Equally contributing first authors.
A neurophysiological marker of impaired preparation in an 11-year follow-up study of attention-deficit/hyperactivity disorder (ADHD)
Article first published online: 13 JUL 2012
© 2012 The Authors. Journal of Child Psychology and Psychiatry © 2012 Association for Child and Adolescent Mental Health.
Journal of Child Psychology and Psychiatry
Volume 54, Issue 3, pages 260–270, March 2013
How to Cite
Doehnert, M., Brandeis, D., Schneider, G., Drechsler, R. and Steinhausen, H.-C. (2013), A neurophysiological marker of impaired preparation in an 11-year follow-up study of attention-deficit/hyperactivity disorder (ADHD). Journal of Child Psychology and Psychiatry, 54: 260–270. doi: 10.1111/j.1469-7610.2012.02572.x
Conflict of interest statement: All authors reported no biomedical financial interests or potential conflicts of interest.
- Issue published online: 11 FEB 2013
- Article first published online: 13 JUL 2012
- Accepted for publication: 08 May 2012Published online: 13 July 2012
Table S1. Cue P300 - peak latency and amplitude at Pz. Analysis of peak latencies and amplitudes at Pz indicated that latency decreased with development (main effect for time). Reduced amplitudes in the ADHD group were observed (but no notable effect for group, significant post hoc t tests for T2). Control subjects amplitudes peaked at the second assessment, which corresponds to the typical nonlinear P300 development.
Table S2. NoGo P300 - peak latency andamplitude at Cz. Analyses of peak latencies and amplitudes at Czrevealed decreasing peak latencies with development (time maineffect) as well as significant group differences regarding peakamplitude (group main effect). Post hoc t tests showed significant group differences for NoGo P300 amplitude at the first three assessments.
Figure S1. Waveforms of ERPs (CNV, Cue P300,NoGo P300) at all four assessments (T1 – T4), which display group differences between ADHD subjects (red lines) and healthy controls (blue lines). Group differences became non-significant in adulthood except for the CNV.
Figure S2. Cue-P300 (microstate 254-578ms) -topographic maps, and t maps; t maps depict the differences between the different assessments and between both groups (attention-deficit/hyperactivity disorder [ADHD] and controls [CTRL]), respectively. The t-maps characterizing ADHD subjects (ADHD minus CTRL) and those characterizing younger subjects (younger minus older; T1 minus T4) showed roughly opposite polarity. The t-maps characterizing the differences between ADHD subjects and healthy controls showed reduced activity for ADHD subjects in left parietal areas at second and fourth assessment. At Time 1 this ADHD effect was localised in central areas.
Figure S3. NoGo –P300 (microstate254-578ms) - topographic maps, and t maps; t mapsdepict the differences between the different assessments andbetween both groups (attention-deficit/hyperactivity disorder[ADHD] and controls [CTRL]), respectively. The NoGo-P3a topographydeveloped from an “immature” parietal towards the typical central positivity. This central positivity was already present at T1 for the control subjects but not before T3 for the ADHD group. The t maps illustrate that the development of the NoGo P300 are particularly prominent and similar for both groups, with highly significant increases at frontocentral, and decreases at posterior electrodes. The t maps characterizing the ADHD effect showed differences between ADHD and control subjects with age mainly at frontocentral sites that strongly resembles the developmental effects. At the fourth assessment t-maps showed a left lateralisation of this ADHD effect.
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