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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.scandinavianjournalpain.com/?rss=yes"><title>Scandinavian Journal of Pain</title><description>Scandinavian Journal of Pain RSS feed: Current Issue. The  Scandinavian Journal of Pain  publishes high quality reports on original experimental and clinical pain research, observational 
studies, and educational case reports. To bring the readership up to date with focused reviews of appropriate topics of interest for 
clinicians and pain researchers. 
 
The journal will also publish abstracts of invited lectures and free presentations at the Scandinavian 
pain meetings. Letters to the Editor commenting on published papers are welcome. The journal will include announcements and comments 
on important pain meetings, educational activities, and research projects related to pain. 
  
The goals of the SASP are exclusively 
educational, scientific and charitable in nature.  The aims are: 
 To connect Scandinavian pain researchers from basic to clinical 
sciences in a multidisciplinary research network acting in close collaboration with the scientific committees of the national pain societies 
and IASP chapters 
 To foster and encourage research on pain mechanisms as well as on diagnosis and treatment of clinical pain 
in order to improve the management of patients with acute and chronic pain 
 To promote educational and training in the area of 
pain research in the Nordic countries 
 To inform physicians, other health professionals and general public of the advances in 
pain research and pain therapy by means of the  Scandinavian Journal of Pain  and dedicated websites for the membership and general 
public 
 To promote the general objectives and goals of the International Association for the Study of Pain (IASP®) on the 
field of pain research. 
 
</description><link>http://www.scandinavianjournalpain.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 Scandinavian Association for the Study of Pain. Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:issn>1877-8860</prism:issn><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:publicationDate>July 2010</prism:publicationDate><prism:copyright> © 2010 Scandinavian Association for the Study of Pain. Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000807/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000832/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000819/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000820/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000108/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000480/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000777/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000753/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000844/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000765/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000509/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000510/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000522/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000534/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000546/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000558/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS187788601000056X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000571/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000583/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000595/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000601/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000613/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000625/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000637/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000649/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000650/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000662/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000674/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000686/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000698/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000704/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000716/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000728/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS187788601000073X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.scandinavianjournalpain.com/article/PIIS1877886010000741/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000807/abstract?rss=yes"><title>Functional brain imaging of acute postoperative pain</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000807/abstract?rss=yes</link><description>Since the early 1990s when modern functional imaging techniques, such as positron emission tomography (PET) suitable for detailed studies on the living human brain and its reactions to external stimuli, were introduced to the study of pain, huge steps have been taken towards understanding the important role of supraspinal systems and mechanisms involved in the perception, cognitive, attentional and emotional processing, as well as top-down modulation of pain in health and disease . PET and, slightly later, functional magnetic resonance imaging (fMRI) have offered non-invasive means to elucidate the relative increases or decreases in regional cerebral blood flow (rCBF; PET and fMRI) or metabolic activity (PET) of different brain areas after pain-inducing or analgesic interventions in comparison to baseline. Depending on the study design, these techniques have allowed evaluation of the effects of emotional and cognitive tasks and states on the activation/deactivation patterns associated to either pain or analgesia.</description><dc:title>Functional brain imaging of acute postoperative pain</dc:title><dc:creator>Satu K. Jääskeläinen</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.033</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section>Editorial comment</prism:section><prism:startingPage>113</prism:startingPage><prism:endingPage>114</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000832/abstract?rss=yes"><title>Brain activation due to postoperative pain from the right hand measured with regional cerebral blood flow using positron emission tomography</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000832/abstract?rss=yes</link><description>Abstract: Background: Brain activation resulting from acute postoperative pain has to our knowledge not previously been studied using positron emission tomography, except from one case study. The aim of this study was to monitor activation in brain sensory pathways during acute pain after surgery of the hand. A secondary aim was to compare brain activation in clinical postoperative pain to that previously reported, by the same research group, for a model of experimental pain from the same body area. Increase in regional cerebral blood flow (rCBF) is presumed to indicate neuronal activation and decrease in blood flow decreased neuronal firing. An increase in blood flow in a brain region may represent stimulatory activity as well as inhibitory.Methods: Brain activity was measured during clinical postoperative pain and a pain free state in six patients with positron emission tomography (PET) as changes in regional cerebral blood flow (rCBF). rCBF during pain from surgery of the right thumb base was compared with a pain free state achieved by regional anaesthesia of the painful area.Results: In postoperative pain, patients had a significantly higher CBF in the contralateral/primary and secondary somatosensory cortices as well as in the contralateral motor cortex compared to the pain free stat during local regional anaesthesia. Relatively lower rCBF during the pain state was observed in clusters in the contralateral tertiary sensory cortex, ipsilateral and contralateral secondary visual cortex, prelimbic cortex, ipsilateral prefrontal as well as anterior cingulate cortex and contralateral secondary somatosensory cortex. The increased rCBF in primary and somatosensory cortices probably correspond to pain localizing processing.We also compared the findings in cerebral activation patterns of the postoperative pain state as described above, with the results from a previously published study by the same research group, using an experimental pain model when pain was inflicted with application of mustard oil in the same location, the thumb base region of the right hand. Since no formal statistical analysis was carried out between the two studies, the data are not very strong, but the differences reported were obvious when comparing the two situations.The comparison gave the following outcome:Digit activation occurred in identical sensory brain areas, i.e. primary and secondary somatosensory cortices, as compared to the changes in this study, supporting that pain localization processes use similar sensory pathways in a nociceptive acute experimental pain model, and in clinical acute postoperative nociceptive pain. Dissimilarities were observed between the models in activation of brain areas coding of the emotional pain qualities, indicating some differences between the experimental and “real” acute nociceptive pain.Conclusion: We have reported a distinct cerebral activation pattern produced by acute postoperative pain following hand surgery. The findings were compared to data obtained in a previously published report of the cerebral activation pattern from an acute experimental pain model in volunteers. We found similarities as well as some differences in the activation pattern between the two situations.</description><dc:title>Brain activation due to postoperative pain from the right hand measured with regional cerebral blood flow using positron emission tomography</dc:title><dc:creator>Torsten Gordh, Bertil Vinnars, Håkan Fischer, Hans Blomberg, Jan Modig, Mats Fredrikson, Per Hartvig</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.036</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section>Editorial comment</prism:section><prism:startingPage>115</prism:startingPage><prism:endingPage>119</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000819/abstract?rss=yes"><title>Long-term low-dose transdermal buprenorphine therapy for chronic noncancer pain</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000819/abstract?rss=yes</link><description>This issue of the Scandinavian Journal of Pain presents the first controlled opioid trial for chronic noncancer pain with a study-duration lasting more than a few months . This double blind placebo-controlled study compares low dose transdermal buprenorphine (LD-TD-BUP) with placebo patches for osteoarthritis (OA) pain. The “world-record” earlier of randomised controlled trials for opioids to patients with chronic non-malignant pain was a four months double blind comparison of tramadol plus paracetamol with placebo for chronic low back pain . Before that, published double blind, placebo-controlled potent-opioid studies lasted only from 3 days up to 2 months .</description><dc:title>Long-term low-dose transdermal buprenorphine therapy for chronic noncancer pain</dc:title><dc:creator>Petter C. Borchgrevink</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.034</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section>Editorial comment</prism:section><prism:startingPage>120</prism:startingPage><prism:endingPage>121</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000820/abstract?rss=yes"><title>A 6-months, randomised, placebo-controlled evaluation of efficacy and tolerability of a low-dose 7-day buprenorphine transdermal patch in osteoarthritis patients naïve to potent opioids</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000820/abstract?rss=yes</link><description>Abstract: Objective: Patients with osteoarthritis (OA) pain often have insufficient pain relief from non-opioid analgesics. The aim of this trial was to study efficacy and tolerability of a low dose 7-day buprenorphine transdermal delivery system, added to a NSAID or coxib regimen, in opioid-naïve patients with moderate to severe OA pain.Methods: A 6 months randomised, double-blind, parallel-group study at 19 centres in Denmark, Finland, Norway, and Sweden, in which OA patients (&gt;40 years) with at least moderate radiographic OA changes and at least moderate pain in a hip and/or knee while on a NSAID or a coxib were randomised to a 7-day buprenorphine patch (n=100) or an identical placebo patch (n=99). The initial patch delivered buprenorphine 5μg/h. This was titrated to 10 or 20μg/h, as needed. Rescue analgesic was paracetamol 0.5–4g daily. Statistical analysis of outcome data was mainly with a general linear model, with treatment as factor, the primary joint of osteoarthritis, baseline scores, and season as covariates.Results: Most patients had OA-radiographic grade II (moderate) or grade III (severe), only 8 in each group had very severe OA (grade IV). The median buprenorphine dose was 10μg/h. 31 buprenorphine-treated patients and 2 placebo-treated patients withdrew because of side effects. Lack of effect caused 12 placebo-treated and 7 buprenorphine-treated patients to withdraw. The differences in effects between treatments: Daytime pain on movement, recorded every evening on a 0–10 numeric rating scale decreased significantly more (P=0.029) in the buprenorphine group. Patients’ Global Impression of Change at the end of the double blind period was significantly improved in the buprenorphine group (P=0.017). The chosen primary effect outcome measure, the Western Ontario and McMaster Universities (WOMAC) OA Index for Pain (P=0.061), and secondary outcome measures, the WOMAC OA score for functional abilities (P=0.055), and the WOMAC total score (P=0.059) indicated more effects from buprenorphine than placebo, but these differences were not statistically significant. In a post-hoc, subgroup analysis with the 16 patients with radiographic grad IV (very severe) excluded, WOMAC OA Index for Pain was significantly (P=0.039) reduced by buprenorphine, compared with placebo. WOMAC OA score for stiffness and the amount of rescue medication taken did not differ. Sleep disturbance, quality of sleep, and quality of life improved in both groups. Side effects: Typical opioid side effects caused withdrawal at a median of 11 days before completing the 168 days double blind trial in 1/3 of the buprenorphine group. Mostly mild local skin reactions occurred equally often (1/3) in both groups.Conclusions: Although the 24hours WOMAC OsteoArthritis Index of pain was not statistically significantly superior to placebo, day-time movement-related pain and patients’ global impression of improvement at the end of the 6-months double blind treatment period were significantly better in patients treated with buprenorphine compared with placebo. Opioid side effects caused 1/3 of the buprenorphine-patients to withdraw before the end of the 6-months double blind study period.Implications: A low dose 7-days buprenorphine patch at 5–20μg/h is a possible means of pain relief in about 2/3 of elderly osteoarthritis patients, in whom pain is opioid-sensitive, surgery is not possible, NSAIDs and coxibs are not recommended, and paracetamol in tolerable doses is not effective enough. Vigilant focus on and management of opioid side effects are essential.</description><dc:title>A 6-months, randomised, placebo-controlled evaluation of efficacy and tolerability of a low-dose 7-day buprenorphine transdermal patch in osteoarthritis patients naïve to potent opioids</dc:title><dc:creator>Harald Breivik, Tone Marte Ljosaa, Kristian Stengaard-Pedersen, Jan Persson, Hannu Aro, John Villumsen, Dorthe Tvinnemose</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.035</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section>Editorial comment</prism:section><prism:startingPage>122</prism:startingPage><prism:endingPage>141</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000108/abstract?rss=yes"><title>Repeated nociceptive stimulation for detecting drug effects</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000108/abstract?rss=yes</link><description>Early seminal studies have revealed that prolonged nociceptive stimulation induces hyperexcitability and prolonged firing of spinal cord nociceptive neurones, both phenomena persisting after cessation of the peripheral stimulus . These observations provoked substantial changes in the understanding of pain pathophysiology. They demonstrated that activity of central pain pathways may persist in the absence of a peripheral nociceptive input, and neural pathways may undergo long-lasting sensitisation. These findings were mirrored by human studies showing that repeated peripheral stimulation at constant intensity evokes an increase in pain sensation during the stimulation train, so that the last stimuli are perceived as painful . This phenomenon is known as temporal summation and is believed to reflect aspects of central sensitisation induced by the peripheral nociceptive input.</description><dc:title>Repeated nociceptive stimulation for detecting drug effects</dc:title><dc:creator>Michele Curatolo</dc:creator><dc:identifier>10.1016/j.sjpain.2010.01.008</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section>Editorial comment</prism:section><prism:startingPage>142</prism:startingPage><prism:endingPage>142</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000480/abstract?rss=yes"><title>The effects of gabapentin in human experimental pain models</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000480/abstract?rss=yes</link><description>Abstract: Background: The antidepressant drugs imipramine and venlafaxine relieve clinical neuropathic pain and have been shown to increase pain thresholds in healthy volunteers during repetitive electrical sural nerve stimulation causing temporal pain summation, whereas pain during the cold pressor test is unaltered by these drugs. If this pattern of effect in experimental pain models reflects potential efficacy in clinical neuropathic pain, the pain summation model may potentially be used to identify new drugs for such pain conditions. Gabapentinoids are evidence-based treatments of clinical neuropathic pain and could contribute with additional knowledge of the usefulness of the pain summation model.The aim of this study: To test the analgesic effect of the gabapentinoid gabapentin in a sural nerve stimulation pain model including temporal pain summation and the cold pressor test.Method: 18 healthy volunteers completed a randomized, double-blind, cross-over trial with medication of 600mg gabapentin orally dosed 3 times over 24h against placebo. Pain tests were performed before and 24h after medication including pain detection and tolerance to single sural nerve stimulation and pain summation threshold to repetitive stimulation (3Hz). Peak pain intensity and discomfort were rated during a cold pressor test.Results: Compared to placebo, gabapentin had a highly significant effect on the threshold of pain summation to repetitive electrical sural nerve stimulation (P=0.009). Gabapentin significantly increased the pain tolerance threshold to single electrical sural nerve stimulation (P=0.04), whereas the pain detection threshold to single electrical sural nerve stimulation tended to be increased (P=0.06). No significant differences were found on pain ratings during the cold pressor test.Conclusion: Gabapentin had a selective hypoalgesic effect in a human experimental pain model of temporal pain summation and the results lend further support to the usefulness of the pain summation model to identify drugs for neuropathic pain.</description><dc:title>The effects of gabapentin in human experimental pain models</dc:title><dc:creator>Thomas P. Enggaard, Søren S. Mikkelsen, Stine T. Zwisler, Niels A. Klitgaard, Søren H. Sindrup</dc:creator><dc:identifier>10.1016/j.sjpain.2010.04.001</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section>Editorial comment</prism:section><prism:startingPage>143</prism:startingPage><prism:endingPage>148</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000777/abstract?rss=yes"><title>Whether the weather influences pain: High prevalence of chronic pain in Iceland and Norway: Common genes? Or lack of sunshine and vitamin D?</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000777/abstract?rss=yes</link><description>In this issue of the Scandinavian Journal of Pain Gunnarsdottir et al.  report the findings of a study on the prevalence and impact of chronic pain in Iceland. The most striking finding is that the prevalence is high, close to 31% and exactly as high as in Norway . The prevalence in Iceland and Norway are higher than in most Southern-European countries (in Spain only 12% ), but also higher than in the other Nordic countries: 20% in Denmark , 18% in Sweden  and 19% in Finland . Is this just an accidental finding caused by flaws in the surveyed samples in Norway and Iceland? Whereas one study found a slightly lower prevalence in Norway, i.e. 25% , two other major health surveys in Norway confirmed a prevalence of chronic pain of moderate-to-severe intensity to be close to 30% .</description><dc:title>Whether the weather influences pain: High prevalence of chronic pain in Iceland and Norway: Common genes? Or lack of sunshine and vitamin D?</dc:title><dc:creator>Harald Breivik</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.030</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section>Editorial comment</prism:section><prism:startingPage>149</prism:startingPage><prism:endingPage>150</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000753/abstract?rss=yes"><title>A population based study of the prevalence of pain in Iceland</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000753/abstract?rss=yes</link><description>Abstract: Prevalence estimates of pain differ depending on how it is defined and measured and on the populations studied. It has been estimated that on a given day, as many as 30–44% of the general population experience some kind of pain. Information about the prevalence of pain in Iceland is not available. The aims of this study were to evaluate the prevalence of pain of various origins among the general population of Iceland, to test hypotheses regarding relationships between pain, quality of life (QOL) and demographic variables, to evaluate participants’ beliefs about causes of their pain, and to evaluate how those who experience pain manage it. A random sample of 1286 adults was drawn from a national registry holding information about all citizens of Iceland. Data were collected with a postal-survey. Pain was evaluated with the Brief Pain Inventory (BPI), with instructions modified to evaluate pain in the past week as opposed to the past 24h. Of 1286 invited, 599 (46.6%) participated, of which, 232 had experienced pain in the past week (40.3%). Participants had a mean (SD) age of 44.94 (17.12) years and 56% were women. Those who had pain perceived their health to be worse than those who had not [B=−0.91, SE=0.15, Wald=38.75, p=0.00], but did not differ on other variables. Of 232 individuals reporting pain, 183 (79.6%) or 30.6% of the total sample had experienced pain for more than three months. On a scale from 0 “no pain” to 10 “pain as bad as I can imagine” the mean (SD) pain severity score (composite of four pain severity scores) for the 232 participants reporting pain was 3.21 (1.73) and pain interference with life activities 2.59 (1.98), also on a 0–10 scale. Pain severity predicted pain interference [B=0.71; F=126.14; df=1,206; p=0.00], which mediated the effects of pain severity on mood and QOL. Between Pain Interference with Life and Positive Affect [B=−0.06; F=4.53; df=1,196; p=0.04], between Pain Interference and Negative Affect [B=0.15; F=23.21; df=1,196; p=0.00], and between Pain Interference and Global Quality of Life [B=−0.18; F=29.11; df=1,196; p=0.00]. Most frequent causes for pain were strain injuries (n=79), resulting from work or sports activity, arthritis (n=39), mechanical problems (e.g. due to birth defects, curvature, slipped discs, etc.) (n=37), various diseases (n=31) and accidents (n=30). Nineteen participants did not know what caused their pain. Treatments for pain varied, but most had used medications alone (n=76) or in combination with other treatments (n=61). The prevalence of pain in the general population of Icelandic adults is similar to what has been reported. Estimates of chronic pain are towards the higher end when compared to data from other European counties, yet comparable to countries such as Norway. This raises questions about possible explanations to be looked for in genetics or cultural point of view. This population based study provides valuable information about the prevalence of pain in Iceland and also supports findings previously reported about pain in the neighboring countries.</description><dc:title>A population based study of the prevalence of pain in Iceland</dc:title><dc:creator>Sigridur Gunnarsdottir, Sandra E. Ward, Ronald C. Serlin</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.028</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section>Editorial comment</prism:section><prism:startingPage>151</prism:startingPage><prism:endingPage>157</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000844/abstract?rss=yes"><title>Swedish nurses are prone to chronic shoulder and back pain because of miserable working conditions and poor leadership?</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000844/abstract?rss=yes</link><description>Nilsson et al. report in this issue of The Scandinavian Journal of Pain that especially registered nurses working in hospitals have a high risk of musculoskeletal pain—mostly shoulder and low back pain . They followed a group of nurses from 2003 to 2006, focusing on pain, disability, and sick leave. About half of the sample reported pain at baseline, and pain at baseline predicted pain and the odds of being disabled at follow up. They also reported significantly more sick days at follow up compared to baseline. It is also interesting that satisfaction with work leaders decreased during the study period .</description><dc:title>Swedish nurses are prone to chronic shoulder and back pain because of miserable working conditions and poor leadership?</dc:title><dc:creator>Tone Rustøen, Sanna Salanterä</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.037</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section>Editorial comment</prism:section><prism:startingPage>158</prism:startingPage><prism:endingPage>159</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000765/abstract?rss=yes"><title>Predicting of pain, disability, and sick leave regarding a non-clinical sample among Swedish nurses</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000765/abstract?rss=yes</link><description>Abstract: Objectives: Health care providers, especially registered nurses (RNs), are a professional group with a high risk of musculoskeletal pain (MSP). This longitudinal study contributes to the literature by describing the prevalence and change in MSP, work-related factors, personal factors, self-reported pain, disability and sick leave (&gt;7 days) among RNs working in a Swedish hospital over a 3-year period. Further, results concerning prediction of pain, disability and sick leave from baseline to a 3-year follow-up are reported.Method: In 2003, a convenience sample of 278 RNs (97.5% women, mean age 43 years) completed a questionnaire. In 2006, 244 RNs (88% of the original sample) were located, and 200 (82%) of these completed a second questionnaire.Results: Logistic regression analyses revealed that pain, disability and sick leave at baseline best predicted pain, disability, and sick leave at follow-up. The personal factors self-rated health and sleep quality during the last week predicted pain at follow-up, while age, self-rated health, and considering yourself as optimist or pessimist predicted disability at follow-up, however weakly. None of the work-related factors contributed significantly to the regression solution.Conclusions: The results support earlier studies showing that a history of pain and disability is predictive of future pain and disability. Attention to individual factors such as personal values may be needed in further research.</description><dc:title>Predicting of pain, disability, and sick leave regarding a non-clinical sample among Swedish nurses</dc:title><dc:creator>Annika Nilsson, Per Lindberg, Eva Denison</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.029</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section>Editorial comment</prism:section><prism:startingPage>160</prism:startingPage><prism:endingPage>166</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000509/abstract?rss=yes"><title>Trigeminal neuralgia or odontogenic pain</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000509/abstract?rss=yes</link><description>Aim: Appreciate the significance of a detailed history in patients with unilateral episodic trigeminal pain.   The commonest cause of pain in the trigeminal region is dental, followed by unilateral temporomandibular disorders and so patients with trigeminal neuralgia (TN) will often seek dental care first. Neurosurgeons have estimated that up to 60% of patients with TN will have undergone irreversible dental treatment and the average duration before referral is around 6 years. It must be noted that dental disease and TN can co exist.</description><dc:title>Trigeminal neuralgia or odontogenic pain</dc:title><dc:creator>Joanna M. Zakrzewska</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.003</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>167</prism:startingPage><prism:endingPage>168</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000510/abstract?rss=yes"><title>What's wrong with animal models of pain?</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000510/abstract?rss=yes</link><description>Recent decades have seen an explosion in our understanding of the molecular and cellular underpinnings of pain, but virtually none of this knowledge has resulted in new clinical therapies. Many pain researchers believe that the problem may lie in the existing animal models of pain, which are reliable but much more complex and subtle than is commonly realized, and of questionable clinical relevance. Most basic science studies of pain continue to rely on the measurement of reflexive, evoked hypersensitivity responses after artificial neuropathic or inflammatory injuries, whereas clinical pain in humans features much spontaneous pain and an important cognitive and emotional overlay.</description><dc:title>What's wrong with animal models of pain?</dc:title><dc:creator>Jeffrey S. Mogil</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.004</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>168</prism:startingPage><prism:endingPage>168</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000522/abstract?rss=yes"><title>Immunotherapy for neuroblastoma elicits a complement dependent whole body allodynia</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000522/abstract?rss=yes</link><description>GD2 ganglioside is found on plasma membranes of tumor cells of neuroectodermal origin, including neuroblastoma cells. A chimeric antibody against GD2 (ch14.18) is currently being used as a treatment for pediatric neuroblastoma. Intravenous administration of the antibody induces severe whole body allodynia in patients which lasts from 24 to 48h. Similar administration of antibody to rats produces tactile, but not thermal sensitivity, whole body touch evoked agitation as well as ectopic activation of identified C nociceptors in the sural nerve. Both the peripheral nerve firing and patient allodynia are sensitive to low dose systemic lidocaine. Pain behavior, in rats and children, is also sensitive to gabapentin.</description><dc:title>Immunotherapy for neuroblastoma elicits a complement dependent whole body allodynia</dc:title><dc:creator>Linda S. Sorkin</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.005</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>168</prism:startingPage><prism:endingPage>168</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000534/abstract?rss=yes"><title>Pain mechanisms in animal models of rheumatoid arthritis</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000534/abstract?rss=yes</link><description>Rheumatoid arthritis (RA) is chronic disease affecting 1% of the population. It is characterized by infiltration of inflammatory cells into the joints, synovial neovascularization and proliferation of fibroblasts and bone erosion. Clinically the disease is evident as joint inflammation, swelling and progressive joint destruction. Of importance, pain is one of the most bothersome symptoms reported by RA patients. Autoantibodies to type II collagen (CII) and glucose-6-phosphate isomerase (GPI) are detected in serum of 70% and 20% of the RA patients, respectively. Intraperitoneal injection of these antibodies to mice rapidly induces arthritis-like symptoms and generates a joint pathology that resembles human RA. While collagen antibody-induced arthritis (CAIA) and K/BxN serum transfer (GPI antibody-mediated) are common models in the rheumatology field, they have not been evaluated as models of arthritis-induced pain. Data from our studies in which pain behavior (tactile and cold allodynia) and the analgesic effect of ketorolac (cyclooxygenase inhibitor), etanercept (TNF inhibitor) and gabapentin were examined will be presented. In brief, we observed that both injection of CII and GPI antibodies caused induction of clinical signs of arthritis including joint swelling and redness of the paws, and that this inflammatory state gave rise to a robust, and reproducible allodynia. Interestingly, the allodynia outlasted the signs of joint inflammation. Of note, while intraperitoneal injection of ketorolac, etanercept and gapapentin attenuated arthritis-induced allodynia during the inflammatory phase, only gabapentin had anti-allodynic effect in the “post-inflammatory” phase. Spinal activation of astrocytes and microglia was assessed as these cells have been implicated to play a role in the maintenance of hypersensitivity in experimental models of persistent pain. Experiments in which microglia and astrocyte activity was assessed using quantitative real time PCR and immunohistochemistry indicated activation of spinal glia in both models.</description><dc:title>Pain mechanisms in animal models of rheumatoid arthritis</dc:title><dc:creator>Christina Christianson, Duygu BalkisBas, Rikard Holmdahl, Nandakumar Kutty Selva, Tony Yaksh, Maripat Corr, Gary Firestein, Camilla I. Svensson</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.006</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>168</prism:startingPage><prism:endingPage>169</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000546/abstract?rss=yes"><title>Translating basic research to pharmacological treatment of neuropathic pain</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000546/abstract?rss=yes</link><description>Despite the major advances in our knowledge of mechanisms involved in neuropathic pain, patients continue to suffer from chronic and disabling neuropathic pain conditions. Over 150 randomized controlled studies have evaluated the effect of pharmacological agents for neuropathic pain conditions, including postherpetic neuralgia, painful polyneuropathy, peripheral nerve injury, and central pain. Despite an increase of about 60% in new randomized placebo-controlled trials in neuropathic pain during the past 5 years, there seems to be no evidence for major changes of the treatment algorithm. Tricyclic antidepressants (TCAs), serotonin noradrenaline reuptake inhibitors (SNRIs), the anticonvulsants gabapentin and pregabalin, and opioids are the drug classes with most consistent efficacy. Topical treatments with lidocaine patch, botulinum toxin A, and high-dose capsaicin are new treatment modalities which seem to have some effect on peripheral neuropathic pain with little or no systemic side effects. Other drug classes seem to relieve neuropathic pain in subgroup of patients, but more trials are needed to evaluate the overall effect and predictors of efficacy of these drugs, which include lamotrigine, oxcarbazepine, carbamazepine, valproate, and lacosamide. Certain drugs do not relieve neuropathic pain despite promising results from basic research. These drugs include NK1-receptor antagonists and the anticonvulsant levetiracetam.</description><dc:title>Translating basic research to pharmacological treatment of neuropathic pain</dc:title><dc:creator>Nanna Brix Finnerup</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.007</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>169</prism:startingPage><prism:endingPage>169</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000558/abstract?rss=yes"><title>Forearm heat pain does not inhibit electrically induced tibialis anterior muscle pain</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000558/abstract?rss=yes</link><description>Objectives: Women report more musculoskeletal pain than men. A dysfunctional pain inhibitory system has been launched as a contributing factor for these gender differences. This study used a diffuse noxious inhibitory controls (DNIC) paradigm and asked the following questions: (1) is electrically induced muscle pain inhibited by a painful heat stimulus to the forearm, and (2) does women show signs of reduced inhibition compared to men?</description><dc:title>Forearm heat pain does not inhibit electrically induced tibialis anterior muscle pain</dc:title><dc:creator>Maria Gullander, Dagfinn Matre</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.008</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>169</prism:startingPage><prism:endingPage>169</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS187788601000056X/abstract?rss=yes"><title>Offset analgesia evoked by non-contact thermal stimulator</title><link>http://www.scandinavianjournalpain.com/article/PIIS187788601000056X/abstract?rss=yes</link><description>Objective: The objective of this study was to test if offset analgesia could be evoked using a noncontact thermal stimulator. Offset analgesia [J. Neurophysiol. 87:2205–2208, 2002] is defined as an unproportionally large decrease in pain intensity following a slight decrease in stimulation intensity. The importance of differences in thermal properties between human hairy and glabrous skin was investigated.</description><dc:title>Offset analgesia evoked by non-contact thermal stimulator</dc:title><dc:creator>K.S. Frahm, O.K. Andersen, L. Arendt-Nielsen, C.D. Mørch</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.009</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>169</prism:startingPage><prism:endingPage>170</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000571/abstract?rss=yes"><title>Inhibition of FAAH reverses spinal LTP</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000571/abstract?rss=yes</link><description>Objectives: Fatty-acid amide hydrolase (FAAH) is an enzyme that metabolizes several endocannabinoids and fatty acid amides important for human pain sensitivity. Here we examine how reduced FAAH activity affects maintenance of spinal long-term potentiation (LTP) and spinal expression of the transcription factor Zif.</description><dc:title>Inhibition of FAAH reverses spinal LTP</dc:title><dc:creator>Guro S. Eriksen, Line M. Jacobsen, Linda M. Pedersen, Johannes Gjerstad</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.010</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>170</prism:startingPage><prism:endingPage>170</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000583/abstract?rss=yes"><title>Hyperexcitable C-nociceptors in human paroxysmal pain</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000583/abstract?rss=yes</link><description>Objectives: Spontaneously occurring paroxysmal pain is an important constituent of the symptomatology of neuropathic pain. While mechanisms of stimulus-evoked pain and also spontaneous ongoing pain have been studied for a long time, little emphasis has been put on the mechanisms of paroxysmal pain. The objective of the present study was to record from single C-nociceptive fibres in a patient presenting with pure paroxysmal pain.</description><dc:title>Hyperexcitable C-nociceptors in human paroxysmal pain</dc:title><dc:creator>I.P. Kleggetveit, B. Namer, R. Schmidt, T. Helås, M. Schmelz, E. Jørum</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.011</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>170</prism:startingPage><prism:endingPage>170</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000595/abstract?rss=yes"><title>Pain sensitivity and experimentally induced sensitization in red haired women</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000595/abstract?rss=yes</link><description>Pain sensitivity has been linked to the melanocortin-1 receptor (MC1R) gene. A mutation in MC1R can result in pale skin and red hair in humans. The aim of this study was to investigate pain sensitivity in redheads. Twenty healthy women with pale skin and red hair (mean age 32 years, range 20–55) and 20 healthy women with blond/dark hair (mean age 31 years, range 20–51) participated in this study. On the left arm pain tolerance threshold to heat and pressure stimulation was determined. On the right arm 0.075% topical capsaicin cream was applied for 30min. Thereafter the secondary hyperalgesic area was estimated with a calibrated filament (von Frey hair, 15g) and the allodynic area by a soft brush. This was done 0, 30, 60 and 90min after removing the cream. There was no difference in either heat or pressure pain tolerance thresholds between the two groups (heat: P=0.8; pressure: P=1.0). The areas to pin-prick were significantly smaller for red haired women than non-red haired women (P=0.014). There were no significantly differences in the allodynic areas. Redheads were less sensitive to capsaicin induced hyperalgesia compared to non-redheads which could be a manifestation of central anti-hyperalgesic involvement of MCR's.</description><dc:title>Pain sensitivity and experimentally induced sensitization in red haired women</dc:title><dc:creator>Trine Andresesn, Lars Arendt-Nielsen, Asbjørn Drewes, Dagmar Lunden</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.012</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>170</prism:startingPage><prism:endingPage>171</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000601/abstract?rss=yes"><title>How are opioids used in Norway? Persistent use, utilization of depot formulation and age profile in non-palliation patients</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000601/abstract?rss=yes</link><description>Objectives: The extent of persistent opioid use in Norway is unknown. We have studied how many persistent opioid users there are in Norway, whether they use long- or short acting opioids and the age distribution of these patients.</description><dc:title>How are opioids used in Norway? Persistent use, utilization of depot formulation and age profile in non-palliation patients</dc:title><dc:creator>Kristian Svendsen, Petter Borchgrevink, Olav Magnus Fredheim, Svetlana Skurtveit</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.013</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>171</prism:startingPage><prism:endingPage>171</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000613/abstract?rss=yes"><title>To which extent does incident and persistent use of weak opioids predict problematic opioid use?</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000613/abstract?rss=yes</link><description>Background: A high consumption of weak opioids may contribute to prescription abuse of opioids, but the risk of development of problematic opioid use in patients starting opioid therapy is not established.</description><dc:title>To which extent does incident and persistent use of weak opioids predict problematic opioid use?</dc:title><dc:creator>S. Skurtveit, K. Furu, M. Handal, P. Borchgrevink, O. Fredheim</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.014</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>171</prism:startingPage><prism:endingPage>171</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000625/abstract?rss=yes"><title>Is transdermal buprenorphine for chronic non-malignant pain used long term without co-medication with other potentially addictive drugs?</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000625/abstract?rss=yes</link><description>Objectives: Guidelines for the appropriate use of opioids to patients with persistent non-cancer pain recommend the use of long-acting opioids. Low dose transdermal buprenorphine (LD-TD-BUP) was introduced as the first depot opioid designed specifically to be used long term to patients with chronic non-malignant pain. Primary aim was to see how many patients prescribed LD-TD-BUP would become long-term users for non-malignant pain. Secondary aim was to see how many patients co-medicated with opioids or other potentially addictive drugs.</description><dc:title>Is transdermal buprenorphine for chronic non-malignant pain used long term without co-medication with other potentially addictive drugs?</dc:title><dc:creator>A. Nordbø, S. Skurtveit, P.C. Borchgrevink, S. Kaasa, O. Fredheim</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.015</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>171</prism:startingPage><prism:endingPage>172</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000637/abstract?rss=yes"><title>Prostaglandin E2 production in synovial tissue and acute postoperative pain after knee arthroscopy</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000637/abstract?rss=yes</link><description>Postsurgical inflammation leads to sensitisation of “sleeping” nociceptors, which enhance pain perception and induce hyperalgesia. Prostaglandin E2 plays a central role in this process. Synovial microdialysis technique allows analyses of biological markers of local inflammation simultaneous with a close follow up of the patient's pain experience. Tissue injury (or surgery) initiates liberation of inflammatory mediators and hyperalgesic substances. This project is translational and aims at exploring the relationship between perceived acute postoperative pain and inflammation. Microdialysis of synovial tissue and pain score after arthroscopy is of special interest to study since the natural pain course and the local inflammation can be observed in patients with no analgesic therapy.</description><dc:title>Prostaglandin E2 production in synovial tissue and acute postoperative pain after knee arthroscopy</dc:title><dc:creator>Nina Solheim, Bente Halvorsen, Leiv Arne Rosseland, Audun Stubhaug</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.016</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>172</prism:startingPage><prism:endingPage>172</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000649/abstract?rss=yes"><title>Girl presenting with oesophageal spasm pain after fundoplication</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000649/abstract?rss=yes</link><description>Introduction: A previously healthy 19-year-old woman, who had symptoms of gastric-oesophagela reflux disease for over one year, was transferred to our specialist hospital three weeks post fundoplication operation at a local hospital. She had several episodes with severe retrosternal pain lasting minutes to hours which was stabbing in character. She persistently experienced what was thought to be episodes of oesophageal spasm associated with food intake or movement. She required gradually escalating doses of opioids, both transdermal, intramuscular and intravenous. She was started on a regime of transdermal opioids in addition to iv opioids for the acute pain episodes. This was later supplemented with a PCA pump. Despite the increase in pain and in CRP, the patient was continued on an opioid reduction regime initiated by the surgeons six weeks post surgery. Two months post fundoplication she developed respiratory failure.</description><dc:title>Girl presenting with oesophageal spasm pain after fundoplication</dc:title><dc:creator>Ewa Gawecka, Oddbjørn Viken</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.017</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>172</prism:startingPage><prism:endingPage>172</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000650/abstract?rss=yes"><title>Epidemiology of persistent postoperative pain: Association of persistent pain and sensory abnormalities</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000650/abstract?rss=yes</link><description>Background: The prevalence of persistent postoperative pain in the general population is poorly documented, but clinical studies indicate that the problem is common.   Aim: The aim of this study was (1) to assess the prevalence of persistent postoperative pain among individuals operated during the last 3 years in a general population and (2) to describe factors associated with chronic postoperative pain.</description><dc:title>Epidemiology of persistent postoperative pain: Association of persistent pain and sensory abnormalities</dc:title><dc:creator>A. Johansen, L. Romundstad, C.S. Nielsen, H. Schirmer, A.E. Eggen, A. Stubhaug</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.018</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>172</prism:startingPage><prism:endingPage>173</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000662/abstract?rss=yes"><title>Cost–benefit of a 13-week multidiciplinary rehabilitation course for chronic non-malignant pain patients</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000662/abstract?rss=yes</link><description>Background: Economy is an important part of chronic pain.   Aim: To describe the economy in chronic non-malignant pain patients attending a 13-week Rehabilitation Program (RP).</description><dc:title>Cost–benefit of a 13-week multidiciplinary rehabilitation course for chronic non-malignant pain patients</dc:title><dc:creator>Villy Meineche-Schmidt</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.019</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>173</prism:startingPage><prism:endingPage>173</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000674/abstract?rss=yes"><title>A novel and effective treatment modality for medically unexplained pain</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000674/abstract?rss=yes</link><description>Medically unexplained pain (MUP) confounds physicians, and the incidence and prevalence of these conditions is poorly documented. This is not least due to the complex nature of MUP and mimicry of morbidity with conditions that have common clinical assessment and treatment modalities, e.g. migraine headaches which stress headaches commonly are misdiagnosed as. Effective treatment modalities for MUP have been more or less non-existent. In the following we present a modality for the assessment, diagnosis and treatment of MUP that in our experience leads to cure, at least in better than half of these cases measured in terms of allowing the individual back to work. These results are at least twice as high as those described hitherto (see below), and yet, our treatment modality is beset with many obstacles, not the least of which is the intransigence of a system that will not and/or can not understand why this modality is so much better than what they are able to offer. The most important obstacle is financing, as this modality requires long term and committed financing to work. The economic implications of not dealing with these issues are described.</description><dc:title>A novel and effective treatment modality for medically unexplained pain</dc:title><dc:creator>Richard Evan Steele</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.020</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>173</prism:startingPage><prism:endingPage>173</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000686/abstract?rss=yes"><title>Somatocognitive therapy in the management of chronic gynaecological pain. A review of current approach and historical background</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000686/abstract?rss=yes</link><description>Introduction: We have developed somatocognitive therapy as a hybrid of Mensendieck physiotherapy and cognitive psychotherapy. Women with chronic pelvic pain (CPP) and vulvodynia (chronic pain of the vulvae and vestibulum, VD) were recruited into two separate treatment protocols as described.</description><dc:title>Somatocognitive therapy in the management of chronic gynaecological pain. A review of current approach and historical background</dc:title><dc:creator>Gro Killi Haugstad, Unni Kirste, Siv Leganger, Elin Haakonsen og Tor S. Haugstad</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.021</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>173</prism:startingPage><prism:endingPage>174</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000698/abstract?rss=yes"><title>The Manual Intervention Trial (MINT)—The effect of various combinations of naprapathic manual therapy. The study protocol of a randomized controlled trial</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000698/abstract?rss=yes</link><description>Objective: Naprapathy is defined as a specific system for examining, diagnostics, manual treatment and rehabilitation of pain/dysfunction in the neuromusculoskeletal system. The therapy aims to reduce pain and dysfunction through treatment of the connective tissue, muscle- and neural tissue in/around the spine and other joints, by a combination of manual techniques. Earlier trials show that Naprapathy is effective for patients with unspecific back/neck pain. The current trial aims to compare the effect of three combinations of Naprapathic manual therapy (NMT) on such pain, to examine prevalence, severity and duration of adverse reactions after NMT, and to identify subgroups of patients who have greater benefit from the treatments.</description><dc:title>The Manual Intervention Trial (MINT)—The effect of various combinations of naprapathic manual therapy. The study protocol of a randomized controlled trial</dc:title><dc:creator>Eva Skillgate, Lena Holm, Helene Schulte</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.022</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>174</prism:startingPage><prism:endingPage>174</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000704/abstract?rss=yes"><title>The experience of chronic pain, loss and grief</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000704/abstract?rss=yes</link><description>Introduction: Based on a theoretical framework which integrates grief theory, cognitive behavioural therapy (CBT) and writing theory, 1–2 an intervention for persons experiencing loss and grief caused by chronic pain or death of someone close is planned. There seems to be lack of understanding of the connections between pain, loss and grief and how these life phenomena can be met in patient care. Understanding the process involved in one sort of grief following loss may help us understand the processes involved in another. Increased understanding of this complexity may contribute to suitable approaches in practice.</description><dc:title>The experience of chronic pain, loss and grief</dc:title><dc:creator>Bodil Furnes, Elin Dysvik</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.023</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>174</prism:startingPage><prism:endingPage>174</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000716/abstract?rss=yes"><title>Effect of buprenorphine and fentanyl in experimental induced superficial, deep and hyperalgesic pain</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000716/abstract?rss=yes</link><description>Chronic pain and hyperalgesia can be difficult to treat with classical opioids acting predominately at the μ-receptor. Some opioids have different receptor binding profiles and different analgesic and anti-hyperalgesic effects. Buprenorphine and its metabolites are believed to exert the analgesic action through μ-, ?- and d-receptors. They may therefore posses another analgesic profile compared to other opioids with a more mono-receptor binding profile such as fentanyl. In the present study 22 healthy volunteers were randomized to treatment with transdermal fentanyl (25μg/h, 72h), buprenorphine (20μg/h, 144h) or placebo in a crossover experimental pain study. The experimental pain tests (phasic and tonic pain, sensitization) involved pressure at the tibial bone, intramuscular nerve growth factor (NGF), UVB burn injury model, cold pressor test, cutaneous electrical and thermal stimulation and intradermal capsaicin induced hyperalgesia. Pain testing was carried out at baseline, 24, 48, 72 and 144h after application of the drugs. Compared to placebo buprenorphine significantly attenuated tibial pressure pain (P=0.007) as well as pressure pain in the UVB induced primary hyperalgesic area (P=0.006). On the other hand fentanyl attenuated cold pressor pain compared to placebo (P=0.005). The two drugs were equipotent and better than placebo to thermal pain stimulation (P=0.0001). They drugs failed to show significant analgesic effect to NGF induced muscle soreness, cutaneous electrical stimulation and to capsaicin induced hyperalgesia. In equipotent doses buprenorphine attenuated bone associated pain and primary hyperalgesia more than fentanyl. These tissue and modality differentiated effects may reflect clinical observations that opioids act differently.</description><dc:title>Effect of buprenorphine and fentanyl in experimental induced superficial, deep and hyperalgesic pain</dc:title><dc:creator>Trine Andresen, Lars Arendt-Nielsen, Asbjørn Drewes, Alexander Oksche, Camilla Staahl</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.024</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>174</prism:startingPage><prism:endingPage>175</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000728/abstract?rss=yes"><title>Pretreatment with opioids enhances afferent induced long-term potentiation in the rat dorsal horn</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000728/abstract?rss=yes</link><description>Objectives: Opioids are increasingly used against chronic non-malignant pain. Long-term opioid treatment may be associated with the development of hyperalgesia. Long term facilitation (LTF) of C-fibre evoked firing of wide dynamic range neurons in the spinal dorsal horn in response to conditioning stimulation (CS) of afferent fibres is a widely studied cellular model of spinal nociceptive sensitization. In a rat model with recording of single neurone responses we have previously demonstrated that seven days of opioid pre-treatment enhances the stimulus-evoked LTF (, Haugan 2008 ). In this study we looked at the effect of long-term pretreatment with morphine on longterm potentiation (LTP) of C-fibre evoked dorsal horn field potentials, a widely used model of spinal hyperexcitability.</description><dc:title>Pretreatment with opioids enhances afferent induced long-term potentiation in the rat dorsal horn</dc:title><dc:creator>Eileen Hauge Kjellsen, Frøydis Haugan, Lars Jørgen Rygh, Arne Tjølsen</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.025</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>175</prism:startingPage><prism:endingPage>175</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS187788601000073X/abstract?rss=yes"><title>Pigs in pain—Porcine behavioural responses towards mechanical nociceptive stimulation directed at the hind legs</title><link>http://www.scandinavianjournalpain.com/article/PIIS187788601000073X/abstract?rss=yes</link><description>Objectives: In recent years, pigs are used increasingly for biomedical translational research and often considered superior to rodent models. However, only very few pain assays for quantification of behavioural nociceptive responses are available for pigs. This experiment is part of a larger project aiming at developing pain assays for pigs, and the present aim was to examine behavioural responses towards mechanical cutaneous stimulation applied to the caudal part of the metatarsus on the hind legs of pigs using an IITC Electronic von Frey Anesthesiometer.</description><dc:title>Pigs in pain—Porcine behavioural responses towards mechanical nociceptive stimulation directed at the hind legs</dc:title><dc:creator>Mette S. Herskin, Julie S. Rasmussen</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.026</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>175</prism:startingPage><prism:endingPage>176</prism:endingPage></item><item rdf:about="http://www.scandinavianjournalpain.com/article/PIIS1877886010000741/abstract?rss=yes"><title>A human experimental bone pain model</title><link>http://www.scandinavianjournalpain.com/article/PIIS1877886010000741/abstract?rss=yes</link><description>Introduction: Bone associated pain from, e.g., metastases is poorly understood. The aim of the study was to develop a human experimental model, which could evoke pain from the periosteum.</description><dc:title>A human experimental bone pain model</dc:title><dc:creator>Trine Andresen, Lars Arendt-Nielsen, Christina Brock, Asbjørn Drewes, Hongling Nie, Anne Olesen</dc:creator><dc:identifier>10.1016/j.sjpain.2010.05.027</dc:identifier><dc:source>Scandinavian Journal of Pain 1, 3 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Scandinavian Journal of Pain</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>1</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1877-8860(10)X0004-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>176</prism:startingPage><prism:endingPage>176</prism:endingPage></item></rdf:RDF>