Executive Function in the Autism and Schizophrenia Spectrums

Friday, May 12, 2017: 5:00 PM-6:30 PM
Golden Gate Ballroom (Marriott Marquis Hotel)
S. Hampton1, R. C. M. Philip2, E. C. Johnstone2, S. M. Lawrie2 and A. C. Stanfield2, (1)University of Cambridge, Cambridge, United Kingdom, (2)University of Edinburgh, Edinburgh, UNITED KINGDOM
Background:  Autism and schizophrenia are known to have overlapping phenotypic features, including difficulties with aspects of executive function such as working memory. Overlaps between autism and schizophrenia are particularly pronounced for higher functioning individuals with autism spectrum disorders (ASD) or schizotypal personality disorder (SPD). It is not known, however, whether these shared features result from common or distinct brain mechanisms. Knowledge of the neural mechanisms involved can help inform how best to address executive function difficulties in each particular condition.

Objectives:  This study aimed to characterise the neural basis of working memory in those with ASD and SPD using functional magnetic resonance imaging (fMRI), in order to explore similarities and differences in the underlying mechanisms involved in both conditions.

Methods:  76 individuals participated in the study: 24 with ASD, 20 with SPD and 32 typically developing controls. While in an MRI scanner, participants completed the n-back task as a measure of working memory. During this task, participants were presented with a sequence of letters and instructed to report whether the letter on the screen matched the one presented n steps earlier in the sequence. Four conditions were employed: 0-back, 1-back, 2-back and 3-back, with each condition placing an increasing load on working memory.

Results:  No significant differences in activation were seen between the ASD and SPD groups. However, significantly less of an increase in activation was seen in the ASD group compared to controls as working memory load increased in a cluster which stretched from the left superior parietal lobule into the cuneus and precuneus and extended into left posterior cingulate. Significantly less of an increase in activation was seen in the SPD group compared to the control group as working memory load increased in a bilateral cluster in posterior cingulate, extending into cuneus, precuneus and lingual gyrus.

Conclusions:  While the ASD and SPD groups showed slightly different activation compared to controls, there were no significant differences between the ASD and SPD groups. Those with ASD and SPD, therefore, do not appear to differ with regard to the brain mechanisms underlying working memory. These findings have implications for therapeutic interventions that target the mechanisms behind difficulties in executive function in these conditions.