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

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and in the response aligned epochs the ®rst 70 ms of each epoch were used as pre-stimulus baseline. NoGo trials were de®ned either as `correct' or ìncorrect.' Trials were designated `correct' when either in the EMG trace for the ®nger extension conditions or in the horizontal EOG trace for the eye movement conditions, motor related activity was completely absent. When motoric activity was evident, trials were de®ned as ìncorrect.' In the averaged ERP pro®les for Go and ìncorrect' NoGo trials, trials were included when motoric response latency was within one standard deviation of mean motoric response latency on Go trials. For both movement modalities, mean motoric response latency was obtained by averaging latency values of motoric response activity on Go trials across subjects and across left and right side movement conditions. No latency limits were imposed for `correct' NoGo trials. Statistical analysis focused on ERP components following the imperative Go/NoGo stimulus, including positive component, P3, negative component, N2, and the èrror related negativity', ERN (Gehring et al., 1993). Components N2 and ERN were evident as negative de¯ections on the initial positive going limb of component P3, on `correct' and ìncorrect' NoGo trials, respectively (Fig. 4). For each subject, determination of latency values of ERP components, from the averaged cortical activity recorded at electrode site Cz, was facilitated by superimposed vertical cursor hairlines. Component latencies were measured relative to imperative stimulus (S2) onset. ERP components analyzed were rather narrow. Therefore, component amplitudes were calculated by averaging ERP data samples also within a narrow time interval, subtending 25 ms centred on peak latency (the latency at which maximum amplitude was recorded). Amplitude of component P3 was measured relative to maximum amplitude of the contingent negative variation (CNV) slow waveform (Grey Walter et al., 1964), recorded across the time interval between computer animation onset and imperative stimulus onset. As the CNV maximum was somewhat broader, CNV amplitude was calculated by averaging ERP data samples across a wider time interval, subtending 160 ms centred on peak CNV latency. The broader CNV time interval was selected to improve accuracy of the amplitude estimate. Amplitude values of components N2 and ERN were measured relative to mean ERP amplitude across a 25 ms interval, centred on the latency at which a negative de¯ection appears on the positive going limb of component P3. Latency and amplitude values were evaluated statistically by means of repeated measures ANOVA. For component P3, analysis of latency values included within-subject variables Movement Modality (®nger extension vs. eye movement) and variable Movement Side (right vs. left ®nger extension, rightward vs. leftward eye movement). In addition, variable Go/NoGo (Go trials vs. `correct' NoGo trials) or variable Correct vs. Incorrect (`correct' NoGo trials vs. ìncorrect' NoGo trials) was included to compare latency values of ERP components between Go and `correct' NoGo trials, D. Van 't Ent, P. Apkarian / Clinical Neurophysiology 110 (1999) 1058±1072 1061 or between `correct' and ìncorrect' NoGo trials. Variable Movement Side was omitted for analysis of ERPs averaged across right and left side movement conditions. Latency values of components N2 and ERN, for `correct' and ìncorrect' NoGo trials, were evaluated in a single repeated measures design with within-subject variables N2 vs. ERN (N2 latency vs. ERN latency) and Movement Modality (®nger extension vs. eye movement). For analysis of component amplitudes, similar statistical pro®les were used. Within-subject variable Electrode (sites FCz, Cz, Pz and O 0 z) was added to evaluate mid-line amplitude topography. Bonferroni's correction method was applied to allow for multiple comparisons in the statistical analyses. When applicable, degrees of freedom were adjusted according to Geisser and Greenhouse (1958). In the present study, uncorrected degrees of freedom are reported to facilitate interpretation of the statistical design. 2.4.3. Error size Motoric actions on ìncorrect' NoGo trials were classi®ed as either small or large errors. For ®nger extension, electromyographic (EMG) activity was integrated (time constant: 0.05 s) over a 200 ms time interval starting at the onset of response related EMG activity. Motoric actions were de®ned as small errors when EMG remained below 20% of the median integrated EMG activity for motoric actions on Go trials. Motor responses were classi®ed as large errors when response related EMG exceeded the 20% threshold. For eye movement, saccade amplitude was determined by calculating the average electro-oculographic (EOG) activity over a time interval, subtending from saccade offset to 80 ms following saccade offset. Saccade amplitude was measured relative to the mean EOG activity across the ®rst 500 ms preceding saccade onset. In general, saccadic eye movements on NoGo trials ceased while close to the saccade target; only a few saccades were substantially hypometric. As such, a higher percentage of EOG activity during eye movement Go trials was employed to classify saccades as small or large errors. When EOG amplitude on NoGo trials was below 85% of the median EOG de¯ection on Go trials, saccades were de®ned as small errors. Saccades with amplitude beyond the 85% limit were speci®ed as large errors. Statistical analysis, by means of repeated measures ANOVA, was performed on the amplitude of component ERN for ìncorrect' NoGo trials with small errors and for ìncorrect' NoGo trials with large errors. To facilitate comparison, analysis also included the amplitude of component N2 on `correct' NoGo trials with no errors. Withinsubject variables included Movement Modality (®nger extension vs. eye movement), Error Size (3 levels: `correct' NoGo trials, ìncorrect' NoGo trials with small errors, ìncorrect' NoGo trials with large errors) and Electrode (mid-line electrode sites FCz, Cz and Pz). In addition, averaged ERP pro®les for `correct' NoGo trials were subtracted from the cortical response pro®les recorded for ìncorrect' NoGo trials with small and large
1062 Table 1 Mean motoric response latency (ms) ^ SEM a errors. Mean size of the amplitude difference between `correct and ìncorrect' NoGo trials was calculated across a 40 ms time interval centred on maximum amplitude of the difference waveform. Mean values were measured relative to the average amplitude across a 250 ms interval preceding onset of the amplitude difference. Calculated difference values were evaluated statistically by repeated measures ANOVA, with within-subject variables Movement Modality (®nger extension vs. eye movement), Error Size (large errors vs. small errors) and Electrode (FCz, Cz, Pz). 2.4.4. Stimulus versus response aligned averaging To examine whether component ERN is time-locked more closely to imperative stimulus onset or to onset of motoric response activity, stimulus aligned and motoric response aligned cortical response pro®les, averaged across ìncorrect' NoGo trials, were compared. Peak amplitude values of component ERN in the stimulus and response aligned waveforms at mid-line electrode sites FCz, Cz and Pz were examined by repeated measures ANOVA, with Alignment (stimulus vs. response synchronized averaging), Movement Modality (®nger vs. eye movement) and Electrode as within-subject variables. For additional analysis, separate averages were constructed for ìncorrect' NoGo trials with early and late onset of motoric activity, respectively. It was hypothesized that if component ERN is time-locked more closely to the imperative stimulus, ERN onset and peak latency would be comparable across trials with early and late motoric response onset in the stimulus aligned averages. Component ERN would occur earlier on trials with late onset of motoric activity in the response locked averages. In contrast, if component ERN is time-locked more closely to motoric response onset, the ERN would appear at a comparable latency in the response synchronized averages and would occur earlier on trials with early onset of motoric activity in the stimulus synchronized averages. Motoric response latency was classi®ed as early or late when onset of motoric activity either preceded or followed median motoric response latency. For both movement modalities, median response latency was determined from the set of motoric response latencies measured on ìncorrect' NoGo trials, across subjects and across right and left side movement conditions. Statistical analysis of ERN latency values, by means of repeated measures ANOVA, was performed separately for stimulus and response synchronized averages. Within-subjects variables included Motoric Response D. Van 't Ent, P. Apkarian / Clinical Neurophysiology 110 (1999) 1058±1072 Right ®nger extension Left ®nger extension Saccades rightward Saccades leftward Go 179 ^ 23 167 ^ 29 211 ^ 22 209 ^ 25 Incorrect NoGo 147 ^ 20 139 ^ 28 194 ^ 36 192 ^ 38 a Mean motoric response latencies (^ standard error of the mean) on Go and ìncorrect' NoGo trials for each movement condition. Latency data for motoric activity on Go trials have been adapted from Van `t Ent and Apkarian (1998). Latency (early vs. late motoric response onset) and Movement Modality (®nger vs. eye movement). 2.4.5. Lateralized readiness potential (LRP) Motor related inter-hemispheric amplitude lateralization was assessed by means of the lateralized readiness potential (LRP) measure derived from stimulus synchronized ERPs (De Jong et al., 1988; Gratton et al., 1988). For statistical evaluation of inter-hemispheric amplitude differences in the LRP, 3 contiguous 100 ms time windows were de®ned across a time interval subtending from 100 ms following stimulus offset (t ˆ 100 ms) to 400 ms following stimulus offset (t ˆ 400 ms). Mean LRP values in each individual time window were calculated for every subject and were examined by means of Wilcoxon's test of paired differences. To account for multiple comparisons, signi®cant inter-hemispheric asymmetry was assumed only when Wilcoxon's probability level was below P ˆ 0:01. 3. Results 3.1. Motoric response latency Onset latencies for motoric activity on Go trials and error responses on ìncorrect' NoGo trials, averaged across mean motoric response latencies for each individual subject, are listed in Table 1. Mean motoric response latency in the eye movement tasks was signi®cantly longer than mean response latency in the ®nger extension tasks (variable Movement Modality; F…1; 9† ˆ52:41, P , 0:001). Furthermore, for both movement modalities, reaction times were shorter on ìncorrect' NoGo trials compared with Go trials (variable Go/NoGo: F…1; 9† ˆ18:50, P ˆ 0:002; interaction Go/NoGo by Movement Modality: not signi®cant). No signi®cant differences were found for mean motoric response latency of right compared with left ®nger extensions or for mean response latency of rightward compared with leftward saccades. 3.2. Event related potentials For Go and ìncorrect' NoGo averages, trials were included when motoric response latency was within 170:8 ^ 60:0 ms (latency range: 110.8±230.8 ms) for ®nger movement and within 209:9 ^ 60:2 ms (latency range: 149.7±270.1 ms) for saccadic eye movement (latency intervals are derived from Van `t Ent and Apkarian, 1998). For
Page 1 and 2: Abstract Motoric response inhibitio
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Page 15: 1072 Pfefferbaum A, Ford JM, Weller

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