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Spontaneous pain is reduced by conditioning pain modulation in peripheral neuropathy but not in fibromyalgia—Implications for different pain mechanisms

  • Eva Kosek
Published/Copyright: July 1, 2012
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Scandinavian Journal of Pain
From the journal Scandinavian Journal of Pain Volume 3 Issue 3

The International Association for the Study of Pain (IASP) has recently redefined neuropathic pain as “pain caused by a lesion or disease of the somatosensory system’, thereby excluding conditions with nervous system dysfunctions, such as fibromyalgia [1]. Although problematic, since neuropathic pain is rarely related to the degree of lesion or disease and rather depends on the resulting dysfunction in the nervous system, the decision can be rational given the ever increasing amount of evidence of aberrant pain modulation, i.e., somatosensory dysfunction, in various nociceptive pain conditions without any known lesions or diseases of the somatosensory system.

Locally increased pain sensitivity in peripheral neuropathic pain vs. generalized increased pain sensitivity in dysfunctional pain, e.g., fibromyalgia. Increased pain sensitivity (allodynia/hyperalgesia) in painful areas has previously been reported in patients with peripheral neuropathic pain [1] as well as nociceptive pain [2] and can hypothetically be explained by abnormal afferent input due to nervous lesions/diseases or peripheral sensitization following tissue damage, respectively. Generalized increases in pain sensitivity outside painful areas have been reported in patients with nociceptive pain such as rheumatoid arthritis or osteoarthritis as well as in patients with dysfunctional pain such as fibromyalgia [2] and these sensory abnormalities are often considered to result from central sensitization, i.e., a bottom-up alteration of pain modulation.

Bottom-up and top-down pain regulations in humans? However, although, bottom-up and top-down pain regulatory mechanisms can be distinguished in animal research, the distinction is not readily made in humans. The situation is further complicated since both bottom-up and top-down pain regulatory mechanisms are generally activated in painful conditions and interact in complex ways. However, noninvasive methods allowing assessment of top-down pain regulation indirectly have been used in humans. One option is to assess pain inhibitory mechanisms, i.e., conditioning pain modulation (CPM), previously referred to as diffuse noxious inhibitory controls (DNIC). CPM implies that normally a painful stimulation in one part of the body reduces pain sensitivity in other parts of the body, most likely through activation of descending pain inhibitory mechanisms, first described by Le Bars and collaborators [3]. Generally, CPM is assessed examining the effects of a tonic, painful, conditioning stimulus on the perception of phasic, painful, test stimuli. Commonly, cold pressor test (extremity in cold water) or tourniquet test (muscle exercise under ischemic conditions) are used as conditioning stimuli and noxious pressure or heat as test stimuli.

Conditional pain modulation (CPM) is dysfunctional in fibromyalgia, but not in peripheral or central neuropathic pain. Previous studies, assessing the effect of noxious conditioning stimulus on noxious test stimuli, have found a dysfunction of CPM in patients with nociceptive pain (osteoarthritis) and dysfunctional pain ( fibromyalgia) [2], but not in neuropathic pain (peripheral or central) [4,5]. However, since the function of CPM is believed to have relevance for development of chronic pain [6] and possibly for response to various treatments, direct assessments of the effect of CPM on the spontaneously ongoing pain in chronic pain patients is of potential clinical interest. To our knowledge, only a few previous studies have addressed this question and with conflicting results. In patients suffering from peripheral neuropathic pain Tuveson et al. [4] found that tourniquet test reduced the intensity of spontaneous pain, while Witting et al. [7] reported that cold pressor test did not. A reduction of spontaneous pain was not seen during a tourniquet test in fibromyalgia patients [8]. Fibromyalgia is often regarded as an extreme end in a continuum of chronic musculoskeletal pain since more than 80% of fibromyalgia patients have localized pain for many years before developing the generalized pain and tenderness of fibromyalgia. It has been suggested that dysfunction of endogenous pain inhibitory mechanisms, such as CPM, could explain the spread of pain in fibromyalgia patients [2]. Furthermore, while various nociceptive and idiopathic pain conditions often precede fibromyalgia, the clinical impression is that peripheral neuropathic pain does not. Therefore it would be of outmost importance to compare the function of CPM in patients with peripheral neuropathic pain and fibromyalgia using the same methods. To our knowledge, no previous studies have addressed this issue.

The first ever direct comparison of CPM in fibromyalgia, neuropathic pain, and human volunteers without pain by Gormsen et al. [9]. Gormsen et al. in this issue of the Scandinavian Journal of Pain [9] set out to compare the function of CPM in patients with fibromyalgia and peripheral neuropathic pain, respectively. They hypothesized that CPM is dysfunctional in fibromyalgia (FM), but intact in patients suffering from neuropathic pain (NP). Thirty patients with peripheral NP pain (14F; 16M), 28 FM patients (26F; 2M) and 26 age-matched controls (21F; 5M) participated. Gender differences were controlled for. All NP patients had a nerve injury and their pain was graded as probable or de finite NP. All FM patients fulfilled the ACR-1990 classification criteria for FM and none had other aetiology for their pain syndrome. Furthermore the groups were adequately matched regarding pain intensity (average corresponding to 6 for FM and 5 for NP patients on a 0–10 numeric rating scale). Quantitative sensory testing (QST) using threshold and suprathreshold pressure and thermal stimuli was performed at baseline and despite slightly inconsistent findings, the authors could draw the conclusion that NP patients had localized hypersensitivity to painful mechanical and thermal stimuli restricted to the affected area of the body, while FM patients had a generalized increase in pain sensitivity.

Cold pressor test as CPM-stimulus decreases spontaneous neuropathic pain, but not spontaneous fibromyalgia pain. Cold pressor test was used as conditioning stimulus and patients rated their spontaneous pain on a visual analogue scale directly before and directly after the cold pressor test. Following the cold pressor test, patients with NP pain rated their spontaneous pain 40% lower, while a minimal difference was seen in FM patients (increased ratings 2.6%). The difference between groups in the change of spontaneous pain intensity following the cold pressor test was statistically significant (p < 0.002). FM patients withdraw their extremity significantly earlier from the cold water than NP patients and healthy controls, but rated the intensity of pain induced by the conditioning stimulus significantly higher than NP patients and controls. The authors concluded that when directly compared, CPM results in reduced spontaneous pain in patients with peripheral NP but not in FM, indicating distinct and separate sensory patterns and pain modulating networks in NP and FM patients, respectively, and therefore justifying that FM is not included as a neuropathic pain condition. Furthermore, they found that their results were consistent with the idea that peripheral neuropathic pain was driven by damaged nerve endings while FM was a central disorder with increased activity in pain-facilitating systems.

Why this difference between neuropathic pain and fibromyalgia? The results of Gormsen et al. [9] are in accordance with previous studies showing that CPM reduced spontaneous pain in patients with peripheral NP [4], but not FM [8]. The authors suggest that the discrepancy between their current results and an earlier study by their group, where they report no reductions in spontaneous pain by CPM [7], could be explained by low baseline pain intensities in the latter, precluding significant pain reductions due to a ceiling effect. Taken together therefore, it seems reasonable to conclude that there is evidence to support that CPM reduces spontaneous pain in patients with peripheral NP but not in FM. The question is why?

CPM-stimulus is applied in painful area in fibromyalgia patients, but not in neuropathic pain patients, triggering pain facilitating mechanisms. As the authors point out, there is no “unaffected” site in FM patients and therefore, the conditioning stimulus was applied to pain affected sites in FM patients but unaffected sites (contralateral and extrasegmental to the most painful area) in NP patients. To our knowledge, there are no previous studies comparing the effects of CPM when the conditioning stimulus is applied within or outside pain afflicted areas.

However, in a study using painful static contractions as conditioning stimulus in myalgia patients, normal extrasegmental pain inhibition was seen when contracting non-afflicted muscles but a lack of inhibition was seen when contracting pain afflicted muscles [10]. The results point to the possibility that conditioning stimuli applied to pain afflicted parts of the body could trigger pain facilitating mechanisms rather than pain inhibition [10]. In the same study FM patents failed to activate pain inhibitory mechanisms during all contractions, which would be in agreement with the suggestion of Gormsen et al. [9], that FM patients activate pain facilitating systems during conditioning stimuli. To our knowledge, it is not known if pain facilitatory mechanisms would also be activated if the conditioning stimuli were applied to the pain affected extremity in patients with peripheral NP.

Can CPM affect central neuropathic pain? Another issue that needs to be considered is the distinction between central pain and peripheral pain. Since CPM is believed to give rise to descending pain inhibitory mechanisms it might well be that CPM does not affect central pain. This is supported by the findings that while CPM using the tourniquet test as conditioning stimulus did influence spontaneous pain in patients with peripheral NP [4], this was not the case in patients with central post stroke NP [5], yet CPM did normally inhibit pain sensitivity to noxious test stimuli (pressure) in both groups. This is different from findings in FM patients where CPM neither reduced spontaneous pain [8; Gormsen et al. [9] this issue of the Scand J Pain], nor had an inhibitory effect on perception of noxious test stimuli [8]. A possible interpretation of these data is that CPM functions normally in neuropathic pain, central and peripheral, but only affects perception of the peripheral pain components. On the other hand, CPM would seem to be truly dysfunctional in FM and in some nociceptive pain conditions, such as osteoarthritis [2]. Furthermore, the function of CPM normalizes following successful treatment of osteoarthritis (hip or knee replacement) indicating that it was initiated and maintained by the nociceptive input [2]. Therefore, contrary to the suggestions of Gormsen et al. [9], the dysfunction of CPM per se should not be regarded to signify a central pain disorder.

Better understanding of dysfunctional CPM will improve treatment of neuropathic pain as well as fibromyalgia. The clinical implications of dysfunctional CPM are not fully understood. Dysfunction of CPM has been related to increased risk to develop chronic pain [6] and it has been suggested that the development of FM is due to the negative influence of nociceptive pain on CPM in susceptible individuals [2]. The importance of early pain treatment to prevent dysfunction of CPM and development of chronic pain has been much discussed, although little is known about the clinical potential of secondary prevention. Furthermore, to our knowledge, there is at present no evidence that also long-standing neuropathic pain can give rise to dysfunction of CPM and increased risk for FM development. Gormsen et al. [9] raise the interesting issue whether serotonin–noradrenaline re-uptake inhibitors (SNRIs) reduce pain through different mechanisms in patients with peripheral NP and FM, respectively. SNRIs are considered to mainly relieve pain through strengthening of descending pain inhibition. Mechanistic studies comparing the effects of SNRIs in peripheral NP and FM would be of great potential value to increase our understanding of the effects of SNRIs, and even more importantly, of pain mechanisms in these pain conditions where really efficient pain treatment is still lacking for most patients.

DOI of refers to article: http://dx.doi.org/10.1016/j.sjpain.2012.01.002.

References

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Published Online: 2012-07-01
Published in Print: 2012-07-01

© 2012 Scandinavian Association for the Study of Pain

Articles in the same Issue

  1. Editorial comment
  2. Spontaneous pain is reduced by conditioning pain modulation in peripheral neuropathy but not in fibromyalgia—Implications for different pain mechanisms
  3. Clinical pain research
  4. Differential pain modulation in patients with peripheral neuropathic pain and fibromyalgia
  5. Editorial comment
  6. Pulsed radiofrequency—Time for a clinical pause and more science
  7. Clinical pain research
  8. Pulsed radiofrequency in peripheral posttraumatic neuropathic pain: A double blind sham controlled randomized clinical trial
  9. Editorial comment
  10. Phantom pains and sensations – how does it feel? Only the patient really knows
  11. Clinical pain research
  12. Phantom phenomena – Their perceived qualities and consequences from the patient’s perspective
  13. Editorial comment
  14. Impact of mental stressor on conditioned pain modulation
  15. Original experimental
  16. The effect of a mental stressor on conditioned pain modulation in healthy subjects
  17. Editorial comment
  18. Pharmacological modulation of chronic pain after whiplash injury
  19. Clinical pain research
  20. Whiplash Associated Disorders (WAD): Responses to pharmacological challenges and psychometric tests
  21. Editorial comment
  22. Why are autonomic responses to pressure pain different from those to heat pain and ischaemic pain?
  23. Original experimental
  24. Cardiovascular responses to and modulation of pressure pain sensitivity in normotensive, pain-free women
  25. Correspondence
  26. Piriformis muscle injection guided by sciatic nerve stimulation: Quick, simple, and safe technique
  27. Correspondence
  28. Musculus piriformis syndrome: Localization and injection therapy—Comment to letter from Mayo-Moldes M et al. [1]
  29. Abstracts
  30. The “pain matrix” reloaded
  31. Abstracts
  32. Endpoints in animal pain models
  33. Abstracts
  34. Evaluating pain-related behavior in spinal cord injury
  35. Abstracts
  36. The role of the amygdala in sensory and emotional-like pain behavior in neuropathic animals
  37. Abstracts
  38. Peripheral and central pain mechanisms—From animal models to clinical research
  39. Abstracts
  40. Human experimental models of central sensitization—Do they bridge the gap between animal models and clinical observations?
  41. Abstracts
  42. Assessment of central sensitization in the clinic. Is it possible?
  43. Abstracts
  44. Migraine neurobiology and treatment
  45. Abstracts
  46. Chronic headaches–Goals and obstacles
  47. Abstracts
  48. Trigeminal neuralgia and other cranial neuralgias
  49. Abstracts
  50. Temporomandibular disorders: Pathophysiology and diagnosis
  51. Abstracts
  52. HIV-associated painful polyneuropathy
  53. Abstracts
  54. Keynote: Neuronal and glial signalling in pain neuroplasticity
  55. Abstracts
  56. Neuropathic pain—From guidelines to clinical practice
  57. Abstracts
  58. Postoperative pain treatment. What’s the evidence—And how to use it?
  59. Abstracts
  60. NSAIDs in postoperative pain
  61. Abstracts
  62. How should we prevent persistent postoperative pain?
  63. Abstracts
  64. Opioids: Genetics and receptors
  65. Abstracts
  66. Chronic pain and sleep disorders
  67. Abstracts
  68. Population-based studies on chronic pain: The role of opioids
  69. Abstracts
  70. Living beyond pain: Acceptance and commitment therapy
  71. Abstracts
  72. Modality specific alterations of esophageal sensitivity caused by longstanding diabetes mellitus
  73. Abstracts
  74. Validation of a porcine behavioural model of UVB induced inflammatory pain
  75. Abstracts
  76. Recovery after a lumbar disc herniation is dependent on a gender and OPRM1 Asn40Asp genotype interaction
  77. Abstracts
  78. Pain sensitivity changes in chronic pain patients with and without spinal cord stimulation assessed by nociceptive withdrawal reflex thresholds and electrical pain thresholds
  79. Abstracts
  80. Acceptance and commitment therapy for fibromyalgia: A randomized controlled trial
  81. Abstracts
  82. Sortilins in neuropathic pain
  83. Abstracts
  84. Systematic review of neuropathic component in persistent post-surgical pain
  85. Abstracts
  86. Pain prevalence in a university hospital in Iceland
  87. Abstracts
  88. The effect of tail-docking neonate piglets on ATF-3 and NR2B immunoreactivity in coccygeal dorsal root ganglia and spinal cord dorsal horn neurons: Preliminary data
  89. Abstracts
  90. Na+/K+-ATPase dependent regulation of astrocyte Ca2+ signalling: A novel mechanism for modulation of long-term pain?
  91. Abstracts
  92. Glutamate attenuates nitric oxide release from isolated trigeminal ganglion satellite glial cells
  93. Abstracts
  94. Acute behavioural responses to tail docking in piglets – Effects of increasing docking length?
  95. Abstracts
  96. Dose and administration-period play a key role in the effect of ceftriaxone on neuropathic pain in CCI-operated rats
  97. Abstracts
  98. Translational aspects of rectal evoked potentials: A comparative study in rats and humans
  99. Abstracts
  100. Time-course of analgesic effects of botulinum neurotoxin type A (BoNTA) on human experimental model of pain induced by injection of glutamate into temporalis muscle
  101. Abstracts
  102. The effect of nerve compression and capsaicin on contact heat evoked potentials (CHEPs) related to Aδ and C fibers
  103. Abstracts
  104. Effect of specific trapezius exercises vs. coordination training on corticomotor control of neck muscles
  105. Abstracts
  106. SNP in TNFα T308G is predictive for persistent postoperative pain following inguinal hernia surgery
  107. Abstracts
  108. Chronic pain in thoracotomy
  109. Abstracts
  110. The variability in thermal threshold-assessments in post-thoracotomy pain syndrome
  111. Abstracts
  112. Persistent pain, sensory disturbances and functional impairment after adjuvant chemotherapy for breast cancer
  113. Abstracts
  114. Neuroplastic alterations in brain responses to painful visceral stimulations reflects individual neuropathic symptoms in diabetes mellitus patients
  115. Abstracts
  116. Exercise and conditioned pain modulation have different effects on cuff pressure pain tolerance in humans
  117. Abstracts
  118. Hyperalgesia in human skin and deep-tissues inside and outside of a UVB irradiated area
  119. Abstracts
  120. Effect of experimental jaw muscle pain on bite force during mastication
  121. Abstracts
  122. Reflex threshold assessment methodology for evaluation of central sensitisation is vulnerable to EMG crosstalk
  123. Abstracts
  124. Cognitive modulation of experimental pain at spinal and cortical levels
  125. Abstracts
  126. Influence of emotionally loaded visual and gustatory stimuli on pain perception
  127. Abstracts
  128. Modulating pain with augmented reality
  129. Abstracts
  130. Offset analgesia: A reproducibility study
  131. Abstracts
  132. Visualization of painful process in peripheral tissue using positron emission tomography and [11C]-D-deprenyl
  133. Abstracts
  134. Mirror-image sensory dysfunction in the post-thoracotomy pain syndrome
  135. Abstracts
  136. Genetic variation in opioid receptor genes and sensitivity to experimental pain in male and female healthy volunteers
  137. Abstracts
  138. Mechanical sensitivity in migraine patients during attack, remission, and pain-free periods:A preliminary study
  139. Abstracts
  140. Multivariate pattern analysis of evoked brain potentials by temporal matching pursuit and support vector machine
  141. Abstracts
  142. Pain following stroke: A prospective study
  143. Abstracts
  144. Chronic thoracic pain in children after cardiac surgery
  145. Abstracts
  146. Chronic pain after breast augmentation is associated with both signs of peripheral nerve injury and central nervous mechanisms
  147. Abstracts
  148. Sensory phenotypes in patients with peripheral neuropathic pain evaluated with quantitative sensory testing
  149. Abstracts
  150. Is health related quality of life related to the pattern of chronic pain?
  151. Abstracts
  152. Comparison between ropivacaine local infiltration analgesia with ketorolac or placebo for total knee replacement surgery
  153. Abstracts
  154. Treatment with topical capsaicin: Experience from a pain clinic
  155. Abstracts
  156. Distribution of concussion related symptoms after whiplash injury in risk strata
  157. Abstracts
  158. HIV/AIDS in different cultures
  159. Abstracts
  160. Pain perception is altered in patients with medication-overuse headache but can improve after detoxification
  161. Abstracts
  162. Detoxification in a structured programme is effective for medication-overuse headache
https://doi.org/10.1016/j.sjpain.2012.04.002

Articles in the same Issue

  1. Editorial comment
  2. Spontaneous pain is reduced by conditioning pain modulation in peripheral neuropathy but not in fibromyalgia—Implications for different pain mechanisms
  3. Clinical pain research
  4. Differential pain modulation in patients with peripheral neuropathic pain and fibromyalgia
  5. Editorial comment
  6. Pulsed radiofrequency—Time for a clinical pause and more science
  7. Clinical pain research
  8. Pulsed radiofrequency in peripheral posttraumatic neuropathic pain: A double blind sham controlled randomized clinical trial
  9. Editorial comment
  10. Phantom pains and sensations – how does it feel? Only the patient really knows
  11. Clinical pain research
  12. Phantom phenomena – Their perceived qualities and consequences from the patient’s perspective
  13. Editorial comment
  14. Impact of mental stressor on conditioned pain modulation
  15. Original experimental
  16. The effect of a mental stressor on conditioned pain modulation in healthy subjects
  17. Editorial comment
  18. Pharmacological modulation of chronic pain after whiplash injury
  19. Clinical pain research
  20. Whiplash Associated Disorders (WAD): Responses to pharmacological challenges and psychometric tests
  21. Editorial comment
  22. Why are autonomic responses to pressure pain different from those to heat pain and ischaemic pain?
  23. Original experimental
  24. Cardiovascular responses to and modulation of pressure pain sensitivity in normotensive, pain-free women
  25. Correspondence
  26. Piriformis muscle injection guided by sciatic nerve stimulation: Quick, simple, and safe technique
  27. Correspondence
  28. Musculus piriformis syndrome: Localization and injection therapy—Comment to letter from Mayo-Moldes M et al. [1]
  29. Abstracts
  30. The “pain matrix” reloaded
  31. Abstracts
  32. Endpoints in animal pain models
  33. Abstracts
  34. Evaluating pain-related behavior in spinal cord injury
  35. Abstracts
  36. The role of the amygdala in sensory and emotional-like pain behavior in neuropathic animals
  37. Abstracts
  38. Peripheral and central pain mechanisms—From animal models to clinical research
  39. Abstracts
  40. Human experimental models of central sensitization—Do they bridge the gap between animal models and clinical observations?
  41. Abstracts
  42. Assessment of central sensitization in the clinic. Is it possible?
  43. Abstracts
  44. Migraine neurobiology and treatment
  45. Abstracts
  46. Chronic headaches–Goals and obstacles
  47. Abstracts
  48. Trigeminal neuralgia and other cranial neuralgias
  49. Abstracts
  50. Temporomandibular disorders: Pathophysiology and diagnosis
  51. Abstracts
  52. HIV-associated painful polyneuropathy
  53. Abstracts
  54. Keynote: Neuronal and glial signalling in pain neuroplasticity
  55. Abstracts
  56. Neuropathic pain—From guidelines to clinical practice
  57. Abstracts
  58. Postoperative pain treatment. What’s the evidence—And how to use it?
  59. Abstracts
  60. NSAIDs in postoperative pain
  61. Abstracts
  62. How should we prevent persistent postoperative pain?
  63. Abstracts
  64. Opioids: Genetics and receptors
  65. Abstracts
  66. Chronic pain and sleep disorders
  67. Abstracts
  68. Population-based studies on chronic pain: The role of opioids
  69. Abstracts
  70. Living beyond pain: Acceptance and commitment therapy
  71. Abstracts
  72. Modality specific alterations of esophageal sensitivity caused by longstanding diabetes mellitus
  73. Abstracts
  74. Validation of a porcine behavioural model of UVB induced inflammatory pain
  75. Abstracts
  76. Recovery after a lumbar disc herniation is dependent on a gender and OPRM1 Asn40Asp genotype interaction
  77. Abstracts
  78. Pain sensitivity changes in chronic pain patients with and without spinal cord stimulation assessed by nociceptive withdrawal reflex thresholds and electrical pain thresholds
  79. Abstracts
  80. Acceptance and commitment therapy for fibromyalgia: A randomized controlled trial
  81. Abstracts
  82. Sortilins in neuropathic pain
  83. Abstracts
  84. Systematic review of neuropathic component in persistent post-surgical pain
  85. Abstracts
  86. Pain prevalence in a university hospital in Iceland
  87. Abstracts
  88. The effect of tail-docking neonate piglets on ATF-3 and NR2B immunoreactivity in coccygeal dorsal root ganglia and spinal cord dorsal horn neurons: Preliminary data
  89. Abstracts
  90. Na+/K+-ATPase dependent regulation of astrocyte Ca2+ signalling: A novel mechanism for modulation of long-term pain?
  91. Abstracts
  92. Glutamate attenuates nitric oxide release from isolated trigeminal ganglion satellite glial cells
  93. Abstracts
  94. Acute behavioural responses to tail docking in piglets – Effects of increasing docking length?
  95. Abstracts
  96. Dose and administration-period play a key role in the effect of ceftriaxone on neuropathic pain in CCI-operated rats
  97. Abstracts
  98. Translational aspects of rectal evoked potentials: A comparative study in rats and humans
  99. Abstracts
  100. Time-course of analgesic effects of botulinum neurotoxin type A (BoNTA) on human experimental model of pain induced by injection of glutamate into temporalis muscle
  101. Abstracts
  102. The effect of nerve compression and capsaicin on contact heat evoked potentials (CHEPs) related to Aδ and C fibers
  103. Abstracts
  104. Effect of specific trapezius exercises vs. coordination training on corticomotor control of neck muscles
  105. Abstracts
  106. SNP in TNFα T308G is predictive for persistent postoperative pain following inguinal hernia surgery
  107. Abstracts
  108. Chronic pain in thoracotomy
  109. Abstracts
  110. The variability in thermal threshold-assessments in post-thoracotomy pain syndrome
  111. Abstracts
  112. Persistent pain, sensory disturbances and functional impairment after adjuvant chemotherapy for breast cancer
  113. Abstracts
  114. Neuroplastic alterations in brain responses to painful visceral stimulations reflects individual neuropathic symptoms in diabetes mellitus patients
  115. Abstracts
  116. Exercise and conditioned pain modulation have different effects on cuff pressure pain tolerance in humans
  117. Abstracts
  118. Hyperalgesia in human skin and deep-tissues inside and outside of a UVB irradiated area
  119. Abstracts
  120. Effect of experimental jaw muscle pain on bite force during mastication
  121. Abstracts
  122. Reflex threshold assessment methodology for evaluation of central sensitisation is vulnerable to EMG crosstalk
  123. Abstracts
  124. Cognitive modulation of experimental pain at spinal and cortical levels
  125. Abstracts
  126. Influence of emotionally loaded visual and gustatory stimuli on pain perception
  127. Abstracts
  128. Modulating pain with augmented reality
  129. Abstracts
  130. Offset analgesia: A reproducibility study
  131. Abstracts
  132. Visualization of painful process in peripheral tissue using positron emission tomography and [11C]-D-deprenyl
  133. Abstracts
  134. Mirror-image sensory dysfunction in the post-thoracotomy pain syndrome
  135. Abstracts
  136. Genetic variation in opioid receptor genes and sensitivity to experimental pain in male and female healthy volunteers
  137. Abstracts
  138. Mechanical sensitivity in migraine patients during attack, remission, and pain-free periods:A preliminary study
  139. Abstracts
  140. Multivariate pattern analysis of evoked brain potentials by temporal matching pursuit and support vector machine
  141. Abstracts
  142. Pain following stroke: A prospective study
  143. Abstracts
  144. Chronic thoracic pain in children after cardiac surgery
  145. Abstracts
  146. Chronic pain after breast augmentation is associated with both signs of peripheral nerve injury and central nervous mechanisms
  147. Abstracts
  148. Sensory phenotypes in patients with peripheral neuropathic pain evaluated with quantitative sensory testing
  149. Abstracts
  150. Is health related quality of life related to the pattern of chronic pain?
  151. Abstracts
  152. Comparison between ropivacaine local infiltration analgesia with ketorolac or placebo for total knee replacement surgery
  153. Abstracts
  154. Treatment with topical capsaicin: Experience from a pain clinic
  155. Abstracts
  156. Distribution of concussion related symptoms after whiplash injury in risk strata
  157. Abstracts
  158. HIV/AIDS in different cultures
  159. Abstracts
  160. Pain perception is altered in patients with medication-overuse headache but can improve after detoxification
  161. Abstracts
  162. Detoxification in a structured programme is effective for medication-overuse headache
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