title: Disconnectivity of the cortical ocular motor control network in autism spectrum disorders.
abstract: Response inhibition, or the suppression of prepotent but contextually inappropriate behaviors, is essential to adaptive, flexible responding. Individuals with autism spectrum disorders (ASD) consistently show deficient response inhibition during antisaccades. In our prior functional MRI study, impaired antisaccade performance was accompanied by reduced functional connectivity between the frontal eye field (FEF) and dorsal anterior cingulate cortex (dACC), regions critical to volitional ocular motor control. Here we employed magnetoencephalography (MEG) to examine the spectral characteristics of this reduced connectivity. We focused on coherence between FEF and dACC during the preparatory period of antisaccade and prosaccade trials, which occurs after the presentation of the task cue and before the imperative stimulus. We found significant group differences in alpha band mediated coherence. Specifically, neurotypical participants showed significant alpha band coherence between the right inferior FEF and right dACC and between the left superior FEF and bilateral dACC across antisaccade, prosaccade, and fixation conditions. Relative to the neurotypical group, ASD participants showed reduced coherence between these regions in all three conditions. Moreover, while neurotypical participants showed increased coherence between the right inferior FEF and the right dACC in preparation for an antisaccade compared to a prosaccade or fixation, ASD participants failed to show a similar increase in preparation for the more demanding antisaccade. These findings demonstrate reduced long-range functional connectivity in ASD, specifically in the alpha band. The failure in the ASD group to increase alpha band coherence with increasing task demand may reflect deficient top-down recruitment of additional neural resources in preparation to perform a difficult task.
authors.affiliation: Department of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA. tal@nmr.mgh.harvard.edu
authors.forename: Tal
authors.initials: T
authors.lastname: Kenet
authors.forename: Elena V
authors.initials: EV
authors.lastname: Orekhova
authors.forename: Hari
authors.initials: H
authors.lastname: Bharadwaj
authors.forename: Nandita R
authors.initials: NR
authors.lastname: Shetty
authors.forename: Emily
authors.initials: E
authors.lastname: Israeli
authors.forename: Adrian K C
authors.initials: AK
authors.lastname: Lee
authors.forename: Yigal
authors.initials: Y
authors.lastname: Agam
authors.forename: Mikael
authors.initials: M
authors.lastname: Elam
authors.forename: Robert M
authors.initials: RM
authors.lastname: Joseph
authors.forename: Matti S
authors.initials: MS
authors.lastname: Hämäläinen
authors.forename: Dara S
authors.initials: DS
authors.lastname: Manoach
mesh_terms: D000328:Adult; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000503:physiopathology*; D002648:Child; D002659:Child Development Disorders, Pervasive / Q000503:physiopathology*; D005260:Female; D006801:Humans; D015225:Magnetoencephalography; D008297:Male; D009434:Neural Pathways / Q000503:physiopathology*; D012438:Saccades / Q000502:physiology