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      Peripherally Induced Reconditioning of the Central Nervous System: A Proposed Mechanistic Theory for Sustained Relief of Chronic Pain with Percutaneous Peripheral Nerve Stimulation

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          Abstract

          Peripheral nerve stimulation (PNS) is an effective tool for the treatment of chronic pain, although its efficacy and utilization have previously been significantly limited by technology. In recent years, purpose-built percutaneous PNS devices have been developed to overcome the limitations of conventional permanently implanted neurostimulation devices. Recent clinical evidence suggests clinically significant and sustained reductions in pain can persist well beyond the PNS treatment period, outcomes that have not previously been observed with conventional permanently implanted neurostimulation devices. This narrative review summarizes mechanistic processes that contribute to chronic pain, and the potential mechanisms by which selective large diameter afferent fiber activation may reverse these changes to induce a prolonged reduction in pain. The interplay of these mechanisms, supported by data in chronic pain states that have been effectively treated with percutaneous PNS, will also be discussed in support of a new theory of pain management in neuromodulation: Peripherally Induced Reconditioning of the Central Nervous System (CNS).

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          Most cited references 187

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          National or state-level estimates on trends in the prevalence of chronic low back pain (LBP) are lacking. The objective of this study was to determine whether the prevalence of chronic LBP and the demographic, health-related, and health care-seeking characteristics of individuals with the condition have changed over the last 14 years. A cross-sectional, telephone survey of a representative sample of North Carolina households was conducted in 1992 and repeated in 2006. A total of 4437 households were contacted in 1992 and 5357 households in 2006 to identify noninstitutionalized adults 21 years or older with chronic (>3 months), impairing LBP or neck pain that limits daily activities. These individuals were interviewed in more detail about their health and health care seeking. The prevalence of chronic, impairing LBP rose significantly over the 14-year interval, from 3.9% (95% confidence interval [CI], 3.4%-4.4%) in 1992 to 10.2% (95% CI, 9.3%-11.0%) in 2006. Increases were seen for all adult age strata, in men and women, and in white and black races. Symptom severity and general health were similar for both years. The proportion of individuals who sought care from a health care provider in the past year increased from 73.1% (95% CI, 65.2%-79.8%) to 84.0% (95% CI, 80.8%-86.8%), while the mean number of visits to all health care providers were similar (19.5 [1992] vs 19.4 [2006]). The prevalence of chronic, impairing LBP has risen significantly in North Carolina, with continuing high levels of disability and health care use. A substantial portion of the rise in LBP care costs over the past 2 decades may be related to this rising prevalence.
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            Cortical plasticity: from synapses to maps.

            It has been clear for almost two decades that cortical representations in adult animals are not fixed entities, but rather, are dynamic and are continuously modified by experience. The cortex can preferentially allocate area to represent the particular peripheral input sources that are proportionally most used. Alterations in cortical representations appear to underlie learning tasks dependent on the use of the behaviorally important peripheral inputs that they represent. The rules governing this cortical representational plasticity following manipulations of inputs, including learning, are increasingly well understood. In parallel with developments in the field of cortical map plasticity, studies of synaptic plasticity have characterized specific elementary forms of plasticity, including associative long-term potentiation and long-term depression of excitatory postsynaptic potentials. Investigators have made many important strides toward understanding the molecular underpinnings of these fundamental plasticity processes and toward defining the learning rules that govern their induction. The fields of cortical synaptic plasticity and cortical map plasticity have been implicitly linked by the hypothesis that synaptic plasticity underlies cortical map reorganization. Recent experimental and theoretical work has provided increasingly stronger support for this hypothesis. The goal of the current paper is to review the fields of both synaptic and cortical map plasticity with an emphasis on the work that attempts to unite both fields. A second objective is to highlight the gaps in our understanding of synaptic and cellular mechanisms underlying cortical representational plasticity.
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              Mechanisms of neuropathic pain.

              Neuropathic pain refers to pain that originates from pathology of the nervous system. Diabetes, infection (herpes zoster), nerve compression, nerve trauma, "channelopathies," and autoimmune disease are examples of diseases that may cause neuropathic pain. The development of both animal models and newer pharmacological strategies has led to an explosion of interest in the underlying mechanisms. Neuropathic pain reflects both peripheral and central sensitization mechanisms. Abnormal signals arise not only from injured axons but also from the intact nociceptors that share the innervation territory of the injured nerve. This review focuses on how both human studies and animal models are helping to elucidate the mechanisms underlying these surprisingly common disorders. The rapid gain in knowledge about abnormal signaling promises breakthroughs in the treatment of these often debilitating disorders.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                jpr
                jpainres
                Journal of Pain Research
                Dove
                1178-7090
                12 March 2021
                2021
                : 14
                : 721-736
                Affiliations
                [1 ]The Spine and Nerve Center of the Virginias , Charleston, WV, USA
                [2 ]Department of Pain Medicine, The James Cook University Hospital , Middlesbrough, UK
                [3 ]Department of Neurosurgery, Neurosurgical Associates of Lancaster , Lancaster, PA, USA
                [4 ]Anesthesiology, Virginia Commonwealth University Medical Center , Richmond, VA, USA
                [5 ]Premier Pain Centers , Shrewsbury, NJ, USA
                [6 ]SPR Therapeutics , Cleveland, OH, USA
                Author notes
                Correspondence: Timothy R Deer The Spine and Nerve Center of the Virginias , 400 Court Street, Suite 100, Charleston, WV, 25301, USATel +1 304/347-6141Fax +1 304/347-6855 Email doctdeer@aol.com
                Article
                297091
                10.2147/JPR.S297091
                7966353
                33737830
                © 2021 Deer et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 4, References: 187, Pages: 16
                Categories
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