Kana RK, Keller TA, Minshew NJ, Just MA. Inhibitory control in high-functioning autism: decreased activation and underconnectivity in inhibition networks. Biol Psychiatry 62: 198-206

Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
Biological Psychiatry (Impact Factor: 10.26). 09/2007; 62(3):198-206. DOI: 10.1016/j.biopsych.2006.08.004
Source: PubMed


Inhibiting prepotent responses is critical to optimal cognitive and behavioral function across many domains. Several behavioral studies have investigated response inhibition in autism, and the findings varied according to the components involved in inhibition. There has been only one published functional magnetic resonance imaging (fMRI) study so far on inhibition in autism, which found greater activation in participants with autism than control participants.
This study investigated the neural basis of response inhibition in 12 high-functioning adults with autism and 12 age- and intelligence quotient (IQ)-matched control participants during a simple response inhibition task and an inhibition task involving working memory.
In both inhibition tasks, the participants with autism showed less brain activation than control participants in areas often found to be active in response inhibition tasks, namely the anterior cingulate cortex. In the more demanding inhibition condition, involving working memory, the participants with autism showed more activation than control participants in the premotor areas. In addition to the activation differences, the participants with autism showed lower levels of synchronization between the inhibition network (anterior cingulate gyrus, middle cingulate gyrus, and insula) and the right middle and inferior frontal and right inferior parietal regions.
The results indicate that the inhibition circuitry in the autism group is activated atypically and is less synchronized, leaving inhibition to be accomplished by strategic control rather than automatically. At the behavioral level, there was no difference between the groups.

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Available from: Kuarmoto Kana
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    • "In addition, extensive neurophysiological and neuroimaging studies reported structural (e.g., Casanova, Buxhoeveden, & Gomez, 2003; Carper & Courchesne, 2005; Casanova et al., 2006, see Teffer & Semendeferi, 2012, for review) and functional abnormalities (Chan et al., 2009; Just, Cherkassky, Keller, & Minshew, 2004; Ohnishi et al., 2000) in the frontal lobes of individuals with ASD. Focal abnormalities in other frontal regions such as the ACC (Chan et al., 2011; Gomot et al., 2006; Hazlett et al., 2005; Haznedar et al., 2000; Kana, Keller, Minshew, & Just, 2007; Schmitz et al., 2006; Thakkar et al., 2008) and pre-SMA (Kana et al., 2007; Muller, Cauich, Rubio, Mizuno, & Courchesne, 2004) were also extensively reported. More importantly, Chan et al. (2009, 2011) found an association between the frontal abnormalities and poor inhibitory control in children with ASD. "
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    • "It is conceivable that lack of inferior frontal/insular activation in the HFA group reflects a more efficient neural processing of response inhibition, as performance was equivalent with controls. However, hypoactivation of VLPFC has been previously related to EF deficits in autism (Dichter and Belger, 2007; Kana et al., 2007; Shafritz et al., 2008). The current findings are in line with these prior results , and provide additional corroborative evidence for hypoactivation during response inhibition even with equivalent performance. "
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    • "Whereas the neurobiological mechanisms associated with ADHD and ASD are still not fully understood (Konrad & Eikoff, 2010; Schaaf & Zoghbi, 2011), it is apparent that there is some overlap in functional dysregulations in the brain for these disorders. Indeed, neuroimaging studies have indicated similar patterns of dysregulation for both ADHD and ASD in the prefrontal cortex (Just, Cherkassky, Keller, Kana, & Minshew, 2007; Smith, Taylor, Brammer, Halari, & Rubia, 2008), anterior cingulate cortex (Kana, Keller, Minshew, & Just, 2007; Smith, Taylor et al., 2008), and large-scale neural networks such as the default-mode network (Assaf et al., 2010; Castellanos et al., 2008) and fronto-parietal circuit (Castellanos & Proal, 2012; Kana et al., 2007). Consonant with such impairments across neural regions and networks involved in regulating goal-directed behavior, deficits in cognitive control— particularly inhibition—are characteristic of children with ADHD and are common in children with autism (Geurts, Verté, Oosterlaan, Roeyers, & Sergeant, 2004; Nydén, Gillberg, Hjelmquist, & Heiman, 1999; Pennington & Ozonoff, 1996). "
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