Home Medicine Brain activation due to postoperative pain from the right hand measured with regional cerebral blood flow using positron emission tomography
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Brain activation due to postoperative pain from the right hand measured with regional cerebral blood flow using positron emission tomography

  • Torsten Gordh EMAIL logo , Bertil Vinnars , Håkan Fischer , Hans Blomberg , Jan Modig , Mats Fredrikson and Per Hartvig
Published/Copyright: July 1, 2010
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Scandinavian Journal of Pain
From the journal Scandinavian Journal of Pain Volume 1 Issue 3

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.

Keywords: Brain imaging; Regional cerebral blood flow; Postoperative pain; Regional nerve block

1 Introduction

Advances in imaging techniques have focused interest to brain signalling in sensory processes.

Sensory activation due to pain has been studied as regional changes in cerebral blood flow using the non-invasive imaging technique positron emission tomography, PET, in several experimental models [1,2,3,4,5,6,7,8]. Consistently, painful stimuli as compared to baseline produce rCBF elevations in contralateral anterior cingulate gyrus, ipsilateral anterior insular and ipsilateral prefrontal cortices [1,2,6,7,9,10,11]. Involvement of primary and secondary somatosensory cortices was also indicated [1,2,4,6,7,12]. Increase in rCBF is presumed to indicate neuronal activation and decrease in blood flow due to decreased neuronal firing. An increase in blood flow in a brain region may represent stimulatory activity as well as inhibitory.

Some years ago, it was possible to confirm a spatial discrimination along the central sulcus as a function of pain induced in the hand or the foot [1]. However, experimental pain differs from clinical pain with respect to several components as to behaviour and effects of treatment. Brain imaging studies in clinical pain states may show different rCBF changes as compared to studies using experimental pain particular with changes of rCBF in thalamus [9]. Different activation in the brain due to different origin of chronic pain states has been discerned as well [12,13], suggesting that clinical and experimental pain may have different central underpinnings. Recently, Kupers and Kehlet emphasized that post-operative pain models are highly appealing since it enables control for many confounding factors, which hamper the interpretation of most current studies [14].

The aim of the present study was to monitor activation in central sensory pathways during a specific clinical acute pain state resulting from surgery in a defined area, i.e. the thumb base of the right hand and to compare the results with a pain free state achieved by local regional anaesthesia. A further, secondary aim was to compare this pattern of brain activation of clinical postoperative pain to that previously reported for an experimental pain model at the same body location, carried out by the same research group [1].

2 Material and methods

2.1 Patients, surgery, and anaesthesia

Seven patients, 1 male and 6 female patients, with pain from the right thumb basal joint with radiographic verified osteoarthritis of the trapeziometacarpal joint took part in the study and were operated by the same surgeon with arthroplasty of the carpometacarpal (CMC) joint. All patients had ASA status I and II and their ages were between 54 and 73 years. The study was approved by the Ethics Review Board of the Medical faculty of Uppsala University and the Radiation Hazards Committee of Uppsala University hospital. All subjects gave their informed consent to participate in accordance with the Declaration of Helsinki. They were informed that pain might be severe after surgery and that analgesic medication (i.v. morphine) was immediately at hand as requested. During pre-operative assessment, which took place the day before surgery, all patients were taught the pain scoring evaluation using a numeric pain scale (NRS) between 0 and 10, in which 0 equals “no-pain” and 10 equals “worst pain ever”. The male patient was excluded due to an unexpected pathological finding (brain tumour) in the frontal lobe at the examination with PET.

Before the surgical procedure, the brachial plexus was blocked via the interscalene route using 40 ml of mepivacaine 15 mg/ml (Carbocain®, AstraZeneca, Sweden) with 2.5 μg/ml epinephrine. Pain from the tourniquet used to obtain a bloodless field was removed by blockade of the intercostobrachial and medial brachial cutaneous nerves with 7 ml of subcutaneous lidocaine (10 mg/ml Xylocain®, AstraZeneca, Sweden) but without epinephrine. All patients were premedicated with 10 mg diazepam (Stesolid®, Dumex, Denmark) 1 h prior to surgery and immediately before surgery an intravenous dose of 1–2 mg of midazolam (Dormicum®, Roche, France). In all patients, the brachial plexus anaesthetics were administered by the same anaesthesiologist.

Surgery time was about 1 h. Patients were brought to the recovery area in the postoperative ward after surgery and were allowed analgesic treatment if necessary until PET. The patients were closely supervised throughout the study by an anaesthesiologist. Ratings of pain were performed at regular intervals, every 10 min, throughout, using the NRS.

2.2 PET-procedure

The patients were brought to PET when the brachial plexus block had worn off about 5 h after surgery on the same day. The patients then experienced at least moderate degrees of postoperative pain, i.e. at least 6 at the NRS scale. Each subject was positioned lying on the back on the couch of the PET camera system and was immobilized with a stereotactic head fixation [1]. A radial artery catheter was inserted (Viggo-Spectramed, Swindon, UK) in the left wrist and another catheter was inserted in a vein at the elbow in the same arm. No significant pain from application of the catheters was reported. The scanning room was dimly lit, the patients had their eyes covered with patches and both ears were plugged. They were again informed about the procedure in order to minimize stress and other factors that could interfere with the PET investigation. Two minutes before the emission scan, the patient was asked to concentrate on the painful hand and try not to think of anything else. They had to close their eyes and were instructed not to move or talk. First, a scan was done with a saline injection in order to calibrate settings of the PET scanner. Thereafter, two baseline scans of rCBF using PET with H215O in the pain state were performed in each subject. Immediately after each scan, patients evaluated ongoing pain with NRS.

After the first PET scan in the painful state had been completed, analgesia was given as an interscalene blockade as described above. After 5 min patients were pain free and two additional PET scans were performed during pain free conditions.

2.3 Blood flow recordings

2.3.1 Scanner

An eight-ring brain PET scanner (GEMS PC2048-15B) with a 10 cm axial field of view was used [15]. The scanner produced 15 slices with 6.5 mm slice spacing and with an axial and transaxial resolution of approximately 6 mm. Subjects were positioned in the scanner such that the planes were parallel to a line between the anterior and posterior commissure, where the most basal slice was one cm above the orbita (anterior brain) and below the calcarina (posterior brain). Next, the subjects were blindfolded and allowed to rest in the scanner for 20 min. Thereafter a transmission scan of 10 min duration was obtained using a rotating 68Ge pin source. Immediately before each emission scan, 600–800 MBq of H215O in 3–4 ml of water (approximately 10 MBq/kg body weight) was injected at 10-min intervals. Following injection, data were collected in fifteen 10-s frames. Each subject had in total four PET scans during two conditions. After the four scans, an additional injection was given during which time the scanner couch was automatically transferred back and forth between two positions 10 cm apart. Data were collected only when in one of these two positions, and never during the transfer. This scan was performed to obtain full axial coverage of the brain, which aids in the stereotactic normalization of PET images.

2.4 Reconstruction of PET data

For each scan, the first frame after arrival of bolus to the brain was identified and relabelled as frame 1. Data were then collected into two summation images consisting of data from frames with odd numbers and from frames with an even number, respectively. Hence, each summed data set consisted of two statistically independent estimates of the radioactivity concentration of the brain from time after arrival of bolus and 60 s forth. It has been shown that, by dividing data from each scan in this manner, significant gains in sensitivity may be achieved [16]. The summation images were reconstructed using the transmission scan to compensate for attenuation, correcting for scattered radiation [17] and using a 15 mm Hanning filter. Note that although data were collected for 2 min, only the first 60 s after bolus arrival to the brain were used.

2.5 Anatomical standardization

Anatomical normalization of all individual CBF images into a standard brain shape [18] was performed automatically [19] by matching the scan with 20 cm axial coverage to an atlas template. The first emission image was then automatically aligned to the 20 cm scan [20] to bring also this scan into the stereotactic space. Then scans two, three and four for each subject was matched to the position of the first to correct for movement of the head between scans and to bring also these scans into the stereotactic space [20]. In all cases, movements between scan 1, 2, 3 and 4 were smaller than 5 mm in any direction, and hence the attenuation correction was deemed satisfactory [20]. The stereotactic space was defined based on the post-mortem slicing of a single subject in which brain contours, gyri, sulci, central structures and Brodmann areas were defined [18]. The reorientation was performed within the same software system as the anatomical standardization [19] and hence only one actual re-sampling of the data was performed. In order to facilitate comparisons between studies the Talairach brain [21] has been mapped into the atlas, allowing results to be communicated in Talairach coordinates.

2.6 Statistical analysis

PET data were fitted to a statistical model described by

i = 1 , 2 ( PAIN, NO-PAIN ) LF i j k GF i j k = u + τ i + γ i + e i j k j = 1 , 2 , . . . , 6 ( subjects ) k = 1 , 2 ( data set for each condition )

GFijk denotes global flow in scan ijk, LFijk denotes local flow (in a given voxel) in scan ijk, u denotes mean pixel value averaged over i, j and k; τ denotes effect of stimulation; γ denotes subject (block) effect; and ε denotes residual error [1]. The model was solved in a least-square sense for estimates of u, τ, γ and ε, and t-values were estimated through linear contrasts.

A single contrast hereafter referred to as the postoperative pain contrast was performed to evaluate rCBF differences between two postoperative states, one painful (PAIN) and one pain free as a result of the anaesthesia block (NO-PAIN) [1 −1]. The contrast generated a t-map with 41 degrees of freedom that was subsequently converted to a z-score map through a probability preserving transformation [22]. The significance of the z-score map was evaluated at an omnibus level using the mean square z-score [23]. Local changes were evaluated using the spatial extent of connected clusters of voxels with a z-score above 2.5 [24]. This test takes into account multiple comparisons and has a cluster-localizing power [25] meaning that the cluster taken as a whole is significantly activated, though no strong statements may be made concerning individual voxels within that cluster.

Fig. 1 PET image (A) showing significantly increased neural activity as a function of postoperative pain (PAIN vs. NO-PAIN) in a cluster of voxels located in the left primary and secondary somatosensory cortices extending into the primary motor cortex. In the coronal image (B) the white line indicates the localization of the horizontal image (A). Yellow contours that outline the brain from the computerised Greitz brain atlas [18]. Note that right corresponds to the left in the brain. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of the article.)
Fig. 1

PET image (A) showing significantly increased neural activity as a function of postoperative pain (PAIN vs. NO-PAIN) in a cluster of voxels located in the left primary and secondary somatosensory cortices extending into the primary motor cortex. In the coronal image (B) the white line indicates the localization of the horizontal image (A). Yellow contours that outline the brain from the computerised Greitz brain atlas [18]. Note that right corresponds to the left in the brain. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of the article.)

3 Results

3.1 Behavioural results

Patients recorded moderate to high pain scores (range 6–10) using the NRS after surgery when the effect of brachial plexus block for the surgical procedure had worn off. All patients rated “no-pain” in the pain free state, demonstrating a successful regional anaesthesia of the brachial plexus. Although possible and encouraged if needed, no patient demanded any analgesic from end of surgery until the end of PET.

3.2 Brain blood flow results

The field of view from which data were evaluated included the entire brain above Talairach [21] z level −14 in the anterior brain and z level 0 in the posterior brain (total brain volume = 64,876 voxels). The postoperative pain contrast, comparing rCBF during postoperative pain and no-pain states, yielded a significant omnibus p-value of less than 0.000001. This indicated a highly significant difference in brain blood flow pattern between the postoperative pain and no-pain conditions. Significant local neural alternations from the postoperative pain contrast are listed in Table 1. As a function of postoperative pain, rCBF was significantly elevated in a cluster (size = 214 voxels) located in the contralateral primary (Brodmann areas 1, 2 and 3), secondary somatosensory cortices (area 7) and the primary motor cortex (area 4) (Fig. 1). A lower rCBF during postoperative pain, as compared to no-pain, was evident in seven clusters with the first one (size = 656 voxels) located in the contralateral tertiary sensory cortex (Brodmann area 40). The second one (size = 632 voxels) was located in the ipsilateral secondary visual cortex (area 18) and the third (size = 447 voxels) was situated in the prelimbic cortex (areas 25 and 33) and the contralateral prefrontal (area 10) as well as in anterior cingulate cortices (area 32). The fourth (size = 275 voxels) was situated in the ipsilateral secondary somatosensory cortex (areas 5 and 7), while the fifth (size = 243 voxels) was located in the contralateral secondary visual cortex (area 19). The sixth (size = 201 voxels) encompassed the ipsilateral prefrontal cortex (area 9) and the seventh in the prefrontal cortex (size = 138 voxels, area 10) on the ipsilateral side.

Table 1

Regional CBF alterations as a function of postoperative pain (i.e. postoperative pain vs. non-pain). Brodmann areas included in each cluster, Talairach coordinates for maximum pixel z-values within each cluster, and cluster p-values for significant increases and decreases in rCBF as well as trends are given. First clusters with increased rCBF are listed (1) using descending p-values and (2) according to cluster size, then clusters with decreased rCBF are given following the same principle.

Brain areas Brodmann areas x y z Maximum pixel z-value Cluster p-value
Regions with higher rCBF during pain Cluster
L parietal cortex 7 –30 –44 62 4.10 .00001
L parietal cortex 1,2,3 –29 –37 62 3.98  
L frontal cortex 4 –36 –18 64 3.41  
Regions with lower rCBF during pain Cluster 1            
L parietal cortex 40 45 –37 22 5.05 .00001
Cluster2            
R occipital cortex 18 19 –79 16 3.99 .00001
Cluster3            
R frontal cortex 25 –07 26 –07 4.30 .00001
L frontal cortex 25 01 24 –07 3.27  
L frontal cortex 10,25,32,33 –20 63 05 3.80  
Cluster4            
R parietal cortex 5,7 12 –42 44 3.41 .0006
Cluster5            
L occipital cortex 19 –24 76 20 3.99 0015
Cluster6            
R frontal cortex 9 26 43 41 4.44 .0051
Cluster 7            
R frontal cortex 10 17 49 –06 3.60 .036

  1. R = right hemisphere.

  2. L = left hemisphere.

  3. _ = where the maximum voxel value is located when several Brodmann areas are lumped together.

  4. The coordinates in millimetres correspond to the stereotactic atlas of Talairach and Tournoux [21]. The x and z coordinates indicate the distance from a line between the anterior and posterior commissures, while the y coordinate indicates the position relative to the anterior commissure. Significance of clusters has been evaluated based on the spatial extent of suprathreshold clusters with z-scores at 2.5 or above [24].

4 Discussion

A prominent increase of rCBF in primary and secondary somatosensory cortices was evident in this study on brain activation as a result of postoperative pain. In response to acute experimental painful stimuli, an increased rCBF has almost invariably been observed in second somatosensory cortex and insular regions as well as in the anterior cingulated cortex and with slightly less consistency also in the thalamus and the primary sensory cortex [10]. Activation of thalamus, primary and secondary somatosensory cortex and insula is thought to relate to sensory-discriminative aspects of the pain process. The majority of studies were performed using different experimental pain models [1,2,3,4,5,6,7,8,26]. Only a few have addressed the activation in clinical pain states [12,13,27,28,29]. Changes of rCBF have been reported to vary with type of experimental pain [7]. The pattern of brain activation differed in clinical pain states, as well. For example, there is a preferential activation of the right anterior cingulate cortex regardless of side in chronic neuropathic pain from the lower extremity [12]. Further, induced cluster headache activated anterior cingulate cortex and temporopolar region also in the right hemisphere [27], which was paralleled by the activation seen in trigeminal neuropathy [28]. Muscle pain and hyperesthesia from the jaw did not show any obvious activation of primary or secondary somatosensory cortices [13].

Brain activation resulting from acute postoperative pain has previously only been sparsely studied using positron emission tomography. The only previous study we have found is a case report by Buvanendran et al. [30]. There the brain activation resulting from pain due to total knee arthroplastic surgery was studied, before and after pain relief from an epidural anaesthesia. They found that postsurgical pain was associated with increased activity in the contralateral primary somatosensory cortex. Other brain regions showing increased postsurgical activity were the contralateral parietal cortex, bilateral pulvinar and ipsilateral medial dorsal nucleus of the thalamus, contralateral putamen, contralateral superior temporal gyrus, ipsilateral fusiform gyrus, ipsilateral posterior lobe, and contralateral anterior cerebellar lobe. That study demonstrated the feasibility of evaluating the central processing of acute postoperative pain using PET scan.

We believe that we add to this knowledge by studying our six subjects using the same methods. It must be born in mind that these kinds of studies are rather difficult to perform, with newly operated patients with pain, complex logistics with transports from recovery rooms to PET scanning, and a high cost for each PET investigation.

In our present study, during acute postoperative pain, activation was observed in the contralateral primary and secondary somatosensory cortices extending into the primary motor cortex. The higher blood flow observed in these areas were in agreement with sensory signalling in different experimental pain models [1,2,4,6,7,9]. Attenuated rCBF during clinical pain in ipsilateral prefrontal as well as in anterior cingulated cortex observed in this study should be viewed in light of the patient returning from intense pain to almost complete anaesthesia of the arm, when discomfort and anxiety might be lower. This effect might reflect anxiety and discomfort which has previously been associated with a diminished prefrontal rCBF during anxiety provocation [31,32,33].

Further, the anterior cingulate cortex did not seem to be involved in the coding of pain signals and location, c.f. Andersson et al. [1]. Instead, alterations in the anterior cingulate cortex appear to participate in both the affective and attentional processes associated with pain [10]. Several studies confirm that blood flow changes in anterior cingulate cortex particularly on the right side are correlated with the unpleasantness of pain [12,28,34]. It is tempting to speculate that the anxiety and discomfort influence brain activity more profoundly than the coding of the emotional pain qualities. Anxiety and fear are associated with an attenuated perfusion [31,32,33]. This may distinguish postoperative pain and experimentally induced pain. Relatively increased activity in the somatosensory cortex and relatively decreased activity in occipital areas may reflect that cortical areas primarily were activated in pain and may suppress other sensory systems. Contralateral primary motor cortex was significantly activated in the present patients, confirming earlier reports [10].

No significant thalamic activation could be discerned in the present study of postoperative pain. However, it must be taken into consideration that no “true” pain free state was included, only the difference in brain activation in the pain state from that of an anaesthetized upper limb. Thus, it is plausible that sensory input from the surgical wound reached the thalamus but that the two conditions were not physiologically or psychologically distinct enough to differentially influence thalamic activity. In an early study on chronic neuropathic pain, an altered pain processing was observed in the thalamus particularly on the side of the affected body part [29], whereas not any change in thalamic activity was reported after block of neuropathic pain from the lower extremity [9,12].

In addition, we cannot rule out that the diazepam medication given to our patients before and during surgery, may have affected the observed activation patterns.

5 Conclusions

In conclusion, somatosensory areas were activated by postoperative pain from the hand as compared to a pain free state achieved through local regional anaesthesia. This pattern of activation is similar to that observed in experimental pain models, and may unify clinical and experimental pain. On the other hand, activity in limbic, paralimbic and subcortical areas was not similar to the pattern evident in experimental nociceptive pain models. Thus, brain activity in real postoperative and experimentally induced pain stemming from the same anatomical location showed similarities and dissimilarities supporting both common and distinct brain mechanisms between the two conditions.

DOI of refers to article: 10.1016/j.sjpain.2010.05.033.

Multidisciplinary Pain Center, Department of Anesthesiology and Intensive Care, Uppsala University Hospital, SE 751 85 Uppsala, Sweden. Tel.: +46 18 611 4876; fax: +46 18 514 621 E-mail:

Acknowledgements

The financial support from the Uppsala County Counsil and the Swedish Medical Research Counsil (grants 8645 and 9077) is gratefully acknowledged. The study was done in cooperation with Uppsala Berzelii Center.

  1. Conflicts of interest: None declared.

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Received: 2009-11-04
Revised: 2010-05-26
Accepted: 2010-05-26
Published Online: 2010-07-01
Published in Print: 2010-07-01

© 2010 Scandinavian Association for the Study of Pain

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  9. Editorial comment
  10. Repeated nociceptive stimulation for detecting drug effects
  11. Original experimental
  12. The effects of gabapentin in human experimental pain models
  13. Editorial comment
  14. Whether the weather influences pain: High prevalence of chronic pain in Iceland and Norway: Common genes? Or lack of sunshine and vitamin D?
  15. Observational studies
  16. A population based study of the prevalence of pain in Iceland
  17. Editorial comment
  18. Swedish nurses are prone to chronic shoulder and back pain because of miserable working conditions and poor leadership?
  19. Observational studies
  20. Predicting of pain, disability, and sick leave regarding a non-clinical sample among Swedish nurses
  21. Abstracts
  22. Trigeminal neuralgia or odontogenic pain
  23. Abstracts
  24. What’s wrong with animal models of pain?
  25. Abstracts
  26. Immunotherapy for neuroblastoma elicits a complement dependent whole body allodynia
  27. Abstracts
  28. Pain mechanisms in animal models of rheumatoid arthritis
  29. Abstracts
  30. Translating basic research to pharmacological treatment of neuropathic pain
  31. Abstracts
  32. Free Poster Presentations: Forearm heat pain does not inhibit electrically induced tibialis anterior muscle pain
  33. Abstracts
  34. Offset analgesia evoked by non-contact thermal stimulator
  35. Abstracts
  36. Inhibition of FAAH reverses spinal LTP
  37. Abstracts
  38. Hyperexcitable C-nociceptors in human paroxysmal pain
  39. Abstracts
  40. Pain sensitivity and experimentally induced sensitization in red haired women
  41. Abstracts
  42. How are opioids used in Norway? Persistent use, utilization of depot formulation and age profile in non-palliation patients
  43. Abstracts
  44. To which extent does incident and persistent use of weak opioids predict problematic opioid use?
  45. Abstracts
  46. Is transdermal buprenorphine for chronic non-malignant pain used long term without co-medication with other potentially addictive drugs?
  47. Abstracts
  48. Prostaglandin E2 production in synovial tissue and acute postoperative pain after knee arthroscopy
  49. Abstracts
  50. Girl presenting with oesophageal spasm pain after fundoplication
  51. Abstracts
  52. Epidemiology of persistent postoperative pain: Association of persistent pain and sensory abnormalities
  53. Abstracts
  54. Cost–benefit of a 13-week multidiciplinary rehabilitation course for chronic non-malignant pain patients
  55. Abstracts
  56. A novel and effective treatment modality for medically unexplained pain
  57. Abstracts
  58. Somatocognitive therapy in the management of chronic gynaecological pain. A review of current approach and historical background
  59. Abstract
  60. The Manual Intervention Trial (MINT)—The effect of various combinations of naprapathic manual therapy. The study protocol of a randomized controlled trial
  61. Abstracts
  62. The experience of chronic pain, loss and grief
  63. Abstracts
  64. Effect of buprenorphine and fentanyl in experimental induced superficial, deep and hyperalgesic pain
  65. Abstract
  66. Pretreatment with opioids enhances afferent induced long-term potentiation in the rat dorsal horn
  67. Abstracts
  68. Pigs in pain—Porcine behavioural responses towards mechanical nociceptive stimulation directed at the hind legs
  69. Abstracts
  70. A human experimental bone pain model
https://doi.org/10.1016/j.sjpain.2010.05.036
Keywords for this article
Brain imaging; Regional cerebral blood flow; Postoperative pain; Regional nerve block

Articles in the same Issue

  1. Editorial comment
  2. Functional brain imaging of acute postoperative pain
  3. Clinical pain research
  4. Brain activation due to postoperative pain from the right hand measured with regional cerebral blood flow using positron emission tomography
  5. Editorial comment
  6. Long-term low-dose transdermal buprenorphine therapy for chronic noncancer pain
  7. Original experimental
  8. 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
  9. Editorial comment
  10. Repeated nociceptive stimulation for detecting drug effects
  11. Original experimental
  12. The effects of gabapentin in human experimental pain models
  13. Editorial comment
  14. Whether the weather influences pain: High prevalence of chronic pain in Iceland and Norway: Common genes? Or lack of sunshine and vitamin D?
  15. Observational studies
  16. A population based study of the prevalence of pain in Iceland
  17. Editorial comment
  18. Swedish nurses are prone to chronic shoulder and back pain because of miserable working conditions and poor leadership?
  19. Observational studies
  20. Predicting of pain, disability, and sick leave regarding a non-clinical sample among Swedish nurses
  21. Abstracts
  22. Trigeminal neuralgia or odontogenic pain
  23. Abstracts
  24. What’s wrong with animal models of pain?
  25. Abstracts
  26. Immunotherapy for neuroblastoma elicits a complement dependent whole body allodynia
  27. Abstracts
  28. Pain mechanisms in animal models of rheumatoid arthritis
  29. Abstracts
  30. Translating basic research to pharmacological treatment of neuropathic pain
  31. Abstracts
  32. Free Poster Presentations: Forearm heat pain does not inhibit electrically induced tibialis anterior muscle pain
  33. Abstracts
  34. Offset analgesia evoked by non-contact thermal stimulator
  35. Abstracts
  36. Inhibition of FAAH reverses spinal LTP
  37. Abstracts
  38. Hyperexcitable C-nociceptors in human paroxysmal pain
  39. Abstracts
  40. Pain sensitivity and experimentally induced sensitization in red haired women
  41. Abstracts
  42. How are opioids used in Norway? Persistent use, utilization of depot formulation and age profile in non-palliation patients
  43. Abstracts
  44. To which extent does incident and persistent use of weak opioids predict problematic opioid use?
  45. Abstracts
  46. Is transdermal buprenorphine for chronic non-malignant pain used long term without co-medication with other potentially addictive drugs?
  47. Abstracts
  48. Prostaglandin E2 production in synovial tissue and acute postoperative pain after knee arthroscopy
  49. Abstracts
  50. Girl presenting with oesophageal spasm pain after fundoplication
  51. Abstracts
  52. Epidemiology of persistent postoperative pain: Association of persistent pain and sensory abnormalities
  53. Abstracts
  54. Cost–benefit of a 13-week multidiciplinary rehabilitation course for chronic non-malignant pain patients
  55. Abstracts
  56. A novel and effective treatment modality for medically unexplained pain
  57. Abstracts
  58. Somatocognitive therapy in the management of chronic gynaecological pain. A review of current approach and historical background
  59. Abstract
  60. The Manual Intervention Trial (MINT)—The effect of various combinations of naprapathic manual therapy. The study protocol of a randomized controlled trial
  61. Abstracts
  62. The experience of chronic pain, loss and grief
  63. Abstracts
  64. Effect of buprenorphine and fentanyl in experimental induced superficial, deep and hyperalgesic pain
  65. Abstract
  66. Pretreatment with opioids enhances afferent induced long-term potentiation in the rat dorsal horn
  67. Abstracts
  68. Pigs in pain—Porcine behavioural responses towards mechanical nociceptive stimulation directed at the hind legs
  69. Abstracts
  70. A human experimental bone pain model
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