Reliability of Long-Interval Cortical Inhibition in Healthy Human Subjects: A TMS–EEG Study

Abstract

Cortical inhibition (CI) is measured by transcranial magnetic stimulation (TMS) combined with electromyography (EMG) through long-interval CI (LICI) and cortical silent period (CSP) paradigms. Recently, we illustrated that LICI can be measured from the dorsolateral prefrontal cortex (DLPFC) through combined TMS with electroencephalography (EEG). We further demonstrated that LICI had different effects on cortical oscillations in the DLPFC compared with motor cortex. The purpose of this study was to establish the validity and reliability of TMS-EEG indices of CI and to replicate our previous findings in an extended sample. The validity of TMS-EEG was examined by evaluating its relationship to standard EMG measures of LICI and the CSP in the left motor cortex in 36 and 16 subjects, respectively. Test-retest reliability was examined in 14 subjects who returned for a repeat session within 7 days of the first session. LICI was applied to the left DLPFC in 30 subjects to compare LICI in the DLPFC with that in the motor cortex. In the motor cortex, EEG measures of LICI correlated with EMG measures of LICI and CSP. All indices of LICI showed high test-retest reliability in motor cortex and DLPFC. Gamma and beta oscillations were significantly inhibited in the DLPFC but not in the motor cortex, confirming previous findings in an extended sample. These findings demonstrate that indexing LICI through TMS combined with EEG is a valid and reliable method to evaluate inhibition from motor and prefrontal regions.

Characterization of GABAB-receptor mediated neurotransmission in the human cortex by paired-pulse TMS–EEG

“…Cronbach's alpha values > 0.7 (Farzan et al, 2010;Neuper et al, 2005) revealed a high level of reproducibility for all single-pulse TEPs and LICI of TEP components across drug conditions (Figures 2C-D), except for LICI of the P25 which showed a low level of reliability (Cronbach's alpha values < 0.7). RMT was not significantly different between drug conditions at baseline before drug intake (diazepam: 44.6 ± 1.3% MSO; baclofen: 44.1 ± 1.3% MSO; placebo: 44.8 ± 1.2% MSO; F (2,28) = 1.12, p = 0.34) and thus cannot account for any of the observed drug-induced changes of LICI (see below).…”

“…Recently, first studies using a combination of TMS and electroencephalography (TMS-EEG) have started to directly investigate mechanisms of LICI at the cortical level (Daskalakis et al, 2008;Farzan et al, 2010;Fitzgerald et al, 2009;Rogasch et al, 2013). It was shown that a conditioning stimulus (LICI protocol) induced a reduction of the averaged TS-evoked EEG potential (TEP) recorded at the C3 electrode, which is located above the stimulated M1 (Daskalakis et al, 2008;Farzan et al, 2010;Fitzgerald et al, 2009;Rogasch et al, 2013).…”

“…It was shown that a conditioning stimulus (LICI protocol) induced a reduction of the averaged TS-evoked EEG potential (TEP) recorded at the C3 electrode, which is located above the stimulated M1 (Daskalakis et al, 2008;Farzan et al, 2010;Fitzgerald et al, 2009;Rogasch et al, 2013).…”

Investigating TMS–EEG Indices of Long-Interval Intracortical Inhibition at Different Interstimulus Intervals

“…Using TMS-EEG, several studies have shown that LICI is associated with reduced excitability in both motor and nonmotor areas of cortex [23,[39][40][41]. For the primary motor cortex, the magnitude of this inhibition correlates with inhibition of the MEP, demonstrating the involvement of mechanisms comparable to those reflected by conventional LICI measurements.…”

Inhibition of the cortex using transcranial magnetic stimulation in psychiatric populations: current and future directions

“…22 Also, long interval cortical inhibition is optimal when the conditioning stimulus precedes the test stimulus by 100-150 ms, 28 comparable to the time course of the GABA B receptor activation, which has been shown to typically peak at around 150-200 ms poststimulus. 15 More recently, a significant positive association has been shown between the suppression of MEP amplitudes in long interval cortical inhibition (with an ISI of 100 ms) and in the cortical silent period in healthy individuals, 29 providing evidence for the mediation of the GABA B receptor in both long interval cortical inhibition and the cortical silent period.…”