The lack of consensus in the literature as to whether children with ADHD or autism have sustained attention and/or response inhibition deficits may reflect differences in task characteristics. By manipulating the predictability of stimulus presentations in the current study, dissociation in error and RT performance was noted between children with ADHD, HFA and controls. The children with ADHD demonstrated clear deficits in response inhibition and sustained attention, as measured by the number of commission and omission errors, the S.D. in RT and the fast, moment-to-moment variability in RT. In addition, they demonstrated waning performance over the course of the task, suggestive of deficits in arousal levels. The children with HFA, in contrast, performed normally on every measure of the SARTs except for the large number of commission errors made on the Random SART. This suggests that children with HFA have intact sustained attention but deficient response inhibition. Since sustained attention is known to be sub-served by fronto-parietal networks of the right-hemisphere (Coull et al., 1998, 1996; Pardo et al., 1991
), as has been demonstrated specifically in imaging studies using the present SART paradigm (Fassbender et al., 2004; O’Connor et al., 2004
), our behavioural data is suggestive of greater dysfunction within these circuits in ADHD than in autism.
The children with ADHD made a greater number of commission errors compared with the children with HFA and control children on the Fixed SART, suggesting sustained attention deficits. In contrast, the HFA group performed comparably with controls, possibly by making use of the externally cued, regular and predictable pattern of the Fixed SART. It is suggested that the children with HFA made special use of the regularly recurring sequence of digits leading up to the no-go “3”, in a systematic way, possibly by utilising compensatory cognitive mechanisms. Schmitz et al. (2006)
recently reported that adults with autism demonstrated normal behavioural performance on executive function tasks, but significantly increased brain activation in the frontal, insular and parietal brain regions. The recruitment of additional areas of the brain to aid in task performance may be occurring in this group of children with HFA, possibly through the use of the external stimuli provided by the Fixed SART.
With the unpredictable stimulus presentation of the Random SART, the children with HFA made as many commission errors as the ADHD group. Indeed, the similarity in the number of commission errors made by the two groups was striking. The nature of response inhibition deficits in participants with HFA appears to be task-dependent. The children with HFA may be demonstrating a response inhibition deficit when external cues are unavailable for use, as the Random SART has a greater response inhibition component, when compared with the Fixed SART (Fassbender et al., 2004
). Response inhibition deficits have previously been shown in children with HFA, particularly if the task tests prepotent inhibition, such as when an alternative response is needed to the primed response. Examples include the circle-drawing task (Geurts et al., 2004
), the oculomotor anti-saccade task (Luna, Doll, Hegedus, Minshew, & Sweeney, 2007
), the oculomotor delayed-response task (Minshew, Luna, & Sweeney, 1999
) and the Go/No-Go task (Ozonoff & McEvoy, 1994
). Children with HFA may not necessarily show deficits in a non-primed response inhibition task, such as the Stroop (Goldberg et al., 2005
) and the visually guided saccade task (Minshew et al., 1999
). Response inhibition deficits are suggestive of prefrontal and possibly parietal cortex dysfunction (Garavan, Ross, & Stein, 1999
The sustained attention deficit of the children with ADHD was clearly shown by the high number of omission errors, made both during the Fixed and Random SARTs. In contrast, the children with HFA and the control children made a similar, lower number of omission errors. All children showed an increase in omission errors as the task progressed, suggesting that a progressive decline in performance is normal at this age.
The ADHD group showed a particular diminution in RT performance over the course of both the Fixed and Random SARTs, which was not shown by either the HFA or the control groups. The children with ADHD slowed in RT over the two halves of the tasks, as demonstrated by the mean RT and the linear regression analyses. The slow frequency variability in RT was significantly higher for the ADHD group. In comparison, the children with HFA and the control group maintained a steady performance across the tasks. The ADHD group may be affected by declining arousal. The SART runs for 5.5 min, which is a considerably shorter period compared with traditional vigilance tasks in which subjects must sustain attention for 15 (Teichner, 1974
), 30 (Mackworth, 1968
) or even 60 min periods (Paus et al., 1997
). Nevertheless it is noteworthy that time-on-tasks effects are apparent even over this relatively short task duration. These results imply that arousal deficits may be one key driver of the ubiquitous findings of RT variability in the ADHD literature. This interpretation is consistent with the hypoarousal (Satterfield, Cantwell, & Satterfield, 1974
) and the Cognitive Energetic models of ADHD (Sergeant, 2005
). EEG, PET and rCBF studies have all provided evidence of cortical hypoarousal in ADHD (e.g. Lou, Henriksen, & Bruhn, 1984
; Lou, Henriksen, Bruhn, Borner, & Neilsen, 1989
), possibly due to dysfunctional sub-cortical areas. For instance, EEG recordings of adolescents with ADHD have shown increased theta activity and reduced beta activity, indicating a continuation of increasing slow wave activity in ADHD (Lazzaro et al., 1999
). A number of recent genetic studies have shown associations between ADHD and allelic variation in genes controlling neurotransmitter systems that regulate arousal, such as noradrenaline (Madras, Miller, & Fischman, 2005
), serotonin (Sheehan et al., 2005
) and corticotrophin (Winsky-Sommerer, Boutrel, & de Lecea, 2005
). Whether slow variability indexes arousal levels and is able to index genetic susceptibility in ADHD will be an important question for future research to address.
The ADHD group performed the Fixed and Random SARTs with greater fast-frequency (moment-to-moment) variability in RT and S.D. of RT than the children with HFA and the control children. The children with HFA and the control children performed the two SARTs with a similar amount of variability. Interestingly, the children with ADHD and control children showed greater fast-frequency variability in the second half of the Random SART compared with the first half, suggesting a time-on-task effect during this more difficult task. The HFA group, in both the Fixed and Random SARTs, appeared to have the capacity to maintain consistent fast-frequency variability in RT over the course of the task. Fast-frequency variation in RT likely reflects lapses in top-down attentional control that occur over relatively short time frames, up to the period of one SART cycle (13 s). There are suggestions that the areas of the fronto-parietal circuit are refreshed over time-spans of between 10 and 40 s (Parasuraman, Warm, & See, 1998
; Pardo et al., 1991; Whitehead, 1991
). The ADHD group's greater fast-frequency variability suggests fluctuating top-down attentional control, which in a harder task is also subject to time-on-task effects. Deficits in sustained attention in ADHD may reflect dysfunction of this executive control system (Silk et al., 2005; Sowell et al., 2003
). The children with HFA did not demonstrate this greater fluctuation in fast-frequency variability, suggesting that they do not have deficits in top-down attentional control.
The ability to sustain attention to a routine task is an important aspect of executive control. There may be at least two different processes involved in the behavioural manifestation of deficient sustained attention: a gradual deterioration in attention to a task and a fast phasic variation in top-down attentional control. An incremental worsening in attention to a task, as reflected by slow-frequency variability in RT (SFAUS), may be linked to a deficit in brain arousal levels, related to the functioning of sub-cortical structures (locus coeruleus, pulvinar, the basal forebrain, thalamus, brain stem reticular formation), the anterior cingulate and neurotransmitter dysfunction (noradrenergic, cholinergic and serotonergic) (Biederman & Spencer, 1999
; Moruzzi & Magoun, 1949
; Paus, 2001; Paus et al., 1997
). These systems might be more dysfunctional in ADHD than in HFA, especially if the task is endogenously taxing. Top-down attentional control may also wax and wane throughout the course of a task in a phasic fashion, affecting the ability to maintain concentration on a task. Sustained attention is thought to reflect the activity of the right-lateralised fronto-parietal attentional networks (Manly et al., 2003
), which may be affected in ADHD to a far greater degree than in HFA. There may be a multisecond oscillatory cycle of sustained attention that is linked to physiological processes such as basal ganglia neuronal activity and cerebral hemodynamic response (Castellanos et al., 2005
). Future research will need to determine the neural substrates of these two distinct processes and their functioning in ADHD and HFA and control children. In addition, it would be interesting to investigate how these two proposed processes vary in the sub-groups of ADHD, to enable a greater understanding of the heterogeneity of this disorder.
The clear distinction in performance between the children with ADHD and HFA on the Fixed and Random SARTs suggests that sustained attention may not be a deficit shared by the two disorders. Response inhibition may be a shared feature of the two disorders, especially in tasks when external cues that provide some structure are unavailable for children with HFA. These clear findings highlight the potential usefulness of CPT-like tasks in the assessment and conceptualisation of children with psychiatric disorders. The response inhibition, sustained attention and arousal deficits of children with ADHD should be addressed when designing cognitive behavioural therapies. The usefulness of external cues in providing a structure for cognition in children with HFA has been highlighted in this comparison of performance on the Fixed and Random SARTs.
This study is limited by the retrospective use of the CPRS-R:S and the ASDI for a sub-group of the children and this must be taken into account when drawing conclusions from the data. It is important to note that 12 (57%) children with HFA scored at least 65 on the Conners’ ADHD Index. Whilst the HFA and ADHD groups differed significantly in their mean ADHD Index scores, some of the children with HFA displayed clinically-relevant ADHD-like behaviours, highlighting the potential comorbidity of these two disorders and the heterogeneity of the HFA group.
In summary, four key findings resulted from the present study. First, the ADHD group showed pervasive deficits in sustained attention in both the Fixed and Random SARTs, particularly when the requirements for endogenous control of attention were high. The clear dissociation in performance of the ADHD group, compared with the HFA and control groups, highlights the potential utility of the SART measures as specific endophenotypes for ADHD. Second, the ADHD group demonstrated a time-on-task effect over the course of the Fixed and Random SARTs, as reflected in the increased slow-frequency variability, mean RT and linear regression of RT, possibly reflecting a decrease in arousal levels. That we found deficits for slow-frequency variability in the ADHD group but not in the HFA group also suggests that variability is not a simple consequence of cerebral disruption (see also MacDonald et al., 2006; Stuss et al., 2003
). Slow-frequency variability in ADHD, rather, may be a consequence of specific disruption within the arousal system. This hypothesis awaits confirmation with neuroimaging. Third, the ADHD and HFA groups both showed heightened levels of commission errors on the Random SART, compared with the control group, suggesting deficits in response inhibition. Interestingly, the finding of a response inhibition deficit in the HFA group that was of comparable effect size to the ADHD group, adds to a burgeoning literature suggesting inhibitory deficits in HFA. Fourth, the HFA group made a normal number of commission errors on the Fixed SART, possibly by utilising the predictable sequence of digits preceding the NoGo “3” stimulus as cues, which is suggestive of a systematizing aptitude. This study provides detailed behavioural evidence of significantly greater sustained attention dysfunction in ADHD than in HFA. This behavioural deficit in ADHD may be underpinned by greater dysfunction within fronto-parietal areas and the subcortical arousal system.