Table 1

TMS-EMG measures

MeasureProtocolSpeculated mechanismPharmacological evidenceReferences
Single-pulse TMS
 Resting motor threshold and active motor thresholdMinimum TMS intensity to elicit an MEP with (usually) 50 μV peak-to-peak amplitude in the target muscle, either at rest (RMT) or during voluntary contraction (AMT)Voltage-gated, sodium-channel-mediated neuronal membrane excitabilityIncreased by voltage-gated sodium channel blockers (e.g., carbamazepine, phenytoin and lamotrigine); decreased by ketamineLang et al.61 (2013)
Menzler et al.62 (2014)
Ziemann et al.63 (1996)
 Amplitude of motor evoked potentialsEvoked by stimulus intensity above the motor thresholdTrans-synaptic activation of corticospinal neurons regulated by glutamatergic, GABAergic and neuromodulating neurotransmittersIncreased by ketamine, noradrenaline agonists (e.g., methylphenidate) and 5-HT agonists (e.g., sertraline); decreased by positive allosteric modulators of GABA receptors (e.g., lorazepam)Ilic et al.64 (2003)
Gerdelat-Mas et al.65 (2005)
Paulus et al.66 (2008)
Boroojerdi et al.30 (2001)
Di Lazzaro et al.67 (2000)
 Duration of cortical silent periodDuration of TMS-induced interruption in voluntary EMG activity of the target muscleMotor cortical inhibition mediated by activation of GABA-A receptors (short CSPs) or GABA-B receptors (long CSPs)Increased by benzodiazepines (short CSPs) and baclofen (specific GABA-B receptor agonist)Inghilleri et al.68 (1996)
Siebner et al.69 (1998)
 Short-latency afferent inhibitionConditioning afferent electrical stimulus to the median or ulnar nerve at the wrist precedes TMS of the contralateral motor cortex by roughly 20 msPhysiologic marker of the integrity and excitability of central cholinergic pathwaysIncreased by acetylcholinesterase inhibitors and nicotine; decreased by scopolamine (acetylcholine antagonist) and lorazepam (benzodiazepine)Di Lazzaro et al.70 (2005)
Di Lazzaro et al.71 (2005)
Di Lazzaro et al.67 (2000)
 Transcallosal inhibitionSingle TMS pulses over the motor cortex ipsilateral to the voluntarily contracted hand muscle to induce a silent period in EMG activityDuration of the silent period is thought to reflect the functioning of the corpus callosum and an inhibitory system in the contralateral motor cortexFerbert et al.34 (1992)
Meyer et al.72 (1998)
Paired-pulse TMS
 Short-interval intracortical inhibitionSubthreshold conditioning stimulus precedes suprathreshold test stimulus by 1~5 msShort-lasting inhibition in regional corticospinal neurons mediated by GABA-A receptors containing α2 or α3 subunitsIncreased by benzodiazepines (positive modulators at α1, α2, α3 or α5 subunits of GABA-A receptors); not affected by zolpidem (specific positive modulator of α1-GABA-A receptor) or S44819 (selective antagonist of α5-GABA-A receptor)Di Lazzaro et al.73 (2007)
Di Lazzaro et al.74 (2006)
 Intracortical facilitationSubthreshold conditioning stimulus precedes suprathreshold test stimulus by 7~20 msNet excitation of an excitatory motor cortical networkIncreased by noradrenergic agonists; decreased by NMDA receptor antagonists and benzodiazepinesZiemann et al.32 (1998)
Ziemann et al.75 (1996)
Boroojerdi et al.30 (2001)
 Long-interval intracortical inhibitionTwo suprathreshold conditioning and test stimuli separated by 50~200 msGABA-B receptor–mediated slow inhibitory postsynaptic potentialsIncreased by baclofen, tiagabine and vigabatrinPierantozzi et al.76 (2004)
Werhahn et al.77 (1999)
McDonnell et al.29 (2006)
  • 5-HT = serotonin; AMT = active motor threshold; CSP = cortical silence period; EMG = electromyography; GABA = γ-aminobutyric acid; MEP = motor evoked potential; NMDA = N-methyl-d-aspartate; RMT = resting motor threshold; TMS = transcranial magnetic stimulation.