Altered cortical excitability in persistent idiopathic facial pain

Cephalalgia ◽  
2018 ◽  
Vol 39 (2) ◽  
pp. 219-228 ◽  
Author(s):  
Ricardo Galhardoni ◽  
Daniel Ciampi de Andrade ◽  
Mariana YT Puerta ◽  
Andre R Brunoni ◽  
Bruna LR Varotto ◽  
...  

Introduction Persistent idiopathic facial pain is a refractory and disabling condition of unknown mechanism and etiology. It has been suggested that persistent idiopathic facial pain patients have not only peripheral generators of pain, but also central nervous system changes that would contribute to the persistence of symptoms. We hypothesized that persistent idiopathic facial pain would have changes in brain cortical excitability as measured by transcranial magnetic stimulation compared to healthy controls. Methods Twenty-nine persistent idiopathic facial pain patients were compared to age- and sex-matched healthy controls and underwent cortical excitability measurements by transcranial magnetic stimulation applied to the cortical representation of the masseter muscle of both hemispheres. Single-pulse stimulation was used to measure the resting motor threshold and suprathreshold motor-evoked potentials. Paired-pulse stimulation was used to assess short intracortical inhibition and intracortical facilitation. Clinical pain and associated symptoms were assessed with validated tools. Results Spontaneous pain was found in 27 (93.1%) and provoked pain was found in two (6.9%) persistent idiopathic facial pain patients. The motor-evoked potentials at 120% and 140% were significantly lower for both hemispheres compared to controls. Persistent idiopathic facial pain patients had lower short-interval intracortical inhibition compared with controls. These changes were correlated with some aspects of quality of life, and higher mood symptoms. These neurophysiological alterations were not influenced by analgesic medication, as similar changes were observed in patients with or without central-acting drugs. Conclusions Persistent idiopathic facial pain is associated with changes in intracortical modulation involving GABAergic mechanisms, which may be related to certain aspects of the pathophysiology of this chronic pain condition. Trial registration: NTC01746355.

Cephalalgia ◽  
2009 ◽  
Vol 30 (1) ◽  
pp. 46-52 ◽  
Author(s):  
F Brighina ◽  
A Palermo ◽  
O Daniele ◽  
A Aloisio ◽  
B Fierro

We showed reduced motor intracortical inhibition (ICI) and paradoxical increase of intracortical facilitation (ICF) to 1 Hz repetitive transcranial magnetic stimulation (rTMS) in patients affected by migraine with aura (MA). In conditions of enhanced excitability due to a reduced inhibition, high-frequency rTMS was found to potentiate intracortical inhibition. Here we explored the conditioning effects of high-frequency priming stimulation of motor cortex with the aim of normalizing excitability reverting paradoxical facilitation by 1 Hz rTMS in MA. Nine patients with MA and nine healthy controls underwent a paired-pulse TMS paradigm to evaluate motor intracortical excitability (ICI and ICF) before and after the following rTMS conditions: 1 Hz alone or preceded by a real or sham conditioning high-frequency (10 Hz) rTMS. Sham was used to control for rTMS specificity. In baseline, ICI was significantly lower in migraineurs with respect to controls. One hertz stimulation reduced motor evoked potential amplitude and ICF in healthy controls, while it caused a significant paradoxical ICF increase in migraineurs. High-frequency rTMS conditioning normalized excitability in migraine, increasing short ICI and so reversing the paradoxical effects of 1 Hz rTMS. These findings raise the possibility that the interictal reduced intracortical inhibition in migraine could be normalized by high-frequency rTMS. This would open perspectives for new treatment strategies in migraine prevention.


2020 ◽  
Vol 123 (5) ◽  
pp. 1969-1978
Author(s):  
Jessica M. D’Amico ◽  
Siobhan C. Dongés ◽  
Janet L. Taylor

In this study, we present a novel, intensity-dependent repetitive transcranial magnetic stimulation (rTMS) protocol that induces lasting, plastic changes within the corticospinal tract. High-intensity rTMS at a frequency of 0.1 Hz induces facilitation of motor evoked potentials (MEPs) lasting at least 35 min. Additionally, these changes are not limited only to small MEPs but occur throughout the recruitment curve. Finally, facilitation of MEPs following high-intensity rTMS does not appear to be due to changes in intracortical inhibition or facilitation.


2009 ◽  
Vol 23 (5) ◽  
pp. 486-493 ◽  
Author(s):  
Jakob Udby Blicher ◽  
Johannes Jakobsen ◽  
Grethe Andersen ◽  
Jørgen Feldbæk Nielsen

Background. A possible role for GABA in regulating cortical plasticity after stroke has been proposed. Objective. To investigate changes in intracortical inhibitory and facilitatory circuits in the affected hemisphere more than 6 months after stroke, as well as modulation of excitability by a single training session. Methods. A total of 22 patients >6 months after stroke were compared to age- and gender-matched healthy participants. Cortical excitability was assessed by transcranial magnetic stimulation (TMS), including paired-pulse stimulation, before and up to 30 minutes after a single 15-minute session of 1 Hz thumb abduction-adduction movements. Results. At baseline, TMS showed decreased intracortical inhibition in the affected hemisphere of patients ( P = .004) compared to healthy participants. After training a short-lasting decline in motor evoked potentials was observed in both patients ( P = .002) and healthy participants ( P = .06). Moreover, in healthy participants, inhibitory activity decreased up to 30 minutes after training whereas no significant change was seen in the patients. Conclusions. The findings indicate that inhibitory intracortical circuits are less active after stroke, and no change in inhibitory activity is evident after a single training session. This may indicate that intracortical disinhibition is beneficial during recovery and that an impaired capacity for modulation remains in the chronic stage of stroke.


2019 ◽  
Vol 121 (2) ◽  
pp. 471-479 ◽  
Author(s):  
Lavender A. Otieno ◽  
George M. Opie ◽  
John G. Semmler ◽  
Michael C. Ridding ◽  
Simranjit K. Sidhu

Fatiguing intermittent single-joint exercise causes an increase in corticospinal excitability and a decrease in intracortical inhibition when measured with peripherally recorded motor evoked potentials (MEPs) after transcranial magnetic stimulation (TMS). Combined TMS and electroencephalography (TMS-EEG) allows for more direct recording of cortical responses through the TMS-evoked potential (TEP). The aim of this study was to investigate the changes in the excitatory and inhibitory components of the TEP during fatiguing single-joint exercise. Twenty-three young (22 ± 2 yr) healthy subjects performed intermittent 30-s maximum voluntary contractions of the right first dorsal interosseous muscle, followed by a 30-s relaxation period repeated for a total of 15 min. Six single-pulse TMSs and one peripheral nerve stimulation (PNS) to evoke maximal M wave (Mmax) were applied during each relaxation period. A total of 90 TMS pulses and 5 PNSs were applied before and after fatiguing exercise to record MEP and TEP. The amplitude of the MEP (normalized to Mmax) increased during fatiguing exercise ( P < 0.001). There were no changes in local and global P30, N45, and P180 of TEPs during the development of intermittent single-joint exercise-induced fatigue. Global analysis, however, revealed a decrease in N100 peak of the TEP during fatiguing exercise compared with before fatiguing exercise ( P = 0.02). The decrease in N100 suggests a fatigue-related decrease in global intracortical GABAB-mediated inhibition. The increase in corticospinal excitability typically observed during single-joint fatiguing exercise may be mediated by a global decrease in intracortical inhibition. NEW & NOTEWORTHY Fatiguing intermittent single-joint exercise causes an increase in corticospinal excitability and a decrease in intracortical inhibition when measured with transcranial magnetic stimulation (TMS)-evoked potentials from the muscle. The present study provides new and direct cortical evidence, using TMS-EEG to demonstrate that during single-joint fatiguing exercise there is a global decrease in intracortical GABAB-mediated inhibition.


2011 ◽  
Vol 105 (2) ◽  
pp. 615-624 ◽  
Author(s):  
Andrew M. Vahabzadeh-Hagh ◽  
Paul A. Muller ◽  
Alvaro Pascual-Leone ◽  
Frances E. Jensen ◽  
Alexander Rotenberg

Paired-pulse transcranial magnetic stimulation (ppTMS) is a noninvasive method to measure cortical inhibition in vivo. Long interpulse interval (50–500 ms) ppTMS (LI-ppTMS) provokes intracortical inhibitory circuits and can reveal pathologically impaired cortical inhibition in disorders such as epilepsy. Adaptation of ppTMS protocols to rodent disease models is highly desirable to facilitate basic and translational research. We previously adapted single-pulse TMS (spTMS) methods to rats, but ppTMS has yet to be applied. Specifically, whether ppTMS elicits an inhibitory response in rodents is unknown. ppTMS in rats also requires anesthesia, a setting under which the preservation of these measures is undetermined. We therefore tested, in anesthetized rats, whether anesthetic choice affects spTMS-motor-evoked potentials (MEPs), LI-ppTMS in rats, as in humans, elicits intracortical inhibition of the MEP, and rat LI-ppTMS inhibition is acutely impaired in a seizure model. Rats were anesthetized with pentobarbital (PB) or ketamine-atropine-xylazine (KAX) and stimulated unilaterally over the motor cortex while recording bilateral brachioradialis MEPs. LI-ppTMS was applied analogous to human long interval intracortical inhibition (LICI) protocols, and acute changes in inhibition were evaluated following injection of the convulsant pentylenetetrazole (PTZ). We find that spTMS-evoked MEPs were reliably present under either anesthetic, and that LI-ppTMS elicits inhibition of the conditioned MEP in rats, similar to human LICI, by as much as 58 ± 12 and 71 ± 11% under PB and KAX anesthesia, respectively. LI-ppTMS inhibition was reduced to as much as 53% of saline controls following PTZ injection, while spTMS-derived measures of corticospinal excitability were unchanged. Our data show that regional inhibition, similar to human LICI, is present in rats, can be elicited under PB or KAX anesthesia, and is reduced following convulsant administration. These results suggest a potential for LI-ppTMS as a biomarker of impaired cortical inhibition in murine disease models.


1997 ◽  
Vol 117 (3) ◽  
pp. 437-443 ◽  
Author(s):  
D. S. Stokic´ ◽  
W. Barry McKay ◽  
Lillian Scott ◽  
Arthur M. Sherwood ◽  
Milan R. Dimitrijevic´

1996 ◽  
Vol 83 (1) ◽  
pp. 288-290 ◽  
Author(s):  
Susumu Yahagi ◽  
Kuniyoshi Shimura ◽  
Tatsuya Kasai

During motor imagery, to estimate changes in excitability of flexor carpi radialis muscle motoneurons of the spinal and cortical levels, electrical stimuli for recording H-reflex and transcranial magnetic stimulation (TMS) for recording motor evoked potentials (MEPs) were used. In the absence of movement or detectable EMG activity during motor magery, there was an increase in cortical excitability with no change in spinal excitability


2019 ◽  
Author(s):  
Marcus T Wilson ◽  
Bahar Moezzi ◽  
Nigel C Rogasch

AbstractObjectiveTo develop a population-based biophysical model of motor-evoked potentials (MEPs) following transcranial magnetic stimulation (TMS).MethodsWe combined an existing MEP model with population-based cortical modeling. Layer 2/3 excitatory and inhibitory neural populations, modeled with neural-field theory, are stimulated with TMS and feed layer 5 corticospinal neurons, which also couple directly but weakly to the TMS pulse. The layer 5 output controls mean motoneuron responses, which generate a series of single motor-unit action potentials that are summed to estimate a MEP.ResultsA MEP waveform was generated comparable to those observed experimentally. The model captured TMS phenomena including a sigmoidal input-output curve, common paired pulse effects (short interval intracortical inhibition, intracortical facilitation, long interval intracortical inhibition) including responses to pharmacological interventions, and a cortical silent period. Changes in MEP amplitude following theta burst paradigms were observed including variability in outcome direction.ConclusionsThe model reproduces effects seen in common TMS paradigms.SignificanceThe model allows population-based modeling of changes in cortical dynamics due to TMS protocols to be assessed in terms of changes in MEPs, thus allowing a clear comparison between population-based modeling predictions and typical experimental outcome measures.HighlightsA model of motor-evoked potential formation gives a realistic electromyogram in response to TMS.The model reproduces effects of SICI, ICF and LICI.A link between existing neural field modeling and realistic outcome measures of TMS is provided.


2021 ◽  
Vol 15 ◽  
Author(s):  
Mitsuhiro Nito ◽  
Natsuki Katagiri ◽  
Kaito Yoshida ◽  
Tadaki Koseki ◽  
Daisuke Kudo ◽  
...  

Repetitive peripheral magnetic stimulation (rPMS) may improve motor function following central nervous system lesions, but the optimal parameters of rPMS to induce neural plasticity and mechanisms underlying its action remain unclear. We examined the effects of rPMS over wrist extensor muscles on neural plasticity and motor performance in 26 healthy volunteers. In separate experiments, the effects of rPMS on motor evoked potentials (MEPs), short-interval intracortical inhibition (SICI), intracortical facilitation (ICF), direct motor response (M-wave), Hoffmann-reflex, and ballistic wrist extension movements were assessed before and after rPMS. First, to examine the effects of stimulus frequency, rPMS was applied at 50, 25, and 10 Hz by setting a fixed total number of stimuli. A significant increase in MEPs of wrist extensors was observed following 50 and 25 Hz rPMS, but not 10 Hz rPMS. Next, we examined the time required to induce plasticity by increasing the number of stimuli, and found that at least 15 min of 50 and 25 Hz rPMS was required. Based on these parameters, lasting effects were evaluated following 15 min of 50 or 25 Hz rPMS. A significant increase in MEP was observed up to 60 min following 50 and 25 Hz rPMS; similarly, an attenuation of SICI and enhancement of ICF were also observed. The maximal M-wave and Hoffmann-reflex did not change, suggesting that the increase in MEP was due to plastic changes at the motor cortex. This was accompanied by increasing force and electromyograms during wrist ballistic extension movements following 50 and 25 Hz rPMS. These findings suggest that 15 min of rPMS with 25 Hz or more induces an increase in cortical excitability of the relevant area rather than altering the excitability of spinal circuits, and has the potential to improve motor output.


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