Motor training‐induced cortical plastic changes and its disruption by chronic pain: A puzzle with more pieces than expected

Andrade, Daniel Ciampi de

doi:10.1002/ejp.531

Cited by 2 publications

(2 citation statements)

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“…This supports the idea that the after-effects of rTMS delivered at frequencies ∼ 10-20Hz are related to the M1 main frequency rather than to effects linked to the stimulation frequency band. This is in line with frequency ranges found to have therapeutic values for chronic pain management by M1 rTMS(see for review [1]).…”

Section: Discussionsupporting

confidence: 87%

“…High-frequency (10 Hz) repetitive transcranial magnetic stimulation (rTMS) to the primary motor cortex (M1) is a non-invasive neuromodulation technique able to induce analgesic effects [1] and has therapeutic potentials in chronic pain, stroke rehabilitation, and movement disorders, among others [2]. Although still unclear, rTMS-induced analgesia may provoke long-lasting cortical plastic changes by repetitively depolarizing myelinated axons in M1 [3], probably via Hebbian synaptic plasticity mechanisms [4].…”

Section: Introductionmentioning

confidence: 99%

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Repetitive transcranial magnetic stimulation to the motor cortex leads to a sequential increase in phase synchronization and power of TMS-evoked electroencephalographic recordings

Martino,

Casali,

Nascimento Couto

et al. 2024

Preprint

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Background: High-frequency (10 Hz) repetitive transcranial magnetic stimulation (rTMS) to the primary motor cortex (M1) is used to treat several neuropsychiatric disorders, but its main mechanism of action remains unclear. Objective: To probe four cortical hubs used for rTMS (M1; dorsolateral-prefrontal cortex, DLPFC; anterior cingulate cortex, ACC; posterosuperior insula, PSI) with TMS coupled with high-density electroencephalography (TMS-EEG) and measure cortical excitability and oscillatory dynamics before and after active and sham rTMS to M1. Methods: Before and immediately after active or sham M1-rTMS (15 min, 3,000 pulses at 10 Hz), single-pulse TMS evoked EEG were recorded at the four targets in 20 healthy individuals. Measures of cortical excitability and oscillatory dynamics were extracted at the main frequency bands (α [8-13 Hz], low-β [14-24 Hz], high-β [25-35 Hz]). Results: Comparing active and sham M1 rTMS, M1 TMS-EEG demonstrated an increase in high-β synchronization in electrodes around M1 stimulation area and remotely in the contralateral hemisphere (p=0.026). The increase in high-β synchronization (48-83 ms after TMS-EEG stimulation) was succeeded by an enhancement in low-β power (86-144 ms after TMS-EEG stimulation) both locally and in the contralateral hemisphere (p=0.006). No significant differences were observed in TMS-EEG responses probing DLPFC, ACC, or PSI. Conclusion: M1-rTMS engaged a sequence of enhanced phase synchronization, followed by an increase in power occurring within M1, that spread to remote areas and was measurable after the end of the stimulation session. These results are relevant to understanding the M1 neuroplastic effects of rTMS and associated changes in cortical activity dynamics.

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Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Repetitive transcranial magnetic stimulation to the motor cortex leads to a sequential increase in phase synchronization and power of TMS-evoked electroencephalographic recordings

Martino,

Casali,

Nascimento Couto

et al. 2024

Preprint

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Temporomandibular disorder and comorbid neck pain: facts and hypotheses regarding pain-induced and rehabilitation-induced motor activity changes

Fougeront

Fleiter

2018

Can. J. Physiol. Pharmacol.

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According to the "pain adaptation model", temporomandibular disorder (TMD)-related pain induces a paradoxical activity of masticatory muscles: an agonistic hypoactivity during jaw closing and an antagonistic activity during jaw opening (agonist/antagonist co-activation). However, this model suffers several weaknesses; notably, it does not explain all types of neck muscle activities in neck pain (NP), which is a very prevalent TMD comorbid condition. In NP, neck muscle antagonistic activity is increased, and agonistic activity is decreased as postulated by the pain adaptation model. However, synergistic and compensatory activity may occur and agonistic activity may be unchanged or even increased as postulated within the "vicious cycle theory". Thus, both theories would apply partly as outlined currently in musculoskeletal disorders (MSD). Besides pain, psychological stress may also induce motor dysfunction in TMD and NP. In NP, rehabilitation may increase agonistic activity and decrease compensatory activity and antagonistic activity, thus inducing a switch from agonist/antagonist co-activation towards reciprocal inhibition. Thus, rehabilitation-induced motor activity changes constitute a new research field that should improve MSD therapeutics. Additionally, immature tongue function (so-called infantile swallow) might be connected to TMD where low agonistic activity of masticatory muscles would be compensated by facial muscle hyperactivity during oropharyngeal phase of deglutition.

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Motor training‐induced cortical plastic changes and its disruption by chronic pain: A puzzle with more pieces than expected

Cited by 2 publications

References 4 publications

Repetitive transcranial magnetic stimulation to the motor cortex leads to a sequential increase in phase synchronization and power of TMS-evoked electroencephalographic recordings

Repetitive transcranial magnetic stimulation to the motor cortex leads to a sequential increase in phase synchronization and power of TMS-evoked electroencephalographic recordings

Temporomandibular disorder and comorbid neck pain: facts and hypotheses regarding pain-induced and rehabilitation-induced motor activity changes

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