Increased Intrinsic Connectivity of the Default Mode Network in Temporal Lobe Epilepsy: Evidence from Resting-State MEG Recordings

PLoS One. 2015 Jun 2;10(6):e0128787. doi: 10.1371/journal.pone.0128787. eCollection 2015.

Abstract

The electrophysiological signature of resting state oscillatory functional connectivity within the default mode network (DMN) during spike-free periods in temporal lobe epilepsy (TLE) remains unclear. Using magnetoencephalographic (MEG) recordings, this study investigated how the connectivity within the DMN was altered in TLE, and we examined the effect of lateralized TLE on functional connectivity. Sixteen medically intractable TLE patients and 22 controls participated in this study. Whole-scalp 306-channel MEG epochs without interictal spikes generated from both MEG and EEG data were analyzed using a minimum norm estimate (MNE) and source-based imaginary coherence analysis. With this processing, we obtained the cortical activation and functional connectivity within the DMN. The functional connectivity was increased between DMN and the right medial temporal (MT) region at the delta band and between DMN and the bilateral anterior cingulate cortex (ACC) regions at the theta band. The functional change was associated with the lateralization of TLE. The right TLE showed enhanced DMN connectivity with the right MT while the left TLE demonstrated increased DMN connectivity with the bilateral MT. There was no lateralization effect of TLE upon the DMN connectivity with ACC. These findings suggest that the resting-state functional connectivity within the DMN is reinforced in temporal lobe epilepsy during spike-free periods. Future studies are needed to examine if the altered functional connectivity can be used as a biomarker for treatment responses, cognitive dysfunction and prognosis in patients with TLE.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Brain Mapping
  • Epilepsy, Temporal Lobe / physiopathology*
  • Female
  • Humans
  • Magnetoencephalography
  • Male
  • Nerve Net / physiopathology*

Grants and funding

This study was supported in part by research grants from Taipei City Hospital (100TPECH04, 102TPECH02), Taipei Veterans General Hospital (V101C-023, V102C-103, VGHUST 102-G7-6-2), Brain Research Center (102AC-B22, 102AC-B7, 103U-001,103AC-B16 and 103AC-B7), and from the National Science Council (NSC 98-2321-B-010-007, NSC 99-2321-B-010-004, NSC 99-2628-B-010 -011-MY3, NSC 100-2218-E-010-002, NSC 100-2321-B-010-004, NSC 101-2314-B-010 -068 -MY3, NSC 101-2314-B-075 -068 -MY2, NSC 102-2221-E-010 -003) in Taipei, Taiwan.