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Saturday, May 9, 2009
Northwest Hall (Chicago Hilton)
11:00 AM
Background: ASD is associated with disturbances of neural connectivity. Connectivity is typically examined within the context of a cognitive task. However, connectivity also exists in the absence of a task. This intrinsic connectivity, known as resting-state connectivity is particularly active in a set of structures called the default network, which includes the posterior cingulate cortex (PCC), retro-splenial cortex, lateral parietal cortex/angular gyrus, medial prefrontal cortex, superior frontal gyrus, temporal lobe, and parahippocampal gyrus. Exploring resting-state connectivity in ASD is of interest as these networks might be active during self-referencing and introspection, domains in which deficits in empathy and social cognition hinge upon. In addition, no prior study has explored resting-state connectivity within adolescents with ASD.
Objectives: We sought to examine resting-state connectivity within the default network in adolescents with ASD and to examine how various measures of symptom severity and adaptive functioning relate to patterns of connectivity. Following the results from a previous resting connectivity study in our lab that showed patterns of weaker and tighter connectivity in adults with ASD, we hypothesized that adolescents with ASD would show weaker coupling between the PCC and the superior frontal gyrus relative to controls. Second, we hypothesized that adolescents with ASD would show tighter coupling between the PCC and the superior temporal gyrus and parahippocampal gyrus relative to controls. Finally, in an exploratory analysis we sought to examine if symptom severity was associated strength of connectivity.
Methods: 12 adolescents with ASD and 12 age-matched controls between the ages of 13-17 took part in a functional MRI study. Participants were instructed to “let your mind wander freely” while looking at a fixation cross displayed in the middle of the screen for 10 minutes during fMRI acquisition. A seed region was placed in the PCC and functional connectivity was examined by obtaining the correlational activity between the PCC and other areas of the default network.
Results: Both ASD and control groups activated the default network of the brain at p<0.05 (whole brain corrected). Analyses of group differences revealed that individuals with ASD relative to controls showed weaker connectivity between the PCC and all regions in the default network (p<0.05 small volume corrected). Moreover, ASD relative to the control groups showed tighter connectivity between the PCC and the superior temporal gyrus. A correlation analysis revealed that poorer social functioning was associated with weaker connectivity between the PCC and left angular gyrus. Greater impairments in the restricted and repetitive behavior domain were associated with weaker connectivity between the PCC and the temporal lobe. Finally, lower overall adaptive functioning in the ASD group was associated with weaker connectivity between the PCC and the angular gyrus.
Conclusions: Relative to the control group, the ASD group showed weaker functional connectivity within the default network in the absence of a task. In addition, more severe symptoms were associated with weaker connectivity within the default network. These findings suggest evidence for altered connectivity within the default network and that connectivity between these structures is associated with core impairments in ASD.
Objectives: We sought to examine resting-state connectivity within the default network in adolescents with ASD and to examine how various measures of symptom severity and adaptive functioning relate to patterns of connectivity. Following the results from a previous resting connectivity study in our lab that showed patterns of weaker and tighter connectivity in adults with ASD, we hypothesized that adolescents with ASD would show weaker coupling between the PCC and the superior frontal gyrus relative to controls. Second, we hypothesized that adolescents with ASD would show tighter coupling between the PCC and the superior temporal gyrus and parahippocampal gyrus relative to controls. Finally, in an exploratory analysis we sought to examine if symptom severity was associated strength of connectivity.
Methods: 12 adolescents with ASD and 12 age-matched controls between the ages of 13-17 took part in a functional MRI study. Participants were instructed to “let your mind wander freely” while looking at a fixation cross displayed in the middle of the screen for 10 minutes during fMRI acquisition. A seed region was placed in the PCC and functional connectivity was examined by obtaining the correlational activity between the PCC and other areas of the default network.
Results: Both ASD and control groups activated the default network of the brain at p<0.05 (whole brain corrected). Analyses of group differences revealed that individuals with ASD relative to controls showed weaker connectivity between the PCC and all regions in the default network (p<0.05 small volume corrected). Moreover, ASD relative to the control groups showed tighter connectivity between the PCC and the superior temporal gyrus. A correlation analysis revealed that poorer social functioning was associated with weaker connectivity between the PCC and left angular gyrus. Greater impairments in the restricted and repetitive behavior domain were associated with weaker connectivity between the PCC and the temporal lobe. Finally, lower overall adaptive functioning in the ASD group was associated with weaker connectivity between the PCC and the angular gyrus.
Conclusions: Relative to the control group, the ASD group showed weaker functional connectivity within the default network in the absence of a task. In addition, more severe symptoms were associated with weaker connectivity within the default network. These findings suggest evidence for altered connectivity within the default network and that connectivity between these structures is associated with core impairments in ASD.