Primary Motor Cortex Organization Is Altered in Persistent Patellofemoral Pain

Te, Maxine; Baptista, Abrahão Fontes; Chipchase, Lucinda S; Schabrun, Siobhan M

doi:10.1093/pm/pnx036

Cited by 51 publications

(56 citation statements)

References 57 publications

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“…Numerous studies have suggested a link between altered corticomotor excitability and the symptoms of chronic musculoskeletal pain (Schabrun, Elgueta-Cancino, & Hodges, 2017;Tsao, Galea, & Hodges, 2008;Te, Baptista, Chipchase, & Schabrun, 2017;Tsao, Danneels, & Hodges, 2011;Schabrun, Hodges, Vicenzino, Jones, & Chipchase, 2015). However, only one study has conducted a longitudinal investigation of this mechanism in response to pain.…”

Section: Discussionmentioning

confidence: 99%

Slow peak alpha frequency and corticomotor depression linked to high pain susceptibility in transition to sustained pain

Seminowicz

Thapa

Furman

et al. 2018

Preprint

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Mechanisms that predict an individual's susceptibility to pain, before pain is present or in the first few days following pain onset, are unknown. We utilised a clinically-relevant human transitional pain model (intramuscular injections of nerve growth factor) to examine brain mechanisms that predict pain susceptibility. Resting state EEG and corticomotor excitability measured by TMS were evaluated longitudinally in healthy individuals as pain developed and resolved over 21 days. Whereas pre-pain central peak alpha frequency (PAF) correlated with peak pain occurring 4-6 days later, altered corticomotor excitability developed several days after pain onset and showed two distinct patterns (facilitation, depression). Individuals with combined slow PAF and corticomotor depression developed more severe pain. These data provide the first evidence of the temporal profile of key brain mechanisms as pain progressively develops. PAF and corticomotor excitability could represent biomarkers for susceptibility to high pain severity and subsequently, the development of chronic pain.

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Section: Discussionmentioning

confidence: 99%

Slow peak alpha frequency and corticomotor depression linked to high pain susceptibility in transition to sustained pain

Seminowicz

Thapa

Furman

et al. 2018

Preprint

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“…Differences in map representations in musculoskeletal pain syndromes are frequently reported (Coppieters et al, 2016). M1 map differences include map size, location, and/or number of peaks, volume, and the overlap between maps for different muscles (Massé-Alarie et al, 2017;Schabrun et al, 2014;Te, Baptista, Chipchase, & Schabrun, 2017;Tsao et al, 2011b;Ziemann & Siebner, 2008). Although the importance of changes in M1 organisation is not yet fully understood, previous research has found associations between differences of some parameters are concurrent with alterations in motor control, such as delayed muscle activations .…”

Section: Motor Cortex Organisation Differs Between Individuals Withmentioning

confidence: 99%

“…In back pain, the representation of superficial lumbar longissimus is more posterior such that it approximates the same location as the deep multifidus muscle (Schabrun et al, 2015;Tsao et al, 2011b). In patellofemoral pain, representations of rectus femoris, vastus lateralis, and vastus medialis are shifted anteriorly with greater overlap (Te et al, 2017). In back pain, greater overlap of M1 representations has been linked with less ability to separately move spine regions (Elgueta-Cancino et al, 2018;Tsao et al, 2011b).…”

Section: Differences In Location Of M1 Representations In Other Body mentioning

confidence: 99%

“…It is important to note that although we observed differences in M1 representation between groups, we cannot conclude they are a precursor to NP, a consequence of NP, or occur in parallel with NP without causal link. As pain can change M1 features (Schabrun et al, 2014;Schabrun et al, 2015;Te et al, 2017;Tsao et al, 2011b), and motor demands change the size of M1 muscle representations (Hund-Georgiadis & von Cramon, 1999;Pascual-Leone et al, 1995;Pascual-Leone, Amedi, Fregni, & Merabet, 2005), it is tempting to speculate that the differences represent an adaptation to pain. Longitudinal studies are required.…”

Section: Differences In Location Of M1 Representations In Other Body mentioning

confidence: 99%

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Motor cortex representation of deep and superficial neck flexor muscles in individuals with and without neck pain

Cancino

Marinovic

Jull

et al. 2019

Human Brain Mapping

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Sensorimotor control of neck muscles differs between individuals with and without pain. Differences in the primary motor cortex (M1) maps of these muscles may be involved. This study compared M1 representations of deep (DNF) and superficial (SNF) neck flexor muscles between 10 individuals with neck pain (NP) and 10 painfree controls. M1 organisation was studied using transcranial magnetic stimulation (TMS) applied to a grid over the skull and surface electromyography of DNF (pharyngeal electrode) and SNF. Three‐dimensional maps of M1 representation of each muscle were generated. Peaks in the SNF map that represented the sternocleidomastoid (SCM) and platysma muscles were identified. Unique centre of gravity (CoG)/map peaks were identified for the three muscles. In comparison to painfree controls, NP participants had more medial location of the CoG/peak of DNF, SCM, and platysma, greater mediolateral variation in DNF CoG (p = 0.02), fewer SNF and DNF map peaks (p = 0.01). These data show that neck flexor muscle M1 maps relate to trunk, neck, and face areas of the motor homunculus. Differences in M1 representation in NP have some similarities and some differences with observations for other musculoskeletal pain conditions. Despite the small sample size, our data did reveal differences and is comparable to other similar studies. The results of this study should be interpreted with consideration of methodological issues.

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“…Moreover, the primary motor cortex representation of the back muscles is shifted posteriorly and displays greater overlap in chronic low back pain using transcranial magnetic stimulation (TMS) [49,50,54,55]. Similar sensorimotor cortical adaptations have also been reported in chronic lateral epicondylalgia [4,44], rotator cuff tears [3], anterior cruciate ligament instability [17] and patello-femoral pain syndrome [32,52] indicating altered corticospinal drive to muscles associated with the painful/damaged structure. Short-term experimental muscle pain models in healthy individuals have been used to study the effect of acute nociception on sensory [37,38,45] and motor cortical excitability [34,51].…”

Section: A N U S C R I P T Introductionmentioning

confidence: 87%

Cortical Somatosensory Excitability Is Modulated in Response to Several Days of Muscle Soreness

Martino

Petrini

Schabrun

et al. 2018

The Journal of Pain

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Changes in excitability of the sensorimotor cortex have been demonstrated in clinical musculoskeletal pain, although the timing is unknown. Eccentric exercise provokes delayed-onset muscle soreness providing a model to study the temporal profile of sensorimotor cortical plasticity during progressively developing muscle soreness. Twelve healthy participants performed eccentric exercise of the wrist extensors. Likert pain scores, pressure pain thresholds at the extensor carpi radialis (ECR) muscle, somatosensory evoked potentials from electrical stimulation of the radial nerve, maximal wrist extension force, and ECR motor evoked potentials to transcranial magnetic stimulation were recorded before (baseline) and at 2 hours (2-h post), 2 days (day 2), and 6 days (day 6) after exercise. Compared with baseline, 1) the Likert pain score was increased at 2-h post and increased further at day 2 (P < .01); 2) the ECR pressure pain thresholds were decreased at day 2 (P < .001); 3) the P45 amplitude of the somatosensory evoked potential from central-parietal recording sites was increased at day 2 (P < .001); 4) maximal wrist extension force was reduced 2-h post and at day 2 (P < .002); and 5) the cortical area from which ECR motor evoked potentials could be elicited was reduced at 2-h post and at day 2 (P < .03). A decrease in the ECR pressure pain thresholds was correlated (P < .027) with an increase in the P45 amplitude at a centroparietal recording site. PERSPECTIVE: These novel data demonstrate that the somatosensory cortical excitability may be affected by muscle soreness developing over days in parallel with a deficit in the motor system. Cortical neuroplasticity may thus develop in the subacute phase and be relevant for understanding neural adaptation in the transition from acute to persistent pain.

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Primary Motor Cortex Organization Is Altered in Persistent Patellofemoral Pain

Cited by 51 publications

References 57 publications

Slow peak alpha frequency and corticomotor depression linked to high pain susceptibility in transition to sustained pain

Slow peak alpha frequency and corticomotor depression linked to high pain susceptibility in transition to sustained pain

Motor cortex representation of deep and superficial neck flexor muscles in individuals with and without neck pain

Cortical Somatosensory Excitability Is Modulated in Response to Several Days of Muscle Soreness

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