Deficient saccadic inhibition in Asperger's disorder and the social-emotional processing disorder

Abstract

Background: Both Asperger's disorder and the social-emotional processing disorder (SEPD), a form of non-verbal learning disability, are associated with executive function deficits. SEPD has been shown to be associated with deficient saccadic inhibition. Objective: To study two executive functions in Asperger's disorder and SEPD, inhibition and task switching, using a single saccadic paradigm. Methods: 22 control subjects and 27 subjects with developmental social processing disorders-SEPD, Asperger's disorder, or both syndromes-performed random sequences of prosaccades and antisaccades. This design resulted in four trial types, prosaccades and antisaccades, that were either repeated or switched. The design allowed the performance costs of inhibition and task switching to be isolated. Results: Subjects with both Asperger's disorder and SEPD showed deficient inhibition, as indicated by increased antisaccade errors and a disproportionate increase in latency for antisaccades relative to prosaccades. In contrast, task switching error and latency costs were normal and unrelated to the costs of inhibition.Conclusions: This study replicates the finding of deficient saccadic inhibition in SEPD, extends it to Asperger's disorder, and implicates prefrontal cortex dysfunction in these syndromes. The finding of intact task switching shows that executive function deficits in Asperger's disorder and SEPD are selective and suggests that inhibition and task switching are mediated by distinct neural networks.

Brief Report: Cognitive Control of Social and Nonsocial Visual Attention in Autism

“…2b suggests a somewhat similar pattern of responses to nonsocial stimuli not related to CIs, suggesting that ASD may be characterized by impaired cognitive control of visual attention in responses to nonsocial stimuli more generally. Additionally, the ASD group showed no differences in prosaccade error rates for any stimulus category, indicating that saccade errors in ASD are most prominent in contexts requiring response inhibition, a finding that is consistent with prior domain-general evidence of relatively greater deficits on anti-relative to prosaccade tasks in ASD (Luna et al 2004; Manoach et al 2004). There were also no differences between the ASD and TD control group in saccade latencies for either the prosaccade or antisaccade conditions.…”

“…A saccadic error was defined as a saccade within 3 degrees of the incorrect onscreen location (Manoach et al 2004). Analyses with and without age, IQ, and the order of condition presentation as covariates yielded nearly identical results, and results without covariates are reported.…”

“…Prosaccade tasks require participants to look towards a cued peripheral target, whereas antisaccade tasks require participants to look to the opposite direction than the cued peripheral target (Hutton 2008). Thus, antisaccade tasks require relatively greater cognitive control, and there is evidence of relatively greater deficits on anti-relative to prosaccade tasks in ASD (Luna et al 2004; Manoach et al 2004). We examined responses to face images as well as to two types of nonsocial stimuli: nonsocial images related to circumscribed interests (CIs) in ASD and nonsocial images unrelated to CIs (Sasson et al 2012).…”

Greater Disruption to Control of Voluntary Saccades in Autistic Disorder than Asperger’s Disorder: Evidence for Greater Cerebellar Involvement in Autism?

“…Correspondingly, both HFA and AD groups demonstrated deficits on the volitional saccades tasks that were attributed to higher level functions. The most striking of these findings was consistently increased response suppression errors in ASD, with variable findings of altered response times and accuracy [30][31][32][42][43][44].…”

“…The neurophysiological loci of dysfunction underpinning these deficits has been postulated to include neocortical circuitry, frontal eye fields (FEF), dorsolateral prefrontal cortex (DLPFC), anterior and posterior cingulate cortices, and fronto-striatal circuitry [30][31][32][42][43][44]. Since the neural circuitry controlling volitional saccades includes projections to and from the cerebellum it is possible that cerebellar motor deficits may have been evident, although unexplored in these previous studies.…”