Muscle Pain Differentially Modulates Short Interval Intracortical Inhibition and Intracortical Facilitation in Primary Motor Cortex

2012 ◽  
Vol 13 (2) ◽  
pp. 187-194 ◽  
Author(s):  
Siobhan M. Schabrun ◽  
Paul W. Hodges
2010 ◽  
Vol 104 (3) ◽  
pp. 1382-1391 ◽  
Author(s):  
Yuichiro Shirota ◽  
Masashi Hamada ◽  
Yasuo Terao ◽  
Hideyuki Matsumoto ◽  
Shinya Ohminami ◽  
...  

Using the paired-pulse paradigm, transcranial magnetic stimulation (TMS) has revealed much about the human primary motor cortex (M1). A preceding subthreshold conditioning stimulus (CS) inhibits the excitability of the motor cortex, which is named short-interval intracortical inhibition (SICI). In contrast, facilitation is observed when the first pulse (S1) is followed by a second one at threshold (S2), named short-interval intracortical facilitation (SICF). SICI and SICF have been considered to be mediated by different neural circuits within M1, but more recent studies reported relations between them. In this study, we performed triple-pulse stimulation consisting of CS-S1-S2 to further explore putative interactions between these two effects. Three intensities of CS (80–120% of active motor threshold: AMT) and two intensities of S2 (120 and 140% AMT) were combined. The SICF in the paired-pulse paradigm exhibited clear facilitatory peaks at ISIs of 1.5 and 3 ms. The second peak at 3 ms was significantly suppressed by triple-pulse stimulation using 120% AMT CS, although the first peak was almost unaffected. Our present results obtained using triple-pulse stimulation suggest that each peak of SICF is differently modulated by different intensities of CS. The suppression of the second peak might be ascribed to the findings in the paired-pulse paradigm that CS mediates SICI by inhibiting later I waves such as I3 waves and that the second peak of SICF is most probably related to I3 waves. We propose that CS might inhibit the second peak of SICF at the interneurons responsible for I3 waves.


2018 ◽  
Vol 120 (6) ◽  
pp. 2858-2867 ◽  
Author(s):  
Harry T. Jordan ◽  
Cathy M. Stinear

Bilateral priming is a rehabilitation adjuvant that can improve upper limb motor recovery poststroke. It uses a table-top device to couple the upper limbs together such that active flexion and extension of one wrist leads to passive movement of the opposite wrist in a mirror symmetric pattern. Bilateral priming increases corticomotor excitability (CME) in the primary motor cortex (M1) of the passively driven wrist; however, the neurophysiological mechanisms underlying this increase remain unclear. This study explored these mechanisms by using transcranial magnetic stimulation over the right M1 and recording motor-evoked potentials from the passively driven left extensor carpi radialis of healthy adults. Intracortical measures were recorded before and 5 and 35 min after a single 15-min session of priming. One-millisecond short-interval intracortical inhibition, long-interval intracortical inhibition, late cortical disinhibition (LCD), and intracortical facilitation were recorded with a posterior-anterior (PA) intracortical current, whereas CME and short-interval intracortical facilitation (SICF) were recorded with both PA and anterior-posterior (AP) currents. CME with PA stimulation was also recorded ~1 h postpriming. PA CME was elevated 35 min postpriming and remained elevated ~1 h postpriming. LCD decreased, and AP SICF increased at both 5 and 35 min postpriming. However, these changes in LCD and AP SICF are unlikely to be the cause of the increased PA CME because of the differing timelines of their effects and AP and PA currents activating separate interneuron circuits. These results suggest that bilateral priming does not increase CME through alterations of the intracortical circuits investigated here. NEW & NOTEWORTHY This is the first study to measure how bilateral priming modulates corticomotor excitability with posterior-anterior and anterior-posterior intracortical currents, 1-ms short-interval intracortical inhibition, late cortical disinhibition, intracortical facilitation, and short-interval intracortical facilitation. We found corticomotor excitability with a posterior-anterior current increased by 35 min until ~1 h postpriming. Short-interval intracortical facilitation with an anterior-posterior current was greater for at least 35 min postpriming. This provides further insight into the neurophysiological mechanisms underlying bilateral priming.


NeuroImage ◽  
2019 ◽  
Vol 203 ◽  
pp. 116194 ◽  
Author(s):  
Jaakko O. Nieminen ◽  
Lari M. Koponen ◽  
Niko Mäkelä ◽  
Victor Hugo Souza ◽  
Matti Stenroos ◽  
...  

2013 ◽  
Vol 110 (5) ◽  
pp. 1158-1166 ◽  
Author(s):  
Mitsuaki Takemi ◽  
Yoshihisa Masakado ◽  
Meigen Liu ◽  
Junichi Ushiba

There is increasing interest in electroencephalogram (EEG)-based brain-computer interface (BCI) as a tool for rehabilitation of upper limb motor functions in hemiplegic stroke patients. This type of BCI often exploits mu and beta oscillations in EEG recorded over the sensorimotor areas, and their event-related desynchronization (ERD) following motor imagery is believed to represent increased sensorimotor cortex excitability. However, it remains unclear whether the sensorimotor cortex excitability is actually correlated with ERD. Thus we assessed the association of ERD with primary motor cortex (M1) excitability during motor imagery of right wrist movement. M1 excitability was tested by motor evoked potentials (MEPs), short-interval intracortical inhibition (SICI), and intracortical facilitation (ICF) with transcranial magnetic stimulation (TMS). Twenty healthy participants were recruited. The participants performed 7 s of rest followed by 5 s of motor imagery and received online visual feedback of the ERD magnitude of the contralateral hand M1 while performing the motor imagery task. TMS was applied to the right hand M1 when ERD exceeded predetermined thresholds during motor imagery. MEP amplitudes, SICI, and ICF were recorded from the agonist muscle of the imagined hand movement. Results showed that the large ERD during wrist motor imagery was associated with significantly increased MEP amplitudes and reduced SICI but no significant changes in ICF. Thus ERD magnitude during wrist motor imagery represents M1 excitability. This study provides electrophysiological evidence that a motor imagery task involving ERD may induce changes in corticospinal excitability similar to changes accompanying actual movements.


2019 ◽  
Author(s):  
Cécilia Neige ◽  
Dylan Rannaud Monany ◽  
Cathy M. Stinear ◽  
Winston D. Byblow ◽  
Charalambos Papaxanthis ◽  
...  

AbstractMotor imagery (MI) is the mental simulation of an action without any apparent muscular contraction. By means of transcranial magnetic stimulation, few studies revealed a decrease of short-interval intracortical inhibition (SICI) within the primary motor cortex. However, this decrease is ambiguous, as one would expect greater inhibition during MI to prevent overt motor output. The current study investigated the extent of SICI modulation during MI through a methodological and a conceptual reconsideration of i) the importance of parameters to assess SICI (Exp.1) and ii) the inhibitory process within the primary motor cortex as an inherent feature of MI (Exp.2). Participants performed two tasks: 1) rest and 2) imagery of isometric abduction of the right index finger. Using transcranial magnetic stimulation, motor evoked potentials were elicited in the right first dorsal interosseous muscle. An adaptive threshold-hunting paradigm was used, where the stimulus intensity required to maintain a fixed motor evoked potential amplitude was quantified. To test SICI, we conditioned the test stimulus with a conditioning stimulus (CS) of different intensities. Results revealed an Intensity by Task interaction showing that SICI decreased during MI as compared to rest only for the higher CS intensity (Exp.1). At the lowest CS intensities, a Task main effect revealed that SICI increased during MI (Exp.2). SICI modulation during MI depends critically on the CS intensity. By optimising CS intensity, we have shown that SICI circuits may increase during MI, revealing a potential mechanism to prevent the production of a movement while the motor system is activated.HighlightsExcitatory and inhibitory neural processes interact during motor imagery, as the motor regions are activated but no movement is produced.The current study investigated the extent of short interval intracortical inhibition modulation (SICI) during motor imagery.When using optimal settings, SICI increased during motor imagery, likely to prevent the production of an overt movement.


2009 ◽  
Vol 120 (1) ◽  
pp. 198-203 ◽  
Author(s):  
Kyohei Takahashi ◽  
Atsuo Maruyama ◽  
Masato Maeda ◽  
Seiji Etoh ◽  
Kohji Hirakoba ◽  
...  

2011 ◽  
Vol 105 (1) ◽  
pp. 100-106 ◽  
Author(s):  
R.F.H. Cash ◽  
U. Ziemann ◽  
G. W. Thickbroom

A suprathreshold pulse of transcranial magnetic stimulation (TMS) delivered to human motor cortex results in a period of long-interval intracortical inhibition (LICI) followed by a briefer period of disinhibition (late cortical disinhibition [LCD]). Short-interval intracortical facilitation (SICF) is mediated by excitatory networks in the motor cortex responsible for the generation of the indirect (I-) wave volleys that are evoked by TMS at a periodicity of about 1.5 ms. Because the excitatory synaptic network responsible for SICF undergoes inhibitory regulation, we hypothesized that SICF will be modulated during periods of inhibition and disinhibition. In particular we were interested to know whether SICF was up-regulated during disinhibition, implying an increase in excitatory synaptic efficacy. We measured SICF, at a paired-pulse interval of 1.5 ms, at various times (100–300 ms) after a suprathreshold priming stimulus (PS) of sufficient strength to evoke LICI and LCD. We found that the strength of SICF was normal during LICI, but was increased during LCD by an average of 64%. SICF onset latency was reduced by one I-wave interval during LCD and was delayed by one I-wave interval during LICI. We conclude that disinhibition, rather than inhibition, modulates the excitatory neuronal networks that underlie SICF, whereas the I-wave targeted is modified by the presence of both inhibition and disinhibition and that there is therefore a dissociation between the strength and site of SICF interaction. The increase in SICF during disinhibition further indicates that this is a promising period to investigate or modulate excitatory synaptic networks while they are less constrained by ongoing levels of inhibition.


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