Response inhibition deficits in externalizing child psychiatric disorders: an ERP-study with the Stop-task

Abstract

Background: Evidence from behavioural studies suggests that impaired motor response inhibition may be common to several externalizing child psychiatric disorders, although it has been proposed to be the core-deficit in AD/HD. Since similar overt behaviour may be accompanied by different covert brain activity, the aim of this study was to investigate both brain-electric-activity and performance measures in three groups of children with externalizing child psychiatric disorders and a group of normal controls.

Methods: A Stop-task was used to measure specific aspects of response inhibition in 10 children with attention-deficit hyperactivity disorder (AD/HD), 8 children with oppositional defiant disorder/conduct disorder (ODD/CD), 11 children with comorbid AD/HD+ODD/CD and 11 normal controls. All children were between 8 and 14 years old. Event-related potentials and behavioural responses were recorded. An initial go-signal related microstate, a subsequent Stop-signal related N200, and performance measures were analyzed using ANCOVA with age as covariate.

Results: Groups did not differ in accuracy or reaction time to the Go-stimuli. However, all clinical groups displayed reduced map strength in a microstate related to initial processing of the Go-stimulus compared to normal controls, whereas topography did not differ. Concerning motor response inhibition, the AD/HD-only and the ODD/CD-only groups displayed slower Stop-signal reaction times (SSRT) and Stop-failure reaction time compared to normal controls. In children with comorbid AD/HD+ODD/CD, Stop-failure reaction-time was longer than in controls, but their SSRT was not slowed. Moreover, SSRT in AD/HD+ODD/CD was faster than in AD/HD-only or ODD/CD-only. The AD/HD-only and ODD/CD-only groups displayed reduced Stop-N200 mean amplitude over right-frontal electrodes. This effect reached only a trend for comorbid AD/HD+ODD/CD.

Conclusion: Following similar attenuations in initial processing of the Go-signal in all clinical groups compared to controls, distinct Stop-signal related deficits became evident in the clinical groups. Both children with AD/HD and ODD/CD showed deficits in behavioural response-inhibition accompanied by decreased central conflict signalling or inhibition processes. Neither behavioural nor neural markers of inhibitory deficits as found in AD/HD-only and ODD/CD-only were additive. Instead, children with comorbid AD/HD+ODD/CD showed similar or even less prominent inhibition deficits than the other clinical groups. Hence, the AD/HD+ODD/CD-group may represent a separate clinical entity.

Figure 1

Mean Amplitudes in the region of interest. Mean amplitudes in the ROI for correct Go-trials and successful Stops. Normal controls (black), AD/HD (red), AD/HD+ODD/CD (green) and ODD/CD (blue).

Figure 2

ERPs for correct Go-trials. Grand-average waveshapes from the region of interest (F4/F8), and spline-interpolated maps for correct Go-trials for normal controls (black), AD/HD (red), AD/HD+ODD/CD (green) and ODD/CD (blue). There were no group-differences and no negative peaks in the region and time window of interest.

Figure 3

ERPs for successful Stop-trials. Grand-average waves in the region of interest and spline-interpolated maps for successful Stop-trials for normal controls (black), AD/HD (red), AD/HD+ODD/CD (green) and ODD/CD (blue). Only normal control children display a negative peak approximately 210 ms after onset of the Stop-signal.

Figure 4

Difference ERPs (successful Stop minus correct Go). Difference waves and spline-interpolated difference maps between event-related potential grand means of successful Stop-correct Go-trials in the region of interest for normal controls (black), AD/HD (red), AD/HD+ODD/CD (green) and ODD/CD (blue). A clear Stop-signal N200 is present only for normal controls.

Figure 5

Microstate estimation according to GFP and Diss. Adaptive segmentation of the total groups grand mean from correct Go (top) and successful Stop (bottom). Microstate boarders were determined by relative minima of GFP (black) together with relative maxima in Diss (red, for better scaling multiplicated with 10) Correct Go-trials revealed five microstates (76–196 ms, 200–272 ms, 276–412 ms, 416–504 ms, 508–640 ms), successful Stops six microstates (76–196 ms, 200–272 ms, 276–428 ms, 432–504 ms, 508–592 ms, 596–724 ms).

Figure 6

Microstate-maps and t-maps for correct Go and successful Stop-trials. Spline-interpolated microstate-maps for normal controls (C), children with AD/HD (A), ODD/CD (O) and AD/HD+ODD/CD (AO) and additional exploratory t-maps with comparisons of clinical groups vs. controls. Unadjusted two-tailed significance-level is reached at t_{(17 to 21)} > 1.7 p < .05.