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Reduced microstructural integrity of the white matter underlying anterior cingulate cortex is associated with increased saccadic latency in schizophrenia.

NeuroImage | 2007

The anterior cingulate cortex (ACC) is a key component of a network that directs both spatial attention and saccadic eye movements, which are tightly linked. Diffusion tensor imaging (DTI) has demonstrated reduced microstructural integrity of the anterior cingulum bundle as indexed by fractional anisotropy (FA) in schizophrenia, but the functional significance of these abnormalities is unclear. Using DTI, we examined the white matter underlying anterior cingulate cortex in schizophrenia to determine whether reduced FA is associated with prolonged latencies of volitional saccades. Seventeen chronic, medicated schizophrenia outpatients and nineteen healthy controls had high-resolution DTI scans. FA maps were registered to structural scans and mapped across participants using a surface-based coordinate system. Cingulate white matter was divided into rostral and dorsal anterior regions and a posterior region. Patients showed reduced FA in cingulate white matter of the right hemisphere. Reduced FA in the white matter underlying anterior cingulate cortex, frontal eye field, and posterior parietal cortex of the right hemisphere was associated with longer saccadic latencies in schizophrenia, though given the relatively small sample size, these relations warrant replication. These findings demonstrate that in schizophrenia, increased latency of volitional saccades is associated with reduced microstructural integrity of the white matter underlying key cortical components of a right-hemisphere dominant network for visuospatial attention and ocular motor control. Moreover, they suggest that anterior cingulate white matter abnormalities contribute to slower performance of volitional saccades and to inter-individual variability of saccadic latency in chronic, medicated schizophrenia.

Pubmed ID: 17590354 RIS Download

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Associated grants

  • Agency: PHS HHS, United States
    Id: BIRN002
  • Agency: PHS HHS, United States
    Id: P01 31154
  • Agency: NCRR NIH HHS, United States
    Id: P41 RR14075
  • Agency: PHS HHS, United States
    Id: R01 31340
  • Agency: PHS HHS, United States
    Id: R01 67720
  • Agency: NIBIB NIH HHS, United States
    Id: R01 EB001550
  • Agency: NCRR NIH HHS, United States
    Id: R01 RR16594-01A1
  • Agency: NCRR NIH HHS, United States
    Id: U24 RR021382
  • Agency: NIBIB NIH HHS, United States
    Id: U54 EB005149

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