Home Medicine Pulsed radiofrequency in peripheral posttraumatic neuropathic pain: A double blind sham controlled randomized clinical trial
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Pulsed radiofrequency in peripheral posttraumatic neuropathic pain: A double blind sham controlled randomized clinical trial

  • Ethem Akural , Voitto Järvimäki , Raija Korhonen , Hannu Kautiainen and Maija Haanpää EMAIL logo
Published/Copyright: July 1, 2012
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Scandinavian Journal of Pain
From the journal Scandinavian Journal of Pain Volume 3 Issue 3

Abstract

Background and purpose

Pulsed radiofrequency (PRF) is widely used for the treatment of chronic pain, although its mechanism of action is not known. The evidence of efficacy of PRF for neuropathic pain (NP) conditions is limited. A double-blind, randomized, sham-controlled parallel study was conducted to evaluate the efficacy and safety of PRF in the treatment of peripheral posttraumatic NP.

Methods

Forty-five patients with peripheral posttraumatic NP in their upper or lower limb were randomly assigned to receive PRF or sham treatment to the injured peripheral nerve (s) causing peripheral posttraumatic NP. Only patients whose pain intensity was at least 5 on numerical rating scale (NRS) 0–10 and who had suffered from their NP for at least 6 months were included. All patients had dynamic mechanical allodynia or pinprick hyperalgesia in their painful area. They had achieved temporary pain relief of at least 50% with a local nerve block performed at a previous visit. The primary efficacy variable was the difference in 3-day mean pain intensity score from the baseline to 3 months. Other variables included response defined as ≥30% reduction in mean pain intensity at 3 months compared to baseline, Neuropathic Pain Scale (NPS) results, health related quality of life (SF-36) and adverse effects. The skin was anesthetized with 1% lidocaine. A radiofrequency needle was introduced through the skin, and then guided to a SMK cannula (52, 100 or 144mm depending on the target nerve) with 4 or 5mm active tip (SMK-C5-4, SMK-C10-5, SMK-C15-5, Radionics®, Burlington, MA, USA). The nerve was located accurately by stimulating at 50 Hz (threshold <0.5 V). Sham treatment or PRF was applied for 120s 1–4 times at each treatment point (Radionics®, Burlington, MA, USA). The total treatment time was up to 8 min. Both patients and clinicians were blinded during the whole treatment and follow-up period.

Results

Forty-three patients were included in the analyses. There was no statistically significant difference between PRF and sham treatment for the primary outcome efficacy variable.

Seven patients (3 in PRF group and 4 in sham treatment group) achieved ≥30% pain relief (difference between groups was not significant). There was no statistically significant difference in the NPS or any dimension of SF-36 between the treatments. Eighteen patients reported adverse effects. They were mild and did not necessitate any treatment. Transient pain was reported by 17 patients, local irritation by 5 patients and local inflammation by 1 patient. There was no significant difference between the groups in the presence of adverse effects.

Conclusions

PRF was well tolerated, but this study failed to show efficacy of PRF over sham treatment for peripheral posttraumatic NP.

Implications

Based on our results, we do not recommend PRF for peripheral posttraumatic NP. More research of the possible use of PRF for various pain conditions is needed to determine its role in the management of prolonged pains.

Keywords: Neuropathic pain; Posttraumatic neuropathic pain; Pulsed radiofrequency; Randomized controlled trial

1 Introduction

Peripheral nerve injury is a common cause of neuropathic pain (NP), i.e. “pain caused by a lesion or disease of the somatosensory system” [1], but the exact prevalence of posttraumatic NP is not known. A peripheral nerve lesion can be caused by a primary trauma or by surgery or other treatments. Iatrogenic NP is probably the most common type of postsurgical persistent pain [2]. In severe cases NP causes suffering, disability and impaired working capacity even when optimally treated [3]. Because many nerve trauma patients are at their best working age, improved treatment might save societal cost of lost working days. Pharmacological treatment is the major choice in NP, although less than 1/3 of patients obtain a pain relief that is better than moderate [4,5]. Only few randomized controlled trials (RCT) showing at least some efficacy of pharmacotherapy have been published on posttraumatic NP [6,7,8,9,10].

In recent years, pulsed radiofrequency (PRF) has gained popularity as a treatment of chronic pain. Its mechanism of action is not fully clarified, but alteration in synaptic transmission is regarded to play a pivotal role. Because it does not cause major nerve damage, it is regarded safer and faster compared to thermal radiofrequency. [11] However, the evidence of efficacy of PRF for any NP condition is limited. An open nonrandomized study with 49 patients reported promising results of PRF for postherpetic neuralgia in 3-month follow-up [12]. We found only case reports of possible utility of PRF given to a peripheral nerve for postsurgical neuralgia [13,14,15,16].

Encouraged by promising results in the case reports, we decided to perform a RCT on PRF for peripheral posttraumatic NP in upper or lower limb.

2 Patients and methods

2.1 Design

To test the hypothesis we conducted a prospective parallel, randomized, double-blind, sham-controlled study. The patients included had tried pharmacotherapy and transcutaneous electrical nerve stimulation. We observed the outcome measures at baseline and at 3 months. The study was performed in accordance with the Helsinki declaration, and approved by the local ethical committee. The assessment and procedures were carried out at the Pain Clinic of Oulu University Hospital. Participants were not offered economic inducements, but the treatment was free of charge. The patients were given written and verbal information about the trial, the potential benefits and risks before giving their written consent.

2.2 Patient selection

General practitioners and colleagues at district hospital refer patients with intractable pain to the Pain Clinic, and our center serves as the only tertiary care center for pain patients in the area. Patients of at least 18 years of age having peripheral posttraumatic NP (caused either a primary nerve trauma or surgery) in upper or lower limb, the NP having lasted for ≥6 months, the pain intensity being ≥5 on numerical rating scale (NRS) 0–10, and consenting to participate were enrolled. The diagnosis of posttraumatic NP was based on history and clinical examination (i.e., distribution of pain and abnormal sensory findings are neuroanatomically plausible) and at least 50% pain relief with local nerve block of the injured nerve (s) in a single session. Only patients with dynamic mechanical allodynia and/or pin-prick hyperalgesia in the painful area were included. All eligible patients were requested to participate. Patients were excluded if they had clinical signs of posttraumatic neuroma, phantom pain, hypersensitivity of local anesthetics, bleeding diathesis, skin lesions at the area of the treatment, untreated severe depression, or any other condition confusing assessment of the NP. Pregnant or lactating women were also excluded.

2.3 Randomization

A computer generated randomization schedule was used to allocate the patients to either the PRF or the sham treatment group. The randomization was stratified according to the location of pain (upper or lower limb). A study nurse who did not participate in the treatment procedure performed the randomization and adjusted the PRF generator to provide either PRF or sham treatment.

2.4 Treatment protocol

Skin was anesthetized with 1% lidocaine (Lidocaine® 10 mg/ml Orion Pharma, Finland). A radiofrequency needle was introduced through the skin, and then guided to a SMK cannula (52, 100 or 144mm depending on the target nerve) with 4 or 5mm active tip (SMK-C5-4, SMK-C10-5, SMK-C15-5, Radionics®, Burlington, MA, USA). The site of the treatment was selected to be the closest possible proximal site of the nerve injury. The nerve was located accurately by stimulating at 50 Hz (threshold <0.5 V). After determining that the needle was in the correct position, PRF at 45 V, 42 degrees was applied to patients (Radionics®, Burlington, MA, USA). Sham treatment or PRF was applied for 120s 1–4 times at each treatment point. The total treatment time was up to 8 min. Either VJ or EA gave the treatment based on the working schedule of the clinic. Both patients and clinicians were blinded during the whole treatment and follow-up period.

2.5 Outcome measurements

Before the treatment session and the 3-months follow-up visit, patients filled in the diary twice daily for 3 days. They assessed their pain at rest and pain after using the affected limb with NRS (0–10). Neuropathic pain scale (NPS) [16] and the Short-Form General Health questionnaire (SF-36) [17] were filled before the treatment and at the 3-month follow-up visit. The NPS results were interpreted by formulating the composite measures NPS 4, NPS 8 and NPS 10 including 4, 8, and 10 out of 10 items of the questionnaire, respectively, and by the measure NPS NA (“non-allodynic”) [17]. The patients were asked about adverse effects of PRF treatment at the 3-month follow-up visit. The primary efficacy variable was the difference in 3-day mean pain intensity score from the baseline to 3 months.

Secondary outcomes were response defined as ≥30% reduction in mean pain intensity at 3 months compared to baseline, NPS results, SF-36 results, and adverse effects. Secondary outcomes were response defined as ≥30% reduction in mean pain intensity at 3 months compared to baseline, NPS results, SF-36 results, and adverse effects.

2.6 Statistical analysis

Power calculation was not possible, because this is the first study to assess the effect of PRF for peripheral posttraumatic pain. The results are expressed as means with standard deviations (SD). Differences in personal variables at baseline between treatment groups were analyzed with the t-test or Fisher–Freeman exact test. The changes in measurement between groups were analyzed by using a bootstrap-type analysis of covariance (ANCOVA). 95% confidence interval obtained by bias corrected bootstrapping (5000 replications). The primary analysis was conducted on the perprotocol population, which was defined as all subjects who received the treatment, filled in the diary and showed up to the control visit.

3 Results

3.1 Demographic data

Between January 2004 and April 2008 1165 patients were referred to Pain Clinic. Of them, 121 patients were screened, and 45 patients with painful peripheral nerve injury in upper or lower limb were recruited (Fig. 1). The most common reasons for the exclusion were the presence of mixed pain (an obvious nociceptive pain in addition to neuropathic pain) and the low intensity of pain achieved by pharmacotherapy. The demographic and clinical features of the participants at baseline are demonstrated in Table 1. The diagnosis of nerve trauma was self-evident in the 8 patients with amputation. Iatrogenic nerve lesion was mentioned in the operation report of 3 patients. Twenty patients had abnormal electroneuromyograpy (ENMG), i.e. objective confirmation of the nerve lesion. Diagnosis of injury of a sensory nerve branch was done on the basis of bedside sensory testing in 14 patients. There was no significant difference between the groups in the demographic and clinical features at baseline. The injured nerves that were treated with PRF are listed in Table 2.

Fig. 1 Flow chart of screened, treated, and evaluated patients.
Fig. 1

Flow chart of screened, treated, and evaluated patients.

Table 1

Demographics of included patients.

Feature PRF group Sham group
Number of recruited patients 22 23
Gender
 Female 9 10
 Male 13 13
Age in years (mean ± SD) 42 ± 11 45 ± 12
Duration of pain
 6-12 months 6 9
 1-2years 5 5
Over 2years 11 9
Location of pain
 Upper limb 12 12
 Lower limb 10 11
Mechanism of nerve trauma
 Amputation 6 2
 Crush 5 12
 Operation 11 9

Table 2

Posttraumatic nerves that were treated.

Upper limb (n = 24)
 Median nerve 4
 Radial nerve 6
 Radial and median nerves 2
 Ulnar nerve 4
 Digital nerve of hand 8
Lower limb (n = 21)
 Femoral nerve 1
 Lateral cutaneous nerve of thigh 1
 Saphenous nerve 7
 Sural nerve 2
 Peroneal nerve 5
 Tibial nerve 2
 Interdigital nerve of foot 3

3.2 Primary outcome

There was no significant difference in the pain intensity at rest or after using the affected limb between the groups at baseline. No significant treatment effect was observed between the groups (Table 3).

Table 3

Pain and neuropathic pain scale (NPS) results.

Variable Baseline Change at 3 months P-value[†]
PRF, mean (SD) Sham, mean (SD) PRF, mean (95% CI) Sham, mean (95% CI)
Pain, NRS
 At rest 6.0 (1.9) 6.1 (1.5) –0.8 (–1.5 to –0.1) –0.6 (–1.1 to 0.1) 0.55
 After using the affected limb, mm 7.9 (1.2) 7.3 (1.2) –0.8 (–1.5 to –0.2) –0.7 (–1.3 to 0.2) 0.95
NPS composite
 NPS 10 52 (14) 56 (13) –4 (–10 to 2) –4 (–10to 2) 0.96
 NPS 8 39 (12) 42 (12) –4 (–9 to 16) –3 (–8 to 2) 0.77
 NPS NA 40 (12) 44 (11) –5 (–11 to 1) –2 (–7 to3) 0.27
 NPS 4 21 (8) 22 (6) –3 (–7 to 1) –1 (–4 to 1) 0.32

  1. Pain values are means of three measurements on subsequent days. NPS = neuropathic pain scale - see text and [16]

3.3 Secondary outcome measures

Seven patients (3 in PRF group and 4 in sham treatment group) achieved ≥30% pain relief (difference between groups was not significant). There was no significant difference between the groups in the NPS scores at the baseline. No significant treatment effect was found in the NPS scores in either group (Table 3). No significant change was observed in any dimension of SF-36 (Fig. 2).

Fig. 2 Short Form (SF)-36 evaluation of health-related quality of life after pulsed radiofrequency (PRF) or sham-treatment.
Fig. 2

Short Form (SF)-36 evaluation of health-related quality of life after pulsed radiofrequency (PRF) or sham-treatment.

Eighteen patients reported adverse effects. They were mild and did not necessitate any treatment. Transient pain was reported by 17 patients, local irritation by 5 patients and local inflammation by 1 patient. There was no significant difference between the groups in the presence of adverse effects.

4 Discussion

This is the first properly designed double-blind comparison of PRF and sham therapy for peripheral posttraumatic NP. Our study failed to show any significant benefit of PRF treatment over sham treatment to the injured peripheral nerves. Actually, more patients in sham group received ≥30% pain reduction, which has been defined as clinically significant pain relief [18]. However, the treatment was safe; only mild and transient adverse effects were reported.

The first report of the use of PRF on peripheral nerves was published by Rohof in 2002, when he reported a retrospective series of 49 patients with chronic shoulder pain treated with PRF with excellent results [19]. The procedure was performed after local anesthesia at the insertion point, and suprascapular nerve was the target of the treatment. Based on promising results, PRF was suggested as an alternative in difficult to treat patients [19]. Munglani reported dramatic reduction of pain after thoracotomy with PRF, and the reduction of symptoms was still present 6 months later [13]. Rozen and Ahn reported 5 patients treated with PRF for ilioinguinal neuralgia secondary to hernioraphy. Four patients reported pain relief 4–9 months after the procedure, while one patient reported no pain relief [14]. We decided to examine the efficacy of PRF for peripheral posttraumatic NP in upper or lower limb in patients refractory to pharmacotherapy and transcutaneous nerve stimulation. The treatment was given to the symptomatic nerve (s) in hope of reduction of abnormal activity in the injured nerve. According to a recent review, the use of PRF to the dorsal root ganglion in cervical radicular pain is compelling, but the evidence for its efficacy for other conditions is weaker [11].

We included only patients with moderate to severe pain, as baseline pain intensity has been shown to be crucial for the sensitivity of analgesic studies [20]. Before the procedure local anesthesia was provided, and the identification of the target nerve was performed similarly in both groups. The procedure was blinded and neither the patient nor the physician could identify whether the treatment was real or sham. However, our patient group was heterogeneous, because patients with upper and lower limb NPs were included and the trauma mechanisms of the nerves were variable. Hence we cannot exclude that the effect might have been beneficial in a certain subgroup – the number of patients in this study was too small to allow subgroup analyses.

5 Conclusion

Our study failed to show efficacy of PRF over sham treatment for peripheral posttraumatic NP. Based on our results we do not recommend PRF for peripheral posttraumatic NP. Larger sham-controlled studies recruiting more homogenous groups of patients are needed to clarify the possible efficacy of PRF for peripheral posttraumatic NP.

DOI of refers to article: http://dx.doi.org/10.1016/j.sjpain.2012.05.071.

Department of Neurosurgery, Helsinki University Central Hospital, P.O. Box 266, 00029 HUS, Helsinki, Finland. Tel.: +358 50 5837722; fax: +358 9 47187560. .

1These authors contributed equally to the study.

Acknowledgements

The study received financial support from the Health Care Foundation of North Finland and research funds of Rehabilitation ORTON.

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Received: 2011-10-12
Revised: 2012-04-30
Accepted: 2012-04-30
Published Online: 2012-07-01
Published in Print: 2012-07-01

© 2012 Scandinavian Association for the Study of Pain

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https://doi.org/10.1016/j.sjpain.2012.04.004
Keywords for this article
Neuropathic pain; Posttraumatic neuropathic pain; Pulsed radiofrequency; Randomized controlled trial

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  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
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  10. Phantom pains and sensations – how does it feel? Only the patient really knows
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  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
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  16. The effect of a mental stressor on conditioned pain modulation in healthy subjects
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  18. Pharmacological modulation of chronic pain after whiplash injury
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  20. Whiplash Associated Disorders (WAD): Responses to pharmacological challenges and psychometric tests
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  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
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  26. Piriformis muscle injection guided by sciatic nerve stimulation: Quick, simple, and safe technique
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  32. Endpoints in animal pain models
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  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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