The prevalence of widespread central hypersensitivity in chronic pain patients

Schliessbach, Jürg; Siegenthaler, Andreas; Streitberger, Konrad; Eichenberger, Urs; Nüesch, Eveline; Jüni, Peter; Arendt-Nielsen, Lars; Curatolo, Michele

doi:10.1002/j.1532-2149.2013.00332.x

Cited by 49 publications

(37 citation statements)

References 39 publications

(49 reference statements)

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“…A reduced CPM response was demonstrated across different pain diagnosis; the proportion of patients with widespread pain was however increased compared with patients with efficient CPM. This is in agreement with a previous study including 464 chronic 13 pain patients demonstrating less than 20% increase in pressure pain threshold after cold pressor test in 60% of patients across different chronic pain conditions [34].…”

Section: Conditioned Pain Modulationsupporting

confidence: 93%

Pain modulatory phenotypes differentiate subgroups with different clinical and experimental pain sensitivity

Vægter

Graven‐Nielsen

2016

PAIN

108

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Pain biomarkers are warranted for individualized pain management. Based on different pain modulatory phenotypes, the objectives of this study were to explore the existence of subgroups within patients with nonmalignant chronic pain and to investigate differences in clinical pain and pain hypersensitivity between subgroups. Cuff algometry was performed on lower legs in 400 patients with chronic pain to assess pressure pain threshold, pressure pain tolerance, temporal summation of pain (TSP: increase in pain scores to 10 repeated stimulations), and conditioned pain modulation (CPM: increase in cuff pressure pain threshold during cuff pain conditioning on the contralateral leg). Heat detection and heat pain thresholds at clinical painful and nonpainful body areas were assessed. Based on TSP and CPM, 4 distinct groups were formed: group 1 (n = 85) had impaired CPM and facilitated TSP; group 2 (n = 148) had impaired CPM and normal TSP; group 3 (n = 45) had normal CPM and facilitated TSP; and group 4 (n = 122) had normal CPM and normal TSP. Group 1 showed more pain regions than the other 3 groups (P < 0.001), indicating that impaired CPM and facilitated TSP play an important role in widespread pain. Groups 1 and 2 compared with group 4 had lower heat pain threshold at nonpainful areas and lower cuff pressure pain tolerance (P < 0.02), indicating that CPM plays a role for widespread hyperalgesia. Moreover, group 1 demonstrated higher clinical pain scores than group 4 (P < 0.05). Although not different between subgroups, patients were profiled on demographics, disability, pain catastrophizing, and fear of movement. Future research should investigate interventions tailored towards these subgroups.

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Section: Conditioned Pain Modulationsupporting

confidence: 93%

Pain modulatory phenotypes differentiate subgroups with different clinical and experimental pain sensitivity

Vægter

Graven‐Nielsen

2016

PAIN

108

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“…When pain patients have impaired CPM, it is not obvious if the inhibition is reduced or the facilitation is increased, but it has been shown in chronic pain patients that the degree of widespread hyperalgesia and reduced CPM are associated (Schliessbach et al, 2013).…”

Section: Descending Pain Modulation (Conditioning Pain Modulation)mentioning

confidence: 99%

Assessment and manifestation of central sensitisation across different chronic pain conditions

Arendt-Nielsen

Morlion

Perrot

et al. 2017

European Journal of Pain

452

445

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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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“…As CPM is a relatively new pain biomarker in humans, few studies have investigated reference values [84] or tested the reproducibility [23,85].…”

Section: Descending Pain Inhibitionmentioning

confidence: 99%

Translational pain biomarkers in the early development of new neurotherapeutics for pain management

Arendt‐Nielsen

Nielsen

Gazerani

2014

Expert Review of Neurotherapeutics

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Translation of the analgesic efficacy of investigational neurotherapeutics from pre-clinical pain models into clinical trial phases is associated with a high risk of failure. Application of human pain biomarkers in early stages of clinical trials can potentially enhance the rate of successful translation, which would eventually reduce both length and costs of drug development after the pre-clinical stage. Human pain biomarkers are based on the standardized activation of pain pathways followed by the assessment of ongoing and paroxysmal pain, plus evoked responses which can be applied to healthy individuals and patients prior to and after pharmacological interventions. This review discusses the rationality and feasibility of advanced human pain biomarkers in early phases of drug development for pain management which is still an unmet medical need.

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The prevalence of widespread central hypersensitivity in chronic pain patients

Cited by 49 publications

References 39 publications

Pain modulatory phenotypes differentiate subgroups with different clinical and experimental pain sensitivity

Pain modulatory phenotypes differentiate subgroups with different clinical and experimental pain sensitivity

Assessment and manifestation of central sensitisation across different chronic pain conditions

Translational pain biomarkers in the early development of new neurotherapeutics for pain management

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