Motoric response inhibition in finger movement and saccadic eye ...

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Fig. 5. Peak amplitude values, at mid-line electrode sites FCz, Cz, Pz and
O 0 z, of ERP components P3 and N2/ERN, following the imperative Go/
NoGo stimulus (S2). Left panels depict ®nger movement, right panels
depict eye movement. Amplitude values also are listed, with standard
deviations, in Table 2. Peak amplitude of component P3 on Go trials
(continuous lines) and `correct' NoGo trials (dashed lines), for each individual
movement condition are depicted (top). Filled and open symbols
represent right and left side movement conditions, respectively. Amplitude
of component P3, at scalp sites FCz and Cz, is enhanced on `correct' NoGo
trials compared with Go trials. The enhancement of P3 amplitude is
observed for both movement modalities. Middle and bottom panels depict
peak amplitude of components N2/ERN and P3 on `correct' and `incorrect'
NoGo trials, determined from ERPs averaged across right and left side
movement conditions. For both movement modalities, ERN amplitude on
`incorrect' NoGo trials (middle; open circles) is enhanced compared with
N2 amplitude on `correct' NoGo trials (middle; ®lled circles), at frontalcentral
electrode sites FCz and Cz. Amplitude of positivity P3 (bottom) is
enhanced on `correct' NoGo trials (®lled symbols) compared with `incorrect'
NoGo trials (open symbols), also primarily at scalp sites FCz and Cz.
Go trials (symbols connected by solid lines) and `correct'
NoGo trials (symbols connected by dashed lines), for each
movement condition, are depicted in the top left and right of
Fig. 5. Corresponding amplitude data are also listed, with
standard deviations, in Table 2 (left). Statistical analysis
showed that the amplitude of component P3 was enhanced
on `correct' NoGo trials compared with Go trials (variable
Go/NoGo: F…1; 9† ˆ12:04, P ˆ 0:014). A signi®cant Go/
NoGo by Electrode interaction (F…3; 27† ˆ39:30,
D. Van 't Ent, P. Apkarian / Clinical Neurophysiology 110 (1999) 1058±1072
P , 0:001) indicated that the increase in P3 amplitude
was observed primarily at frontal-central electrode sites,
FCz and Cz. Interactions Go/NoGo by Movement Modality
and Go/NoGo by Movement Side were non-signi®cant.
Further, no inter- or intra-modality differences in P3 amplitude
were found, neither between ®nger extension and
saccadic eye movement, between right and left ®nger extension
nor between right- and leftward saccades (variables
Movement Modality, Movement Side and their interaction:
non-signi®cant). A signi®cant Go/NoGo by Movement
Modality by Movement Side interaction was found
(F…1; 9† ˆ7:51, P ˆ 0.046). The latter interaction is
explained by the fact that on `correct' NoGo trials for eye
movement, component P3 is slightly enhanced on rightward
compared to leftward saccades (Fig. 5: top right).
Peak latency values of component P3 are also listed in
Table 2 (left). P3 latency was prolonged on `correct' NoGo
trials compared with Go trials (variable Go/NoGo:
F…1; 9† ˆ224:85, P , 0:001). A signi®cant main effect
for variable Movement Modality (F…1; 9† ˆ13:08,
P ˆ 0:012) also indicated that P3 latency was longer for
eye movement, compared with ®nger movement. The interaction
Go/NoGo by Movement Modality was not signi®cant.
P3 latency was comparable for right and left ®nger
extension as well as for right- and leftward saccades (variable
Movement Side and interactions with variable Movement
Side: not signi®cant).
3.2.2. `Correct'/`incorrect' NoGo trials
As the number of `incorrect' NoGo trials was relatively
small, for subsequent analysis, ERPs were averaged across
right and left side movement conditions. The averaged cortical
activity, recorded at scalp site FCz, on `incorrect' NoGo
trials is also depicted in Fig. 4. For ®nger extension as well
as saccadic eye movement, a negative component labelled
ERN, is evident at a similar latency as observed for component
N2 on `correct' NoGo trials. Scalp distributions of
components ERN and N2 also appeared comparable.
Components N2 / ERN: Peak amplitude values of component
N2 on `correct' NoGo trials and component ERN on
`incorrect' NoGo trials are depicted in Fig. 5 (middle left
and right) and in the upper right of Table 2. Amplitude data
are displayed for mid-line electrode sites FCz, Cz and Pz;
components N2 and ERN could not be identi®ed at occipital
sites. In the statistical analysis, a signi®cant main effect for
variable Electrode was found (F…2; 18† ˆ27:64,
P , 0:001). Analysis by means of univariate F-tests indicated
that N2 and ERN amplitude values were enhanced at
frontal-central electrode sites FCz and Cz, compared with
parietal site Pz (FCz/Cz vs. Pz: F…1; 9† ˆ31:02,
P , 0:001). Peak amplitudes at electrode sites FCz and
Cz were not signi®cantly different. Amplitude of component
ERN was enhanced compared with N2 amplitude (variable
N2 vs. ERN: F…1; 9† ˆ26:01, P ˆ 0:001), primarily at frontal-central
electrode sites (N2 vs. ERN by Electrode interaction:
F…2; 18† ˆ29:69, P , 0:001). N2 and ERN