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Human brain cortical correlates of short-latency afferent inhibition: a combined EEG-TMS study.
J Neurophysiol 2012; 108(1):314-23JN

Abstract

When linking in time electrical stimulation of the peripheral nerve with transcranial magnetic stimulation (TMS), the excitability of the motor cortex can be modulated to evoke clear inhibition, as reflected by the amplitude decrement in the motor-evoked potentials (MEPs). This specific property, designated short-latency afferent inhibition (SAI), occurs when the nerve-TMS interstimulus interval (ISI) is approximately 25 ms and is considered to be a corticothalamic phenomenon. The aim of the present study was to use the electroencephalographic (EEG) responses to navigated-TMS coregistration to better characterize the neuronal circuits underlying SAI. The present experimental set included magnetic resonance imaging (MRI)-navigated TMS and 60-channel TMS-compatible EEG devices. TMS-evoked EEG responses and MEPs were analyzed in eight healthy volunteers; ISIs between median nerve and cortical stimulation were determined relative to the latency of the individual N20 component of the somatosensory-evoked potential (SEP) obtained after stimulation of the median nerve. ISIs from the latency of the N20 plus 3 ms and N20 plus 10 ms were investigated. In all experimental conditions, TMS-evoked EEG responses were characterized by a sequence of negative deflections peaking at approximately 7, 44, and 100 ms alternating with positive peaks at approximately 30, 60, and 180 ms post-TMS. Moreover, ISI N20+3 ms modulated both EEG-evoked activity and MEPs. In particular, it inhibited MEP amplitudes, attenuated cortical P60 and N100 responses, and induced motor cortex beta rhythm selective decrement of phase locking. The findings of the present experiment suggest the cortical origin of SAI that could result from the cortico-cortical activation of GABAergic-mediated inhibition onto the corticospinal neurons modulated by cholinergic activation able to reducing intralaminar inhibition and promoting intracolumnar inhibition.

Authors+Show Affiliations

Department of Clinical Neurophysiology, Kuopio University Hospital, University of Eastern Finland, Kuopio, Finland. f.ferreri@unicampus.itNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22457460

Citation

Ferreri, Florinda, et al. "Human Brain Cortical Correlates of Short-latency Afferent Inhibition: a Combined EEG-TMS Study." Journal of Neurophysiology, vol. 108, no. 1, 2012, pp. 314-23.
Ferreri F, Ponzo D, Hukkanen T, et al. Human brain cortical correlates of short-latency afferent inhibition: a combined EEG-TMS study. J Neurophysiol. 2012;108(1):314-23.
Ferreri, F., Ponzo, D., Hukkanen, T., Mervaala, E., Könönen, M., Pasqualetti, P., ... Määttä, S. (2012). Human brain cortical correlates of short-latency afferent inhibition: a combined EEG-TMS study. Journal of Neurophysiology, 108(1), pp. 314-23. doi:10.1152/jn.00796.2011.
Ferreri F, et al. Human Brain Cortical Correlates of Short-latency Afferent Inhibition: a Combined EEG-TMS Study. J Neurophysiol. 2012;108(1):314-23. PubMed PMID: 22457460.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Human brain cortical correlates of short-latency afferent inhibition: a combined EEG-TMS study. AU - Ferreri,Florinda, AU - Ponzo,David, AU - Hukkanen,Taina, AU - Mervaala,Esa, AU - Könönen,Mervi, AU - Pasqualetti,Patrizio, AU - Vecchio,Fabrizio, AU - Rossini,Paolo Maria, AU - Määttä,Sara, Y1 - 2012/03/28/ PY - 2012/3/30/entrez PY - 2012/3/30/pubmed PY - 2012/12/10/medline SP - 314 EP - 23 JF - Journal of neurophysiology JO - J. Neurophysiol. VL - 108 IS - 1 N2 - When linking in time electrical stimulation of the peripheral nerve with transcranial magnetic stimulation (TMS), the excitability of the motor cortex can be modulated to evoke clear inhibition, as reflected by the amplitude decrement in the motor-evoked potentials (MEPs). This specific property, designated short-latency afferent inhibition (SAI), occurs when the nerve-TMS interstimulus interval (ISI) is approximately 25 ms and is considered to be a corticothalamic phenomenon. The aim of the present study was to use the electroencephalographic (EEG) responses to navigated-TMS coregistration to better characterize the neuronal circuits underlying SAI. The present experimental set included magnetic resonance imaging (MRI)-navigated TMS and 60-channel TMS-compatible EEG devices. TMS-evoked EEG responses and MEPs were analyzed in eight healthy volunteers; ISIs between median nerve and cortical stimulation were determined relative to the latency of the individual N20 component of the somatosensory-evoked potential (SEP) obtained after stimulation of the median nerve. ISIs from the latency of the N20 plus 3 ms and N20 plus 10 ms were investigated. In all experimental conditions, TMS-evoked EEG responses were characterized by a sequence of negative deflections peaking at approximately 7, 44, and 100 ms alternating with positive peaks at approximately 30, 60, and 180 ms post-TMS. Moreover, ISI N20+3 ms modulated both EEG-evoked activity and MEPs. In particular, it inhibited MEP amplitudes, attenuated cortical P60 and N100 responses, and induced motor cortex beta rhythm selective decrement of phase locking. The findings of the present experiment suggest the cortical origin of SAI that could result from the cortico-cortical activation of GABAergic-mediated inhibition onto the corticospinal neurons modulated by cholinergic activation able to reducing intralaminar inhibition and promoting intracolumnar inhibition. SN - 1522-1598 UR - https://www.unboundmedicine.com/medline/citation/22457460/Human_brain_cortical_correlates_of_short_latency_afferent_inhibition:_a_combined_EEG_TMS_study_ L2 - http://www.physiology.org/doi/full/10.1152/jn.00796.2011?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -