1993
DOI: 10.1007/bf00230207
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On the origin of the postexcitatory inhibition seen after transcranial magnetic brain stimulation in awake human subjects

Abstract: Non-invasive transcranial magnetic stimulation (TMS) of motor cortex induces motor evoked potentials in contralateral muscles which are thought to be conducted by the corticospinal tract. Furthermore, inhibitory actions can be elicited by TMS which appear directly after the motor evoked potential (postexcitatory inhibition, PI) and can be visualized by blockade of tonic voluntary EMG activity. It was the aim of the present study to answer the questions of whether this inhibitory action is mainly of cortical or… Show more

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Cited by 280 publications
(115 citation statements)
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“…Furthermore, Roick et al (1993) also demonstrated that SP duration was not modulated by any changes of finger or ankle joint position. It was identical irrespective of whether muscle actions were isometric or dynamic, with or without joint fixation.…”
Section: Silent Period (Sp) Tms Of Human Motor Cortex During a Volunmentioning
confidence: 85%
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“…Furthermore, Roick et al (1993) also demonstrated that SP duration was not modulated by any changes of finger or ankle joint position. It was identical irrespective of whether muscle actions were isometric or dynamic, with or without joint fixation.…”
Section: Silent Period (Sp) Tms Of Human Motor Cortex During a Volunmentioning
confidence: 85%
“…SP duration progressively increases with increasing TMS intensity. Roick et al (1993) reported that for first dorsal interosseous muscle, SP increased concomitantly with stimulation intensity from 30 to 100% of maximum stimulator output, unlike the MEPs which plateaued at 60-70%. Interestingly, muscle activation had a negligible role on the duration of SP; Säisänen et al (2008) reported that varying from 20 to 80% of MVC for the thenar musculature had no effect on SP.…”
Section: Silent Period (Sp) Tms Of Human Motor Cortex During a Volunmentioning
confidence: 95%
See 1 more Smart Citation
“…[15][16][17][18] For instance, administration of tiagabine, a GABA reuptake inhibitor, leads to an increased concentration of GABA in the synaptic cleft and predominantly activates GABA B receptors, 19 which has been reported to result in a dose-dependent prolongation of the cortical silent period. 16 Furthermore, baclofen, a potentiator of GABA B receptor-mediated inhibitory neurotransmission, has also been found to lengthen the cortical silent period.…”
Section: Cortical Silent Periodmentioning
confidence: 99%
“…10,38 Evidence has been given for the existence of supraspinal inhibition due to intracortical inhibitory interneurons because MEPs and CoSPs are variable in different cortical and subcortical lesions. 2,4,34 The CoSPs can be used for prediction of recovery in deficient motor systems poststroke and for judgment of callosal function. 18,43 The present study demonstrates that CoSPs can correspond well to motor deficits in syringomyelia and are superior in specificity than MEPs (86% vs 72%, respectively), although this is statistically not significant.…”
Section: 13mentioning
confidence: 99%