Dysfunctional pain inhibition in patients with chronic whiplash-associated disorders: an experimental study

Daenen, Liesbeth; Nijs, Jo; Roussel, Nathalie; Wouters, Kristien; Loo, Michel Van; Cras, Patrick

doi:10.1007/s10067-012-2085-2

Cited by 70 publications

(63 citation statements)

References 81 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Patients with whiplash-associated disorder had reduced CPM. 17 For rheumatoid arthritis, Meeus et al 53 found normal exerciseinduced analgesia, whereas Lee et al 49 reported reduced CPM, noting that the association might have been mediated by sleep disturbances.…”

Section: Nociceptivementioning

confidence: 96%

“…This observation was shown for fibromyalgia (FM), 40,46 irritable bowel syndrome (IBS), 12 migraine, 80 tensionheadache, 82 temporomandibular disorder (TMD), 51 osteoarthritis (OA) and muscle pain, 41 and whiplash 17,61 ; see also the review by Lewis et al 50 Typically, a CPM protocol includes a test stimulus that is given 1 time as a stand-alone, and 1 time during, or immediately after, a conditioning stimulus. The CPM effect is the net change in pain rating, obtained psychophysically or neurophysiologically, between the 2.…”

mentioning

confidence: 92%

See 1 more Smart Citation

Role of endogenous pain modulation in chronic pain mechanisms and treatment

Yarnitsky

2015

Pain

291

214

View full text Add to dashboard Cite

Development and application of psychophysical test paradigms to assess endogenous pain modulation in healthy controls and in patients yielded large body of data over the last 2 decades. These tests can assist in predicting pain acquisition, in characterizing pain syndromes and related dysfunctions of pain modulation, and in predicting response to treatment. This chapter reviews the development of thought on pain modulation in the clinical setup, focusing on conditioned pain modulation, and update on accumulated data regarding the mechanism, protocols of administration, and applications in the clinic.

show abstract

Section: Nociceptivementioning

confidence: 96%

mentioning

confidence: 92%

Role of endogenous pain modulation in chronic pain mechanisms and treatment

Yarnitsky

2015

Pain

291

214

View full text Add to dashboard Cite

show abstract

“…myofascial temporomandibular joint pain (Bragdon et al, 2002), chronic LBP (Peters et al, 1992;Mlekusch et al, 2016), whiplash (Daenen et al, 2013(Daenen et al, , 2014De Kooning et al, 2015), long-standing patellofemoral pain (Rathleff et al, 2016), myofascial pain (Hilgenberg-Sydney et al, 2016), fibromyalgia (Kosek and Hansson, 1997;Staud, 2009), painful knee OA (Arendt- , chronic LBP (Correa et al, 2015), frequent episodic tension-type headache (Drummond and Knudsen, 2011), chronic tension-type headaches (Sandrini et al, 2006), chronic daily headache (Hilgenberg-Sydney et al, 2016), endotoxemia (Karshikoff et al, 2015), interstitial cystitis (Ness et al, 2014), irritable bowel syndrome (Wilder-Smith and Robert-Yap, 2007;Williams et al, 2013), and chronic pancreatitis (Olesen et al, 2010).…”

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

517

494

View full text Add to dashboard Cite

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.

show abstract

“…Patients with chronic WAD have decreased pressure pain thresholds (PPTs) in response to exercise [9] and demonstrate dysfunctional pain inhibition [10], providing evidence for the presence of central sensitization in this population.…”

Section: Introductionmentioning

confidence: 99%

Endogenous pain inhibition is unrelated to autonomic responses in acute whiplash-associated disorders

Kooning

Daenen

Roussel³

et al. 2015

J Rehabil Res Dev

Self Cite

View full text Add to dashboard Cite

Abstract-Patients with acute whiplash-associated disorder (WAD) demonstrate an inefficient endogenous pain inhibition and may experience a dysfunction in autonomic nervous system reactivity to pain. This study compared the autonomic response to painful stimuli between patients with acute and chronic WAD and healthy controls. In addition, the role of the autonomic nervous system for explaining inefficient endogenous pain inhibition was examined in acute WAD. Seventeen patients with acute WAD, 30 patients with chronic WAD, and 31 healthy controls participated in an experiment evaluating the autonomic nervous system at rest and during painful stimuli. Skin conductance and heart rate variability (HRV) parameters were monitored continuously during conditioned pain modulation. A significant autonomic response to pain was present for skin conductance and two HRV parameters in all experimental groups. There was an interaction effect in the skin conductance response to pain but not in HRV responses in any of the groups. In patients with acute WAD, no significant correlations were present between pain, pressure pain thresholds, pain inhibition, and any of the autonomic parameters. This study refutes autonomic dysfunction at rest and in response to pain in acute WAD. The dysfunctional conditioned pain modulation appears unrelated to autonomic responses to pain.

show abstract

Dysfunctional pain inhibition in patients with chronic whiplash-associated disorders: an experimental study

Cited by 70 publications

References 81 publications

Role of endogenous pain modulation in chronic pain mechanisms and treatment

Role of endogenous pain modulation in chronic pain mechanisms and treatment

Assessment and manifestation of central sensitisation across different chronic pain conditions

Endogenous pain inhibition is unrelated to autonomic responses in acute whiplash-associated disorders

Contact Info

Product

Resources

About