Insights About the Neuroplasticity State on the Effect of Intramuscular Electrical Stimulation in Pain and Disability Associated With Chronic Myofascial Pain Syndrome (MPS): A Double-Blind, Randomized, Sham-Controlled Trial

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Abstract

Background: There is limited evidence concerning the effect of intramuscular electrical stimulation (EIMS) on the neural mechanisms of pain and disability associated with chronic Myofascial Pain Syndrome (MPS).

Objectives: To provide new insights into the EIMS long-term effect on pain and disability related to chronic MPS (primary outcomes). To assess if the neuroplasticity state at baseline could predict the long-term impact of EIMS on disability due to MPS we examined the relationship between the serum brain-derived-neurotrophic-factor (BDNF) and by motor evoked potential (MEP). Also, we evaluated if the EIMS could improve the descending pain modulatory system (DPMS) and the cortical excitability measured by transcranial magnetic stimulation (TMS) parameters.

Methods: We included 24 right-handed female with chronic MPS, 19–65 years old. They were randomically allocated to receive ten sessions of EIMS, 2 Hz at the cervical paraspinal region or a sham intervention ( n = 12).

Results: A mixed model analysis of variance revealed that EIMS decreased daily pain scores by -73.02% [95% confidence interval (CI) = -95.28 to -52.30] and disability due to pain -43.19 (95%CI, -57.23 to -29.39) at 3 months of follow up. The relative risk for using analgesics was 2.95 (95% CI, 1.36 to 6.30) in the sham group. In the EIMS and sham, the change on the Numerical Pain Scale (NPS0-10) throughout CPM-task was -2.04 (0.79) vs. -0.94 (1.18), respectively, ( P = 0.01). EIMS reduced the MEP -28.79 (-53.44 to -4.15), while improved DPMS and intracortical inhibition. The MEP amplitude before treatment [(Beta = -0.61, (-0.58 to -0.26)] and a more significant change from pre- to post-treatment on serum BDNF) (Beta = 0.67; CI95% = 0.07 to 1.26) were predictors to EIMS effect on pain and disability due to pain.

Conclusion: These findings suggest that a bottom–up effect induced by the EIMS reduced the analgesic use, improved pain, and disability due to chronic MPS. This effect might be mediated by an enhancing of corticospinal inhibition as seen by an increase in IC and a decrease in MEP amplitude. Likewise, the MEP amplitude before treatment and the changes induced by the EIMS in the serum BDNF predicted it’s long-term clinical impact on pain and disability due MPS.

The trial is recorded in ClinicalTrials.gov : NCT02381171.

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Most cited references 41

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Descending control of pain.

Mark J Millan (2002)

Upon receipt in the dorsal horn (DH) of the spinal cord, nociceptive (pain-signalling) information from the viscera, skin and other organs is subject to extensive processing by a diversity of mechanisms, certain of which enhance, and certain of which inhibit, its transfer to higher centres. In this regard, a network of descending pathways projecting from cerebral structures to the DH plays a complex and crucial role. Specific centrifugal pathways either suppress (descending inhibition) or potentiate (descending facilitation) passage of nociceptive messages to the brain. Engagement of descending inhibition by the opioid analgesic, morphine, fulfils an important role in its pain-relieving properties, while induction of analgesia by the adrenergic agonist, clonidine, reflects actions at alpha(2)-adrenoceptors (alpha(2)-ARs) in the DH normally recruited by descending pathways. However, opioids and adrenergic agents exploit but a tiny fraction of the vast panoply of mechanisms now known to be involved in the induction and/or expression of descending controls. For example, no drug interfering with descending facilitation is currently available for clinical use. The present review focuses on: (1) the organisation of descending pathways and their pathophysiological significance; (2) the role of individual transmitters and specific receptor types in the modulation and expression of mechanisms of descending inhibition and facilitation and (3) the advantages and limitations of established and innovative analgesic strategies which act by manipulation of descending controls. Knowledge of descending pathways has increased exponentially in recent years, so this is an opportune moment to survey their operation and therapeutic relevance to the improved management of pain.

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Modern pain-control theory predicts that a loss of inhibition (disinhibition) in the dorsal horn of the spinal cord is a crucial substrate for chronic pain syndromes. However, the nature of the mechanisms that underlie such disinhibition has remained controversial. Here we present evidence for a novel mechanism of disinhibition following peripheral nerve injury. It involves a trans-synaptic reduction in the expression of the potassium-chloride exporter KCC2, and the consequent disruption of anion homeostasis in neurons of lamina I of the superficial dorsal horn, one of the main spinal nociceptive output pathways. In our experiments, the resulting shift in the transmembrane anion gradient caused normally inhibitory anionic synaptic currents to be excitatory, substantially driving up the net excitability of lamina I neurons. Local blockade or knock-down of the spinal KCC2 exporter in intact rats markedly reduced the nociceptive threshold, confirming that the reported disruption of anion homeostasis in lamina I neurons was sufficient to cause neuropathic pain.

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Brain-derived neurotrophic factor.

Devin K Binder, Helen Scharfman (2004)

Since the purification of BDNF in 1982, a great deal of evidence has mounted for its central roles in brain development, physiology, and pathology. Aside from its importance in neural development and cell survival, BDNF appears essential to molecular mechanisms of synaptic plasticity. Basic activity-related changes in the central nervous system are thought to depend on BDNF modification of synaptic transmission, especially in the hippocampus and neocortex. Pathologic levels of BDNF-dependent synaptic plasticity may contribute to conditions such as epilepsy and chronic pain sensitization, whereas application of the trophic properties of BDNF may lead to novel therapeutic options in neurodegenerative diseases and perhaps even in neuropsychiatric disorders.

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Author and article information

Contributors

Leonardo Botelho: URI : http://loop.frontiersin.org/people/284483/overview

Letícia Angoleri: URI : http://loop.frontiersin.org/people/616008/overview

Maxciel Zortea: URI : http://loop.frontiersin.org/people/528063/overview

Alicia Deitos: URI : http://loop.frontiersin.org/people/75553/overview

Aline Brietzke: URI : http://loop.frontiersin.org/people/294110/overview

Iraci L. S. Torres: URI : http://loop.frontiersin.org/people/52437/overview

Felipe Fregni: URI : http://loop.frontiersin.org/people/12651/overview

Wolnei Caumo: URI : http://loop.frontiersin.org/people/39494/overview

Journal

Journal ID (nlm-ta): Front Hum Neurosci

Journal ID (iso-abbrev): Front Hum Neurosci

Journal ID (publisher-id): Front. Hum. Neurosci.

Title: Frontiers in Human Neuroscience

Publisher: Frontiers Media S.A.

ISSN (Electronic): 1662-5161

Publication date (Electronic): 16 October 2018

Publication date Collection: 2018

Volume: 12

Electronic Location Identifier: 388

Affiliations

[1] ¹Post-Graduate Program in Medical Sciences, School of Medicine, Universidade Federal do Rio Grande do Sul , Porto Alegre, Brazil

[2] ²Laboratory of Pain and Neuromodulation, Hospital de Clínicas de Porto Alegre , Porto Alegre, Brazil

[3] ³Anesthesia and Perioperative Pain Medicine, Hospital de Clínicas de Porto Alegre , Porto Alegre, Brazil

[4] ⁴Pain and Palliative Care Service at Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul , Porto Alegre, Brazil

[5] ⁵Department of Pharmacology, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul , Porto Alegre, Brazil

[6] ⁶Spaulding Center of Neuromodulation, Department of Physical Medicine and Rehabilitation, Harvard Medical School , Boston, MA, United States

[7] ⁷Department of Surgery, School of Medicine, Universidade Federal do Rio Grande do Sul , Porto Alegre, Brazil

Author notes

Edited by: Filippo Brighina, Università degli Studi di Palermo, Italy

Reviewed by: Gianluca Coppola, Fondazione G.B. Bietti (IRCCS), Italy; Carmelo Attilio Costa, Humanitas Centro Catanese di Oncologia, Italy

*Correspondence: Wolnei Caumo, wcaumo@ 123456hcpa.edu.br

Article

DOI: 10.3389/fnhum.2018.00388

PMC ID: 6232764

PubMed ID: 30459575

SO-VID: d50b5fed-6713-4b60-a3b8-588e0cb0564a

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

History

Date received : 03 June 2018

Date accepted : 06 September 2018

Page count

Figures: 5, Tables: 4, Equations: 0, References: 48, Pages: 13, Words: 0

Funding

Funded by: Coordenação de Aperfeiçoamento de Pessoal de Nível Superior 10.13039/501100003593

Award ID: No 04/2015

Funded by: Conselho Nacional de Desenvolvimento Científico e Tecnológico 10.13039/501100003593

Insights About the Neuroplasticity State on the Effect of Intramuscular Electrical Stimulation in Pain and Disability Associated With Chronic Myofascial Pain Syndrome (MPS): A Double-Blind, Randomized, Sham-Controlled Trial

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Abstract

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Functional role of amyloid

Most cited references 41

Descending control of pain.

Trans-synaptic shift in anion gradient in spinal lamina I neurons as a mechanism of neuropathic pain.

Brain-derived neurotrophic factor.

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