report a minimum of one of the
following: SSRT in the Stop-Signal task, No-Go Commission errors, Go Omission Errors,
Go RT in the GNG task, and BIS-Motor Impulsiveness, (h) calculate SSRT if a stop-signal
task is used, rather than calculating the percentage of inhibited responses at various stop
signal delays, and (i) provide sufficient information for effect size calculation. Although
there were no included studies with adolescent samples, no age limit was applied to the
exclusion/inclusion criteria. We included studies that had No-Go and Go trials of all
relative frequencies. Samples where there were no PGs which satisfied criteria for sub-
stance use disorder, or where both groups did not differ in substance use, were included.
Samples with comorbid ADHD were not excluded because there are a limited number of
studies excluding ADHD psychopathology or making comparisons between comorbid and
non-comorbid PGs, which would result in low statistical power for the meta-analysis.

Calculating Effect Sizes

We used http://www.campbellcollaboration.org/resources/effect_size_input.php to calcu-

late Cohen’s d and inverse variance weights (Lipsey and Wilson 2001). We used means
and SDs, or F and t values to calculate effect sizes. Where multiple gambling groups
existed (e.g. PG alone vs. PG with comorbid ADHD) or where repeated measures were
taken (e.g. across different blocks of the GNG task), the means and SDs of those groups or
repeated measures were combined. For the stop-signal task, we calculated the effect sizes
for SSRT. Other measures from this task (e.g. Go RT, error rates) were not analysed as
they are rarely reported. For the GNG task, we calculated the effect size for errors of
commission, errors of omission, and Go RT. For the BIS, we calculated the effect size for
the score on BIS-Motor Impulsiveness. Positive effect sizes were indicative of lower
SSRT, fewer commission errors, fewer omission errors, quicker Go RTs and lower BIS-
Motor Impulsiveness in the control group.

Performing the Meta-Analyses

The meta-analyses were conducted using the Comprehensive Meta-Analysis Software

(Version 3; Biostat, Englewood, NJ, 2014). We used a random effects model to calculate
the weighted mean effect size of each measure (Borenstein et al. 2007), although we also
indicate when the results differ if a fixed effects model is used. Each effect size was
assigned a weight, and the weighted k effect sizes were summed. This total was divided by

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the sum of the weights of the k studies to obtain the weighted mean effect size. We also
computed the standard error and variance of the weighted mean effect size as well as the
95% confidence interval of the effect size. We then carried out a z-transformation to test
the null hypotheses that the weighted mean effect size was 0, with two-tailed significance
set at a p value of 0.05. Under a fixed effects model, we also computed the Q-statistic to
test whether there was significant heterogeneity amongst the effect sizes Significance was
assessed against a k-1 degrees of freedom Chi squared distribution. A Q-statistic with a
p \ 0.05 suggests that the dispersion of effect sizes between the k studies is substantial.
We also computed the I2 statistic, an estimate of the percentage of variability due to effect
size heterogeneity (Borenstein et al. 2009).

Results

As shown in Fig. 2, partial text screening identified 46 studies comparing a gambling group
with a control group on a measure of motor impulsivity. After full text screening, 12
studies were not included as comorbid substance use disorder was not an exclusion cri-
terion, 6 studies using the BIS-11 were excluded as data on the motor impulsiveness
subscale were not available, 4 studies were excluded as percentage inhibited response was
used in the stop signal task analysis rather than SSRT (although 1 of these studies was still
eligible for a comparison of BIS Motor Impulsiveness), 3 studies were excluded as the
gambling group did not meet criteria for PG, 1 study was excluded as the control groups’
gambling habits were not significantly different from the PG group, and 1 study was
excluded as there were insufficient data to calculate the desired effect size. This led to the
exclusion of 26 studies, leaving 20 studies for the meta-analysis.
Of the studies which met inclusion criteria, 5 studies reported SSRT differences (with a
total of 179 PGs and 188 Controls) and 7 studies reported GNG Commission Differences
(with a total 328 PGs and 350 controls). Although 4 studies reported GNG Omission
differences, the effect size of 5.89 obtained from Zhou et al. (2016) was considered an
outlier, and likely to reflect an error in their reporting, and was therefore excluded, leaving
3 studies for the final analysis (with a total of 189 PGs and 181 Controls). Five studies
reported GNG Go RT differences (with a total of 225 PGs and 261 Controls) and 12 studies
included analysis of the BIS-11 Motor Impulsiveness Subscale (with a total of 410 PGs and
464 Controls). Refer to Tables 1, 2 and 3 for the characteristics of the included studies.
Of the 5 studies reporting SSRT differences, 4 involved choice reaction time tasks (e.g.
responding with left or right arrows based on the direction of stimuli), with an auditory (Grant
et al. 2010; Goudriaan et al. 2005, 2006) or visual (Kraplin et al. 2015; Rodriguez-Jimenez
et al. 2006) stop signal presented at a staircased interval after the appearance of the go-signal
on 25% of the trials. One study (Billieux et al. 2012) involved a matching task where
participants were instructed to respond when a target stimulus matched a cue stimulus; on
25% of the trials, the target stimuli would turn red at a certain interval after its onset, to which
participants would have to withhold their response. Four out of 5 studies reported significantly
slower SSRTs in PGs compared to control. A meta-analysis of SSRT differences between
PGs and Controls revealed an overall moderate-large effect size of 0.57, in adherence with
Cohen’s (1992) effect size classifications of small (0.2), medium (0.5) and large (0.8).
Among the 7 studies reporting on the GNG task, 2 studies (Goudriaan et al. 2005; Zhou
et al. 2016) involved responding and withholding responses to a one of numerous go and
no-go stimuli (e.g. withhold a response to one of four two-digit numbers), 4 studies

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Fig. 2 Flow chart representing the process in which the papers included in the meta-analysis were
identified

(Kertzman et al. 2008, 2011, Fuentes et al. 2006, van Holst et al. 2012) involved
responding and withholding responses to only one go and one no-go stimulus (e.g. a certain
coloured square) and another study (Rodriguez-Jimenez et al. 2006) involved responding

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 Table 1 Characteristics of study samples and effect sizes, for papers which use the stop signal task
123
Study Control group
N (male) Mean Criteria
age
Goudriaan et al. 50 (35) 35.6 No history of substance use or
(2006) dependence, no major psychiatric
disorders, no physical conditions
which could affect cognitive and
motor performance, Dutch as first
language, no current use of
psychotropic medication which
could not be discontinued, negative
urinalysis for alcohol, cannabis and
benzodiazepines, age between 18
and 60
Rodriguez-Jimenez 40 (40) 32.0 Absence of pathological gambling,
et al. (2006) SOGS \ 4, no substance use in the
previous year (except caffeine and
nicotine), no ADHD, no psychotic or
affective disorders, no organic
mental disorders, no somatic
disorders which would interfere with
testing, no illiteracy, no IQ \ 70
Gambling group Effect size (Cohen’s d),
notes
N (male) Mean Criteria
age
49 (40) 37.3 DSM-IV pathological gambling 0.64
(DIS)a, no current treatment except
for PG, no history of substance use/
dependence (except nicotine), no
major psychiatric disorders except
for manic disorders, OCD, ADHD
and anti-social personality disorder,
no physical conditions which could
affect cognitive and motor
performance, Dutch as first
language, no current use of
psychotropic medication which
could not be discontinued, negative
urinalysis for alcohol, cannabis and
benzodiazepines, age between 18
and 60. Gamblers were seeking
treatment
55 (55) 33.2 DSM-IV pathological gambling -0.15
(SOGS), no substance use in the Combined the means and
previous year (except caffeine and SDs of the ADHD and
nicotine), no psychotic or affective non-ADHD group
disorders, no organic mental
disorders, no somatic disorders
which would interfere with testing,
no illiteracy, no IQ \ 70. Gamblers
were seeking treatment
J Gambl Stud
 Table 1 continued
Study Control group
N (male) Mean Criteria
age
Grant et al. (2010) 26 (10) 50.4 Absence of a history of psychiatric
illness
Billieux et al. (2012) 20 (17) 38.30 No past or present gambling activity,
no history of psychiatric or
neurological disorder
Kraplin et al. (2015) 52 (21) 25.69 Irregular and unproblematic gambling,
smoked less than 20 cigarettes in
life, no current treatment for mental
or personality disorders, no other
mental disorders in the previous
12 months, no physical conditions
which could affect cognitive and
motor performance (e.g. ADHD),
German as first language, no use of
psychotropic medication in the
previous two weeks, negative
urinalysis for cocaine, ecstasy,
methamphetamines, opioids or
cannabis, no other mental disorders,
age between 18 and 25
a
Diagnostic instrument used to assess pathological gambling, such as the South Oaks Gambling Screen (SOGS), Diagnostic Interview Schedule (DIS), Structured Clinical
Interview for DSM (SCID) and the NORC Diagnostic Screen for Gambling Problems (NODS)
123
Gambling group Effect size (Cohen’s d),
notes
N (male) Mean Criteria
J Gambl Stud
age
29 (11) 50.4 DSM-IV pathological gambling (SCI- 0.81
PG), no current substance abuse or Baseline data were used
dependence (except nicotine), no for gamblers and
lifetime bipolar disorder, no control
dementia, no psychotic disorder.
Gamblers were recruited from the
community via advertisements
20 (17) 44.1 DSM-IV pathological gambling 1.10
(SOGS), no substance use disorder,
no reported history of neurological
disorders. Gamblers were seeking
treatment
26 (20) 29.89 DSM-IV pathological gambling in 0.64
previous 12 months, no current None of the participants
treatment for mental or personality in the PG group met
disorders, no physical conditions criteria for DSM-IV
which could affect cognitive and substance use disorder
motor performance (e.g. ADHD), in the past 12 months
German as first language, no use of Combined the means and
psychotropic medication in the SDs of the PG and PG/
previous two weeks, negative ND group
urinalysis for cocaine, ecstasy,
methamphetamines, opioids or
cannabis, no other mental disorders,
age between 18 and 25. Gamblers
were recruited from the community
via advertisements
 Table 2 Characteristics of study samples and effect sizes, for papers which use the Go/No-Go task

123
Study Control group Gambling group Go/No-Go Effect size (Cohen’s d), notes
proportions
N (male) Mean Criteria N (male) Mean Criteria Commission Omission Go
age age RT

Goudriaan 49 (34) 35.8 No lifetime substance abuse or
et al. dependence, no history of
(2005) psychosis, no treatment for a
mental disorder in past
3 years, physical conditions
which could affect cognitive
and motor performance, use
of psychotropic medication
which could not be
discontinued, negative
urinalysis for alcohol,
cannabis and
benzodiazepines
Fuentes 82 (45) 40.9 Did not meet criteria for any
et al. psychiatric disorders (e.g.
(2006) substance abuse) or lifetime
diagnosis of a recurrent
psychiatric syndrome
48 (40) 39.0 DSM-IV pathological Equiprobable 0.51 – –
gambling (DIS), no lifetime Go and No-
substance abuse or Go Trials
dependence, no history of
psychosis, no current
treatment for mental
disorders except for those
under study, physical
conditions which could
affect cognitive and motor
performance, use of
psychotropic medication
which could not be
discontinued, negative
urinalysis for alcohol,
cannabis and
benzodiazepines. Gamblers
were treatment seeking
52 40.1 DSM-IV pathological Equiprobable 0.80 – -0.20
gambling (SOGS). non- Go and No- Use the means and SDs of the
comorbid Pathological Go Trials Non-Comorbid Pathological
Gambling Group did not Gamblers
meet criteria for any
psychiatric disorders (e.g. Combined the means and SDs of
substance abuse). Gamblers the visual and auditory version
were treatment seeking of the GNG task
J Gambl Stud
 Table 2 continued

Study Control group Gambling group Go/No-Go Effect size (Cohen’s d), notes
proportions
N (male) Mean Criteria N (male) Mean Criteria Commission Omission Go
J Gambl Stud

age age RT

Rodriguez- 40 (40) 32.0 Absence of pathological
Jimenez gambling, SOGS \ 4, no
et al. substance use in the previous
(2006) year (except caffeine and
nicotine), no ADHD, no
psychotic or affective
disorders, no organic mental
disorders, no somatic
disorders which would
interfere with testing, no
illiteracy, no IQ \ 70
Kertzman 84 (56) 36.8 No current psychiatric
et al. disorder, no lifetime
(2008) diagnosis of schizophrenia,
no bipolar disorder, no
ADHD, no OCD, no
substance-related disorders,
no neurological disorders
55 (55) 33.2 DSM-IV pathological Equiprobable 0.08 0.24 –
gambling (SOGS), no Go and No- Combined the means and SDs of
substance use in the previous Go Trials the ADHD and non-ADHD
year (except caffeine and group
nicotine), no psychotic or
affective disorders, no
organic mental disorders, no
somatic disorders which
would interfere with testing,
no illiteracy, no IQ \ 70
Gamblers were seeking
treatment
83 (56) 39.5 DSM-IV pathological Both Rare No- 0.21 0.34 0.70
gambling (Semi-Structured Go Blocks Combined the means and SDs of
Interview, SOGS), no and Rare Go all four blocks of the GNG task
ongoing psychiatric Blocks
treatment, no alcohol and
substance use/dependence,
no major psychiatric
disorders, no neurological
disorder, no mental
retardation, no use of
psychotropic medication in
the previous month.
Gamblers were seeking
treatment

123
 Table 2 continued

Study Control group Gambling group Go/No-Go Effect size (Cohen’s d), notes
proportions
N (male) Mean Criteria N (male) Mean Criteria Commission Omission Go

123
age age RT

Kertzman 57 (36) 37.70 No current psychiatric 51 (35) 39.51 DSM-IV pathological Both Rare No- -0.07 0.34 0.57
et al. disorder, no lifetime DSM- gambling (Semi-Structured Go Blocks Combined the means and SDs of
(2011) IV Axis 1 disorder such as Interview), o alcohol and and Rare Go all four blocks of the GNG task
schizophrenia, bipolar substance use/dependence, Blocks
disorder, no ADHD, no no major psychiatric
OCD, no substance-related disorders, no neurological
disorder disorder, no mental
retardation, no use of
psychotropic medication in
the previous month.
Gamblers were seeking
treatment
J Gambl Stud
 Table 2 continued
Study Control group
N (male) Mean Criteria
age
van Holst 15 (15) 36.20 Gamble less than 3 times a
et al. year, no treatment for any
(2012) mental disorder other than
PG, no alcohol or substance
use disorder, no lifetime
diagnosis of schizophrenia/
psychotic episodes, no
manic disorder, no OCD, no
PTSD, no history or current
treatment for neurological
disorders, no internal
disorders, no brain trauma,
no exposure to neurotoxic
factors, no use of
psychotropic medication, no
difficulty reading Dutch,
negative urinalysis for
alcohol, amphetamines,
benzodiazepines, opioids
and cocaine
123
Gambling group Go/No-Go Effect size (Cohen’s d), notes
proportions
N (male) Mean Criteria Commission Omission Go
J Gambl Stud
age RT
16 (16) 34.38 DSM-IV pathological Rare No-Go -0.11 – 0.72
gambling (DIS, SOGS), no Trials One participant did not meet
treatment for any mental criteria for DSM-IV criteria
disorder other than PG, no according to the DIS, but all
alcohol or substance use had scores higher than 5 on the
disorder, no lifetime SOGS
diagnosis of schizophrenia/
psychotic episodes, no
manic disorder, no OCD, no
PTSD, no history or current
treatment for neurological
disorders, no internal
disorders, no brain trauma,
no exposure to neurotoxic
factors, no use of
psychotropic medication, no
difficulty reading Dutch,
negative urinalysis for
alcohol, amphetamines,
benzodiazepines, opioids
and cocaine. Gamblers were
seeking treatment
 Table 2 continued

Study Control group Gambling group Go/No-Go Effect size (Cohen’s d), notes
proportions
N (male) Mean Criteria N (male) Mean Criteria Commission Omission Go

123
age age RT

Zhou et al. 23 (16) 28 No diagnosis of PG or IAD, no 23 (18) 29 DSM-IV pathological Equiprobable 0.80 5.89 0.02
(2016) alcohol dependence, no gambling, no alcohol- Go and No-
diagnosis of substance dependence, no diagnosis of Go Trials
dependence, no neurological substance of alcohol or
disorder, no history of head substance dependence, were
injury, no systemic disease non-smokers, no
that affects the CNS neurological disorder, no
history of head injury.
Gamblers were seeking
treatment
J Gambl Stud
 Table 3 Characteristics of study samples and effect sizes, for papers which report on the motor-impulsiveness subscale of the Barratt Impulsivity Scale
Study Control group Gambling group Effect size (Cohen’s d),
notes
J Gambl Stud

N (male) Mean Criteria N (male) Mean Criteria

age age

Rodriguez- 40 (40) 32.0 Absence of pathological gambling,
Jimenez SOGS \ 4, no substance use in the
et al. previous year (except caffeine and
(2006) nicotine), no ADHD, no psychotic or
affective disorders, no organic mental
disorders, no somatic disorders which
would interfere with testing, no
illiteracy, no IQ \ 70
Ledgerwood 41 (17) 45.7 NODS \=1, no substance dependence
et al. within past 12 months (excluding
(2009) caffeine and nicotine), no acute and
severe psychiatric disorders (i.e. acute
suicidality, uncontrolled psychosis), no
non-English speakers, no individuals
who could not provide informed
consent, negative toxicology screen for
marijuana, alcohol, cocaine, opioids
Lai et al. 40 (40) 35.61 No neurological, psychiatric or
(2011) psychological disorders, no score
higher than 29 on the Beck-Depression
Inventory
55 (55) 33.2 DSM-IV pathological gambling (SOGS), 1.52
no substance use in the previous year Combined the means and
(except caffeine and nicotine), no SDs of the ADHD and
psychotic or affective disorders, no non-ADHD group
organic mental disorders, no somatic
disorders which would interfere with
testing, no illiteracy, no IQ \ 70.
Gamblers were seeking treatment
30 (14) 48.4 DSM-IV pathological gambling (NODS), 0.54
had gambled in past 2 months, no
substance dependence within past
12 months (excluding caffeine and
nicotine), no acute and severe
psychiatric disorders (i.e. acute
suicidality, uncontrolled psychosis), no
non-English speakers, no individuals
who could not provide informed
consent, negative toxicology screen for
marijuana, alcohol, cocaine, opioids.
Half of the gamblers were seeking
treatment, and half were recruited from
the community via advertisements
37 (37) 36.42 DSM-IV pathological gambling (SCID, 0.74
SOGS), no neurological, psychiatric or No significant differences
psychological disorders other than PG, between pathological
no score higher than 29 on the Beck- gamblers and control
Depression Inventory. Gamblers were groups in alcohol use and
seeking treatment other substance use

123
 Table 3 continued
Study Control group
N (male) Mean Criteria
123
age
Hwang et al. 33 (33) 24.9 No Axis 1 diagnosis, No history of
(2012) substance use, no psychotic disorders,
no neurological disorder, no significant
head injury and no mental retardation
Black et al. 54 (27) 47.5 Score of 0 on the NODS and SOGS, No
(2013) substance use disorder within the last
3 months (except tobacco), no current
or past diagnosis of schizophrenia, no
bipolar I and II disorder, no primary
neurological disorder, no major
depressive episode in last three months,
no significant evidence of cognitive
impairment (MMSE \ 23), no history
of head injury (with loss of
consciousness [ 10 min)
De Wilde 31 (27) 28.06 No Signs of pathological gambling, No
et al. signs of lifetime substance use
(2013) disorders (except caffeine or nicotine
abuse or dependence), no psychotic
disorders, no organic deterioration or
amnesic disorders, no physical
handicaps, no severe somatic disorders
Gambling group Effect size (Cohen’s d),
notes
N (male) Mean Criteria
age
15 (15) 28.1 DSM-IV pathological gambling (SOGS). 1.25
No history of substance use, no
psychotic disorders, no neurological
disorder, no significant head injury and
no mental retardation. Gamblers were
seeking treatment
54 (19) 45.3 DSM-IV pathological gambling (NODS, 0.89
SOGS), No substance use disorder
within the last 3 months (except
tobacco), no current or past diagnosis
of schizophrenia, no bipolar I and II
disorder, no primary neurological
disorder, no major depressive episode
in last three months, no significant
evidence of cognitive impairment
(MMSE \ 23), no history of head
injury (with loss of
consciousness [ 10 min). Gamblers
were recruited from the community via
advertisements, a gambling registry
and word-of-mouth
22 (20) 33.50 DSM-IV Pathological Gambling (SCID, 1.59
SOGS), No signs of lifetime substance Combined the means and
use disorders (except caffeine or SDs of abstinent and non-
nicotine abuse or dependence), no abstinent pathological
psychotic disorders, no organic gamblers
deterioration or amnesic disorders, no
physical handicaps, no severe somatic
disorders. Gamblers were seeking
treatment
J Gambl Stud
 Table 3 continued

Study Control group Gambling group Effect size (Cohen’s d),

notes
N (male) Mean Criteria N (male) Mean Criteria
J Gambl Stud

age age

Giorgetta 20 (17) 37.15 No history of psychiatric or neurological 20 (17) 36.45 DSM-IV Pathological gambling, no 0.98
et al. disorders alcohol or substance use disorder, no
(2014) current major depressive episodes, no
neurological or medical illnesses, no
history of traumatic brain injury.
Gamblers were seeking treatment
Grecucci 23 (20) 37.48 No substance use disorders, no physical, 23 (20) 35.61 DSM-IV Pathological Gambling, no 1.23
et al. psychiatric or neurological problems substance use disorders, no physical,
(2014) psychiatric or neurological problems,
no other comorbid disorders (such as
anxiety disorders), no cognitive
impairment. Gamblers were seeking
treatment
Kraplin et al. 53 (32) 36.74 No history of substance use or 51 (44) 37.82 DSM-IV pathological gambling (DIS), 0.95
(2014) dependence, no major psychiatric no current treatment except for PG, no
disorders, no physical conditions which history of substance use/dependence
could affect cognitive and motor (except nicotine), no major psychiatric
performance, Dutch as first language, disorders except for manic disorders,
no current use of psychotropic OCD, ADHD and anti-social
medication which could not be personality disorder, no physical
discontinued, negative urinalysis for conditions which could affect cognitive
alcohol, cannabis and benzodiazepines, and motor performance, Dutch as first
age between 18 and 60 language, no current use of
psychotropic medication which could
not be discontinued, negative urinalysis
for alcohol, cannabis and
benzodiazepines, age between 18 and
60. Gamblers were seeking treatment

123
 Table 3 continued

Study Control group Gambling group Effect size (Cohen’s d),

notes
N (male) Mean Criteria N (male) Mean Criteria

123
age age

Kraplin et al. 52 (21) 25.69 Irregular and unproblematic gambling,
(2015) smoked less than 20 cigarettes in life,
no current treatment for mental or
personality disorders, no other mental
disorders in the previous 12 months, no
physical conditions which could affect
cognitive and motor performance (e.g.
ADHD), German as first language, no
use of psychotropic medication in the
previous two weeks, negative
urinalysis for cocaine, ecstasy,
methamphetamines, opioids or
cannabis, no other mental disorders,
age between 18 and 25
Ciccarelli 54 (54) 41.56 No pre-existing psychiatric or
et al. neurological disorder, no pre-existing
(2016) problem gambling
Zhou et al. 23 (16) 28 No diagnosis of PG or IAD, no alcohol
(2016) dependence, no diagnosis of substance
dependence, no neurological disorder,
no history of head injury, no systemic
disease that affects the CNS
26 (20) 29.89 DSM-IV pathological gambling in 0.45
previous 12 months, no current None of participants in the
treatment for mental or personality PG group met criteria for
disorders, no physical conditions which DSM-IV substance use
could affect cognitive and motor disorder in the past
performance (e.g. ADHD), German as 12 months
first language, no use of psychotropic Combined the means and
medication in the previous two weeks, SDs of the PG and PG/
negative urinalysis for cocaine, ecstasy, ND group
methamphetamines, opioids or
cannabis, no other mental disorders,
age between 18 and 25. Gamblers were
recruited from the community via
advertisements
54 (54) 41.56 DSM-V pathological gambling, no 0.99
alcohol or substance use, no
neurological or medical illness, no
pharmacological treatment, no
comorbid Axis-I or Axis-II disorders.
Gamblers were seeking treatment
23 (18) 29 DSM-IV pathological gambling, no 1.05
alcohol-dependence, no diagnosis of
substance of alcohol or substance
dependence, were non-smokers, no
neurological disorder, no history of
head injury. Gamblers were seeking
treatment
J Gambl Stud
J Gambl Stud

to a letter only if it was preceded by a specific letter. The relative proportions of go and no-
go stimuli in each of these studies are reported in Table 2. Four out of 7 studies reporting
commission errors found a significantly higher commission error rate in PGs compared to
controls, with a meta-analysis revealing an overall small-moderate effect size of 0.32.
Upon exclusion of the effect size obtained from Zhou et al. (2016), two out of 3 studies
reporting omission errors found a significantly higher omission error rate in PGs compared
to controls, with a meta-analysis revealing an overall small-moderate effect size of 0.31.
Three out of 5 studies reporting Go RT found significantly slower Go RT in PGs compared
to control, with a meta-analysis revealing an overall non-significant small-moderate effect
size of 0.35, although this effect size was significant when a fixed effects model was used.
Of the 12 studies included in the analysis that used the BIS-Motor Impulsiveness
subscale, all found significantly higher self-reported motor impulsiveness in PGs compared
to controls. A meta-analysis revealed overall a large effect size of 0.96.
Heterogeneity Analyses computing the Q statistic revealed significant heterogeneity in
effect sizes for SSRT, GNG Commission errors and GNG Go RT, with no significant
differences in effect sizes for BIS-Motor Impulsiveness and GNG Omission errors.
Analysis of the I2 statistic showed that there was moderate-high heterogeneity for SSRT
and GNG commission errors, high heterogeneity for GNG Go RT and low-moderate
heterogeneity for BIS-Motor Impulsiveness, in adherence with the classification system
(Higgins et al. 2003) of low (25%), moderate (50%) and high (75%). Refer to Table 4 for a
summary of the meta-analysis, and to Fig. 3 for the forest plots of the effect sizes.

Discussion

On the whole, the results of our meta-analysis suggest that PGs without comorbid sub-
stance use disorder have elevated motor impulsivity. Compared to controls, PGs rate
themselves higher on self-reported motor impulsiveness (with large effect sizes), require
more time to stop an already initiated response (with moderate to large effect sizes) and are
more likely to fail to withhold a response to a no-go stimulus (with small to moderate
effect sizes). Interestingly, PGs are also more likely to fail to execute a response to a go
stimulus (with small to moderate effect sizes), pointing towards deficits in sustained
attention, and in some cases, are slower at responding to a go stimulus (with small to
moderate effect sizes). Our findings for the SSRT measure are consistent with Smith et al.
(2014), where a similar overall moderate effect size for SSRT was also found for PGs. In
contrast, Lipszyc and Schachar (2010) did not find a significant overall effect size for
SSRT, although their analysis was based on only two studies. Our findings for the GNG
measures are inconsistent with Smith et al. (2014), as their analysis revealed non-signifi-
cant effect sizes for commission and omission errors for PGs, although their analysis was
limited to two studies, whereas our analysis had higher statistical power. Nevertheless,
there appears to be more evidence of behavioural motor impulsivity in PGs in the stop
signal task compared to the GNG task.

Heterogeneity of Effect Sizes

Our analysis revealed significant heterogeneity in effect sizes for most behavioural mea-
sures of motor impulsivity. The significant heterogeneity in the SSRT measure was greatly
driven by the negative effect size obtained from Rodriguez-Jimenez et al. (2006), where a
PG group without ADHD showed a lower (albeit non-significant) SSRT than the control

123
123
Table 4 Results of the effect size and heterogeneity analysis
Measure Effect size analysis Heterogeneity analysis

k d Mix–max Variance SE CI lower CI upper z p I2 Q df p

Stop Signal Task - SSRT 5 0.57 -0.15 to 1.10 0.05 0.22 0.15 1.00 2.66 0.008 73.20 14.92 4 0.005
GNG Commission errors 7 0.32 -0.11 to 0.80 0.02 0.14 0.05 0.59 2.30 0.022 65.60 17.44 6 0.008
GNG Omission errors 3 0.31 0.24–0.34 0.01 0.11 0.11 0.52 2.97 0.003 0.00 0.16 2 0.92
GNG Go RT 5 0.35 -0.20 to 0.72 0.04 0.21 -0.06 0.76 1.68 0.092 77.61 17.87 4 0.001
Barratt Motor Impulsiveness Subscale 12 0.98 0.45–1.59 0.01 0.10 0.78 1.18 9.78 <0.001 42.89 19.26 11 0.056
Values in bold reflect significant p values
J Gambl Stud
J Gambl Stud

Fig. 3 Forest plots of the effect sizes for SSRT, GNG Commission errors, GNG Omission Errors, GNG Go
RT and BIS Motor Impulsiveness

group. This emphasizes the need for more studies looking at the effects of comorbid
ADHD on motor impulsivity. Another potential factor that may contribute to heterogeneity
of the SSRT measure is variation in the Go RTs in the Stop Signal task. If participants
progressively slow their response to the go signal as a strategy to avoid stopping errors, this
can increase the probability of stopping above the targeted 50% success rate, leading to an
underestimation of the SSRT. Hence, it would be beneficial for future researchers to report
the probability of stopping along with mean Go RT, in order to determine whether any
SSRT measures are affected by strategic slowing.
There are a few possible reasons for the heterogeneity in GNG measures. One is to do
with variations in the nature of the GNG tasks (types of stimuli used/number of stimuli
requiring a response) and variations in the proportions of Go and No-Go trials. In addition,
there may be differences between studies in the characteristics of the samples studied. For
example, some comorbid psychopathologies may be over-represented in some samples
relative to others. Nonetheless, it may simply be the case that heterogeneity in a charac-
teristic such as motor impulsivity will always exist, with no one factor accounting for all
cases of PG. It rests on future research to understand the task conditions and sample
characteristics which relate to deficits in inhibitory control.

Implications

Motor Impulsivity

On the whole, our findings suggest that PGs are impaired on behavioural and self-reported
measures of motor impulsivity (SSRT, commission error rate and BIS-motor

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impulsiveness). Thus, one reason for the failed attempts to control gambling in PG may be
a general deficit in inhibitory control. Gamblers receive many internal (cognitions, emo-
tions) and external signals to pursue gambling (e.g. advertisements for betting on a sports
team) and to cease gambling (e.g. a friend advising them to stop gambling) in their daily
lives. Our results suggest that gamblers who are highly motor impulsive may be at greater
risk of PG, as they are more likely to gamble even when cued to cease gambling, and are
less likely (or take much longer) to interrupt gambling once they have already begun. Of
course, it should be acknowledged that behavioural measures collected in the laboratory
are limited in their applicability towards such real-world situations as they tap into pro-
cesses in the millisecond range and contain generic cues, whereas the failure to inhibit
gambling would occur over a larger time frame and involve a more complex set of cues.
Nonetheless, we believe that the results of these tasks are important as they attempt to
isolate a specific cognitive mechanism (inhibitory control). Therefore, assessing whether
this mechanism is impaired in PGs can inform us about aetiology at a basic level. It is
likely that this is one mechanism, amongst many others (e.g. associative learning, cognitive
biases) that may contribute to the failure to inhibit gambling. It also worth noting that our
focus on motor impulsivity does not address differences in the compulsion to gamble, and
thus understanding the relationship between compulsivity and impulsivity may be an
important consideration.
Further work is required on the applicability of behavioural measures to PG. For
instance, stronger conclusions may be made through the use of GNG tasks and Stop-Signal
tasks which contain gambling relevant stimuli. Furthermore, future studies should inves-
tigate the reliability of GNG measures and Stop-Signal measures throughout time or
throughout treatment, as this may provide information as to whether such measures are
indeed state measures of impulsivity or whether they may reflect stable and generalizable
trait measures. For the BIS-motor impulsiveness measure, further caution should be
exercised in interpreting this as a true measure of motor impulsivity reflecting inhibitory
control, particularly because none of the items on this subscale explicitly ask questions
related to difficulties ‘‘stopping’’ or ‘‘withholding’’ inappropriate actions. The question-
naire also has items which may be considered irrelevant to motor impulsivity, such as
one’s tendency to change jobs or residence. Another concern with this measure is the
inherent circularity of using questionnaires on gamblers, such that the leading nature of the
questions coupled with recent involvement in gambling activities is likely to overinflate
self-reported motor impulsiveness, which may be contributing to the large effect sizes. It
would be more informative if such individuals judged themselves as impulsive on the basis
of behaviours outside of gambling contexts, which could perhaps be communicated upon
administration of the questionnaire.

Cause or Consequence?

There is ongoing debate as to whether it is impulsivity which predisposes an individual to

gambling or whether it is gambling that leads to the development of impulsivity. Recent
evidence, suggests that PG in adulthood is predicted by impulsivity in childhood and
adolescence (Auger et al. 2010; Dussault et al. 2011; Pagani et al. 2009). In relation to our
analyses, this suggests that it is the core inhibitory control deficits that acts as a vulner-
ability factor for predisposing early gamblers towards a pattern of pathological gambling,
as opposed to the deficits themselves being a product of increasing gambling frequency and
intensity. Nevertheless, it is likely that the relationship between PG and motor impulsivity
is bidirectional and varies between individuals.

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J Gambl Stud

Attention Deficits

Our analysis revealed a higher rate of omission errors in PGs than controls, pointing
towards a deficit in sustained attention alongside the deficit in inhibitory control. However,
conclusions made about the specific deficits in the GNG task are difficult to make, as the
relative proportions of Go and No-Go trials are thought to reveal different sorts of
information about underlying deficits (Smith et al. 2014). Tasks with Frequent Go and Rare
No-Go trials are thought to be the best test of inhibition deficits, as the Go Response
becomes the pre-potent/automatic response that must be withheld on No-Go trials. In
contrast, tasks with frequent No-Go and Rare Go trials are thought to be the best test of
sustained attention, as the No-Go Response is the pre-potent/automatic response that must
be overridden on Go trials. The underlying deficit (inhibition vs. inattention) in
equiprobable GNG tasks is difficult to disentangle and may instead reflect general response
selection or discrimination deficits. Our analysis mostly found significant group differences
in commission error rates in equiprobable GNG tasks; whilst only one out of three studies
using Rare No-go trials revealed significant group differences in commission errors,
suggesting evidence of inhibition per se may not be as strong as expected. Significant
group differences in omission errors, in contrast, were found on GNG tasks with both
equiprobable and Rare No-Go trials, providing good evidence for deficits in sustained
attention. A further note of caution for conclusions about attention deficits must also be
made as our samples did not exclude comorbid ADHD. Therefore, there is no clear
evidence of attention deficits in PG that are not mediated by ADHD.

A Generalised Executive/Cognitive Control Deficit

The finding of significantly slower Go RT for PGs in some studies is somewhat para-
doxical. Intuitively, impulsive individuals are expected to respond quickly (or rashly) to
stimuli, although the contrary was found in our meta-analysis. Alongside the finding of
significantly more omission errors, this pattern of results may suggest that the core psy-
chopathology in PG is not specifically motor impulsivity, but it may be a generalised
deficit in executive or cognitive control (Wright et al. 2014) which consists of inhibitory
control, attentional control, cognitive flexibility and working memory (Diamond 2013).
This generalised deficit results in an inability to resolve conflicts between ‘‘stimulus-
driven/automatic’’ and ‘‘voluntary’’ responses, leading to slow processing. Consequently,
in tasks where there are differing proportions of Go and No-Go trials, there is conflict
between the automatic tendency to execute a response and the voluntary tendency to
withhold a response, leading impulsive individuals to be more susceptible to slow Go RTs
(Kertzman et al. 2008). This explanation fits in with our results, as significant Go RT effect
sizes were only observed in studies with differing proportions of Go and No-Go trials
(when conflict was present), in contrast to equiprobable GNG tasks wherein there is no
strong bias for going or stopping.

Clinical Implications

An enriched understanding of the aetiology of PG has clinical implications. Laboratory and

self-report measures of motor impulsivity may be used to distinguish different types of
gamblers to help guide treatment. For example, Blaszczynski and Nower’s (1998) model
categorises gamblers into three overlapping aetiological pathways; one where PG is caused

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purely by associative learning principles, one where PG is caused by associative learning

as well as mood disturbances, and another where impulsivity is a predisposing factor in
addition to emotional and behavioural factors. It is possible that those in the impulsivity
pathway are more impaired on SSRT and GNG measures relative to those in the purely
behavioural pathway or those in the mood-disturbance pathway. Hence, using these
measures may help identify certain groups of gamblers, which may then guide treatment
strategies, particularly whether the inability to inhibit inappropriate thoughts, behaviours
and emotions should be a core target of intervention. Such measures may also be used as
indicators of treatment resistance, treatment attrition, and the likelihood of relapse into PG.

Limitations of Current Research/Areas for Future Research

To further strengthen conclusions about the relationship between PG and motor impul-
sivity, there are a number of gaps in the identified studies that require consideration. First,
more acknowledgement of heterogeneity amongst PGs is required, including those who
gamble for different reasons (to remove aversive mood states or those who relieve bore-
dom/increase arousal), and/or those who fit in different pathways according to
Blaszczynski and Nower’s (1998) model. More research is also required comparing motor
impulsivity in PGs with and without ADHD. As the results of Rodriguez-Jimenez et al.
(2006) would suggest, comorbid ADHD is likely to influence measures of motor impul-
sivity, and thus, the isolated effects of PGs on motor impulsivity are still unclear. Fur-
thermore, the PG and control samples in the studies reported were mostly males. Although
this is consistent with gender biases in the PG population, this limits generalizability to
females. There is also little research on the relationship between the severity of gambling
symptoms and performance on state and trait measures of motor impulsivity. For instance,
it may be that ‘‘problem’’ gamblers, which are a less severe population of gamblers than
PGs, may be less impaired on measures of inhibitory control. Lastly, more research is
required on the neural basis for motor impulsivity in problem and pathological gamblers.
Investigating whether the neural processes involved in inhibitory control are also impaired
in such populations would provide a multidimensional account about PG aetiology
alongside self-reported and behavioural measures.

Limitations of Current Meta-Analyses

Alongside limitations of studies, our meta-analysis itself has several limitations. For the
Stop Signal task, we did not include studies which measured the percentage of inhibited
responses at different stop-signal delays (e.g. 50, 150, 250 and 350 ms). Of the 4 excluded
studies which used this measure, 3 of these studies did not find significant differences
between PGs and controls, suggesting that conclusions made about motor impulsivity in
PGs may change depending on the measure that is used. Nonetheless, we did not include
this measure as it does not consider the ‘‘race’’ between Go and Stop Processes. Therefore,
the lack of differences may be due to the slowing of responses to the Go Signal (as results
from the GNG task would suggest), such that longer SSDs need to be presented to PGs
relative to controls to find failed inhibition. Another limitation of this meta-analysis is that
for the GNG measures, we combined the means and SDs of different task conditions (e.g.
different frequencies of Go and No-Go trials, different blocks of the GNG task), which is
problematic as it is likely to be a cause of substantial heterogeneity between effect sizes on
these measures. Comparing effects across different task conditions may have been bene-
ficial and will become possible as the number of studies investigating inhibitory deficits in

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PGs grows. Lastly, the meta-analysis could have benefited from the inclusion of other
subscales of the BIS-11, such as the attentional subscale, as this could have complemented
omission error rates as a measure of sustained attention. Moreover, analysis of subscales
from other questionnaires such as the UPPS Urgency Subscale, which may reflect a similar
concept of motor impulsivity (Billieux et al. 2010), would have complemented the BIS-11
Motor Impulsiveness subscale as another self-report measure.

Conclusion

In conclusion, our meta-analysis provides evidence that PGs without comorbid substance
use have elevated motor impulsivity on both a behavioural and self-report level, suggesting
that this is one feature of their psychopathology and may account for their difficulties
controlling the urge to gamble in the face of negative consequences. However, future
research must address the gaps in the current measures of motor impulsivity, the gaps in
previous research, and the gaps in our meta-analysis in order reach a more solid
conclusion.
Compliance with Ethical Standards

Conflict of interest The authors declare that they have no conflict of interest.

Research Involving Human Participants This article does not contain any studies with human partici-
pants performed by any of the authors.

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