Electrophysiological correlates of short-latency afferent inhibition: a combined EEG and TMS study

被引:47
|
作者
Bikmullina, Rozaliya [2 ]
Kicic, Dubravko [1 ,2 ]
Carlson, Synnoeve [3 ,4 ,5 ]
Nikulin, Vadim V. [6 ,7 ]
机构
[1] Aalto Univ, Dept Biomed Engn & Computat Sci, Espoo 02015, TKK, Finland
[2] Hosp Dist Helsinki & Uusimaa, BioMag Lab HUSLAB, Helsinki, Finland
[3] Univ Helsinki, Neurosci Unit, Inst Biomed Physiol, Helsinki, Finland
[4] Aalto Univ, Low Temp Lab, Brain Res Unit, FIN-02150 Espoo, Finland
[5] Univ Tampere, Sch Med, FIN-33101 Tampere, Finland
[6] Charite, Neurophys Grp, Dept Neurol & Clin Neurophysiol, D-13353 Berlin, Germany
[7] Bernstein Ctr Computat Neurosci, Berlin, Germany
基金
芬兰科学院;
关键词
Short-latency afferent inhibition; TMS-evoked EEG response; Motor cortex; TRANSCRANIAL MAGNETIC STIMULATION; HUMAN MOTOR CORTEX; CORTICAL STIMULATION; CUTANEOMOTOR INTEGRATION; EVOKED-POTENTIALS; HUMAN HAND; GABA-A; RESPONSES; EXCITABILITY; BRAIN;
D O I
10.1007/s00221-009-1723-7
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Cutaneous stimulation produces short-latency afferent inhibition (SAI) of motor-evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS). Since the demonstration of SAI is primarily based on the attenuation of MEPs, its cortical origin is not yet fully understood. In the present study we combined TMS with concurrent electroencephalography (EEG) in order to obtain direct cortical correlates of SAI. TMS-evoked EEG responses and MEPs were analysed with and without preceding electrical stimulation of the index finger cutaneous afferents in ten healthy volunteers. We show that the attenuation of MEPs by cutaneous stimulation has its counterpart in the attenuation of the N100 EEG response. Moreover, the attenuation of the cortical N100 component correlated positively with the strength of SAI, indicating that the transient changes in cortical excitability can be reflected in the amplitude dynamics of MEPs. We hypothesize that the hyperpolarization of the pyramidal cells due to SAI lowers the capacity of TMS to induce the inhibitory current needed to elicit N100, thus leading to its attenuation. We suggest that the observed interaction of two inhibitory processes, SAI and N100, provides further evidence for the cortical origin of SAI.
引用
收藏
页码:517 / 526
页数:10
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