High frequency repetitive transcranial magnetic stimulation to the left dorsolateral prefrontal cortex modulates sensorimotor cortex function in the transition to sustained muscle pain

Martino, Enrico De; Seminowicz, David A.; Schabrun, Siobhan M; Petrini, Laura; Graven‐Nielsen, Thomas

doi:10.1016/j.neuroimage.2018.10.076

Cited by 35 publications

(37 citation statements)

References 74 publications

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“…Moreover, previous research in healthy pain-free individuals demonstrated that network-tDCS (Fischer et al, 2017), bilateral M1 tDCS (Maezawa et al, 2019), single-site M1 tDCS (Nitsche et al, 2005) and repeated-TMS (rTMS) to M1 increased corticomotor excitability above baseline values. Results are also in agreement with rTMS studies in experimental pain (De Martino et al, 2019;Fierro et al, 2010) and chronic disorders (De Andrade et al, 2011;Mhalla et al, 2011;Moisset et al, 2016) where pain-related changes in corticomotor excitability were reverted to normal levels, but not beyond them, when targeting DLPFC or M1. These pieces of evidence suggest that tDCS effects on the corticomotor excitability show a state dependency (i.e.…”

Section: Counteraction Of Pain-related Corticomotor Inhibition After Network-tdcssupporting

confidence: 88%

Effects of multifocal transcranial direct current stimulation targeting the motor network during prolonged experimental pain

Gregoret

Zamorano

Graven‐Nielsen

2021

European Journal of Pain

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Background Antinociceptive effects of transcranial direct current stimulation (tDCS) over the primary motor cortex (M1) have been extensively studied in the past years. However, M1 does not work in isolation, but it rather interacts within a network, the so‐called resting‐state motor network. Objective To explore the anti‐nociceptive effects of a new multifocal tDCS approach administered to regions linked to the resting state motor network (network‐tDCS) compared to sham tDCS. Methods Healthy individuals were included in this randomized, parallel and double‐blinded study comprising two consecutive interventions with 24‐hr interval of either active (n = 19) or sham (n = 19) network‐tDCS. Prolonged pain was induced by application of topical capsaicin on the dorsum of the hand during a 24‐hr period. Assessments of corticomotor excitability (transcranial magnetic stimulation), pain ratings (numerical rating scale, NRS), skin pain sensitivity on the arm (heat and mechanical), temporal summation of pain (TSP) and conditioned pain modulation (CPM) were performed at baseline (Day1‐baseline), after 25 min of capsaicin application and before the first tDCS session (Day1‐post‐cap), and after the second tDCS session (Day2). Results Comparing Day2 to Day1‐baseline measures, there was reduced corticomotor excitability (p < .05) and impaired CPM‐effect (p < .05) after sham but not after active network‐tDCS. Pain NRS ratings increased at Day2 compared to Day1‐post‐cap (p < .01) in both groups whereas no significant changes were found in pain sensitivity and TSP. Conclusions Present findings demonstrate that tDCS applied over regions linked to the resting state motor network reverts the inhibition of corticomotor excitability and CPM impairment both provoked by prolonged experimental pain for 24 hr. Significance These findings highlight that the stimulation of the resting state motor network with multifocal tDCS may represent a potential cortical target to treat chronic pain, particularly in patients exhibiting maladaptive corticomotor excitability and impaired conditioned pain modulation effects.

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Section: Counteraction Of Pain-related Corticomotor Inhibition After Network-tdcssupporting

confidence: 88%

Effects of multifocal transcranial direct current stimulation targeting the motor network during prolonged experimental pain

Gregoret

Zamorano

Graven‐Nielsen

2021

European Journal of Pain

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“…The DLPFC is involved in many cognitive and regulatory functions and connected to different functional brain networks (Seminowicz & Moayedi, ). Regarding tonic experimental pain, modulatory effects of the DLPFC on the excitability of the sensorimotor cortex were reported (De Martino, Seminowicz, Schabrun, Petrini, & Graven‐Nielsen, ). The present observation of increased connectivity between sensorimotor and lateral prefrontal cortex would be, in principle, well compatible with these observations of an important role of dorsolateral prefrontal‐sensorimotor connectivity in tonic pain.…”

Section: Discussionmentioning

confidence: 99%

Neural oscillations and connectivity characterizing the state of tonic experimental pain in humans

Nickel

Dinh

et al. 2019

Human Brain Mapping

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Pain is a complex phenomenon that is served by neural oscillations and connectivity involving different brain areas and frequencies. Here, we aimed to systematically and comprehensively assess the pattern of neural oscillations and connectivity characterizing the state of tonic experimental pain in humans. To this end, we applied 10‐min heat pain stimuli consecutively to the right and left hand of 39 healthy participants and recorded electroencephalography. We systematically analyzed global and local measures of oscillatory brain activity, connectivity, and graph theory‐based network measures during tonic pain and compared them to a nonpainful control condition. Local measures showed suppressions of oscillatory activity at alpha frequencies together with stronger connectivity at alpha and beta frequencies in sensorimotor areas during tonic pain. Furthermore, sensorimotor areas contralateral to stimulation showed significantly increased connectivity to a common area in the medial prefrontal cortex at alpha frequencies. Together, these observations indicate that the state of tonic experimental pain is associated with a sensorimotor‐prefrontal network connected at alpha frequencies. These findings represent a step further toward understanding the brain mechanisms underlying long‐lasting pain states in health and disease.

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“…Overall, our findings that suggest decreased corticomotor excitability direct oppose the vicious cycle theory (Travell et al, ). Nonetheless, recent studies have presented the opposite effect for the spinal innervation, i.e., increased corticomotor excitability following repeated injections of NFG into the extensor carpi radialis brevis (ECRB), which is likely explained as a motor learning effect that results from the search for a new moment strategy in the affected limb (De Martino, Seminowicz, Schabrun, Petrini, & Graven‐Nielsen, ; De Martino, Zandalasini, Schabrun, Petrini, & Graven‐Nielsen, ; Schabrun, Christensen, Mrachacz‐Kersting, & Graven‐Nielsen, ). There are some important methodological differences that could account for these contradictory findings, besides the need of the above‐mentioned pre‐activation level: (a) the tonic muscle contractions could have facilitated nociceptive inputs in the NGF injected masseter.…”

Section: Discussionmentioning

confidence: 99%

Masseter corticomotor excitability is decreased after intramuscular administration of nerve growth factor

Costa

Exposto

Kothari

et al. 2019

European Journal of Pain

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Background Quantification of motor‐evoked potentials (MEPs) can contribute to better elucidate the central modulation of motor pathways in response to nociceptive inputs. The primary aim of this study was to assess the modulatory effects of nerve growth factor (NGF) injection on masseter corticomotor excitability. Methods The healthy participants of this randomized, double blind placebo‐controlled experiment were assigned to have injected into the right masseter muscle either NGF (n = 25) or isotonic saline (IS, n = 17). The following variables were assessed at baseline and 48 hr after the injection: right masseter MEP amplitude and corticomotor mapping and clinical assessment of jaw pain intensity and function. Repeated Measures ANOVA was applied to the data. Results NGF caused jaw pain and increased jaw functional disability after the injection (p < 0.050). Also, the participants in the NGF group decreased the MEP amplitude (p < 0.001) but the IS group did not present any significant modulation after the injection (p > 0.050). Likewise, the participants in the NGF group reduced corticomotor map area and volume (p < 0.001), but the IS group did not show any significant corticomotor mapping changes after the injection (p > 0.050). Finally, there was a significant correlation between the magnitude of decreased corticomotor excitability and jaw pain intensity on chewing 48 hr after the NGF injection (r = −0.51, p = 0.009). Conclusion NGF‐induced masseter muscle soreness can significantly reduce jaw muscle corticomotor excitability, which in turn is associated with lower jaw pain intensity and substantiates the occurrence of central changes that most likely aim to protect the musculoskeletal orofacial structures. Significance Intramuscular administration of nerve growth factor into masseter muscle causes inhibitory corticomotor plasticity, which likely occurs to prevent further damage and seems associated with lower pain intensity on function.

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High frequency repetitive transcranial magnetic stimulation to the left dorsolateral prefrontal cortex modulates sensorimotor cortex function in the transition to sustained muscle pain

Abstract: 2019) High frequency repetitive transcranial magnetic stimulation to the left dorsolateral prefrontal cortex modulates sensorimotor cortex function in the transition to sustained muscle pain. NeuroImage,

Cited by 35 publications

References 74 publications

Effects of multifocal transcranial direct current stimulation targeting the motor network during prolonged experimental pain

Effects of multifocal transcranial direct current stimulation targeting the motor network during prolonged experimental pain

Neural oscillations and connectivity characterizing the state of tonic experimental pain in humans

Masseter corticomotor excitability is decreased after intramuscular administration of nerve growth factor

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