Neuroscience Letters 485 (2010) 138–142

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Neuroscience Letters
journal homepage: www.elsevier.com/locate/neulet

Impulse inhibition in people with Internet addiction disorder:

Electrophysiological evidence from a Go/NoGo study
Guangheng Dong a,∗ , Qilin Lu b,c , Hui Zhou a , Xuan Zhao a
a
Department of Psychology, Zhejiang Normal University, PR China
b
Institute of Neuroinformatics, Dalian University of Technology, PR China
c
Courtesy Research Assistant, University of Oregon, United States

a r t i c l e i n f o a b s t r a c t

Article history: We investigated response inhibition in people with Internet addiction disorder (IAD) by recording event-
Received 17 January 2010 related brain potentials during a Go/NoGo task. Twelve IAD-afflicted and 12 normal university students
Received in revised form 2 July 2010 participated in the study. Results show that the IAD group exhibited lower NoGo-N2 amplitude, higher
Accepted 1 September 2010
NoGo-P3 amplitude, and longer NoGo-P3 peak latency than the normal group. The results also suggest
that the IAD students had lower activation in the conflict detection stage than the normal group; thus,
Keywords:
they had to engage in more cognitive endeavors to complete the inhibition task in the late stage. In
Event-related potentials
addition, the IAD students showed less efficiency in information processing and lower impulse control
Go/NoGo
Impulse control ability
than their normal peers.
Internet addiction disorder © 2010 Elsevier Ireland Ltd. All rights reserved.

Internet addiction disorder (IAD), also described as pathological
Internet use, is the inability of an individual to control his or her
use of the Internet, eventually causing psychological, social, and/or
work difficulties [11,30]. Studies reveal the correlation between
low impulse control and other addictive behaviors, such as patho-
logical gambling, substance abuse, and alcohol abuse. Barnes et al.
found that lower impulse control is a significant predictor of alco-
hol misuse for females and delinquency for males [1]. Vitaro et
al. used a prospective-longitudinal design to investigate whether
measuring low impulse control in 12–14-year-olds could predict
engagement in gambling in late adolescence [29]. Moeller et al.
found that impulsivity is a significant predictor of cocaine use
and treatment retention [25]. Cavedini et al. also explored the
relationship between the ventromedial orbitofrontal circuits and
pathological gambling [10].
Researchers believe that Internet addiction is an impulse dis-
order or at least related to impulse control disorder [2,30] because
pathological gamblers, drug addicts, and alcohol abusers may share
similar neuropsychological and personality characteristics with
Internet addicts. Using questionnaires, Cao showed a specific rela-
tionship between impulse control and Internet addiction [9]. In
the current study, the neuroactivity of the impulse control pro-
cess in IAD was explored to determine whether impulse control is
∗ Corresponding author at: Department of Psychology, Zhejiang Normal Univer-
sity, 688 Yingbin Road, Jinhua City, Zhejiang Province, Postal Code 321004, PR China.
Tel.: +86 579 8228 2961; fax: +86 579 8228 2549.
E-mail address: dongguangheng@zjnu.edu.cn (G. Dong).
impaired in people with IAD. If IAD is related to lower impulse con-
trol, this research is likely to demonstrate that neuropsychological
characteristics of IAD may be similar to those of other disorders.
However, few electrophysiological studies about the relationship
between IAD and impulse control have been done. Thus, this study
aims to assess whether Internet addiction is related to impaired
impulse control based on electrophysiological evidence.
A useful way to assess response inhibition is through Go/NoGo
tasks, which always consist of two stimuli: a Go stimulus requiring a
response (usually a button press) and a NoGo stimulus that requires
the inhibition of the response [13,21,23]. To elicit the response
impulse, more Go trials were conducted than NoGo trials. Two
major components of event-related potentials (ERPs) have been
consistently linked with the response inhibition in Go/NoGo tasks.
The first is an enhanced negative component (NoGo-N2) at approx-
imately 200 ms post-stimulus onset in response to NoGo stimuli,
and is maximal in the frontal areas [5]. N2 may represent response
inhibition [18] or the process of conflict monitoring [28]. The sec-
ond major ERP component is an enhanced wave (NoGo-P3) elicited
within a 300–500 ms time window [6]. NoGo-P3 shows a fronto-
central maximum as opposed to the centro-parietal maximum of
Go-P3 [6]. Infrequent stimuli-related P3 is an important compo-
nent in oddball tasks. NoGo-P3 is also believed to be related to
response inhibition and indexing a late stage of the inhibitory pro-
cess, such as, response evaluation or successful response inhibition
[14,16,31].
With regard to the relation between brain activity and impulse
control, Kenemans et al. believed that the direct reflections of brain
activity suggest that the mechanisms of expectation and atten-

0304-3940/$ – see front matter © 2010 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.neulet.2010.09.002
 G. Dong et al. / Neuroscience Letters 485 (2010) 138–142
tion govern behavioral manifestations of impulsivity [22]. Studies
on attention-deficit hyperactivity disorder also reveal that atten-
tion deficiency is an important factor in lower impulse control
[3]. IAD-afflicted people show some attention deficiency features
[15]. Thus, we believe that impulse control in IAD-afflicted indi-
viduals differs from that in normal people and can be detected
by psycho-physiological evidence. The present study aims to
find a neural index underlying the response inhibition difference
between Internet-addicted and normal people by using an ERP
technique. The mechanism that caused the behavior of the par-
ticipants was explored. As discussed, N2 is believed to be related
to the process of conflict monitoring, and P3 to response eval-
uation. These two mental processes are fundamental abilities in
the impulse inhibition process. Internet-addicted participants were
expected to show some difference in N2 and P3 compared with their
normal peers.
Twenty-four healthy right-handed (determined by digitizing
tablet method) university students participated in this study. All
participants were paid 30 dollars for their participation. The IAD
group (12 males, 20.47 ± 4.12 years old) were selected by Young’s
Internet addiction test (IAT) [30] in which 8 items were presented,
and only those who scored 5 or higher were considered Internet
addicts. A strict selection criterion was used: only those who scored
7 or higher were allowed to participate. The students from the nor-
mal group (12 males, 20.19 ± 4.47 years old) were recruited from
the same university and scored lower than 4 in the IAT. All partic-
ipants had normal or corrected-to-normal vision and were free of
neurological or psychiatric disorders. To control the pathological
variables that may confuse the results, the psychological test data
(SCL-90 and 16PF) obtained when the students entered the univer-
sity were checked. Mental states of the IAD group members prior to
Internet addiction were verified further by conducting interviews
with their classmates and tutors. The experiment procedure is in
accordance with the ethical principles of the 1964 Declaration of
Helsinki (World Medical Organization).
Stimuli for the Go/NoGo task were the capital letters “O” and “S.”
Stimuli were presented at the center of the screen. Each trial started
with a small white cross (+) at the center of the screen against a
black background for 250 ms, followed by a stimulus letter. Stimuli
were presented for 500 ms and then terminated by a key press. After
a 500 ms black screen appears, the next trial is initiated. During each
trial, one of the two letters was presented, and either a response
(Go) or the withholding of a response (NoGo) was required.
After an initial practice block of 40 stimuli, four experimental
blocks each consisting of 80 stimuli (25% NoGo probability) were
completed with 1–2 min breaks between blocks. The “S” and “O” in
Go and NoGo cues were counter-balanced among these four blocks.
The stimuli procedure and behavioral data were collected using the
E-prime software system.
Two methods were used to stimulate the impulse of partici-
pants to respond. First, more Go trials were conducted than NoGo
trials (4:1). Most of the trials were Go cues; thus, when the NoGo
cues appeared, participants had to control their impulse to respond,
inducing the impulse inhibition process. Second, participants were
informed before the task that the six best-performing (shorter reac-
tion time, accurate rate ≥90%) participants would be rewarded with
an additional 30 dollars.
Participants were seated in a dimly lit, electrically shielded,
and sound-attenuated room. Participants were positioned approx-
imately 100 cm away from a computer screen (DELL 17-in. LCD
monitor) with horizontal and vertical visual angles of less than
5◦ . All participants were instructed to keep their eyes fixed at the
center of the screen throughout the entire task.
High-density ERPs of each participant were recorded using a
128-channel geodesic sensor net (EGI system, Electrical Geodesics
Inc., Eugene, OR, USA), coupled to a high-input impedance ampli-
139
fier. The electroencephalogram was continuously recorded with
a sample rate of 250 Hz. Whenever possible, impedances were
reduced to less than 5 k before recording with vertical elec-
trooculograms recorded at the left orbital rim, and horizontal
electrooculograms recorded at the right orbital rim.
EEG epochs of 800 ms, including 200 ms of pre-stimulus time as
baseline, were offline averaged only using correct trials according
to the stimuli (Go and NoGo). Epochs with artifacts exceeding
±50 ␮V at any electrode were omitted from further analysis.
The peak latencies were calculated by the software Netstation
(Electrical Geodesics Inc., Eugene, OR, USA). The N2 amplitude was
calculated at the negative maximum between 180 and 220 ms
and the P3 amplitude was calculated at the positive maximum
between 250 and 450 ms. Because the number of trials in Go
and NoGo conditions was not equal (4:1), we selected only one
quarter of the Go trials randomly for further comparison. The
following sites were chosen for statistical analysis: Fz, F1, F2,
F3, F4 (5 frontal sites), FCz, FC1, FC2, FC3, FC4 (5 frontal-central
sites), Cz, C1, C2, C3, C4 (5 central sites), CPz, CP1, CP2, CP3, CP4 (5
central-parietal sites), and Pz, P1, P2, P3, P4 (5 parietal sites). The
frontal and central sites (15 sites) were selected for comparison
in N2. All of the 25 sites were selected for comparison in P3. ERP
amplitudes and latencies were analyzed using repeated measures
ANOVA with electrode sites (frontal/central/parietal) × stimulus
(Go/NoGo) as within-subject factors and group (Internet
addicted/normal) as a between-subjects factor. Post hoc (LSD)
was used when necessary. Bonferroni correction was used when
appropriate.
The reaction time (RT) in Go trials, and the error rate (ER) in
NoGo trials from both groups were subjected to t-tests. There was
no difference between these two groups in Go-RTs (t(1,22) = 0.29,
p > 0.05. IAD, 306.2 ± 30.7; normal, 297.9 ± 30.5). There was no
difference between these two groups in ERs in NoGo condition
(t(1,22) = 0.13, p > 0.05. IAD, 0.088 ± 0.009; normal, 0.090 ± 0.014).
No significant difference was found in behavioral performance
between these two groups.
Fig. 1 shows the ERP waveforms at Fz, Cz, and Pz electrode sites.
Table 1 shows the mean amplitudes and peak latencies in N2 and
P3.
The significant stimulus main effect in the mean amplitude of N2
was larger for NoGo than Go condition in both IAD [F(1,11) = 5.04,
p < 0.05] and normal groups [F(1,11) = 5.18, p < 0.05]. Significant
difference was found between IAD and normal groups in NoGo
condition, the IAD group elicited significant lower N2 mean ampli-
tude than normal group [F(1,22) = 6.92, p < 0.05]. The difference was
largest at the central sites (1.21 ␮V), as compared with frontal sites
(0.76 ␮V) and parietal sites (0.69 ␮V). No significant difference was
found between these two groups in Go condition [F(1,22) = 1.21,
p > 0.05]. The peak latencies in NoGo conditions were significant
longer than Go conditions in both IAD group [F(1,11) = 5.22, p < 0.05]
and normal group [F(1,11) = 4.96, p < 0.05]. However, in N2 peak
latency, group main effect was not found in Go [F(1,22) = 1.35,
p > 0.05] or NoGo conditions [F(1,22) = 2.19, p > 0.05] when com-
pared IAD and normal groups. The interaction of group and stimulus
was not significant in N2 mean amplitude [F(1,22) = 1.41, p > 0.05]
and peak latency [F(1,22) = 1.61, p > 0.05].
The significant main effect of stimulus indicated P3 amplitudes
were larger for the NoGo than the Go stimulus in IAD [F(1,11) = 7.18,
p < 0.05] and normal [F(1,11) = 6.20, p < 0.05] group. Further analysis
between groups showed that IAD group showed significant higher
P3 amplitude than normal group in NoGo items [F(1,22) = 6.43,
p < 0.05]. No significant main effect was found in Go trials between
these two groups [F(1,22) = 1.18, p > 0.05]. In peak latencies of P3,
IAD group elicited significant longer P3 latency than normal group
in NoGo condition [F(1,22) = 4.88, p < 0.05], but no significant dif-
ference was found in Go condition [F(1,22) = 1.21, p > 0.05]. The
140 G. Dong et al. / Neuroscience Letters 485 (2010) 138–142

Fig. 1. The grand-average ERP waveforms at Fz, Cz, and Pz electrode sites in different groups. N2 and P3 components were found in both groups. The IAD group elicited lower
N2 and higher P3 amplitude than normal group in impulse control condition (NoGo trials).
 G. Dong et al. / Neuroscience Letters 485 (2010) 138–142
Table 1
Mean amplitude and peak latencies in Go/NoGo conditions in different groups.
Go, mean amplitude NoGo, mean amplitude
IAD Normal IAD Normal
N2
M 0.87 0.81 1.12 1.43
SD 0.15 0.15 0.25 0.27
P3
M 1.18 1.23 1.92 2.42
SD 0.22 0.24 0.41 0.46
Notes: M, arithmetic mean; SD, standard deviation; IAD, Internet addiction disorder group; Normal, normal group.
interaction of group and stimulus was not significant in P3 mean
amplitude [F(1,22) = 1.87, p > 0.05] and peak latency [F(1,22) = 2.02,
p > 0.05]. The relation between mean amplitude (P3) and the ER
in NoGo condition was 0.053 (p > 0.05) in IAD and 0.048 (p > 0.05)
in normal group. In RTs, the relation between mean amplitude (P3)
and RT in Go conditions was 0.076 (p > 0.05) in IAD group and 0.068
(p > 0.05) in normal group. No significant correlation was found
during these analyses.
In the present study, ERPs were used to investigate the response
inhibition difference between IAD-afflicted and normal students
during a Go/NoGo task, by focusing on the NoGo-N2 and NoGo-
P3 components related to the impulse inhibition. In the behavioral
performances, no significant difference was found between the IAD
and normal groups. This may indicate that behavioral results were
not sensitive enough to allow for measurement of the difference
between the two groups. Our main findings could be summarized
as follows. The mean amplitude was lower in N2, but higher in P3
in NoGo conditions in the IAD group compared with the normal
group. The peak latency was longer in P3 in NoGo conditions in the
IAD group than in the normal group.
All participants (IAD and normal) showed a distinct NoGo-N2
effect, that is, the NoGo stimuli elicited larger N2 amplitude com-
pared with the Go stimuli. The NoGo-N2 effect reported in this
study is consistent with that of previous studies [14,16,20]. How-
ever, the NoGo-N2 in the IAD group was significantly lower than
in the normal group. Findings from previous Go/NoGo studies
support the hypothesis that the NoGo-N2 is driven by inhibi-
tion of a planned response [18]. Researchers also believe that
the NoGo-N2 reflects the conflict monitoring process, and the
increase of NoGo-N2 amplitude could be interpreted as reflecting
higher demands on inhibitory control [22]. The NoGo-N2 amplitude
could reflect the association between amplitude and successful
response inhibition [17]. In summary, the N2 may be used to
detect conflict and the insistence of participants on controlling their
impulses.
In the present study, the IAD group showed lower N2 amplitude
than the normal group, suggesting that their attention and ability
to detect conflict were impaired. The NoGo stimuli elicited signifi-
cantly higher P3 amplitude than the Go stimuli in all participants.
This result can be explained by the characteristics of the present
research task. The number of Go and NoGo trials was in the 4:1
ratio; thus, the NoGo trials are similar to the infrequent targets in
oddball tasks [12].
The IAD group elicited higher P3 amplitude than the nor-
mal group. The posterior P3 is an index of the inhibition of
task-irrelevant information, and representation of later conscious
categorization, decision-making, and premotor response-related
activities [7,8,19]. NoGo-P3 is also believed to be an index of
response inhibition [6,14,28]. Thus, the size of P3 amplitudes in the
present experiment might reflect the degree of cognitive endeav-
ors when the participants successfully inhibited their impulse to
respond. The IAD group elicited higher P3 amplitude than the nor-
mal group. This result may reflect the need for more cognitive
141
Go, peak latency NoGo, peak latency
IAD Normal IAD Normal
168.3 177.9 197.6 203.1
23.1 25.8 33.0 35.4
301.9 304.6 369.8 321.4
50.1 56.6 57.3 56.5
endeavors for participants to successfully inhibit their response
impulses.
The NoGo-P3 latency was longer in IAD-afflicted participants
compared with that of normal subjects. Peak latency is associated
with cognitive efficiency. P3 latency is an indicator of processing
speed [24,26] suggesting that IAD-afflicted students had less effi-
cient information processing function than their normal peers. On
the other hand, the longer P3 amplitude may be related to impaired
impulse control. Evidence from studies on impaired inhibitory abil-
ity shows that PTSD and Parkinson’s disease groups have longer
NoGo-P3 latency compared with control groups [4,27].
In summary, IAD-afflicted participants displayed less efficient
brain function not only with respect to information processing, but
also response inhibition.
Taking all features of N2 and P3 components into considera-
tion, we can comprehensively understand impulse control in the
IAD-afflicted students. N2 may represent the detection of response
conflict [14] or recognition of the need for inhibition [28]. NoGo-
P3 is associated with response evaluation or successful response
inhibition [6]. Peak latency is associated with processing efficiency
during the cognitive processes [24,26]. The IAD-afflicted students
showed a lower activation in detecting response conflict (lower N2
amplitude) than normal students. As a result, they had to engage in
more cognitive endeavors to complete the inhibition task (higher
P3 amplitude). They were less efficient during these processes than
the normal participants (longer P3 peak latency).
Limitations of the present research should be noted. First, all the
participants were right-handed students as is the case in most ERP
studies. Second, all the participants were male students because
few females are addicted to the Internet. Consequently, our findings
only apply to right-handed male individuals.
The present results show that the conflict detection ability of
IAD-afflicted students was impaired as recorded by indexing of
the lower NoGo-N2 mean amplitude. These students had lower
inhibitory ability and slower speed as indexed by higher NoGo-
P3 amplitude and shorter NoGo-P3 latency. The inferior response
inhibition ability of the IAD group might have come from the first
stages of conflict detection to the later stage of response evaluation
or successful response inhibition. This result provides evidence for
the assumption that inhibitory ability is impaired in IAD-afflicted
people.
Acknowledgement
This research was supported by National Science Foundation of
China (30900405).
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