A Framework for Understanding the Relationship between Descending Pain Modulation, Motor Corticospinal, and Neuroplasticity Regulation Systems in Chronic Myofascial Pain

Abstract

Myofascial pain syndrome (MPS) is a leading cause of chronic musculoskeletal pain. However, its neurobiological mechanisms are not entirely elucidated. Given the complex interaction between the networks involved in pain process, our approach, to providing insights into the neural mechanisms of pain, was to investigate the relationship between neurophysiological, neurochemical and clinical outcomes such as corticospinal excitability. Recent evidence has demonstrated that three neural systems are affected in chronic pain: (i) motor corticospinal system; (ii) internal descending pain modulation system; and (iii) the system regulating neuroplasticity. In this cross-sectional study, we aimed to examine the relationship between these three central systems in patients with chronic MPS of whom do/do not respond to the Conditioned Pain Modulation Task (CPM-task). The CPM-task was to immerse her non-dominant hand in cold water (0−1°C) to produce a heterotopic nociceptive stimulus. Corticospinal excitability was the primary outcome; specifically, the motor evoked potential (MEP) and intracortical facilitation (ICF) as assessed by transcranial magnetic stimulation (TMS). Secondary outcomes were the cortical excitability parameters [current silent period (CSP) and short intracortical inhibition (SICI)], serum brain-derived neurotrophic factor (BDNF), heat pain threshold (HPT), and the disability related to pain (DRP). We included 33 women, (18–65 years old). The MANCOVA model using Bonferroni's Multiple Comparison Test revealed that non-responders (n = 10) compared to responders (n = 23) presented increased intracortical facilitation (ICF; mean ± SD) 1.43 (0.3) vs. 1.11 (0.12), greater motor-evoked potential amplitude (μV) 1.93 (0.54) vs. 1.40 (0.27), as well a higher serum BDNF (pg/Ml) 32.56 (9.95) vs. 25.59 (10.24), (P < 0.05 for all). Also, non-responders presented a higher level of DRP and decreased HPT (P < 0.05 for all). These findings suggest that the loss of net descending pain inhibition was associated with an increase in ICF, serum BDNF levels, and DRP. We propose a framework to explain the relationship and potential directionality of these factors. In this framework we hypothesize that increased central sensitization leads to a loss of descending pain inhibition that triggers compensatory mechanisms as shown by increased motor cortical excitability.

Delayed pain decrease following M1 tDCS in spinal cord injury: A randomized controlled clinical trial

“…The authors explained that lack of effects is likely due to refractoriness of pain and duration of disease since most of the patients enrolled had injury durations of 10 or more years. In addition, the limited number of [19][20][21][22][23][24][25][26] sessions and small sample size, may not have been sufficient to observe significant effects at follow-up. The second study, on low back pain, even though the sample size was large (n = 135), did not show significant differences between sham and active tDCS [58].…”

“…Several studies have shown that M1 stimulation leads to local and distant effects that result in pain reduction. For instance, stimulating M1 may counteract the lack of inhibition from M1, that could also be associated with pain reduction [22,23]. In addition, it also leads to changes in thalamic and cingulate activity [24], known to be related to pain processing.…”

Access to pain management for cancer patients treated under the Brazilian private healthcare system

“…In addition, it is essential to understand the pain in a broader setting. Aspects such as psychological vulnerabilities, which include anxiety, depression, catastrophism (Syrjala et al, 2014), and previous chronic pain, which may change the integrity of descending modulatory endogenous pathways (Botelho et al, 2016), impact on development, maintenance, and response to treatment.…”

myoActivation: A Structured Process for Chronic Pain Resolution

“…Chemical changes within the muscle may also lead to peripheral sensitization. MTPs can generate continual nociceptive traffic to induce central sensitization, cortical re-organization, and alterations in descending inhibitory pain pathways [32][33][34][35][36]. MTPs are associated with muscles in sustained contraction causing limited movement across joints [37].…”