The Efficacy of Systemic Lidocaine in the Management of Chronic Pain: A Literature Review

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Abstract

Context

Despite recent advances in the understanding of the chronic pain concept, its diagnosis and management remains a daily challenge for clinicians and patients. Based on the published literature, this review discusses and tries to organize the current knowledge and the up-to-date clinical experience about the efficacy and safety of the use of intravenous lidocaine in treatment and prevention of chronic pain.

Evidence Acquisition

To prepare this narrative review, we performed an in depth literature review using the PubMed searching engine. We extracted all relevant articles published in English, up to April 2016.

Results

Lidocaine, administered as transdermal patch or intravenous lidocaine, is a safe and effective modality in the treatment of post-herpetic neuralgia (PHN), complex regional pain syndrome, as well and for prevention of chronic pain. It may be effective in the management of neuropathic pain syndromes, chronic pain, post-operative pain, and refractory cancer pain.

Conclusions

Intravenous lidocaine and lidocaine patch are effective and safe for the treatment of several chronic or neuropathic pain syndromes. The use of lidocaine during surgery could prevent the development of some chronic post-surgical pain syndromes.

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Most cited references 68

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The role of the immune system in the generation of neuropathic pain.

Margarita Calvo, John Dawes, David Bennett (2012)

Persistent pain is a sequela of several neurological conditions with a primary immune basis, such as Guillain-Barré syndrome and multiple sclerosis. Additionally, diverse forms of injury to the peripheral or the central nervous systems--whether traumatic, metabolic, or toxic--result in substantial recruitment and activation of immune cells. This response involves the innate immune system, but evidence also exists of T-lymphocyte recruitment, and in some patient cohorts antibodies to neuronal antigens have been reported. Mediators released by immune cells, such as cytokines, sensitise nociceptive signalling in the peripheral and central nervous systems. Preclinical data suggest an immune pathogenesis of neuropathic pain, but clinical evidence of a central role of the immune system is less clear. An important challenge for the future is to establish to what extent this immune response initiates or maintains neuropathic pain in patients and thus whether it is amenable to therapy. Copyright © 2012 Elsevier Ltd. All rights reserved.

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Importance of glial activation in neuropathic pain.

Katarzyna Popiołek, Ewelina Rojewska, Joanna Mika … (2013)

Glia plays a crucial role in the maintenance of neuronal homeostasis in the central nervous system. The microglial production of immune factors is believed to play an important role in nociceptive transmission. Pain may now be considered a neuro-immune disorder, since it is known that the activation of immune and immune-like glial cells in the dorsal root ganglia and spinal cord results in the release of both pro- and anti-inflammatory cytokines, as well as algesic and analgesic mediators. In this review we presented an important role of cytokines (IL-1alfa, IL-1beta, IL-2, IL-4, IL-6, IL-10, IL-15, IL-18, TNFalpha, IFNgamma, TGF-beta 1, fractalkine and CCL2); complement components (C1q, C3, C5); metaloproteinases (MMP-2,-9) and many other factors, which become activated on spinal cord and DRG level under neuropathic pain. We discussed the role of the immune system in modulating chronic pain. At present, unsatisfactory treatment of neuropathic pain will seek alternative targets for new drugs and it is possible that anti-inflammatory factors like IL-10, IL-4, IL-1alpha, TGF-beta 1 would fulfill this role. Another novel approach for controlling neuropathic pain can be pharmacological attenuation of glial and immune cell activation. It has been found that propentofylline, pentoxifylline, minocycline and fluorocitrate suppress the development of neuropathic pain. The other way of pain control can be the decrease of pro-nociceptive agents like transcription factor synthesis (NF-kappaB, AP-1); kinase synthesis (MEK, p38MAPK, JNK) and protease activation (cathepsin S, MMP9, MMP2). Additionally, since it is known that the opioid-induced glial activation opposes opioid analgesia, some glial inhibitors, which are safe and clinically well tolerated, are proposed as potential useful ko-analgesic agents for opioid treatment of neuropathic pain. This review pointed to some important mechanisms underlying the development of neuropathic pain, which led to identify some possible new approaches to the treatment of neuropathic pain, based on the more comprehensive knowledge of the interaction between the nervous system and glial and immune cells. © 2013 Elsevier B.V. All rights reserved.

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When does acute pain become chronic?

C Voscopoulos, M. Lema (2010)

The transition from acute to chronic pain appears to occur in discrete pathophysiological and histopathological steps. Stimuli initiating a nociceptive response vary, but receptors and endogenous defence mechanisms in the periphery interact in a similar manner regardless of the insult. Chemical, mechanical, and thermal receptors, along with leucocytes and macrophages, determine the intensity, location, and duration of noxious events. Noxious stimuli are transduced to the dorsal horn of the spinal cord, where amino acid and peptide transmitters activate second-order neurones. Spinal neurones then transmit signals to the brain. The resultant actions by the individual involve sensory-discriminative, motivational-affective, and modulatory processes in an attempt to limit or stop the painful process. Under normal conditions, noxious stimuli diminish as healing progresses and pain sensation lessens until minimal or no pain is detected. Persistent, intense pain, however, activates secondary mechanisms both at the periphery and within the central nervous system that cause allodynia, hyperalgesia, and hyperpathia that can diminish normal functioning. These changes begin in the periphery with upregulation of cyclo-oxygenase-2 and interleukin-1β-sensitizing first-order neurones, which eventually sensitize second-order spinal neurones by activating N-methyl-d-aspartic acid channels and signalling microglia to alter neuronal cytoarchitecture. Throughout these processes, prostaglandins, endocannabinoids, ion-specific channels, and scavenger cells all play a key role in the transformation of acute to chronic pain. A better understanding of the interplay among these substances will assist in the development of agents designed to ameliorate or reverse chronic pain.

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Author and article information

Journal

Journal ID (nlm-ta): Anesth Pain Med

Journal ID (iso-abbrev): Anesth Pain Med

Journal ID (doi): 10.5812/aapm.

Journal ID (publisher-id): Kowsar

Title: Anesthesiology and Pain Medicine

Publisher: Kowsar

ISSN (Print): 2228-7523

ISSN (Electronic): 2228-7531

Publication date (Electronic): 22 April 2017

Publication date Collection: June 2017

Volume: 7

Issue: 3

Electronic Location Identifier: e44732

Affiliations

[1 ]Department of Anesthesiology, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran

[2 ]Brain and Spinal Cord Injury Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran

[3 ]Assistant Professor, Department of Anesthesia, McGill University Health Centre, Montreal, QC, Canada

[4 ]Professor, Department of Anesthesia, McGill University Health Centre, Montreal, QC, Canada

Author notes

[* ]Corresponding author: Juan Francisco Asenjo, Montreal General Hospital, 1650 Cedar Avenue, D10-144, Montreal, QC, Canada. E-mail: jfasenjog@ 123456yahoo.com

Article

DOI: 10.5812/aapm.44732

PMC ID: 5561441

PubMed ID: 28856112

SO-VID: 1ea3cd2a-1fd3-4e8d-b451-7b8a1b7b0212

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License ( http://creativecommons.org/licenses/by-nc/4.0/) which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited.

History

Date received : 13 December 2016

Date revision received : 05 February 2017

Date accepted : 11 March 2017

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The Efficacy of Systemic Lidocaine in the Management of Chronic Pain: A Literature Review

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Abstract

Context

Evidence Acquisition

Results

Conclusions

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Efficacy of Communicating Science

Most cited references 68

The role of the immune system in the generation of neuropathic pain.

Importance of glial activation in neuropathic pain.

When does acute pain become chronic?

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