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Rapid‐rate paired associative stimulation of the median nerve and motor cortex can produce long‐lasting changes in motor cortical excitability in humans
Author(s) -
Quartarone Angelo,
Rizzo Vincenzo,
Bagnato Sergio,
Morgante Francesca,
Sant'Angelo Antonino,
Girlanda Paolo,
Roman Siebner Hartwig
Publication year - 2006
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2006.114025
Subject(s) - transcranial magnetic stimulation , motor cortex , interstimulus interval , stimulation , neuroscience , evoked potential , stimulus (psychology) , medicine , psychology , psychotherapist
Repetitive transcranial magnetic stimulation (rTMS) or repetitive electrical peripheral nerve stimulation (rENS) can induce changes in the excitability of the human motor cortex (M1) that is often short‐lasting and variable, and occurs only after prolonged periods of stimulation. In 10 healthy volunteers, we used a new repetitive paired associative stimulation (rPAS) protocol to facilitate and prolong the effects of rENS and rTMS on cortical excitability. Sub‐motor threshold 5 Hz rENS of the right median nerve was synchronized with submotor threshold 5 Hz rTMS of the left M1 at a constant interval for 2 min. The interstimulus interval (ISI) between the peripheral stimulus and the transcranial stimulation was set at 10 ms (5 Hz rPAS 10ms ) or 25 ms (5 Hz rPAS 25ms ). TMS was given over the hot spot of the right abductor pollicis brevis (APB) muscle. Before and after rPAS, we measured the amplitude of the unconditioned motor evoked potential (MEP), intracortical inhibition (ICI) and facilitation (ICF), short‐ and long‐latency afferent inhibition (SAI and LAI) in the conditioned M1. The 5 Hz rPAS 25ms protocol but not the 5 Hz rPAS10 ms protocol caused a somatotopically specific increase in mean MEP amplitudes in the relaxed APB muscle. The 5 Hz rPAS 25ms protocol also led to a loss of SAI, but there was no correlation between individual changes in SAI and corticospinal excitability. These after‐effects were still present 6 h after 5 Hz rPAS 25ms . There was no consistent effect on ICI, ICF and LAI. The 5 Hz rENS and 5 Hz rTMS protocols failed to induce any change in corticospinal excitability when given alone. These findings show that 2 min of 5 Hz rPAS 25ms produce a long‐lasting and somatotopically specific increase in corticospinal excitability, presumably by sensorimotor disinhibition.