Adolescents and Young Adults with Autism Spectrum Disorder Show Differences in Dynamics and Recruitment of Cognitive Control Networks

Poster Presentation
Saturday, May 12, 2018: 11:30 AM-1:30 PM
Hall Grote Zaal (de Doelen ICC Rotterdam)
M. Solomon1,2,3, M. K. Krug4, C. C. Coleman4, M. V. Elliott5, J. Hogeveen6, T. A. Niendam7, J. D. Ragland7 and C. S. Carter8, (1)MIND Institute, Sacramento, CA, (2)Imaging Research Center, UC Davis, Sacramento, CA, (3)Department of Psychiatry & Behavioral Sciences, UC Davis MIND Institute, Sacramento, CA, (4)Department of Psychiatry & Behavioral Sciences, The Medical Investigation of Neurodevelopmental Disorders (MIND) Institute, University of California, Davis, Sacramento, CA, (5)Department of Psychology, University of California, Berkeley, Berkeley, CA, (6)Department of Psychiatry & Behavioral Sciences, UC Davis, Sacramento, CA, (7)Imaging Research Center, Sacramento, CA, (8)Department of Psychiatry and Behavioral Sciences, University of California Davis, Sacramento, CA

Individuals with Autism Spectrum Disorder (ASD) exhibit cognitive control (CC) deficits that appear to persist into adolescence and adulthood (Ozonoff et al, 1991, Solomon et al, 2017). CC deficits may be associated with the difficulties in social functioning, adaptive functioning and restricted and repetitive behaviors that are characteristic of individuals with ASD. Previous fMRI studies with slow event-related versions of the preparing to overcome prepotency (POP) task found evidence that typically developing (TYP) individuals develop a mature LPFC/parietal network in adolescence; however, individuals with ASD may continue to rely more heavily on a less mature dACC/LPFC network when presented with a situation that requires the implementation of CC (Solomon et al, 2009, Solomon et at, 2014).


(1) Investigate potential group differences in CC by looking at behavioral performance in a rapid event-related version of the POP task in participants aged 12-22 years old. (2) Associate behavioral measures with recruitment of brain regions known to play a role in implementation of CC. (3) Examine age-related changes in CC network recruitment and connectivity.


Participants included 46 ASD (mean age=17.2 years; mean IQ=103) diagnosed using gold standard measures and 46 TYP (mean age=16.7 years; mean IQ=109). They completed four 28 trial runs of the Rapid Preparing to Overcome Prepotency (rPOP) task in the fMRI environment. For each trial of rPOP, a color cue was presented, followed by an arrow probe. For green cues, participants were instructed to press a button on the same side as the arrow probe. For red cues, participants were instructed to press a button on the opposite side of the arrow. Data was acquired using a 3 Tesla Siemens Tim Trio with a 32 channel head coil. Data were preprocessed and analyzed using SPM12. Functional connectivity analyses used CONN toolbox (http://www.nitrc.org /projects/conn).


Behavioral performance was assessed by calculating inverse efficiency score (IES; RT(ms)/accuracy; larger values indicate inefficient performance).There was a main effect of both cue type and diagnosis and a significant cue type X diagnosis interaction (F=10.17,p<.005), indicating that the ASD group was less efficient at the task. Whole brain analysis indicated that recruitment of BA 32 was greater for red cue trials compared to green cue in both groups (p-FDR<.05). In the ASD versus the TYP group, there was significantly stronger functional connectivity between the dACC and the DLPFC at the cue phase (Figure 1), which was negatively associated with task performance (Figure 2). This connectivity pattern negatively correlated with age in TYP, but there was no relationship in ASD.


Our findings suggest a possible neural mechanism underlying the CC impairment evidenced by poor behavioral performance in ASD on the rPOP task. The developmental dissociation between TYP and ASD in this consequential network is also of great interest, and may provide an explanation for the persistence of CC deficits into young adulthood in ASD. Future analyses will investigate how these CC networks develop longitudinally, and their relationships to relevant clinical and adaptive functioning outcomes in young adults with ASD.