scholarly journals Interactions between short-interval intracortical inhibition and short-latency afferent inhibition in human motor cortex

2009 ◽  
Vol 587 (21) ◽  
pp. 5163-5176 ◽  
Author(s):  
Henrik Alle ◽  
Tonio Heidegger ◽  
Lucia Kriváneková ◽  
Ulf Ziemann
Keyword(s):  
Motor Cortex ◽  
Short Interval ◽  
Intracortical Inhibition ◽  
Short Latency ◽  
Human Motor Cortex ◽  
Short Latency Afferent Inhibition ◽  
Afferent Inhibition ◽  
Human Motor

scholarly journals Two forms of short-interval intracortical inhibition in human motor cortex

2021 ◽  
Author(s):  
Po-Yu Fong ◽  
Danny Spampinato ◽  
Lorenzo Rocchi ◽  
Ricci Hannah ◽  
Yinghui Teng ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Short Interval ◽  
Intracortical Inhibition ◽  
Human Motor Cortex ◽  
Human Motor

Late Cortical Disinhibition in Human Motor Cortex: A Triple-Pulse Transcranial Magnetic Stimulation Study

2010 ◽  
Vol 103 (1) ◽  
pp. 511-518 ◽  
Author(s):  
R. F. H. Cash ◽  
U. Ziemann ◽  
K. Murray ◽  
G. W. Thickbroom
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Motor Cortex ◽  
Magnetic Stimulation ◽  
Short Interval ◽  
Motor Evoked Potential ◽  
Silent Period ◽  
Intracortical Inhibition ◽  
Human Motor Cortex ◽  
Acid Type ◽  
Human Motor

In human motor cortex transcranial magnetic stimulation (TMS) has been used to identify short-interval intracortical inhibition (SICI) corresponding to γ-aminobutyric acid type A (GABAA) effects and long-interval intracortical inhibition (LICI) and the cortical silent period (SP) corresponding to postsynaptic GABAB effects. Presynaptic GABAB effects, corresponding to disinhibition, can also be identified with TMS and have been shown to be acting during LICI by measuring SICI after a suprathreshold priming stimulus (PS). The duration of disinhibition is not certain and, guided by studies in experimental preparations, we hypothesized that it may be longer-lasting than postsynaptic inhibition, leading to a period of late cortical disinhibition and consequently a net increase in corticospinal excitability. We tested this first by measuring the motor-evoked potential (MEP) to a test stimulus (TS), delivered after a PS at interpulse intervals (IPIs) ≤300 ms that encompassed the period of PS-induced LICI and its aftermath. MEP amplitude was initially decreased, but then increased at IPIs of 190–210 ms, reaching 160 ± 17% of baseline 200 ms after PS ( P < 0.05). SP duration was 181 ± 5 ms. A second experiment established that the onset of the later period of increased excitability correlated with PS intensity ( r2 = 0.99) and with the duration of the SP ( r2 = 0.99). The third and main experiment demonstrated that SICI was significantly reduced in strength at all IPIs ≤220 ms after PS. We conclude that TMS-induced LICI is associated with a period of disinhibition that is at first masked by LICI, but that outlasts LICI and gives rise to a period during which disinhibition predominates and net excitability is raised. Identification of this late period of disinhibition in human motor cortex may provide an opportunity to explore or modulate the behavior of excitatory networks at a time when inhibitory effects are restrained.

Inhibitory and Disinhibitory Effects on I-Wave Facilitation in Motor Cortex

2011 ◽  
Vol 105 (1) ◽  
pp. 100-106 ◽  
Author(s):  
R.F.H. Cash ◽  
U. Ziemann ◽  
G. W. Thickbroom
Keyword(s):  
Motor Cortex ◽  
Short Interval ◽  
Intracortical Inhibition ◽  
Pulse Interval ◽  
Onset Latency ◽  
Intracortical Facilitation ◽  
Human Motor Cortex ◽  
Human Motor ◽  
Sufficient Strength ◽  
Inhibitory Regulation

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.

Effects of short-latency afferent inhibition on short-interval intracortical inhibition

2014 ◽  
Vol 111 (6) ◽  
pp. 1350-1361 ◽  
Author(s):  
Kaviraja Udupa ◽  
Zhen Ni ◽  
Carolyn Gunraj ◽  
Robert Chen
Keyword(s):  
Short Interval ◽  
Conditioning Stimulus ◽  
Intracortical Inhibition ◽  
Short Latency ◽  
Short Latency Afferent Inhibition ◽  
Afferent Inhibition ◽  
First Dorsal Interosseous Muscle ◽  
Active Motor ◽  
Inhibitory Interactions ◽  
Dorsal Interosseous Muscle

Peripheral nerve stimulation inhibits the motor cortex, and the process has been termed short-latency afferent inhibition (SAI) at interstimulus intervals (ISIs) of ∼20 ms. The objective of the present study was to test how SAI interacts with short-interval intracortical inhibition (SICI) under different stimulation conditions. We studied 20 healthy volunteers. Surface electromyogram was recorded from the first dorsal interosseous muscle. Using paired- and triple-pulse paradigms, we investigated how SAI interacts with SICI under these different conditions. The effects of different conditioning stimulus (CS) intensities (0.6–0.9 active motor threshold), SAI latencies (23 and 25 ms), and ISIs (2 and 3 ms) for SICI were examined in rest and active conditions. SAI had inhibitory interactions with SICI at different CS intensities for rest or active SICI, at SAI latencies of 23 and 25 ms. This interaction occurred at weak CS intensities for SICI when there was no inhibition, and SICI became facilitatory in the presence of SAI. This can be explained by SICI inhibiting SAI and not by saturation of inhibition. The interaction between SAI and SICI was greater for SICI at ISI of 3 ms than for ISI of 2 ms, suggesting that different circuits may be activated at these ISIs. We conclude that SAI and SICI have inhibitory interactions that are influenced by factors such as ISI and muscle activities, which should be considered in design and interpretation of cortical interaction studies.

Reorganisation in human motor cortex

1995 ◽  
Vol 73 (2) ◽  
pp. 218-222 ◽  
Author(s):  
M. C. Ridding ◽  
J. C Rothwell
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Motor Cortex ◽  
Magnetic Stimulation ◽  
Voluntary Contraction ◽  
Short Latency ◽  
Human Motor Cortex ◽  
Amputation Stump ◽  
Human Motor

Transcranial magnetic stimulation over the motor cortex was used to construct a map of the effective sites on the scalp from which short-latency electromyogram responses could be evoked in muscles proximal to either an amputation stump (two subjects) or an ischemically anesthetized forearm (two subjects). At rest, the maps were larger and the responses bigger when stimulating contralateral to the amputated arm or after anesthesia than they were in the intact arm or before anesthesia. However, this difference disappeared when the maps were constructed during a small tonic voluntary contraction of the target muscle. We conclude that reorganisation of the corticospinal projection to a muscle at rest may no longer be present during activity. If so, this calls into question the possible functional benefits of such reorganisation in the control of movement after peripheral damage.Key words: motor cortex, magnetic stimulation, amputation, ischemia.

scholarly journals Short-latency afferent inhibition and somato-sensory evoked potentials during the migraine cycle: surrogate markers of a cycling cholinergic thalamo-cortical drive?

2020 ◽  
Author(s):  
Gianluca Coppola ◽  
Davide Di Lenola ◽  
Chiara Abagnale ◽  
Fabio Ferrandes ◽  
Gabriele Sebastianelli ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Evoked Potentials ◽  
Motor Evoked Potential ◽  
Short Latency ◽  
Excitatory Effect ◽  
Sensory Afferents ◽  
Short Latency Afferent Inhibition ◽  
Afferent Inhibition ◽  
Cycle Dependent ◽  
Sensory Evoked

Abstract Background: Short-latency afferent inhibition (SAI) consists of motor cortex inhibition induced by sensory afferents and depends on the excitatory effect of cholinergic thalamocortical projections on inhibitory GABAergic cortical networks. Given the electrophysiological evidence for thalamo-cortical dysrhythmia in migraine, we studied SAI in migraineurs during and between attacks and searched for correlations with somatosensory habituation, thalamocortical activation, and clinical features.Methods: SAI was obtained by conditioning the transcranial magnetic stimulation-induced motor evoked potential (MEP) with an electric stimulus on the median nerve at the wrist with random stimulus intervals corresponding to the latency of individual somatosensory evoked potentials (SSEP) N20 plus 2, 4, 6, or 8 ms. We recruited 30 migraine without aura patients, 16 between (MO), 14 during an attack (MI), and 16 healthy volunteers (HV). We calculated the slope of the linear regression between the unconditioned MEP amplitude and the 4-conditioned MEPs as a measure of SAI. We also measured SSEP amplitude habituation, and high-frequency oscillations (HFO) as an index of thalamo-cortical activation.Results: Compared to HV, SAI, SSEP habituation and early SSEP HFOs were significantly reduced in MO patients between attacks, but enhanced during an attack. There was a positive correlation between degree of SAI and amplitude of early HFOs in HV, but not in MO or MI. When the two patient groups were pooled, both the MEP SAI slope and the SSEP habituation slope correlated positively with the number of days elapsed since the last migraine attack.Conclusions: The migraine cycle-dependent variations of SAI and SSEP HFOs are further evidence that facilitatory thalamocortical activation (of GABAergic networks in the motor cortex for SAI), likely to be cholinergic, is reduced in migraine at a distance from an attack, but increased ictally.

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