Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder that starts in childhood and frequently persists in adults. Several theories postulate deficits in ADHD that have effects across many executive functions or in more narrowly defined aspects, such as response inhibition. Electrophysiological studies on children, however, indicate that ADHD is not associated with a core deficit of response inhibition, as abnormal inhibitory processing is typically preceded or accompanied by other processing deficits. It is not yet known if this pattern of abnormal processing is evident in adult ADHD. The objective of this paper was to investigate event-related potential indices of preparatory states and subsequent response inhibition processing in adults with ADHD. Two cued continuous performance tasks were presented to 21 adults meeting current criteria for adult ADHD and combined type ADHD in childhood, and 20 controls. The ADHD group exhibited significantly weaker orienting attention to cues, cognitive preparation processes and inhibitory processing. In addition, we observed a strong correlation between the resources allocated to orienting to cues and the strength of the subsequent response strength control processes, suggesting that orienting deficits partly predict and determine response control deficits in ADHD. These findings closely resemble those previously found in children with ADHD, which indicate that there is not a core response inhibition deficit in ADHD. These findings therefore suggest the possibility of developmental stability into adulthood of the underlying abnormal processes in ADHD.

Background: Patients with attention deficit-hyperactivity disorder (ADHD) exhibit difficulties in multiple attentional functions. Although high heritability rates suggest a strong genetic impact, aetiological pathways from genes and environmental factors to the ADHD phenotype are not well understood. Tracking the time course of deviant task processing using event-related electrophysiological brain activity should characterize the impact of familiality on the sequence of cognitive functions from preparation to response control in ADHD.Method: Preparation and response control were assessed using behavioural and electrophysiological parameters of two versions of a cued continuous performance test with varying attentional load in boys with ADHD combined type (n = 97), their non-affected siblings (n = 27) and control children without a family history of ADHD (n = 43).Results: Children with ADHD and non-affected siblings showed more variable performance and made more omission errors than controls. The preparatory Cue-P3 and contingent negative variation (CNV) following cues were reduced in both ADHD children and their non-affected siblings compared with controls. The NoGo-P3 was diminished in ADHD compared with controls whilst non-affected siblings were located intermediate but did not differ from both other groups. No clear familiality effects were found for the Go-P3. Better task performance was further associated with higher CNV and P3 amplitudes.Conclusions: Impairments in performance and electrophysiological parameters reflecting preparatory processes and to some extend also for inhibitory response control, especially under high attentional load, appeared to be familially driven in ADHD and may thus constitute functionally relevant endophenotypes for the disorder.

Inhibitory deficits are often a matter of debate in the pathophysiology of Tourette syndrome (TS). Previous neuropsychological studies on behavioral inhibition revealed equivocal results.

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.