Electrophysiology as a tool to unravel the origin of pancreatic pain

Lelic, Dina; Olesen, Søren Schou; Graversen, Carina; Brock, Christina; Valeriani, Massimiliano; Drewes, Asbjørn Mohr

doi:10.4291/wjgp.v5.i1.33

Cited by 12 publications

(7 citation statements)

References 27 publications

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“…Interference of chronic pain on cognitive performance has also been examined by qEEG [ 67 ]. Data suggest that qEEG associated with sensoriomotor standardized protocols can help to improve the diagnosis of the mechanisms involved in the chronification process of pain over time [ 2 , 68 ].…”

Section: Discussionmentioning

confidence: 99%

“…Recent findings have repeatedly suggested that this phenomenon is fundamental for the chronification of pain symptoms [ 6 ]. Quantitative EEG may be used not only to identify some aspects of maladaptive plasticity, but it may also be a feasible, low cost alternative in the management of patients with chronic pain [ 68 ].…”

Section: Discussionmentioning

confidence: 99%

“…Imaging tools may help researchers and clinicians to assess the mechanisms and the efficacy of therapeutic interventions [ 71 ]. The recording of sensory and cognitive ERPs, for instance, has become a reliable biomarker for assessing the effects of various analgesic drugs [ 68 , 72 , 73 ]. Quantitative EEG can also document the inhibitory activity of the cortex in patients undergoing treatment with those therapies.…”

Section: Discussionmentioning

confidence: 99%

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Electroencephalographic Patterns in Chronic Pain: A Systematic Review of the Literature

et al. 2016

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The main objective of this study is to review and summarize recent findings on electroencephalographic patterns in individuals with chronic pain. We also discuss recent advances in the use of quantitative Electroencephalography (qEEG) for the assessment of pathophysiology and biopsychosocial factors involved in its maintenance over time. Data collection took place from February 2014 to July 2015 in PubMed, SciELO and PEDro databases. Data from cross-sectional studies and longitudinal studies, as well as clinical trials involving chronic pain participants were incorporated into the final analysis. Our primary findings related to chronic pain were an increase of theta and alpha EEG power at rest, and a decrease in the amplitude of evoked potentials after sensory stimulation and cognitive tasks. This review suggests that qEEG could be considered as a simple and objective tool for the study of brain mechanisms involved in chronic pain, as well as for identifying the specific characteristics of chronic pain condition. In addition, results show that qEEG probably is a relevant outcome measure for assessing changes in therapeutic studies.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Electroencephalographic Patterns in Chronic Pain: A Systematic Review of the Literature

et al. 2016

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“…These phenomena are closely associated with increased abdominal pain sensation in the respective patients (8). Of note is that the central nervous system might also play a role in pain sensation in CP (27). The detailed mechanism needs to be further investigated.…”

Section: Discussionmentioning

confidence: 99%

Adrenergic signaling mediates mechanical hyperalgesia through activation of P2X3 receptors in primary sensory neurons of rats with chronic pancreatitis

Wang

Zhu

Jin

et al. 2015

American Journal of Physiology-Gastrointestinal and Liver Physi

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. Adrenergic signaling mediates mechanical hyperalgesia through activation of P2X3 receptors in primary sensory neurons of rats with chronic pancreatitis. Am J Physiol Gastrointest Liver Physiol 308: G710 -G719, 2015. First published January 29, 2015; doi:10.1152/ajpgi.00395.2014.-The mechanism of pain in chronic pancreatitis (CP) is poorly understood. The aim of this study was designed to investigate roles of norepinephrine (NE) and P2X receptor (P2XR) signaling pathway in the pathogenesis of hyperalgesia in a rat model of CP. CP was induced in male adult rats by intraductal injection of trinitrobenzene sulfonic acid (TNBS). Mechanical hyperalgesia was assessed by referred somatic behaviors to mechanical stimulation of rat abdomen. P2XR-mediated responses of pancreatic dorsal root ganglion (DRG) neurons were measured utilizing calcium imaging and whole cell patch-clamp-recording techniques. Western blot analysis and immunofluorescence were performed to examine protein expression. TNBS injection produced a significant upregulation of P2X3R expression and an increase in ATP-evoked responses of pancreatic DRG neurons. The sensitization of P2X3Rs was reversed by administration of ␤-adrenergic receptor antagonist propranolol. Incubation of DRG neurons with NE significantly enhanced ATPinduced intracellular calcium signals, which were abolished by propranolol, and partially blocked by protein kinase A inhibitor H-89. Interestingly, TNBS injection led to a significant elevation of NE concentration in DRGs and the pancreas, an upregulation of ␤ 2-adrenergic receptor expression in DRGs, and amplification of the NE-induced potentiation of ATP responses. Importantly, pancreatic hyperalgesia was markedly attenuated by administration of purinergic receptor antagonist suramin or A317491 or ␤ 2-adrenergic receptor antagonist butoxamine. Sensitization of P2X3Rs, which was likely mediated by adrenergic signaling in primary sensory neurons, contributes to pancreatic pain, thus identifying a potential target for treating pancreatic pain caused by inflammation. chronic pancreatitis; dorsal root ganglion; purinergic receptors; norepinephrine; protein kinase A CHRONIC PANCREATITIS (CP) is a progressive inflammatory disorder characterized by repeated attacks of abdominal pain, fibrosis, and destruction of the glandular pancreas (15,29,39). Pain is a cardinal feature of CP, featured as burning, intermittent, and shooting pain (13). It is, not only the most frequent and dominant symptom of patients with CP, but also the most difficult to treat (1,3,22,35). Our lack of knowledge about what causes pain in pancreatitis has been a serious obstacle to treatment on these patients, with pain frequently relapsing or persisting (1, 31). Basic research of pancreatic nerves and experimental human pain studies have provided evidence that pain processing is abnormal in these patients and in many conditions resembles that seen in neuropathic pain disorders (34). Despite much speculation, little is known about the detailed pathophysiology of pain in ...

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“…Besides, standard clinical and sensory testing, neuroimaging (e.g. Alomar and Bakhaidar, ; Morton et al., ) and electrophysiological (Lelic et al., ; Pinheiro et al., ) assessments have been suggested as tools for evaluating sensitisation processes, but these options are not further discussed in the present paper.…”

Section: Defining and Assessing Sensitisationmentioning

confidence: 99%

Assessment and manifestation of central sensitisation across different chronic pain conditions

Arendt-Nielsen

Morlion

Perrot

et al. 2017

European Journal of Pain

492

494

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Different neuroplastic processes can occur along the nociceptive pathways and may be important in the transition from acute to chronic pain and for diagnosis and development of optimal management strategies. The neuroplastic processes may result in gain (sensitisation) or loss (desensitisation) of function in relation to the incoming nociceptive signals. Such processes play important roles in chronic pain, and although the clinical manifestations differ across condition processes, they share some common mechanistic features. The fundamental understanding and quantitative assessment of particularly some of the central sensitisation mechanisms can be translated from preclinical studies into the clinic. The clinical perspectives are implementation of such novel information into diagnostics, mechanistic phenotyping, prevention, personalised treatment, and drug development. The aims of this paper are to introduce and discuss (1) some common fundamental central pain mechanisms, (2) how they may translate into the clinical signs and symptoms across different chronic pain conditions, (3) how to evaluate gain and loss of function using quantitative pain assessment tools, and (4) the implications for optimising prevention and management of pain. The chronic pain conditions selected for the paper are neuropathic pain in general, musculoskeletal pain (chronic low back pain and osteoarthritic pain in particular), and visceral pain (irritable bowel syndrome in particular). The translational mechanisms addressed are local and widespread sensitisation, central summation, and descending pain modulation. Significance Central sensitisation is an important manifestation involved in many different chronic pain conditions. Central sensitisation can be different to assess and evaluate as the manifestations vary from pain condition to pain condition. Understanding central sensitisation may promote better profiling and diagnosis of pain patients and development of new regimes for mechanism based therapy. Some of the mechanisms underlying central sensitisation can be translated from animals to humans providing new options in development of therapies and profiling drugs under development.

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Electrophysiology as a tool to unravel the origin of pancreatic pain

Cited by 12 publications

References 27 publications

Electroencephalographic Patterns in Chronic Pain: A Systematic Review of the Literature

Electroencephalographic Patterns in Chronic Pain: A Systematic Review of the Literature

Adrenergic signaling mediates mechanical hyperalgesia through activation of P2X3 receptors in primary sensory neurons of rats with chronic pancreatitis

Assessment and manifestation of central sensitisation across different chronic pain conditions

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