scholarly journals Effectiveness and Safety of Dorsal Root Ganglion Stimulation for the Treatment of Chronic Pain: A Pooled Analysis

2019 ◽  
Vol 23 (2) ◽  
pp. 213-221 ◽  
Author(s):  
Frank J.P.M. Huygen ◽  
Jan Willem Kallewaard ◽  
Harold Nijhuis ◽  
Liong Liem ◽  
Jan Vesper ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Pooled Analysis

scholarly journals Quantitative Sensory Testing of Spinal Cord and Dorsal Root Ganglion Stimulation in Chronic Pain Patients

2021 ◽  
Author(s):  
Vishwanath Sankarasubramanian ◽  
Srinivas Chiravuri ◽  
Ehsan Mirzakhalili ◽  
Carlos J. Anaya ◽  
John Ryan Scott ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Chronic Pain ◽  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Quantitative Sensory Testing ◽  
Sensory Testing ◽  
Chronic Pain Patients ◽  
Pain Patients

Dorsal Root Ganglion Neuron Types and Their Functional Specialization

2018 ◽  
pp. 127-155 ◽  
Author(s):  
Edward C. Emery ◽  
Patrik Ernfors
Keyword(s):  
Chronic Pain ◽  
Dorsal Root Ganglion ◽  
Sensory Neurons ◽  
Dorsal Root ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Drg Neurons ◽  
Low Threshold

Primary sensory neurons of the dorsal root ganglion (DRG) respond and relay sensations that are felt, such as those for touch, pain, temperature, itch, and more. The ability to discriminate between the various types of stimuli is reflected by the existence of specialized DRG neurons tuned to respond to specific stimuli. Because of this, a comprehensive classification of DRG neurons is critical for determining exactly how somatosensation works and for providing insights into cell types involved during chronic pain. This article reviews the recent advances in unbiased classification of molecular types of DRG neurons in the perspective of known functions as well as predicted functions based on gene expression profiles. The data show that sensory neurons are organized in a basal structure of three cold-sensitive neuron types, five mechano-heat sensitive nociceptor types, four A-Low threshold mechanoreceptor types, five itch-mechano-heat–sensitive nociceptor types and a single C–low-threshold mechanoreceptor type with a strong relation between molecular neuron types and functional types. As a general feature, each neuron type displays a unique and predicable response profile; at the same time, most neuron types convey multiple modalities and intensities. Therefore, sensation is likely determined by the summation of ensembles of active primary afferent types. The new classification scheme will be instructive in determining the exact cellular and molecular mechanisms underlying somatosensation, facilitating the development of rational strategies to identify causes for chronic pain.

Dorsal root ganglion stimulation lead fractures: potential mechanisms and ways to avoid

2021 ◽  
Vol 14 (5) ◽  
pp. e241353
Author(s):  
Gaurav Chauhan ◽  
Brandon I Roth ◽  
Nagy Mekhail
Keyword(s):  
Spinal Cord ◽  
Chronic Pain ◽  
Case Report ◽  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Unusual Case ◽  
Pain Syndrome ◽  
Structural Instability ◽  
Probable Mechanism ◽  
Lead Fracture

Dorsal root ganglion stimulation (DRGS) therapy is a rapidly emerging tool being used by pain physicians in the treatment of chronic pain. Complex regional pain syndrome (CRPS), a debilitating disease whose mechanism is still has yet to be fully elucidated, is a common pathology targeted by DRGS therapy, often better results than traditional spinal cord stimulation. DRGS therapy, however, is not bereft of complications. Lead migration and fracture are two examples in particular that are among the most common of these complications. The authors report an unusual case of lost efficacy due to lead fractures in patients with CRPS treated with DRGS. The case report narrates identification, management and probable mechanism of DRGS lead fracture. The structural instability of DRGS leads can yield distressing symptoms at any point during the therapy, and physicians should be cognisant of the complications of DRGS therapy.

scholarly journals Noncoding RNAs

2014 ◽  
Vol 121 (2) ◽  
pp. 409-417 ◽  
Author(s):  
Brianna Marie Lutz ◽  
Alex Bekker ◽  
Yuan-Xiang Tao
Keyword(s):  
Chronic Pain ◽  
Dorsal Root Ganglion ◽  
Antisense Rna ◽  
Dorsal Root ◽  
Molecular Mechanisms ◽  
Noncoding Rnas ◽  
Current Evidence ◽  
Noxious Stimuli ◽  
Chronic Pain Conditions ◽  
Novel Therapeutic Strategies

Abstract Chronic pain, a common clinical symptom, is often treated inadequately or ineffectively in part due to the incomplete understanding of molecular mechanisms that initiate and maintain this disorder. Newly identified noncoding RNAs govern gene expression. Recent studies have shown that peripheral noxious stimuli drive expressional changes in noncoding RNAs and that these changes are associated with pain hypersensitivity under chronic pain conditions. This review first presents current evidence for the peripheral inflammation/nerve injury–induced change in the expression of two types of noncoding RNAs, microRNAs, and Kcna2 antisense RNA, in pain-related regions, particularly in the dorsal root ganglion. The authors then discuss how peripheral noxious stimuli induce such changes. The authors finally explore potential mechanisms of how expressional changes in dorsal root ganglion microRNAs and Kcna2 antisense RNA contribute to the development and maintenance of chronic pain. An understanding of these mechanisms may propose novel therapeutic strategies for preventing and/or treating chronic pain.

scholarly journals Nerve Injury-Induced Chronic Pain Is Associated with Persistent DNA Methylation Reprogramming in Dorsal Root Ganglion

2018 ◽  
Vol 38 (27) ◽  
pp. 6090-6101 ◽  
Author(s):  
Judit Garriga ◽  
Geoffroy Laumet ◽  
Shao-Rui Chen ◽  
Yuhao Zhang ◽  
Jozef Madzo ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Chronic Pain ◽  
Dorsal Root Ganglion ◽  
Nerve Injury ◽  
Dorsal Root

scholarly journals Activation of STAT3-mediated CXCL12 up-regulation in the dorsal root ganglion contributes to oxaliplatin-induced chronic pain

2017 ◽  
Vol 13 ◽  
pp. 174480691774742 ◽  
Author(s):  
Yong-Yong Li ◽  
He Li ◽  
Ze-Long Liu ◽  
Qiong Li ◽  
Hua-Wen Qiu ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Dorsal Root Ganglion ◽  
Dorsal Root

Perspectives in Pain Research 2014: Neuroinflammation and glial cell activation: The cause of transition from acute to chronic pain?

2015 ◽  
Vol 6 (1) ◽  
pp. 3-6 ◽  
Author(s):  
Brian E. Cairns ◽  
Lars Arendt-Nielsen ◽  
Paola Sacerdote
Keyword(s):  
Spinal Cord ◽  
Chronic Pain ◽  
Dorsal Root Ganglion ◽  
Glial Cell ◽  
Schwann Cells ◽  
Glial Cells ◽  
Proinflammatory Cytokines ◽  
Immune Cells ◽  
Dorsal Root ◽  
Satellite Glial Cells

AbstractBackgroundIt is unknown why an acute pain condition under various circumstances can transition into a chronic pain condition.There has been a shift towards neuroinflammation and hence glial cell activations specifically in the dorsal root ganglion and spinal cord as a mechanism possibly driving the transition to chronic pain. This has led to a focus on non-neuronal cells in the peripheral and central nervous system. Besides infiltrating macrophages, Schwann cells and satellite glial cells release cytokines and therefore important mechanisms in the maintenance of pain. Activated Schwann cells, satellite glial cells, microglia, and astrocytes may contribute to pain sensitivity by releasing cytokines leading to altered neuronal function in the direction of sensitisation.Aims of this perspective paper1) Highlight the complex but important recent achievement in the area of neuroinflammation and pain at spinal cord level and in the dorsal root ganglion.2) Encourage further research which hopefully may provide better understanding of new key elements driving the transition from acute to chronic pain.Recent results in the area of neuroinflammation and painFollowing a sciatic nerve injury, local macrophages, and Schwann cells trigger an immune response immediately followed by recruitment of blood-derived immune cells. Schwann cells, active resident, and infiltrating macrophages release proinflammatory cytokines. Proinflammatory cytokines contribute to axonal damage and also stimulate spontaneous nociceptor activity. This results in activation of satellite glial cells leading to an immune response in the dorsal root ganglia driven by macrophages, lymphocytes and satellite cells. The anterograde signalling progresses centrally to activate spinal microglia with possible up regulation of glial-derived proinflammatory/pronociceptive mediators.An important aspect is extrasegmental spreading sensitisation where bilateral elevations in TNF-α, IL-6, and IL-10 are found in dorsal root ganglion in neuropathic models. Similarly in inflammatory pain models, bilateral up regulation occurs for TNF-α, IL-1 β, and p38 MAPK. Bilateral alterations in cytokine levels in the DRG and spinal cord may underlie the spread of pain to the uninjured side.An important aspect is how the opioids may interact with immune cells as opioid receptors are expressed by peripheral immune cells and thus can induce immune signaling changes. Furthermore, opioids may stimulate microglia cells to produce proinflammatory cytokines such as IL-1.ConclusionsThe present perspective paper indicates that neuroinflammation and the associated release of pro-inflammatory cytokines in dorsal root ganglion and at the spinal cord contribute to the transition from acute to chronic pain. Neuroinflammatory changes have not only been identified in the spinal cord and brainstem, but more recently, in the sensory ganglia and in the nerves as well. The glial cell activation may be responsible for contralateral spreading and possible widespread sensitisation.ImplicationsCommunication between glia and neurons is proposed to be a critical component of neuroinflammatory changes that may lead to chronic pain. Sensory ganglia neurons are surrounded by satellite glial cells but how communication between the cells contributes to altered pain sensitivity is still unknown. Better understanding may lead to new possibilities for (1) preventing development of chronic pain and (2) better pain management.

scholarly journals The causal role of magnesium deficiency in the neuroinflammation, pain hypersensitivity and memory/emotional deficits in ovariectomized and aging mice

2021 ◽  
Author(s):  
Xian-guo Liu ◽  
Jun Zhang ◽  
Chun-lin Mai ◽  
Ying Xiong ◽  
Zhen-Jia Lin ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Dorsal Root Ganglion ◽  
Dorsal Horn ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Emotional Deficits ◽  
Ganglion Neurons ◽  
Neuronal Disorders

Abstract Background: Postmenopausal women often suffer from chronic pain, memory decline and mood depression. The mechanisms underlying the neuronal disorders are not fully understood and effective treatment is still lacking.Methods: Oral administration of magnesium-L-threonate was tested to treat the neuronal disorders in ovariectomized and aging mice. The pain hypersensitivity, memory function and depression were measured with a set of behavioral tests. Western blots and immunochemistry were used to assess molecular changes.Results: Chronic oral administration of magnesium-L-threonate substantially prevented or reversed the chronic pain, and memory/emotional deficits in both ovariectomized and aging female mice. We found that phospho-p65, an active form of nuclear factor-kappaB, tumor necrosis factor-alpha and interleukin-1beta were significantly upregulated in the neurons of dorsal root ganglion, spinal dorsal horn and hippocampus in ovariectomized and aging mice. The microglia and astrocytes were activated in spinal dorsal horn and hippocampus. The peptidergic C-fibers in dorsal horn were increased, which are associated with potentiation of C-fiber-mediated synaptic transmission in the model mice. In parallel with neuroinflammation and synaptic potentiation, free Mg2+ levels in plasma, cerebrospinal fluid and dorsal root ganglion neurons were significantly reduced. Oral magnesium-L-threonate normalized the neuroinflammation, synaptic potentiation and Mg2+ deficiency, but did not affect the estrogen decline in ovariectomized and aging mice. Furthermore, in cultured dorsal root ganglion neurons estrogen elevated intracellular Mg2+, and depressed the upregulation of phospho-p65, tumor necrosis factor-alpha and interleukin-1beta exclusively in the presence of extracellular Mg2+.Conclusions: Estrogen decline in menopause causes neuroinflammation by reducing intracellular Mg2+ in neurons, leading to chronic pain, memory/emotional deficits. Thus, supplement Mg2+ by oral magnesium-L-threonate may be a novel approach for treating menopause-related neuronal disorders.

scholarly journals GPER/β-Alanine Positive Interaction in The Dorsal Root Ganglion Uncovers Potential Mechanisms: Mediating Continuous Neuronal Sensitisation and Neuroinflammation Responses in Neuropathic Pain

2021 ◽  
Author(s):  
Zhenzhen Xu ◽  
Wanli Xie ◽  
Yiqi Feng ◽  
Yanting Wang ◽  
Yuyao He ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Estrogen Receptor ◽  
Neuropathic Pain ◽  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Neuronal Response ◽  
Male Rats ◽  
Patch Clamp Technique ◽  
Positive Interaction ◽  
The Impact

Abstract Background: The pathogenesis of neuropathic pain and the reasons for the prolonged unhealing are still unknown. Increasing evidence suggests that estrogen sex differences play a role in pain sensitivity, but few studies focused on the role of estrogen receptor which maybe an important molecular component contributing to peripheral pain transduction. We aimed to investigate the impact of oestrogen receptors in nociceptive neuronal response in the dorsal root ganglion (DRG) and spinal dorsal horn using a spared nerve injury (SNI) rat model of chronic pain. Methods: We used a class of estrogen receptors antagonists and agonists intrathecal (i.t.) administrated to male rats with SNI or normal rats to identify the main receptor. Moreover, we applied genes identified through genomic metabolic analysis to determine the key metabolism point and elucidate potential mechanisms mediating continuous neuronal sensitisation and neuroinflammation responses in neuropathic pain. The excitability of DRG neurons was detected using the patch clamp technique. Immunohistochemistry, Western blotting, qPCR and behavioral testing were used to assess the expressions, cellular distributions, and actions of main receptor and its related signaling molecules.Results: Increasing the expression and function of G protein-coupled estrogen receptor (GPER), but not estrogen receptor-α (ERα) and estrogen receptor-β (ERβ), in the DRG, but not the dorsal spinal cord, contributed to SNI-induced neuronal sensitisation. Inhibiting GPER expression in the DRG alleviated SNI-induced pain behaviours and neuroinflammation by downregulating IL-1β and IL-6 expression as well as restoring GABAα2 expression simultaneously. Additionally, the positive interaction between GPER and β-alanine, β-alanine accumulation enhances pain sensation and promotes chronic pain development. Conclusion: GPER activation in the DRG causes a positive interaction of β-alanine with IL-1β and IL-6 expression and represses GABAα2 involved in post-SNI neuropathic pain development. Blocking GPER and eliminating β-alanine in the DRG may prevent neuropathic pain development.

scholarly journals Dorsal Root Ganglion Stimulation for the Management of Chronic Neuropathic Pain: A Retrospective Case Series during Four Years follow-up in a Single Center

2020 ◽  
Vol 13 (1) ◽  
pp. 35-41
Author(s):  
Alfonso Papa ◽  
Elisabetta Saracco ◽  
Maria Teresa Di Dato ◽  
Pietro Buonavolontà ◽  
Anna Maria Salzano ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Neuropathic Pain ◽  
Dorsal Root Ganglion ◽  
Data Collection ◽  
Dorsal Root ◽  
Case Series ◽  
Chronic Neuropathic Pain ◽  
Neuropathic Pain Syndrome

Objectives: The dorsal root ganglion (DRG) is involved in the transduction of pain signals to the central nervous system (CNS) and undergoes a number of physiopathological changes during chronic pain. The purpose of this data collection was to evaluate the long-term safety and efficacy of DRG stimulation for the treatment of chronic pain and its impact on functional aspects. Materials and Methods: Forty-four subjects with non-reactive chronic neuropathic pain syndrome were implanted with DRG stimulation. Patients were evaluated at baseline as well as at 15, and 30 days, and at 3, 6, 12, 24, 36 and 48 months after medical intervention/surgery using the Visual Analogic Scale (VAS), which measures pain intensity, and the Oswestry Scale, for the estimation of disability (ODI). Results: After four years of simulation, VAS and ODI showed a statistically significant reduction throughout the follow-up period. The average pain relief obtained after 48 months of treatment was 74.1% ± 3.4. Conclusion: The results of this data collection demonstrate the feasibility of DRG stimulation, the correspondence between the clinical indications at the DRG implant and what is commonly found in the literature on this technique.(18,20) Patients defined as clinical responders to DRG stimulation and so implanted with definitive IPG showed a sustained and long term efficacy. Eight patients had previously been implanted with a traditional SCS without any clinically relevant efficacy; they were then explained for unsatisfactory results. Six of them (75%) were later implanted with DRG, with long-term effectiveness. Another advantage of this therapy is the absence of positional effects and lead migration. The adverse events proved to be independent of the anatomical level of insertion; moreover, this series of cases show a lower incidence of lead migration than reported in the literature. In summary, DRGs have been ignored for too long, probably due to the technical difficulty of reaching their deep, almost extra-spinal anatomical position.

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