Frontiers in Computational Neuroscience (Sep 2017)

Altered Local Spatiotemporal Consistency of Resting-State BOLD Signals in Patients with Generalized Tonic-Clonic Seizures

  • Shuai Ma,
  • Sisi Jiang,
  • Rui Peng,
  • Qiong Zhu,
  • Hongbin Sun,
  • Jianfu Li,
  • Xiaoyan Jia,
  • Ilan Goldberg,
  • Liang Yu,
  • Cheng Luo

DOI
https://doi.org/10.3389/fncom.2017.00090
Journal volume & issue
Vol. 11

Abstract

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The purpose of this study was to evaluate the spatiotemporal Consistency of spontaneous activities in local brain regions in patients with generalized tonic-clonic seizures (GTCS). The resting-state fMRI data were acquired from nineteen patients with GTCS and twenty-two matched healthy subjects. FOur-dimensional (spatiotemporal) Consistency of local neural Activities (FOCA) metric was used to analyze the spontaneous activity in whole brain. The FOCA difference between two groups were detected using a two sample t-test analysis. Correlations between the FOCA values and features of seizures were analyzed. The findings of this study showed that patients had significantly increased FOCA in motor-related cortex regions, including bilateral supplementary motor area, paracentral lobule, precentral gyrus and left basal ganglia, as well as a substantial reduction of FOCA in regions of default mode network (DMN) and parietal lobe. In addition, several brain regions in DMN demonstrated more reduction with longer duration of epilepsy and later onset age, and the motor-related regions showed higher FOCA value in accompany with later onset age. These findings implicated the abnormality of motor-related cortical network in GTCS which were associated with the genesis and propagation of epileptiform activity. And the decreased FOCA in DMN might reflect the intrinsic disturbance of brain activity. Moreover, our study supported that the FOCA might be potential tool to investigate local brain spontaneous activity related with the epileptic activity, and to provide important insights into understanding the underlying pathophysiological mechanisms of GTCS.

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