Table 1.
TMS-EMG measures
| Measure | Protocol | Speculated mechanism | Pharmacological evidence | References |
|---|---|---|---|---|
| Single-pulse TMS | ||||
| Resting motor threshold and active motor threshold | Minimum 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 excitability | Increased by voltage-gated sodium channel blockers (e.g., carbamazepine, phenytoin and lamotrigine); decreased by ketamine | Lang et al.61 (2013) Menzler et al.62 (2014) Ziemann et al.63 (1996) |
| Amplitude of motor evoked potentials | Evoked by stimulus intensity above the motor threshold | Trans-synaptic activation of corticospinal neurons regulated by glutamatergic, GABAergic and neuromodulating neurotransmitters | Increased 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 period | Duration of TMS-induced interruption in voluntary EMG activity of the target muscle | Motor 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 inhibition | Conditioning afferent electrical stimulus to the median or ulnar nerve at the wrist precedes TMS of the contralateral motor cortex by roughly 20 ms | Physiologic marker of the integrity and excitability of central cholinergic pathways | Increased 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 inhibition | Single TMS pulses over the motor cortex ipsilateral to the voluntarily contracted hand muscle to induce a silent period in EMG activity | Duration of the silent period is thought to reflect the functioning of the corpus callosum and an inhibitory system in the contralateral motor cortex | Ferbert et al.34 (1992) Meyer et al.72 (1998) |
|
| Paired-pulse TMS | ||||
| Short-interval intracortical inhibition | Subthreshold conditioning stimulus precedes suprathreshold test stimulus by 1~5 ms | Short-lasting inhibition in regional corticospinal neurons mediated by GABA-A receptors containing α2 or α3 subunits | Increased 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 facilitation | Subthreshold conditioning stimulus precedes suprathreshold test stimulus by 7~20 ms | Net excitation of an excitatory motor cortical network | Increased by noradrenergic agonists; decreased by NMDA receptor antagonists and benzodiazepines | Ziemann et al.32 (1998) Ziemann et al.75 (1996) Boroojerdi et al.30 (2001) |
| Long-interval intracortical inhibition | Two suprathreshold conditioning and test stimuli separated by 50~200 ms | GABA-B receptor–mediated slow inhibitory postsynaptic potentials | Increased by baclofen, tiagabine and vigabatrin | Pierantozzi 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.