Muscle Pain Differentially Modulates Short Interval Intracortical Inhibition and Intracortical Facilitation in Primary Motor Cortex

The University of Queensland, NHMRC Centre of Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Science, St Lucia, Australia.
The journal of pain: official journal of the American Pain Society (Impact Factor: 4.01). 02/2012; 13(2):187-94. DOI: 10.1016/j.jpain.2011.10.013
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Excitability of the motor cortex can be suppressed during muscle pain. Yet the mechanisms are largely unknown. Short interval intracortical inhibition (SICI) and intracortical facilitation (ICF) were examined as possible candidate mechanisms to underpin this change. SICI and ICF were investigated in 11 healthy individuals before, during and after infusion of hypertonic saline into right first dorsal interosseous (FDI). Using paired-pulse transcranial magnetic stimulation (TMS), interstimulus intervals of 2, 3, and 13 ms were investigated. Pain intensity and quality were recorded using a 10-cm visual analogue scale and the McGill Pain Questionnaire. Resting motor threshold and motor-evoked potentials (MEPs) to single TMS stimuli were recorded before and after pain. Electromyographic recordings were made from right FDI and abductor digiti minimi. Participants reported an average pain intensity of 5.8 (1.6) cm. MEP amplitudes decreased in both muscles. Compared with the pre-pain condition, SICI was increased following pain, but not during. ICF was decreased both during and after pain when compared with the pre-pain condition. These findings suggest that muscle pain differentially modulates SICI and ICF. Although the functional relevance is unknown, we hypothesize decreased facilitation and increased inhibition may contribute to the restriction of movement of a painful body part. PERSPECTIVE: This article provides evidence for decreased intracortical facilitation and increased short interval intracortical inhibition in response to muscle pain. This finding is relevant to clinicians as a mechanism which may underlie restricted movement in acute and chronic pain.

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Available from: Siobhan Schabrun, Oct 05, 2015
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    • "Increased corticomotor excitability was observed during and after acute muscle pain, and this effect was accompanied by a reduction in ICF, but no change in SICI, during pain. The reduction in ICF, and no change in SICI, during pain is consistent with previous studies of hypertonic saline injection in healthy individuals (Schabrun and Hodges 2012). Why corticomotor excitability was increased in the NGF sensitized system is unclear. "
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    ABSTRACT: Primary motor cortical (M1) adaptation has not been investigated in the transition to sustained muscle pain. Daily injection of nerve growth factor (NGF) induces hyperalgesia reminiscent of musculoskeletal pain and provides a novel model to study M1 in response to progressively developing muscle soreness. Twelve healthy individuals were injected with NGF into right extensor carpi radialis brevis (ECRB) on Days 0 and 2 and with hypertonic saline on Day 4. Quantitative sensory and motor testing and assessment of M1 organization and function using transcranial magnetic stimulation were performed prior to injection on Days 0, 2, and 4 and again on Day 14. Pain and disability increased at Day 2 and increased further at Day 4. Reorganization of M1 was evident at Day 4 and was characterized by increased map excitability. These changes were accompanied by reduced intracortical inhibition and increased intracortical facilitation. Interhemispheric inhibition was reduced from the "affected" to the "unaffected" hemisphere on Day 4, and this was associated with increased pressure sensitivity in left ECRB. These data provide the first evidence of M1 adaptation in the transition to sustained muscle pain and have relevance for the development of therapies that seek to target M1 in musculoskeletal pain. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail:
    Cerebral Cortex 01/2015; DOI:10.1093/cercor/bhu319 · 8.67 Impact Factor
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    • "In the clinical setting, subjects who frequently experience stress and anxiety have higher predisposition to develop trigger points, which can lead to myofascial pain syndrome (MPS) [8]. According to epidemiologic studies, the myofascial trigger points (MTrPs) might be a source of nociceptive inputs in 30% to 85% of the patients seeking pain relief [9,10]. "
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    ABSTRACT: This study aimed to answer three questions related to chronic myofascial pain syndrome (MPS): 1) Is the motor cortex excitability, as assessed by transcranial magnetic stimulation parameters (TMS), related to state-trait anxiety? 2) Does anxiety modulate corticospinal excitability changes after evoked pain by Quantitative Sensory Testing (QST)? 3) Does the state-trait anxiety predict the response to pain evoked by QST if simultaneously receiving a heterotopic stimulus [Conditional Pain Modulation (CPM)]? We included females with chronic MPS (n = 47) and healthy controls (n = 11), aged 19 to 65 years. Motor cortex excitability was assessed by TMS, and anxiety was assessed based on the State-Trait Anxiety Inventory. The disability related to pain (DRP) was assessed by the Profile of Chronic Pain scale for the Brazilian population (B:PCP:S), and the psychophysical pain measurements were measured by the QST and CPM. In patients, trait-anxiety was positively correlated to intracortical facilitation (ICF) at baseline and after QST evoked pain (beta = 0.05 and beta = 0.04, respectively) and negatively correlated to the cortical silent period (CSP) (beta = -1.17 and beta = -1.23, respectively) (P <0.05 for all comparisons). After QST evoked pain, the DRP was positively correlated to ICF (beta = 0.02) (P < 0.05). Pain scores during CPM were positively correlated with trait-anxiety when it was concurrently with high DRP (beta = 0.39; P = 0.02). Controls' cortical excitability remained unchanged after QST. These findings suggest that, in chronic MPS, the imbalance between excitatory and inhibitory descending systems of the corticospinal tract is associated with higher trait-anxiety concurrent with higher DRP.
    BMC Neuroscience 03/2014; 15(1):42. DOI:10.1186/1471-2202-15-42 · 2.67 Impact Factor
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    • "First, the time-course of the M1 response to pain differs between muscles and between pain protocols (Romaniello et al., 2000; Le Pera et al., 2001; Svensson et al., 2003; Tsao et al., 2011) and individual variation is high (Tsao et al., 2011) and this may conceal or reveal changes in some studies. Furthermore, depression of MEP amplitudes is more profound after peak-pain than during (Le Pera et al., 2001), possibly due to the activation of intracortical inhibitory mechanisms in the post-pain phase (Schabrun and Hodges, 2012). Given these variables, our absence of reduced MEP amplitude during experimental pain is not unexpected. "
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    ABSTRACT: Background: Integration of information between multiple cortical regions is thought to underpin the experience of pain. Yet studies tend to focus on pain related changes in discrete cortical regions. Although altered processing in the primary motor (M1) and sensory cortex (S1) is implicated in pain, the temporal relationship between these regions is unknown and may provide insight into the interaction between them. Methods: We used recordings of somatosensory-evoked potentials (SEPs) and transcranial magnetic stimulation to investigate the temporal relationship between altered excitability of the primary sensory cortex and corticomotor output during and after muscle pain induced by hypertonic saline infusion into the right first dorsal interosseous. SEPs and motor-evoked potentials (MEPs) were recorded in 12 healthy individuals. Results: Participants reported an average pain intensity of 5.4 (0.5) on a 10-cm visual analogue scale. The area of the N20-P25-N33 complex of the SEP was reduced during and after pain, but MEP amplitudes were suppressed only after pain had resolved. Conclusions: Our data show that pain reduces sensory processing before motor output is altered. This temporal dispersion, coupled with the lack of correlation between pain-induced changes in S1 and M1 excitability, imply either that independent processes are involved, or that reduced excitability of S1 during acute experimental muscle pain mediates latent reductions in motor output via processes that are non-linear and potentially involve activation of a wider brain network.
    Neuroscience 01/2013; 235. DOI:10.1016/j.neuroscience.2012.12.072 · 3.36 Impact Factor
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