Journal of Behavioral and Brain Science, 2011, 1, 234-241
doi:10.4236/jbbs.2011.14030 Published Online November 2011 (http://www.SciRP.org/journal/jbbs)
Motor and Nonmotor Components of Event-Brain Potential
in Preparation of Motor Response
Yasunori Kotani1, Yoshimi Ohgami1, Jun-ichiro Arai2, Shigeru Kiryu3, Yusuke Inoue4
1Department of Human Syst em Science , Department of Social Engi neering, Tokyo Instit ute of Technology , Tokyo, Japan
2Technology Innovation Center Development Department, Daikin Industries, Ltd., Tokyo, Japan
3The Institute of Medical Science, The University of Tokyo, Tokyo, Japan
4Department of Diagnostic Radiology, Kitasato University School of Medicine, Kanagawa, Japan
Received August 5, 2011; revised October 13, 2011; acce pt ed October 31, 2011
Abstract
Stimulus-preceding negativity (SPN), readiness potential (RP), and contingent negative variation (CNV)
were recorded to verify the hypothesis that the CNV late wave is the sum of the RP and the SPN. SPN and
RP were elicited using a time-estimation task, and the CNV was recorded using a warned reaction-time task.
A “virtual CNV” was calculated by superimposing the SPN on the RP. Then the real and virtual CNVs were
compared to evaluate the hypothesis. Although an amplitude difference between the real and virtual CNV
late waves was observed at the frontal site, the amplitudes at the central and parietal sites were not different
between the two. These results suggest that the CNV late wave and the SPN might have a common underly-
ing physiological mechanism in the parietal area, and that these potentials might be related to attentional
systems.
Keywords: Contingent Negative Variation, Stimulus-Preceding Negativity
1. Introduction
Contingent negative variation (CNV) is an even-related
brain potential (ERP) that relates to motor preparation and
anticipatory behavior [1]; it can be elicited in a warned re-
action-time paradigm. In such a task, a warning stimulus
is presented preceding a response stimulus, and a partici-
pant has to make a motor response as quickly as possible
after the response stimulus appears. A slow negative shift
can be observed between the warning stimulus and the
response stimulus, and this negative shift is termed the
CNV [1]. The CNV has at least two compon en ts : an ea r ly
wave and a late wave [2]. Although the early wave seems
to be related to the salience and signal value of the
warning stimulus [3], the functional significance of the
late wave is more complicated. After activations in the
primary motor cortex, anterior cingulate cortex, and sup -
plementary motor area (SMA) were confirmed in both a
magnetic field encephalography (MEG) study [4] and a
functional magnetic resonance imaging (fMRI) study [5],
it became evident that a motor preparation process is
involved when a motor response is required after a re-
sponse stimulus. However, how nonmotor processes in-
cluding anticipation contribute to the late wave is un-
clear.
In order to clarify this issue, Damen and Brunia [6]
developed a time estimation task to temporally separate
nonmotor processes from motor preparation. In their task,
a participant has to press a button when she or he thinks
an instructed time, for example 6 seconds, has elapsed. A
few seconds after the button press, a feedback stimulus
conveying information about the correctness of the par-
ticipant’s timing is presented. They found two different
slow potentials in this task [6]. One is the readiness po-
tential [7] preceding the bu tton press, and the other is the
stimulus-preceding negativity (SPN) before the feed-
back stimulus. The amplitude of the RP was largest at the
precentral and postcentral area contralateral to the respond-
ing hand, whereas the SPN showed a right hemisphere
preponderance regardless of which hand was used for re-
sponding. Based on these distributions, they concluded
that the RP reflects motor preparation and the SPN re-
flects stimulus anticipation. After conducting several
studies to confirm the existence of the SPN, they con-
cluded that the CNV late wave is the sum of the RP and
the SPN [6,8,9]. After this theory became better known,

235 Y. KOTANI ET AL.
many researchers investigated SPN to clarify the antici-
pation mechanism [10].
Although Brunia’s [9] hypothesis (that the CNV late
wave is the sum of the RP and the SPN) is intriguing,
there is a countervailing point of view. Employing the
dipole models of RP, SPN, and CNV, Böcker [11] found
that the SPN could be modeled by bilateral frontal di-
poles, whereas the CNV did not contain such dipoles. Re-
garding the components of the SPN, van Boxtel and Böc-
ker [12] suggested that there could be two components
when the SPN is recorded preceding a feedback stimulus.
One is a frontal dominant component that relates to an-
ticipation of the feedback stimulus process, and the other
is a parietal dominant component related to perceptual
anticipation. Concerning the frontal dominant SPN, sev-
eral studies investigated the effect of emotion on the SPN,
and showed that such an effect was mainly found at the
frontal area [13-15]. For instance, Ohgami et al. [13] re-
vealed that a monetary reward increased the left frontal
SPN, whereas a monetary punishment did not affect the
SPN amplitude. Kotani et al. [15] also suggests that the
SPN reflects emotional anticipation.
On the other hand, the parietal-dominant component is
affected by the modality of the stimulus that is antici-
pated [14,16]. The SPN in the parietal area increased
mor e wh en it prec ed ed visua l feedb ack s timu li than wh en it
preceded auditory feedback stimuli. This result indicates
that the parietal component reflects perceptual anticipa-
tion. Perceptual anticipation is a preparatory process, based
on the modality of anticipated stimulus. The perceptual
anticipation could be also involved in the CNV paradigm
because subjects have to prepare for the input of respon-
se stimulus. In addition, recent fMRI studies of CNV [5]
and SPN [17,18]. have indicated that the inferior parietal
lobule was activated in both CNV and SPN tasks. These
studies suggest that the CNV and the SPN have a com-
mon neural mechanism in the parietal area, that is involve d
in attention process. Taking these into account, one can
conclude tentatively that the CNV late wave is the sum
of the RP and the parietal-dominant SPN, although there
might be some functional differences at the frontal area.
One of the methods used to investigate CNV late wav e
components is the composition of their waveforms. It is
possible to virtually compose the CNV late wave (the vir-
tual CNV) by superimposing the pre-feedback SPN on
the RP. On the other hand, the real CNV can be elicited
in a warned reaction-time paradigm. If the virtual CNV
is compared to the real CNV, it might be possible to ver-
ify the hypothesis that the CNV late wave is the sum of
the RP and the parietal dominant SPN that reflects per-
ceptual anticipation .
A method by which two different waves are combined
to compare the sum to an actual waveform was used by
Rohrbaugh, Syndulko, and Lindsley [19]. They recorded
two different event-related potentials (ERPs). One was the
ERP elicited by acoustic tones; the other was the ERP
elicited by motor responses. They combined these ERPs
in order to compare the co mbination with the actua l CNV
that was recorded in the warned reaction-time task. In-
deed, they verified this hypothesis. Therefore, this wave-
combination method would probably be useful to invest-
tigate various CNV components.
In the present study, the real CNV and the virtual CNV
were compared to confirm the hypothesis that the CNV
late wave is the sum of the RP and the parietal dominant
SPN. The real CNV was obtained using a warned reac-
tion-time task, and the virtual CNV was obtained by su-
perimposing the SPN on the RP in a time-estimation task.
If the hypothesis is correct, there should be no amplitude
difference between the real and the virtual CNV late waves
at the parietal area. On the other hand, at the frontal area,
there might be some amplitude differences because the
frontal SPN can be affected by emotional properties of
the stimuli; dipo le models of CNV and SPN have sh own
such a difference in the frontal area [12].
2. Methods
2.1. Participants
Fifteen right-handed males began this experiment. Data
from three participants was discarded because of an in-
sufficient number of trials available for analysis. The re-
maining participants were 12 males with ages ranging
from 20 to 25 (mean age: 22.8 years). Hand preferences
were assessed using an abridged version of the Edin-
burgh Inventory [20]. All participants had normal hear-
ing and no history of head injury. They were paid 1000
yen/hr (US $8/hr). The experimental procedure was ap-
proved by the Research Ethics Committees of the De-
partment of Human System Science at Tokyo Institu te of
Technology, and written informed consent was obtained
from all of the participants.
2.2. Apparatus
After providing informed consent and receiving an over-
view of the experimental procedures, participants were
seated in a comfortable chair in a sound attenuating and
electrically shielded room under faint lighting. They were
supervised through a video camera in order to check body
movements.
2.3. Warned Reaction-Time Task
As mentioned above, we used two tasks in the present

Y. KOTANI ET AL.
236
study to study the compostion of the CNV late wave. In
the warned reaction-time task, an acoustic tone was pre-
sented three seconds after a light-emitting diode (LED)
was switched on. The LED served as a warning stimulus.
A 15 × 8 cm panel containing five LEDs was placed on a
fixed tripod 1.5 m in front of the participant. The five 2
mm red LEDs were arranged in a plus-sign pattern (2 × 2
cm) just below eye level. A vertical bar (formed by illu-
minating three of the LEDs) served as the warning stimu-
lus; its duration was 200 ms. The central LED served as
an eye fixation point and was illumina ted throughout the
entire block of trials.
The response stimulus for a single trial consisted of
either a low (500 Hz) or high (1000 Hz) computer-gen-
erated acoustic tone (duration 100 ms, 70 dB(A)). A
speaker located 1 m behind the participan t presented this
response stimulus. Participants were instructed to press a
button in response to the high tone, but to refrain from
responding to the low tone. They were told that the high
tone would be presente d in 50% of the trials.
2.4. Time Estimation Task
In the time estimation task, the offset of the visual stimu-
lus indicated to participants when to start time estimation.
The LEDs acted so as to instruct participants which length
of time should be estimated. When a “minus-sign” was
presented, the time interval between offset of the LED
and the right index finger movement was supposed to be
as close as possible to 6 s; the “vertical-bar” corresponded
to an interval of 8 s, and the “plus-sign” indicated 10 s.
In each case, the length of this instruction stimulus was 2
s, which was long enough to be detected even if the p ar-
ticipant blinked. Particip ants were asked to push the but-
ton when the instructed time had elapsed. Three seconds
after the participant pressed the response button, a tone
conveying feedback information was presented (duration
100 ms, 70 dB(A)). A one-thousand-hertz high tone was
presented when the response reflected a correct time es-
timate, and a low tone (500 Hz) indicated an incorrect
estimate. The width of the time interval considered to be
correct was individually adjusted to obtain about 40%
correct trials.
The movement in the warned reaction-time task reflects a
go/no-go paradigm, whereas the movement in the time
estimation task is a self-paced voluntary movement. Even
so, Cavina-Pratesi et al. [21] revealed that there is no sig-
nificant difference of activation in the motor related cor-
tical area between the two movement paradigms.
In both tasks, the inter-trial interval (from offset of the
acoustic stimulus to onset of the visual stimulus) varied
between 6 and 10 s in steps of 1 sec.
2.5. Procedure
To practice the task and to learn eye movement control,
subjects participated in a training session at least one day
before the experimental session. Participants received about
half of the trials in each condition in the training session.
To reduce contamination of the EEG by eye movement
and blinking, participants were instructed to fix their eyes
on the central LED of the panel from 3 s preceding until
4 s following the button press in th e ti me-estimation task ,
and from 1 s preceding the warning stimulus until 1 s
following the response stimulus in the warned reaction-
time task.
In the experimental session, each task consisted of 2
blocks of 36 trials each. Thus, a complete record consisted
of 4 blocks (2 conditions × 2 blocks) of 36 trials. The or-
der of the experimental tasks was counterbalanced be-
tween partic ipants. In every task, each block was followed
by a rest of 2 to 3 minutes; between the tasks a longer
break was allowed .
In the warned reaction-time task, participants received
feedback about their performance after each block of 36
trials. In the time-estimation task, participants were in-
structed to flex their right index finger rapidly, and w ere
also requested to refrain from coun ting or any other rhy-
th mic activity during time estimation. Although they were
not informed of the actual target length until the experi-
ment was finished, participants acquired the target leng th
during the training session.
In both tasks, participan ts were encouraged to produ ce
as many correct estimates or responses as possible, and
instructed to produce the same kind of finger movement
throughout. At the end of each block, they were informed
of their percentage of correct responses.
2.6. Physiological Recording
An electroencephalogram (EEG) was recorded using Ag-
AgCl electrodes (8 mm) located on the scalp at F3, F4,
C3, C4, P3, and P4, placed according to the international
10 - 20 system with the mastoids reference. The number of
EEG electrodes was restricted to these 6 locations since
the impedances of the electrodes were carefully main-
tained at less than 2 kohm to precisely record slow po-
tentials without contamination. Two Ag-AgCl electrodes
(4 mm) were used to record the electro-oculogram (EOG).
One was fixed directly above, and the other laterally be-
low, the left eye. An electromyogram (EMG) was recorded
from the dorsal interosseus I muscle of the right hand by
two 4 mm Ag-AgCl electrodes 1 cm apart. The EMG was
amplified (5.3 - 1000 Hz), full-wave rectified, low-pass
filtered at 50 Hz, and digitized at 100 Hz. All EEG and
EOG signals were amplified ( time constan t 10 s), low-pa ss

237 Y. KOTANI ET AL.
filtered at 30 Hz (Butterworth, 6 dB per octave roll-off)
and digitized on line at 100 Hz. Stimulus control and mea-
surement of performance data were managed by a com-
puter. All signals were segmented from 2.5 s preceding
until 4 s following switch closure by a second computer
and a 12-bit A/D converter.
2.7. Data Analysis
Only trials fulfilling the following criteria were accepted
for averaging: 1) the change in EEG and EOG ampli-
tudes did not exceed 60 µV; 2) obvious body movements
were not observed through the video camera; 3) the EMG
production was not extremely large or small compared
with other trials; 4) the produced time estimation was not
less than 3 s in the time-estimation task, and the reac-
tion time was not longer than 1 s in the warned reaction-
time task. The data of each participant with at least 30
acceptable trials in each task were analyzed. We employed
the strictest 60 µV criteria of EEG and EOG for averag-
ing [22,23] to prevent EEG contamination. In the warned
reaction-time task, the average during the 1 s period be-
fore the warning stimulus was used as the baseline. In the
time-estimation task, the mean amplitude from 2.5 s to 1.75
s preceding the button press was used as the baseline.
2.8. Real and Virtual CNV Late Waves
To compose the virtual CNV from the sum of the RP and
the SPN in the time-estimation task, the averaged EEG
from 2500 ms before the onset of the feedback stimulus
to 500 ms after the onset was superimposed on the aver-
aged EEG during the interval from 2500 ms before to
500 ms after the button press. Because there was no re-
sponse stimulus in the time estimation task, the onset
time of the feedback stimulus was defined as the time of
the virtual response stimulus for the virtual CNV. The
late wave of the real CNV was calculated as the mean
amplitude of the EEG in the interval of 300 ms before
the response stimulus. The late wave of the virtual CNV
was likewise the mean amplitude of the EEG in the in-
terval of 300 ms before the virtual response stimulus. To
examine whether there is a difference between the real
and the virtual CNV, the CNV late waves were subjected
to a repeated measures analysis of variance (ANOVA)
with CNV type (Real, Virtual), Hemisphere (Left, Right),
and Electrode (Frontal, Central, Parietal) as factors.
In order to investigate whether the early wave over-
lapped the late wave, the mean amplitudes of every 500
ms interval from the warning stimulus to the response
stimulus were calculated. There were five time windows:
from 501 ms to 1000 ms after the warning stimulus (ter-
med the “1000 ms window”), from 1001 ms to 1500 ms
(the 1500 ms window), from 1501 ms to 2000 ms (the 2000
ms window), from 2001 ms to 2500 ms (the 2500 ms win-
dow), and from 2501 ms to 3000 ms (the 3000 ms win-
dow). The mean CNV amplitudes in each time window
were subjected to a repeated measures ANOVA with CNV
type (Real, Virtual), Hemisphere (Left, Right), Electrode
(Frontal, Central, Parietal), and Window (1000 ms win-
dow, 1500 ms window, 2000 ms window, 2500 ms win-
dow, 3000 ms window) as factors.
When an interaction of CNV type by electrode posi-
tion was significant, a normalization procedure [24] was
conducted for testing interactions. Follow-up analyses were
conducted, where appropriate, using univariate ANOVAs
and paired-sample t tests. Greenhouse-Geisser and Bon-
ferroni corrections were applied when appropr i ate.
In the time est imation task, a virtual EOG was al so cal-
culated, by superimposing the EOG preceding the feed-
back stimulus upon the EOG before the button press. The
mean amplitudes of the virtual EOG and the real EOG
(in the 300 ms interval before the warning stimulus) were
subjected to a repeated measures ANOVA with CNV
type (Real, Virtual) as a factor in order to estimate the
effect of EOG amplitude on CNV amplitude.
All statistical analyses were conducted at a significance
level of 5%.
3. Results
3.1. Task Performance
In the warned reaction-time task, the mean reaction time
was 308.6 ± 68.5 (S.D.) ms, and the mean correct ratio
for the warned reaction was 97.2% ± 2.6%. In the time
estimation task, the averaged percentage of correct time
estimation was 52.7% ± 12.7%. The averaged widths of
(time-interval defined) accurate time estimation were 641
± 300 ms for 6 s, 825 ± 408 ms for 8 s, and 1108 ± 742
ms for 10 s.
3.2. Slow Potentials
Figure 1 shows the grand averag es of the slow poten tials
in the warned reaction-time task, and in the time-estima-
tion task. CNV was indeed elicited between the warning
stimulus and the response stimulus, and the RP and the
SPN can be clearly observed before the button press (BP)
and feedback stimuli (FB), respectively.
3.3. The Real and Virtual CNV Late Wave
Recall that the virtual CNV late wave was calculated from
the SPN and the RP, and the real CNV late wave was
actually recorded in the warned reaction-time task. The

Y. KOTANI ET AL.
238
Figure 1. Grand averaged waveforms of CNV in the warned reaction-time task, and SPN and RP in the time estimation task.
WS = warning stimulus; RS = response stimulus; BP = button press; FB = feedback stimulus.
grand averaged waveforms of the real and virtual CNV
late waves are presented in Figure 2. Analysis of the
CNV late wave showed that the main effect of CNV type
was not significant, F(1, 11) = 2.30. However, the analy-
sis revealed significant interactions of CNV Type × Elec-
trode, F(2, 22) = 4.19,
 = 0.73, p = 0.04, and CNV Type
× Electrode × Hemisphere, F(2, 22)=4.62,
 = 0.75, p =
0.03. The normalization procedur e [24] conf irmed th e same
si g n ifican t interaction s. The fo llow-up un ivariate ANOVAs
for the CNV Type × Electrode interaction showed that
the mean amplitude of the real CNV late wave at the
frontal site was significantly larger than that of the vir-
tual CNV late wave, F(1, 11) = 5.10, p = 0.04, whereas
there were no significant differences between the real
and virtual CNV late waves at the central, F(1, 11) =
2.18, and the parietal, F(1, 11) = 0.52, sites. Regarding
the interaction of CNV Type × Electrode × Hemisphere,
the simple interaction analysis and follow-up univariate
ANOVAs revealed that the real CNV at F3 was signifi-
cantly larger than the virtual CNV at F3, F(1, 11) = 6.22,
p = 0.03. At the right frontal area, there was a strong
tendency for the real CNV at F4 to be larger than the
virtual CNV at F4, F(1, 11) = 3.73, p = 0.08 (Figure 3).
The EOG amplitude difference between the real CNV
(2.97 µV) and the virtual CNV (7.16 µV) was not statis-
tically significant, F(1, 11) = 2. 41. Figure 2. Grand averaged waveforms of the real and virtual
CNV late waves. RS = response stimulus press.

239 Y. KOTANI ET AL.
Figure 3. Mean amplitudes and standard errors of the real
CNV late wave and the virtual CNV late wave at the left
hemisphere and the right hemisphere as a function of elec-
trode site.
The ANOVA performed on the CNV amplitude in each
time window revealed a significant interaction of CNV
type × Electrode × Window, F(8, 88) = 5.58,
 = 0.32, p
= 0.005, in addition to main ef f ects of Electrod e, F(2 , 22)
= 6.28,
 = 0.63, p = 0.02, and Window, F(4, 44) = 37.14,
 = 0.37, p = 0.0001. Th e interactio n of Electrode × Win-
dow was also statistically significant, F(8, 88) = 20.91,
 = 0.32, p = 0.0001. The results of follow-up ANOVAs
of CNV type × Electrode × Window are presented in
Table 1. Table 1 shows that the main effect of Electrode
reached statistical significance in the 2001 - 2500 ms time
window, whereas the effect of CNV type did not show
any statistically significant differences between the real
and virtual CNVs throughout the time course. Concern-
ing the interaction of CNV type × Electrode, statistically
Table 1. Summary of follow-up ANOVAs for the interaction
of CNV type × Electrode × Window on the mean CNV ampli-
tudes from 501 ms to 3000 ms after the warning stimulus.
501 -1000
ms 1001 -1500 ms 1501 - 2000 ms 2001 - 2500 ms 2501 -3000 ms
F =8.07F = 1.87F = 4.04 F = 6.85F = 17.32
Electrode
(E) p = 0.008n. s. n. s. p = 0.01 p = 0.0001
F = 0.94F = 2.94F = 3.15 F = 2.35F = 2.67 Type
(T) n. s. n. s. n. s. n. s. n. s.
F = 2.19F = 2.62F = 0.45 F = 0.63F = 3.89
T × En. s. n. s. n. s. n. s. p = 0.05
Note: T × E = CNV type × Electrode; n. s. = not significant.
significant interactions were observed in the 2501-3000
ms time window, F(2, 22) = 3.89,
 = 0.74, p = 0.05.
Results of the 2501 - 3000 ms ti me window were almost
identical to the results of the CNV late wave analysis on
the mean amplitude in the 300 ms interval before the re-
sponse stimulus. These results suggest that the observed
difference in the 300 ms interval before the response sti-
mulus is not due to the effect of the early wave, because
the significant interaction of CNV type × Electrode was
found only in the 2501 - 3000 ms time window.
4. Discussion
This study investigated the hypothesis that the CNV late
wave is the sum of the RP and SPN in a straightforward
manner. The actual CNV was recorded in the w arned reac-
tion-time task, and the virtual CNV was composed by su-
perimposing the RP on the SPN in accord with Brunia’s
hypothesis [9]. It is evident that the real CNV late wave
contains components related to motor preparation, becau-
se participants were requested to produce motor reactions.
In addition to su ch motor-related components , there shoul d
be components reflecting anticipation of the appearance
of the response stimulus. The lack of any significant am-
plitude difference at the parietal area between the CNV
types suggests that the CNV late wave includes a com-
ponent sharing its common underlying neural substrates
with the SPN. Regarding physiological sources of the
CNV, in an fMRI experiment, Nagai, Critchley, Feather-
stone, Fenwick, Trimble, and Dolan [5] found activation s
in the inferior parietal lobule and occipitoparietal junc-
tion in a CNV paradigm. In fMRI studies investigating
the physiological sources of SPN [17,18], activations in
the bilateral inferior parietal lobule as well as the visual
cortex were also found. Recent functional imaging studies
revealed that the inferior parietal lobule—especially the
temporoparietal junction—is involved in the ventral at-
tention system [25]. Different from the dorsal attention

Y. KOTANI ET AL.
240
system that is engaged in goal orienting and voluntary
attentional orientation, the ventral attention system is re-
lated to processing salient stimuli and involuntary atten-
tion orientation. Regarding the ventral attention system,
Ecker et al. [26] showed that the dorsal attention system
is modulated by the anterior insular cortex that belongs
to the ventral attention system. Intriguingly, fMRI stud-
ies of both the CNV [5] and the SPN [17] found activa-
tions in the insula cortex, suggesting that both the dorsal
and the ventral attention systems could contribute to the
CNV late waves. Taking these into account, the CNV and
the SPN might have common neural substrates in the pa-
rietal regions that would relate to the ventral attention
system interacting with the dorsal attention system.
Although the real and the virtual CNVs were not dif-
ferent at the central and parietal areas, an amplitude dif-
ference was found at the frontal site: The real CNV late
wave at the frontal area was larger than that of the virtual
CNV. One possible reason for the observed amplitude
difference at the frontal area is EOG amplitudes. The EOG
might affect EEG amplitudes, especially in the frontal area.
However, statistical analysis of EOG amplitudes of the
real and the virtual CNVs rev ealed that there was no EOG
amplitude difference between them. Furthermore, the elec-
trode impedances were strictly controlled (keeping them
less than 2 kohms), and the trials where EEG or EOG
amplitudes exceeded the 60 µV criterion were rejected
for EEG averaging. Therefore, EOG amplitude effects or
other artifacts of frontal ERP amplitude should have been
negligible.
Another possible reason for the difference in the fron-
tal area could be activation of medial and superior frontal
areas in the CNV task. Gómez, Flores, and Ledesma [27]
estimated physiological sources of the CNV using low-
resolution brain electromagnetic tomography (LORETA),
and found activations in the medial and superior frontal
areas in addition to fronto-parietal lateral areas and ex-
trastriate visual cortex. Th ey concluded that activation of
fronto-parietal networks involved in endogenous atten-
tional effort is a main contr ibutor to th e CNV. This notion
is in agreement with fMRI findings that activities in the
bilateral thalamus, anterior cingulate, and supplementary
motor cortex were modulated by CNV amplitude [5].
Regarding frontal activations in the time estimation
task, Ohgami et al. [13] calculated topography maps of
SPN using high density electrodes, and found that SPN
showed more activation at fronto-temporal areas than at
fronto-medial areas. Furthermore, they found that the fron-
tal SPN was affected by monetary reward, suggesting that
the frontal SPN is more responsive to emotional antici-
pation than perceptual anticipation. The fact that there is
a frontal amplitude difference between the real and the
virtual CNVs suggests that the SPN and the CNV have
different neural substrates in the frontal area. As Gómez
et al. [27] suggested, the CNV could contain the medial
and superior frontal activations that are related to the
fronto-parietal attention network. On the other hand, the
SPN involves more lateral frontal activation that is re-
lated to processing emotional and salient stimuli. These
functional differences in the frontal area between the
CNV and the SPN could be related to the frontal ampli-
tude difference between the real and the virtual CNVs.
5. Conclusions
In the present study, the real and virtual CNVs were com-
pared to verify the hypothesis that the CNV late wave is
the sum of the RP and the SPN. The finding that no am-
plitude difference was found at the central and parietal
areas suggests that the CNV and the SPN could share
common neural substrates pertaining to attention systems.
At the frontal area, the real CNV showed a larger ampli-
tude than the virtual CNV, probably due to the medial and
superior frontal activations related to the fronto-parietal
attenti o n ne t work.
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