scholarly journals Short interval cortical inhibition – literature review of methodology aspects and recommendations

2021 ◽  
Vol 14 (6) ◽  
pp. 1650
Author(s):  
Martin Horký ◽  
Tomáš Svěrák ◽  
Pavla Linhartová ◽  
Tomáš Kašpárek
eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Anton Fomenko ◽  
Kai-Hsiang Stanley Chen ◽  
Jean-François Nankoo ◽  
James Saravanamuttu ◽  
Yanqiu Wang ◽  
...  

Low-intensity transcranial ultrasound (TUS) can non-invasively modulate human neural activity. We investigated how different fundamental sonication parameters influence the effects of TUS on the motor cortex (M1) of 16 healthy subjects by probing cortico-cortical excitability and behavior. A low-intensity 500 kHz TUS transducer was coupled to a transcranial magnetic stimulation (TMS) coil. TMS was delivered 10 ms before the end of TUS to the left M1 hotspot of the first dorsal interosseous muscle. Varying acoustic parameters (pulse repetition frequency, duty cycle, and sonication duration) on motor-evoked potential amplitude were examined. Paired-pulse measures of cortical inhibition and facilitation, and performance on a visuomotor task was also assessed. TUS safely suppressed TMS-elicited motor cortical activity, with longer sonication durations and shorter duty cycles when delivered in a blocked paradigm. TUS increased GABAA-mediated short-interval intracortical inhibition and decreased reaction time on visuomotor task but not when controlled with TUS at near-somatosensory threshold intensity.


Author(s):  
Daisuke Sato ◽  
Koya Yamashiro ◽  
Yudai Yamazaki ◽  
Koyuki Ikarashi ◽  
Hideaki Onishi ◽  
...  

We aimed to verify whether indirect-wave (I-wave) recruitment and cortical inhibition can regulate or predict the plastic response to paired associative stimulation with an inter-stimulus interval of 25 ms (PAS25), and also whether water immersion (WI) can facilitate the subsequent PAS25-induced plasticity. To address the first question, we applied transcranial magnetic stimulation (TMS) to the M1 hand area, while alternating the direction of the induced current between posterior-to-anterior and anterior-to-posterior to activate two independent synaptic inputs to the corticospinal neurons. Moreover, we used a paired stimulation paradigm to evaluate the short-latency afferent inhibition (SAI) and short-interval intracortical inhibition (SICI). To address the second question, we examined the motor evoked potential (MEP) amplitudes before and after PAS25, with and without WI, and used the SAI, SICI, and MEP recruitment curves to determine the mechanism underlying priming by WI on PAS25. We demonstrated that SAI, with an inter-stimulus interval of 25 ms, might serve as a predictor of the response to PAS25, whereas I-wave recruitment evaluated by the MEP latency difference was not predictive of the PAS25 response, and found that 15 min WI prior to PAS25 facilitated long-term potentiation (LTP)-like plasticity due to a homeostatic increase in cholinergic activity.


Author(s):  
Zafiris J. Daskalakis ◽  
Robert Chen

Transcranial magnetic stimulation was first introduced in the late 1980s. Numerous studies have used TMS as an investigational tool to elucidate cortical physiology and to probe cognitive processes. This article introduces TMS paradigms and presents information gathered on cortical neuronal connectivity. TMS paradigms that demonstrate intracortical inhibition include short-interval cortical inhibition (SICI), cortical silence period (cSP) and long interval cortical inhibition (LICI). There are two types of cortical inhibitions from the stimulation of other brain areas, interhemispheric inhibition and cerebellum inhibition. The inhibition of the motor cortex can also be induced through the stimulation of peripheral nerves. This article talks about studies that describe interaction between inhibitory and facilitatory paradigms, the results of which are discussed in terms of cortical physiology and connectivity. The study of the interactions among cortical inhibitory and excitatory circuits may help to elucidate pathophysiology of neurological and psychiatric diseases.


Neurology ◽  
2019 ◽  
Vol 93 (6) ◽  
pp. e599-e610 ◽  
Author(s):  
Donald L. Gilbert ◽  
David A. Huddleston ◽  
Steve W. Wu ◽  
Ernest V. Pedapati ◽  
Paul S. Horn ◽  
...  

ObjectiveCompared to typically developing (TD) peers, children with attention-deficit/hyperactivity disorder (ADHD) consistently demonstrate impaired transcranial magnetic stimulation (TMS)-evoked short interval cortical inhibition (SICI) of motor evoked potentials (MEPs) in resting motor cortex (M1). To determine whether perturbed M1 physiology also reflects clinically relevant behavioral dysfunction, we evaluated M1 physiology during a cognitive control task taxing motor response selection/inhibition.MethodsIn this case-control study, behavioral ratings, motor skill (assessed using standardized examination), and left M1 physiology were evaluated in 131 right-handed, 8- to 12-year-old children (66 ADHD: mean 10.5 years, 43 male; 65 TD: mean 10.6 years, 42 male). The primary outcomes were MEP amplitudes and SICI, evaluated during rest and during a modified “racecar” Slater-Hammel stop signal reaction task, with TMS pulses administered 150 ms prior to the target go action and after the dynamic stop cue.ResultsGo responses were significantly slower (p = 0.01) and more variable (p = 0.002) in ADHD. Children with ADHD showed less M1 SICI at rest (p = 0.02) and during go (p = 0.03) and stop trials (p = 0.02). Rest M1 excitability increased during response inhibition task engagement (p < 0.0001). This Task-Related Up-Modulation (TRUM) was less robust across and within groups, with diminished task upmodulation associated with significantly more severe ADHD behavioral ratings and slower stop signal reaction times.ConclusionChildren with ADHD show anomalous motor cortex physiology, with deficient SICI across behavioral states and less TRUM from rest to action selection. Associations of these physiologic measures with ADHD symptoms and cognitive control measures support further investigation into biological mechanisms.


2005 ◽  
Vol 170 (2) ◽  
pp. 191-198 ◽  
Author(s):  
Nicola M. Benwell ◽  
Paul Sacco ◽  
Geoff R. Hammond ◽  
Michelle L. Byrnes ◽  
Frank L. Mastaglia ◽  
...  

2019 ◽  
Vol 12 (2) ◽  
pp. 445
Author(s):  
N. Chowdhury ◽  
E. Livesey ◽  
J. Harris

2019 ◽  
Vol 22 (7) ◽  
pp. 435-444 ◽  
Author(s):  
Deniz Doruk Camsari ◽  
Charles P Lewis ◽  
Ayse Irem Sonmez ◽  
Aiswarya Laks Nandakumar ◽  
Marjorie A Gresbrink ◽  
...  

Abstract Background The goal of this study was to examine baseline transcranial magnetic stimulation measures of cortical inhibition and excitability in depressed patients and characterize their longitudinal posttreatment changes. Methods Fifteen adolescents (age 13–17 years) with moderate to severe major depressive disorder and 22 healthy controls (age 9–17) underwent single- and paired-pulse transcranial magnetic stimulation and clinical assessments. Transcranial magnetic stimulation measures included short-interval intracortical inhibition (2 and 4 milliseconds), long-interval intracortical inhibition (100, 150, and 200 milliseconds), cortical silent period, and intracortical facilitation (10, 15, and 20 milliseconds). Ten participants with major depressive disorder initiated antidepressant treatment or had dose adjustments. These participants were reassessed after treatment. Depression symptom severity was measured with the Children’s Depression Rating Scale, Revised. Robust regression modeling compared healthy and depressed adolescents at baseline. Relationships between changes in cortical inhibition and changes in depressive symptom severity were assessed in the depressed adolescents receiving antidepressant treatment. Results Our results revealed that at baseline, short-interval intracortical inhibition-2 was significantly reduced (Padj = .01) in depressed participants, suggesting impaired cortical inhibition compared with healthy controls. At follow-up, improvement in Children’s Depression Rating Scale, Revised scores correlated with improvement in short-interval intracortical inhibition-4 amplitude (greater inhibition) after antidepressant treatment (R2 = 0.63; P = .01). Conclusions These results suggest that cortical inhibition measures may have promise as biomarkers in adolescents treated for depression.


2013 ◽  
Vol 109 (1) ◽  
pp. 106-112 ◽  
Author(s):  
R. F. H. Cash ◽  
F. L. Mastaglia ◽  
G. W. Thickbroom

A single transcranial magnetic stimulation (TMS) pulse typically evokes a short series of spikes in corticospinal neurons [known as indirect (I)-waves] which are thought to arise from transynaptic input. Delivering a second pulse at inter-pulse intervals (IPIs) corresponding to the timing of these I-waves leads to a facilitation of the response, and if stimulus pairs are delivered repeatedly, a persistent LTP-like increase in excitability can occur. This has been demonstrated at an IPI of 1.5 ms, which corresponds to the first I-wave interval, in an intervention referred to as ITMS (I-wave TMS), and it has been argued that this may have similarities with timing-dependent plasticity models. Consequently, we hypothesized that if the second stimulus is delivered so as not to coincide with I-wave timing, it should lead to LTD. We performed a crossover study in 10 subjects in which TMS doublets were timed to coincide (1.5-ms IPI, ITMS1.5) or not coincide (2-ms IPI, ITMS2) with I-wave firing. Single pulse motor-evoked potential (MEP) amplitude, resting motor threshold (RMT), and short-interval cortical inhibition (SICI) were measured from the first dorsal interosseous (FDI) muscle. After ITMS1.5 corticomotor excitability was increased by ∼60% for 15 min ( P < 0.05) and returned to baseline by 20 min. Increasing the IPI by just 500 μs to 2 ms reversed the aftereffect, and MEP amplitude was significantly reduced (∼35%, P < 0.05) for 15 min before returning to baseline. This reduction was not associated with an increase in SICI, suggesting a reduction in excitatory transmission rather than an increase in inhibitory efficacy. RMT also remained unchanged, suggesting that these changes were not due to changes in membrane excitability. Amplitude-matching ITMS2 did not modulate excitability. The results are consistent with timing-dependent synaptic LTP/D-like effects and suggest that there are plasticity mechanisms operating in the human motor cortex with a temporal resolution of the order of a few hundreds of microseconds.


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