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.
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.
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.
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.
