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  • 1. Ahmed, Aisha S
    et al.
    Li, Jian
    Erlandsson-Harris, Helena
    Stark, André
    Bakalkin, Georgy
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaceutisk biovetenskap.
    Mahmood, Ahmed
    Suppression of pain and joint destruction by inhibition of the proteasome system in experimental osteoarthritis2012Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 153, nr 1, s. 18-26Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Osteoarthritis is a degenerative joint disease with pain and loss of joint function as major pathological features. Recent studies show that proteasome inhibitors reduce pain in various pathological conditions. We evaluated the effects of MG132, a reversible proteasome inhibitor on pain and joint destruction in a rat model of osteoarthritis. Osteoarthritis was induced by intraarticular injection of monosodium iodoacetate into the rat knee. Knee joint stiffness was scored and nociception was evaluated by mechanical pressure applied to the respective hind paw. Knee joint destruction was assessed by radiological and histological analyses. Expression of matrix metalloproteinase-3 (MMP-3) was analyzed by quantitative reverse transcription polymerase chain reaction in the knee articular cartilage. Expression of substance P (SP) and calcitonin gene-related peptide (CGRP) was studied in the dorsal root ganglia (L4–L6) by quantitative reverse transcription polymerase chain reaction and in the knee joints by immunohistochemistry. Our results indicate that daily treatment of osteoarthritic rats with MG132 significantly increases their mobility while the swelling, pain thresholds, and pathological features of the affected joints were reduced. Furthermore, the upregulated expression of MMP-3, SP, and CGRP in the arthritic rats was normalized by MG132 administration. We conclude that the proteasome inhibitor MG132 reduces pain and joint destruction, probably by involving the peripheral nervous system, and that changes in SP and CGRP expression correlate with alterations in behavioural responses. Our findings suggest that nontoxic proteasome inhibitors may represent a novel pharmacotherapy for osteoarthritis.

  • 2.
    Amandusson, Åsa
    et al.
    Klin o experimentell medicin.
    Hallbeck, M
    Hallbeck, AL
    Hermansson, O
    Blomqvist, A
    Estrogen-induced alterations of spinal cord enkephalin gene expression1999Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 83, nr 2, s. 243-248Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Enkephalin-synthesizing neurons in the superficial laminae of the spinal and trigeminal dorsal horn are critical components of the endogenous pain-modulatory system. We have previously demonstrated that these neurons display intracellular estrogen receptors, suggesting that estrogen can potentially influence their enkephalin expression. By using Northern blot, we now show that a bolus injection of estrogen results in a rapid increase in spinal cord enkephalin mRNA levels in ovariectomized female rats. Thus, 4 h after estrogen administration the enkephalin mRNA-expression in the lumbar spinal cord was on average 68% higher (P<0.05) than in control animals injected with vehicle only. A small increase in the amount of enkephalin mRNA was also seen after 8 h (P<0.05), whereas no difference between estrogen-injected and control animals was found after 24 h or at time periods shorter than 4 h. Taken together with the previous anatomical data, the present findings imply that estrogen has an acute effect on spinal opioid levels in areas involved in the transmission of nociceptive information.

  • 3.
    Aresh, Bejan
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Genetisk utvecklingsbiologi.
    Freitag, Fabio B.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Genetisk utvecklingsbiologi.
    Perry, Sharn
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Genetisk utvecklingsbiologi.
    Blümel, Edda
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Genetisk utvecklingsbiologi.
    Lau, Joey
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk cellbiologi.
    Franck, Marina C.M.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Genetisk utvecklingsbiologi.
    Lagerström, Malin C.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Genetisk utvecklingsbiologi.
    Spinal Cord Interneurons Expressing the Gastrin-Releasing Peptide Receptor Convey Itch Through VGLUT2-Mediated Signaling2017Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 158, nr 5, s. 945-961Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Itch is a sensation that promotes the desire to scratch, which can be evoked by mechanical and chemical stimuli. In the spinal cord, neurons expressing the gastrin-releasing peptide receptor (GRPR) have been identified as specific mediators of itch. However, our understanding of the GRPR population in the spinal cord, and thus how these neurons exercise their functions, is limited. For this purpose, we constructed a Cre line designed to target the GRPR population of neurons (Grpr-Cre). Our analysis revealed that Grpr-Cre cells in the spinal cord are predominantly excitatory interneurons that are found in the dorsal lamina, especially in laminae II-IV. Application of the specific agonist gastrin-releasing peptide induced spike responses in 43.3% of the patched Grpr-Cre neurons, where the majority of the cells displayed a tonic firing property. Additionally, our analysis showed that the Grpr-Cre population expresses Vglut2 mRNA, and mice ablated of Vglut2 in Grpr-Cre cells (Vglut2-lox; Grpr-Cre mice) displayed less spontaneous itch and attenuated responses to both histaminergic and nonhistaminergic agents. We could also show that application of the itch-inducing peptide, natriuretic polypeptide B, induces calcium influx in a subpopulation of Grpr-Cre neurons. To summarize, our data indicate that the Grpr-Cre spinal cord neural population is composed of interneurons that use VGLUT2-mediated signaling for transmitting chemical and spontaneous itch stimuli to the next, currently unknown, neurons in the labeled line of itch.

  • 4. Barr, Travis P.
    et al.
    Hrnjic, Alen
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaceutisk biovetenskap.
    Khodorova, Alla
    Sprague, Jared M.
    Strichartz, Gary R.
    Sensitization of cutaneous neuronal purinergic receptors contributes to endothelin-1-induced mechanical hypersensitivity2014Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 155, nr 6, s. 1091-1101Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Endothelin (ET-1), an endogenous peptide with a prominent role in cutaneous pain, causes mechanical hypersensitivity in the rat hind paw, partly through mechanisms involving local release of algogenic molecules in the skin. The present study investigated involvement of cutaneous ATP, which contributes to pain in numerous animal models. Pre-exposure of ND7/104 immortalized sensory neurons to ET-1 (30 nM) for 10 min increased the proportion of cells responding to ATP (2 mu M) with an increase in intracellular calcium, an effect prevented by the ETA receptor-selective antagonist BQ-123. ET-1 (3 nM) pre-exposure also increased the proportion of isolated mouse dorsal root ganglion neurons responding to ATP (0.2-0.4 mu M). Blocking ET-1-evoked increases in intracellular calcium with the IP3 receptor antagonist 2-APB did not inhibit sensitization to ATP, indicating a mechanism independent of ET-1-mediated intracellular calcium increases. ET-1-sensitized ATP calcium responses were largely abolished in the absence of extracellular calcium, implicating ionotropic P2X receptors. Experiments using quantitative polymerase chain reaction and receptor-selective ligands in ND7/104 showed that ET-1-induced sensitization most likely involves the P2X4 receptor subtype. ET-1-sensitized calcium responses to ATP were strongly inhibited by broad-spectrum (TNP-ATP) and P2X4-selective (5-BDBD) antagonists, but not antagonists for other P2X subtypes. TNP-ATP and 5-BDBD also significantly inhibited ET-1-induced mechanical sensitization in the rat hind paw, supporting a role for purinergic receptor sensitization in vivo. These data provide evidence that mechanical hypersensitivity caused by cutaneous ET-1 involves an increase in the neuronal sensitivity to ATP in the skin, possibly due to sensitization of P2X4 receptors.

  • 5.
    Bjelland, Elisabeth Krefting
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Allmänmedicin och preventivmedicin.
    Owe, Katrine Mari
    Pingel, Ronnie
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Allmänmedicin och preventivmedicin.
    Kristiansson, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Allmänmedicin och preventivmedicin.
    Vangen, Siri
    Eberhard-Gran, Malin
    Pelvic pain after childbirth: a longitudinal population study2016Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 157, nr 3, s. 710-716Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    In this longitudinal population study, the aims were to study associations of mode of delivery with new onset of pelvic pain and changes in pelvic pain scores up to 7-18 months after childbirth. We included 20,248 participants enrolled in the Norwegian Mother and Child Cohort Study (1999-2008) without preexisting pelvic pain in pregnancy. Data were obtained by four self-administered questionnaires and linked to the Medical Birth Registry of Norway. A total of 4.5% of the women reported new onset of pelvic pain 0-3 months postpartum. Compared to unassisted vaginal delivery, operative vaginal delivery was associated with increased odds of pelvic pain (adjusted odds ratio 1.30; 95% confidence interval: 1.06-1.59). Planned and emergency cesarean deliveries were associated with reduced odds of pelvic pain (adjusted odds ratio 0.48; 95% confidence interval: 0.31-0.74 and adjusted odds ratio 0.65; 95% confidence interval: 0.49-0.87, respectively). Planned cesarean delivery, young maternal age, and low Symptom Checklist-8 scores were associated with low pelvic pain scores after childbirth. A history of pain was the only factor associated with increased pelvic pain scores over time (P=0.047). We conclude that new onset of pelvic pain after childbirth was not commonly reported, particularly following cesarean delivery. Overall, pelvic pain scores were rather low at all time points and women with a history of pain reported increased pelvic pain scores over time. Hence, clinicians should follow up women with pelvic pain after a difficult childbirth experience, particularly if they have a history of pain.

  • 6.
    Brattberg, Gunilla
    et al.
    Department of Social Work, Stockholm University, Stockholm, Sweden.
    Parker, Marti G
    Thorslund, Mats
    The prevalence of pain among the oldest old in Sweden1996Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 67, nr 1, s. 29-34Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Although there is information available about pain in elderly persons, there have been very few studies about pain among the oldest old. In Sweden, 8% of the population is older than 74 years, and 2% is older than 84 years. It is the group over 74 which is growing fastest in proportion to the entire population. The aims of the present study are (a) to analyze if pain increases or decreases with age in the oldest age groups and (b) to study gender differences regarding pain. The present study of a random sample (n = 537) of the oldest old in Sweden shows that there is some evidence of decreased musculoskeletal pain with age. Among women, total reported pain decreases with age. Among men, there is an increase of reported severe pain with age. Including the results from another Swedish population survey of individuals aged 18-84, there is evidence that the prevalence of pain among the older elderly is comparable to the prevalence of pain among the middle-aged (45-64) and is higher than the prevalence among the younger elderly (65-75). Musculoskeletal pain is more common among old women than old men but for chest pain and abdominal pain there is no difference. The sex difference is more pronounced for multiple and severe pain complaints. The prevalence of mild or severe pain in any of the studied locations in the whole study group (77+) was 73% and for individuals over 85 years, 68%. For multiple pain, the figures were 47% for all older elderly (77+) and 46% for individuals over 85 years of age. For severe pain in at least one location, corresponding figures were 33% and 35%.

  • 7.
    Buhrman, Monica
    et al.
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Fältenhag, Sofia
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Ström, Lars
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Andersson, Gerhard
    Controlled trial of Internet-based treatment with telephone support for chronic back pain2004Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 111, nr 3, s. 368-377Artikel i tidskrift (Refereegranskat)
  • 8.
    Butler, Stephen
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Allmänmedicin och preventivmedicin.
    The IMMPACT factor or IMMPACT strikes again!2013Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 154, nr 11, s. 2243-2244Artikel i tidskrift (Övrigt vetenskapligt)
  • 9.
    Butler, Stephen H.
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Jonzon, Bror
    Branting-Ekenback, Christina
    Wadell, Cecilia
    Farahmand, Bahman
    Predictors of severe pain in a cohort of 5271 individuals with self-reported neuropathic pain2013Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 154, nr 1, s. 141-146Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The influence of pain descriptors and mechanical hypersensitivity on pain severity in neuropathic pain has not been well researched and is poorly understood. The aim of this study was to determine the relationship between pain severity and other factors describing chronic neuropathic pain in a large cohort of patients with self-reported neuropathic pain potentially recruited as subjects for a Phase IIa study. A questionnaire specific to the study parameters covering demographics and pain characteristics was sent to potential participants. Overall, 9185 questionnaires were returned from potential subjects who self-reported neuropathic pain. Adjusted odds ratios with 95% confidence intervals were used as a measure of association. These were estimated by unconditional logistic regression. Pain descriptors in the questionnaire were: burning, shooting, shocking, and aching. The presence of self-reported allodynia and hyperalgesia was strongly indicative of both moderate and severe pain, with a significant interaction of both factors in moderate and severe pain. Having 3 or 4 pain descriptors was also strongly indicative of both moderate and severe pain. Female gender, age, and history of serious mental disorders were found to be weaker indicators of both moderate and severe pain. Given the large and varied population with many neuropathic pain diagnoses in the study, the findings are not likely to be merely chance, but are likely to reflect important relationships between pain severity and other factors in those who suffer from chronic neuropathic pain.

  • 10.
    Butler, Stephen H.
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Allmänmedicin och preventivmedicin. Norwegian Univ Sci & Technol, Fac Med, Dept Circulat & Med Imaging, Trondheim, Norway..
    Landmark, Tormod
    St Olavs Univ Hosp, Natl Competence Ctr Complex Symptom Disorders, Trondheim, Norway..
    Glette, Mari
    Norwegian Univ Sci & Technol, Fac Med, Dept Circulat & Med Imaging, Trondheim, Norway..
    Borchgrevink, Petter
    Norwegian Univ Sci & Technol, Fac Med, Dept Circulat & Med Imaging, Trondheim, Norway.;St Olavs Univ Hosp, Natl Competence Ctr Complex Symptom Disorders, Trondheim, Norway..
    Woodhouse, Astrid
    St Olavs Univ Hosp, Natl Competence Ctr Complex Symptom Disorders, Trondheim, Norway.;Norwegian Univ Sci & Technol, Fac Med, Dept Publ Hlth & Gen Practice, Trondheim, Norway..
    How widespread should pain be to be defined as widespread?: Reply2016Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 157, nr 8, s. 1832-1833Artikel i tidskrift (Refereegranskat)
  • 11.
    Butler, Stephen
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Allmänmedicin och preventivmedicin. Norwegian Univ Sci & Technol, Fac Med, Dept Circulat & Med Imaging, N-7034 Trondheim, Norway; Univ Uppsala Hosp, Pain Ctr, ING 79,2 TR, S-75185 Uppsala, Sweden.
    Landmark, Tormod
    St Olavs Univ Hosp, Natl Competence Ctr Complex Symptom Disorders, Trondheim, Norway.
    Glette, Mari
    Norwegian Univ Sci & Technol, Fac Med, Dept Circulat & Med Imaging, N-7034 Trondheim, Norway.
    Borchgrevink, Petter
    Norwegian Univ Sci & Technol, Fac Med, Dept Circulat & Med Imaging, N-7034 Trondheim, Norway; St Olavs Univ Hosp, Natl Competence Ctr Complex Symptom Disorders, Trondheim, Norway.
    Woodhouse, Astrid
    St Olavs Univ Hosp, Natl Competence Ctr Complex Symptom Disorders, Trondheim, Norway; Norwegian Univ Sci & Technol, Fac Med, Dept Publ Hlth & Gen Practice, N-7034 Trondheim, Norway.
    Chronic widespread pain - the need for a standard definition2016Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 157, nr 3, s. 541-543Artikel, forskningsöversikt (Refereegranskat)
  • 12. Bäckryd, Emmanuel
    et al.
    Lind, Anne-Li
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Uppsala Berzelii Technology Center for Neurodiagnostics, Uppsala University, Uppsala, Sweden.
    Thulin, Måns
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Statistiska institutionen.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk kemi.
    Gerdle, Björn
    Gordh, Torsten
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Uppsala Berzelii Technology Center for Neurodiagnostics, Uppsala University, Uppsala, Sweden.
    High levels of cerebrospinal fluid chemokines point to the presence of neuroinflammation in peripheral neuropathic pain: a cross-sectional study of 2 cohorts of patients compared with healthy controls2017Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 158, nr 12, s. 2487-2495Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Animal models suggest that chemokines are important mediators in the pathophysiology of neuropathic pain. Indeed, these substances have been called "gliotransmitters," a term that illustrates the close interplay between glial cells and neurons in the context of neuroinflammation and pain. However, evidence in humans is scarce. The aim of the study was to determine a comprehensive cerebrospinal fluid (CSF) inflammatory profile of patients with neuropathic pain. Our hypothesis was that we would thereby find indications of a postulated on-going process of central neuroinflammation. Samples of CSF were collected from 2 cohorts of patients with neuropathic pain (n = 11 and n = 16, respectively) and healthy control subjects (n = 11). The samples were analyzed with a multiplex proximity extension assay in which 92 inflammation-related proteins were measured simultaneously (Proseek Multiplex Inflammation I; Olink Bioscience, Uppsala, Sweden). Univariate testing with control of false discovery rate, as well as orthogonal partial least squares discriminant analysis, were used for statistical analyses. Levels of chemokines CXCL6, CXCL10, CCL8, CCL11, CCL23 in CSF, as well as protein LAPTGF-beta-1, were significantly higher in both neuropathic pain cohorts compared with healthy controls, pointing to neuroinflammation in patients. These 6 proteins were also major results in a recent similar study in patients with fibromyalgia. The findings need to be confirmed in larger cohorts, and the question of causality remains to be settled. Because it has been suggested that prevalent comorbidities to chronic pain (eg, depression, anxiety, poor sleep, and tiredness) also are associated with neuroinflammation, it will be important to determine whether neuroinflammation is a common mediator.

  • 13.
    Denison, Eva
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Åsenlöf, P.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Lindberg, P.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Self-efficacy, fear avoidance, and pain intensity as predictors of disability in subacute and chronic musculoskeletal pain patients in primary health care2004Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 111, nr 3, s. 245-252Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    This study examined the relations between disability, as measured by the Pain Disability Index (PDI) and self-efficacy, fear avoidance variables (kinesiophobia and catastrophizing), and pain intensity, using a prospective design. Two primary health care samples (n1=210; n2=161) of patients with subacute, chronic or recurring musculoskeletal pain completed sets of questionnaires at the beginning of a physiotherapy treatment period. Multiple hierarchial regression analyses showed that self-efficacy explained a considerably larger proportion of the variance in disability scores than the fear avoidance variables in the first sample. This finding was replicated in the second sample. Pain intensity explained a small, but significant proportion of the variance in disability scores in one sample only. Gender, age, and pain duration were not related to disability. These findings suggest that self-efficacy beliefs are more important determinants of disability than fear avoidance beliefs in primary health care patients with musculoskeletal pain. The findings also suggest that pain-related beliefs, such as self-efficacy and fear avoidance, in turn, are more important determinants of disability than pain intensity and pain duration in these patients.

  • 14. Dominguez, Cecilia A.
    et al.
    Kalliomaki, Maija
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper.
    Gunnarsson, Ulf
    Moen, Aurora
    Sandblom, Gabriel
    Kockum, Ingrid
    Lavant, Ewa
    Olsson, Tomas
    Nyberg, Fred
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaceutisk biovetenskap.
    Rygh, Lars Jorgen
    Roe, Cecilie
    Gjerstad, Johannes
    Gordh, Torsten
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Piehl, Fredrik
    The DQB1*03:02 HLA haplotype is associated with increased risk of chronic pain after inguinal hernia surgery and lumbar disc herniation2013Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 154, nr 3, s. 427-433Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Neuropathic pain conditions are common after nerve injuries and are suggested to be regulated in part by genetic factors. We have previously demonstrated a strong genetic influence of the rat major histocompatibility complex on development of neuropathic pain behavior after peripheral nerve injury. In order to study if the corresponding human leukocyte antigen complex (HLA) also influences susceptibility to pain, we performed an association study in patients that had undergone surgery for inguinal hernia (n = 189). One group had developed a chronic pain state following the surgical procedure, while the control group had undergone the same type of operation, without any persistent pain. HLA DRB1genotyping revealed a significantly increased proportion of patients in the pain group carrying DRB1*04 compared to patients in the pain-free group. Additional typing of the DQB1 gene further strengthened the association; carriers of the DQB1*03:02 allele together with DRB1*04 displayed an increased risk of postsurgery pain with an odds risk of 3.16 (1.61-6.22) compared to noncarriers. This finding was subsequently replicated in the clinical material of patients with lumbar disc herniation (n = 258), where carriers of the DQB1*03:02 allele displayed a slower recovery and increased pain. In conclusion, we here for the first time demonstrate that there is an HLA-dependent risk of developing pain after surgery or lumbar disc herniation; mediated by the DRB1*04 - DQB1*03:02 haplotype. Further experimental and clinical studies are needed to fine-map the HLA effect and to address underlying mechanisms.

  • 15.
    Eccleston, Christopher
    et al.
    Univ Bath, Ctr Pain Res, Bath BA2 7AY, Avon, England;Univ Ghent, Dept Clin & Hlth Psychol, Ghent, Belgium.
    Fisher, Emma
    Univ Bath, Ctr Pain Res, Bath BA2 7AY, Avon, England;Oxford Univ Hosp, Pain Palliat & Support Care, Oxford, England.
    Cooper, Tess E.
    Univ Sydney, Fac Med & Hlth, Sch Publ Hlth, Sydney, NSW, Australia.
    Gregoire, Marie-Claude
    Dalhousie Univ, Dept Pediat, Halifax, NS, Canada.
    Heathcote, Lauren C.
    Stanford Univ, Sch Med, Dept Anesthesiol Perioperat & Pain Med, Palo Alto, CA 94304 USA.
    Krane, Elliot
    Stanford Univ, Sch Med, Dept Anesthesiol Perioperat & Pain Med, Perintnv, Palo Alto, CA 94304 USA.
    Lord, Susan M.
    Hunter Med Res Inst, Childrens Complex Pain Serv, John Hunter Childrens Hosp, Newcastle, NSW, Australia;Univ Newcastle, Fac Hlth & Med, Newcastle, NSW, Australia.
    Sethna, Navil F.
    Harvard Med Sch, Boston Childrens Hosp, Dept Anesthesiol Crit Care & Pain Med, Boston, MA 02115 USA.
    Anderson, Anna-Karenia
    Royal Marsden Hosp, London, England.
    Anderson, Brian
    Univ Auckland, Dept Anaesthesiol, Auckland, New Zealand.
    Clinch, Jacqueline
    Univ Bristol, Bristol Royal Childrens Hosp, Bristol, Avon, England;Royal Natl Hosp Rheumat Dis, Bath, Avon, England.
    Gray, Andrew L.
    Univ KwaZulu Natal, Div Pharmacol, Discipline Pharmaceut Sci, Durban, South Africa.
    Gold, Jeffrey, I
    Univ Southern Calif, Keck Sch Med, Anesthesiol Pediat & Psychiat & Behav Sci, Los Angeles, CA USA;Childrens Hosp Los Angeles, Pediat Pain Management Clin, Los Angeles, CA 90027 USA.
    Howard, Richard F.
    Great Ormond St Hosp Sick Children, Dept Anaesthesia & Pain Med, London, England.
    Ljungman, Gustaf
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Forskargrupper (Inst. för kvinnor och barns hälsa), Barnneurologi/Barnonkologi.
    Moore, R. Andrew
    Univ Oxford, Churchill, Dept Clin Neurosci, Pain Res,Nuffield, Oxford, England.
    Schechter, Neil
    Harvard Med Sch, Boston Childrens Hosp, Dept Anesthesiol, Boston, MA 02115 USA.
    Wiffen, Philip J.
    Univ Oxford, Churchill, Dept Clin Neurosci, Pain Res,Nuffield, Oxford, England.
    Wilkinson, Nick M. R.
    Kings Coll London, Evelina London Childrens Hosp, Dept Paediat, London, England.
    William, David G.
    Great Ormond St Hosp Children NHS Fdn Trust, Anaesthet Dept, London, England.
    Wood, Chantal
    Univ Limoges, Univ Hosp Limoges, Chron Pain Ctr, Dept Rheumatol, Haute Vienne, France.
    van Tilburg, Miranda A. L.
    Campbell Univ, Coll Pharm & Hlth Sci, Buies Creek, NC 27506 USA;Univ N Carolina, Div Gastroenterol & Hepatol, Chapel Hill, NC 27515 USA.
    Zernikow, Boris
    Childrens & Adolescents Hosp, German Paediat Pain Ctr, Datteln, Germany;Witten Herdecke Univ, Childrens Pain Therapy & Paediat Palliat Care, Fac Hlth, Sch Med, Witten, Germany.
    Pharmacological interventions for chronic pain in children: an overview of systematic reviews2019Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 160, nr 8, s. 1698-1707Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    We know little about the safety or efficacy of pharmacological medicines for children and adolescents with chronic pain, despite their common use. Our aim was to conduct an overview review of systematic reviews of pharmacological interventions that purport to reduce pain in children with chronic noncancer pain (CNCP) or chronic cancer-related pain (CCRP). We searched the Cochrane Database of Systematic Reviews, Medline, EMBASE, and DARE for systematic reviews from inception to March 2018. We conducted reference and citation searches of included reviews. We included children (0-18 years of age) with CNCP or CCRP. We extracted the review characteristics and primary outcomes of >= 30% participant-reported pain relief and patient global impression of change. We sifted 704 abstracts and included 23 systematic reviews investigating children with CNCP or CCRP. Seven of those 23 reviews included 6 trials that involved children with CNCP. There were no randomised controlled trials in reviews relating to reducing pain in CCRP. We were unable to combine data in a meta-analysis. Overall, the quality of evidence was very low, and we have very little confidence in the effect estimates. The state of evidence of randomized controlled trials in this field is poor; we have no evidence from randomised controlled trials for pharmacological interventions in children with cancer-related pain, yet cannot deny individual children access to potential pain relief.

  • 16.
    Ericson, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
    Cerebrospinal fluid biomarkers of inflammation in trigeminal neuralgia patients operated with microvascular decompression.2019Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 160, nr 11, s. 2603-2611Artikel i tidskrift (Refereegranskat)
  • 17.
    Faria, Vanda
    et al.
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi. Harvard Univ, Sch Med, Boston Childrens Hosp, Ctr Pain & Brain,Dept Anesthesiol Perioperat & Pa, Boston, MA USA..
    Erpelding, Nathalie
    Harvard Univ, Sch Med, Boston Childrens Hosp, Ctr Pain & Brain,Dept Anesthesiol Perioperat & Pa, Boston, MA USA..
    Lebel, Alyssa
    Harvard Univ, Sch Med, Boston Childrens Hosp, Ctr Pain & Brain,Dept Anesthesiol Perioperat & Pa, Boston, MA USA.;Harvard Univ, Sch Med, Boston Childrens Hosp, Chron Headache Program, Boston, MA USA..
    Johnson, Adriana
    Harvard Univ, Sch Med, Boston Childrens Hosp, Ctr Pain & Brain,Dept Anesthesiol Perioperat & Pa, Boston, MA USA..
    Wolff, Robert
    Harvard Univ, Sch Med, Boston Childrens Hosp, Dept Neurol, Boston, MA USA..
    Fair, Damien
    Oregon Hlth & Sci Univ, Sch Med, Dept Behav Neurosci, Portland, OR 97201 USA.;Oregon Hlth & Sci Univ, Sch Med, Dept Psychiat, Portland, OR 97201 USA..
    Burstein, Rami
    Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Anesthesia & Crit Care, Boston, MA 02215 USA..
    Becerra, Lino
    Harvard Univ, Sch Med, Boston Childrens Hosp, Ctr Pain & Brain,Dept Anesthesiol Perioperat & Pa, Boston, MA USA..
    Borsook, David
    Harvard Univ, Sch Med, Boston Childrens Hosp, Ctr Pain & Brain,Dept Anesthesiol Perioperat & Pa, Boston, MA USA.;Harvard Univ, Sch Med, Boston Childrens Hosp, Chron Headache Program, Boston, MA USA..
    The migraine brain in transition: girls vs boys2015Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 156, nr 11, s. 2212-2221Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The prevalence of migraine has an exponential trajectory that is most obvious in young females between puberty and early adulthood. Adult females are affected twice as much as males. During development, hormonal changes may act on predetermined brain circuits, increasing the probability of migraine. However, little is known about the pediatric migraine brain and migraine evolution. Using magnetic resonance. imaging, we evaluated 28 children with migraine (14 females and 14 males) and 28 sex-matched healthy controls to determine differences in brain structure and function between (1) females and males with migraine and (2) females and males with migraine during earlier (10-11 years) vs later (14-16 years) developmental stages compared with matched healthy controls. Compared with males, females had more gray matter in the primary somatosensory cortex (Si), supplementary motor area, precuneus, basal ganglia, and amygdala, as well as greater precuneus resting state functional connectivity to the thalamus, amygdala, and basal ganglia and greater amygdala resting state functional connectivity to the thalamus, anterior midcingulate cortex, and supplementary motor area. Moreover, older females with migraine had more gray matter in the Si, amygdala, and caudate compared to older males with migraine and matched healthy controls. This is the first study showing sex and developmental differences in pediatric migraineurs in brain regions associated with sensory, motor, and affective functions, providing insight into the neural mechanisms underlying distinct migraine sex phenotypes and their evolution that could result in important clinical implications increasing treatment effectiveness.

  • 18. Galer, Bradley S.
    et al.
    Jensen, Mark
    Butler, Stephen
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Neglect-like signs and symptoms in CRPS2013Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 154, nr 6, s. 961-962Artikel i tidskrift (Refereegranskat)
  • 19.
    Gordh, Torsten
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Chu, Haichen
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Sharma, Hari Shanker
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Spinal nerve lesion alters blood-spinal cord barrier function and activates astrocytes in the rat2006Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 124, nr 1-2, s. 211-221Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Alterations in the spinal cord microenvironment in a neuropathic pain model in rats comprising right L-4 spinal nerve lesion were examined following 1, 2, 4 and 10 weeks using albumin and glial fibrillary acidic protein (GFAP) immunoreactivity. Rats subjected to nerve lesion showed pronounced activation of GFAP indicating astrocyte activation, and exhibited marked leakage of albumin, suggesting defects of the blood-spinal cord barrier (BSCB) function in the corresponding spinal cord segment. The intensities of these changes were most prominent in the gray matter of the lesioned side compared to them contralateral cord in both the dorsal and ventral horns. The most marked changes in albumin and GFAP inummoreaction were seen after 2 weeks and persisted with mild intensities even after 10 weeks. Distortion of nerve cells, loss of neurons and general sponginess were evident in the gray matter of the spinal cord corresponding to the lesion side. These nerve cell and glial cell changes are mainly evident in the areas showing leakage of endogenous albumin in the spinal cord. These novel observations indicate that chronic nerve lesion has the capacity to induce a selective increase in local BSCB permeability that could be instrumental in nerve cell and glial cell activation. These findings may be relevant to our current understanding on the pathophysiology of neuropathic pain.

  • 20.
    Gordh, Torsten E
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Stubhaug, Audun
    Jensen, Troels S
    Arnèr, Staffan
    Biber, Björn
    Boivie, Jörgen
    Mannheimer, Clas
    Kalliomäki, Jarkko
    Kalso, Eija
    Gabapentin in traumatic nerve injury pain: a randomized, double-blind, placebo-controlled, cross-over, multi-center study2008Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 138, nr 2, s. 255-266Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    A double-blind, randomized, placebo-controlled cross-over multi-center study was conducted to evaluate the efficacy and safety of gabapentin in the treatment of neuropathic pain caused by traumatic or postsurgical peripheral nerve injury, using doses up to 2400 mg/day. The study comprised a run-in period of two weeks, two treatment periods of five weeks separated by a three weeks' washout period. The primary efficacy variable was the change in the mean pain intensity score from baseline to the last week of treatment. Other variables included pain relief, health related quality of life (SF-36), interference of sleep by pain, Clinician and Patient Global Impression of Change, and adverse effects. Nine centers randomized a total of 120 patients, 22 of whom withdrew. There was no statistically significant difference between the treatments for the primary outcome efficacy variable. However, gabapentin provided significantly better pain relief (p=0.015) compared with placebo. More patients had at least a 30% pain reduction with gabapentin compared with placebo (p=0.040) and pain interfered significantly less with sleep during gabapentin treatment compared with placebo (p=0.0016). Both the Patient (p=0.023) and Clinician (p=0.037) Global Impression of Change indicated a better response with gabapentin compared with placebo. Gabapentin was well tolerated. The most common adverse effects were dizziness and tiredness.

  • 21. Gustavsson, A.
    et al.
    Björkman, J.
    Ljungcrantz, C.
    Rhodin, Annika
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Rivano-Fischer, M.
    Sjölund, K. -F
    Mannheimer, C.
    Pharmaceutical treatment patterns for patients with a diagnosis related to chronic pain initiating a slow-release strong opioid treatment in Sweden2012Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 153, nr 12, s. 2325-2331Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Slow-release strong opioids (SRSO) are indicated in patients with severe chronic pain. Side effects, lack of efficacy and risk of dependency limit their use in clinical practice. The aim of this study was to explore prescription patterns of SRSO in Swedish real-world data on patients with a diagnosis related to chronic pain (DRCP). Patient-level data were extracted from the national prescriptions register and a regional register with diagnosis codes. The prescription sequences, switches, co-medications, and strengths over time were analyzed for cancer and noncancer patients. Of 840,000 patients with a DRCP, 16,257 initiated treatment with an SRSO in 2007 to 2008. They were 71 years old on average; 60% were female and 34% had cancer. The most common first prescription was oxycodone (54%) followed by fentanyl (19%), buprenorphine (14%), and morphine (13%). 63% refilled their prescription within 6 months, and 12% switched to another SRSO, most commonly fentanyl. After 3 years, 51% of cancer and 27% of noncancer patients still being in contact with health care remained on any SRSO. Of noncancer patients, 35% had a psychiatric co-medication (SSRI or benzodiazepine). In conclusion, fewer patients remain on SRSO in the long-term in clinical practice than reported in previous clinical trials. Oxycodone is the most common first SRSO prescription and one-third of patients get a prescription indicating psychiatric comorbidity. Our interpretation of these findings are that there is need for better treatment options for these patients, and that more effort is needed to improve treatment guidelines and to ascertain that these guidelines are followed.

  • 22. Hallström, Hélène
    et al.
    Norrbrink, Cecilia
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Sjukgymnastik.
    Screening tools for neuropathic pain: Can they be of use in individuals with spinal cord injury?2011Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 152, nr 4, s. 772-779Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Pain of both neuropathic and nociceptive aetiology is common after spinal cord injury (SCI), and classifying pain is sometimes a challenge. The objective of this study was to test the usefulness of the Swedish version of the screening tools Douleur Neuropathique 4 questions (DN4), the Leeds Assessment of Neuropathic Symptoms and Signs (LANSS), the Neuropathic Pain Questionnaire (NPQ), and the painDETECT Questionnaire (PD-Q) in individuals with SCI and pain. A further objective was to define pain descriptors able to discriminate neuropathic pain from nonneuropathic pain. Forty individuals with SCI ⩾1year and pain ⩾6months were examined by a specialised physician and assessed twice using the 4 screening tools. The analysis included tests of reliability (test-retest) and validity (calculation of sensitivity, specificity, and overall agreement), an explorative analysis of the cutoff scores and regression analysis for identifying predictors of diagnostic accuracy. Our results indicate that reliability was good to very good for 3 of the screening tools, DN4, LANSS, and NPQ with a Cohen's kappa coefficient between 0.70 and 1.00. DN4 showed the highest sensitivity (93%), followed by PD-Q (68%), NPQ (50%), and LANSS (36%). LANSS and NPQ demonstrated the highest specificity (100%), followed by PD-Q (83%) and DN4 (75%). Diagnostic accuracy for the tools was for DN4 88%, PD-Q 78%, NPQ 65%, and LANSS 55%. A final model showed that 3 items, hypoesthesia to touch, burning pain, and numbness, could discriminate pain in this cohort of individuals with SCI with a high goodness of fit. This study indicates that the Douleur Neuropathique 4 (Swedish version) has high reliability and validity and can be used as screening tool for neuropathic pain in spinal cord injury.

  • 23. Jörum, E.
    et al.
    Örstavik, K.
    Schmidt, Roland
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Klinisk neurofysiologi.
    Namer, Berit
    Carr, R. W.
    Kvarstein, G.
    Hilliges, M.
    Handwerker, H.
    Torebjörk, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Klinisk neurofysiologi.
    Schmelz, M.
    Catecholamine-induced excitation of nociceptors in sympathetically maintained pain2007Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 127, nr 3, s. 296-301Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Sympathetically maintained pain could either be mediated by ephaptic interactions between sympathetic efferent and afferent nociceptive fibers or by catecholamine-induced activation of nociceptive nerve endings. We report here single fiber recordings from C nociceptors in a patient with sympathetically maintained pain, in whom sympathetic blockade had repeatedly eliminated the ongoing pain in both legs. We classified eight C-fibers as mechano-responsive and six as mechano-insensitive nociceptors according to their mechanical responsiveness and activity-dependent slowing of conduction velocity (latency increase of 0.5±1.1 vs. 7.1±2.0ms for 20 pulses at 0.125Hz). Two C-fibers were activated with a delay of several seconds following strong endogenous sympathetic bursts; they were also excited for about 3min following the injection of norepinephrine (10μl, 0.05%) into their innervation territory. In these two fibers, a prolonged activation by injection of low pH solution (phosphate buffer, pH 6.0, 10μl) and sensitization of their heat response following prostaglandin E2 injection were recorded, evidencing their afferent nature. Moreover, their activity-dependent slowing was typical for mechano-insensitive nociceptors. We conclude that sensitized mechano-insensitive nociceptors can be activated by endogenously released catecholamines and thereby may contribute to sympathetically maintained pain. No evidence for ephaptic interaction between sympathetic efferent and nociceptive afferent fibers was found.

  • 24. Kleggetveit, Inge Petter
    et al.
    Namer, Barbara
    Schmidt, Roland
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Klinisk neurofysiologi.
    Helas, Tormod
    Rueckel, Michael
    Orstavik, Kristin
    Schmelz, Martin
    Jorum, Ellen
    High spontaneous activity of C-nociceptors in painful polyneuropathy2012Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 153, nr 10, s. 2040-2047Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Polyneuropathy can be linked to chronic pain but also to reduced pain sensitivity. We investigated peripheral C-nociceptors in painful and painless polyneuropathy patients to identify pain-specific changes. Eleven polyneuropathy patients with persistent spontaneous pain and 8 polyneuropathy patients without spontaneous pain were investigated by routine clinical methods. For a specific examination of nociceptor function, action potentials from single C-fibres including 214 C-nociceptors were recorded by microneurography. Patients with and without pain were distinguished by the occurrence of spontaneous activity and mechanical sensitization in C-nociceptors. The mean percentage of C-nociceptors being spontaneously active or mechanically sensitized was significantly higher in patients with pain (mean 40.5% and 14.6%, respectively, P = .02). The difference was mainly due to more spontaneously active mechanoinsensitive C-nociceptors (operationally defined by their mechanical insensitivity and their axonal characteristics) in the pain patients (19 of 56 vs 6 of 43; P = .02). The percentage of sensitized mechanoinsensitive C-nociceptors correlated to the percentage of spontaneously active mechanoinsensitive C-nociceptors (Kendall's tau = .55, P = .004). Moreover, spontaneous activity of mechanoinsensitive C-nociceptors correlated to less pronounced activity-dependent slowing of conduction (Kendall's tau = -.48, P = .009), suggesting that axons were included in the sensitization process. Hyperexcitability in mechanoinsensitive C-nociceptors was significantly higher in patients with polyneuropathy and pain compared to patients with polyneuropathy without pain, while the difference was much less prominent in mechanosensitive (polymodal) C-nociceptors. This hyperexcitability may be a major underlying mechanism for the pain experienced by patients with painful peripheral neuropathy.

  • 25. Kåreholt, Ingemar
    et al.
    Brattberg, Gunilla
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Socialmedicin.
    Pain and mortality risk among elderly persons in Sweden1998Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 77, nr 3, s. 271-278Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The aim of this study is to analyse how the mortality risk varies with mild or severe pain in different locations: chest, back and hips, shoulders, the extremities, abdomen, rectum and head. A Swedish nationally representative sample of 1930 persons born 1892-1915 were interviewed in 1968 (ages 53-76). Survivors were also interviewed in 1974 and 1981 if they had not passed the age of 75 years. Proportional hazard regression was used to analyze mortality risk among persons ages 53-98 years for the period 1968-1991. Relationships were found between mortality risk and headache, chest pain, abdominal pain, pain in the extremities and rectal pain. No relationships were found between mortality and pain in back and hips or in shoulders. There was a correlation between chest pain and increased mortality among both men and women, but the association was significantly stronger among men. There was a significant association between severe rectal pain and mortality among men but no similar association among women. Significant associations between mortality and chest pain and abdominal pain were found among persons younger than 80 years, but not among those older than 80 years. Pain is an indicator of the quality of life and a symptom of underlying medical conditions. The finding that there are relationships between mortality risk and pain in the chest, abdomen, rectum, the extremities and head may be of clinical relevance. These results, however, must be further investigated since the relationships between reported pain and mortality do not imply that pain in these locations is necessarily symptomatic of lethal diseases. Abdominal pain, rectal pain and headache may be indicators of diseases but can also be side effects of treatments for other diseases correlated with higher mortality.

  • 26.
    Leino-Arjas, Päivi
    et al.
    Finnish Inst Occupat Hlth, Helsinki, Finland..
    Rajaleid, Kristiina
    Stockholm Univ, Stress Res Inst, Stockholm, Sweden.;Stockholm Univ, Karolinska Inst, Ctr Hlth Equ Studies, Stockholm, Sweden..
    Mekuria, Gashaw
    Univ Tampere, Sch Informat Sci, Tampere, Finland..
    Nummi, Tapio
    Univ Tampere, Sch Informat Sci, Tampere, Finland..
    Virtanen, Pekka
    Univ Tampere, Sch Hlth Sci, Tampere, Finland..
    Hammarström, Anne
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Folkhälsovetenskap.
    Trajectories of musculoskeletal pain from adolescence to middle age: the role of early depressive symptoms, a 27-year follow-up of the Northern Swedish Cohort2018Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 159, nr 1, s. 67-74Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Depression and musculoskeletal pain are associated, but long-term follow-up studies are rare. We aimed to examine the relationship of early depressive symptoms with developmental patterns of musculoskeletal pain from adolescence to middle age. Adolescents ending compulsory school (age 16) in Lulea, Northern Sweden, in 1981 (n = 1083) were studied and followed up in 1986, 1995, and 2008 (age 43) for musculoskeletal pain. Attrition was very low. Indicators for any and severe pain were based on pain in the neck-shoulders, low back, and the extremities. Latent class growth analyses were performed on 563 men and 503 women. Associations of a depressive symptoms score (DSS, range 0.0-2.0) at age 16 with pain trajectory membership were assessed by logistic and multinomial regression, adjusting for parental socioeconomic status, social adversities, smoking, exercise, body mass index, and alcohol consumption at age 16. For any pain, 3 trajectories emerged: high-stable (women 71%, men 61%), moderate (11%, 17%), and low-increasing (18%, 22%). With the low-increasing trajectory as reference, for each 0.1-point increase in the DSS, the odds ratio of belonging to the high-stable trajectory was 1.25 (95% confidence interval 1.11-1.41) in women and 1.23 (1.10-1.37) in men. For severe pain, 2 trajectories were found: moderate-increasing (women 19%, men 9%) and low-stable. For each 0.1-point increase in the DSS, the odds ratio of membership in the moderate-increasing trajectory was 1.14 (1.04-1.25) in women and 1.17 (1.04-1.31) in men in the fully adjusted model. Thus, depressive symptoms at baseline are strongly associated with pain trajectory membership.

  • 27.
    Lin, Jiaxi
    et al.
    University of Freiburg.
    Klatt, L
    Leibniz Research Centre for Working Environment and Human Factors.
    McCracken, Lance
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Baumeister, H
    University of Ulm.
    Psychological flexibility mediates the effect of an online-based acceptance and commitment therapy for chronic pain: An investigation of change processes2018Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 159, nr 4, s. 663-672Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    One way to improve treatment effects of chronic pain is to identify and improve control over mechanisms of therapeutic change. One treatment approach that includes a specific proposed mechanism is acceptance and commitment therapy (ACT) with its focus on increasing psychological flexibility (PF). The aim of the present study was to examine the role of PF as a mechanism of change in ACT. This is based on mediation analyses of data from a previously reported randomized controlled trial, evaluating the effectiveness of an ACT-based online intervention for chronic pain (ACTonPain). We performed secondary analyses on pretreatment, posttreatment, and follow-up data from 302 adults, receiving a guided (n = 100) or unguided (n = 101) version of ACTonPain, or allocated to the waitlist control group (n = 101). Structural equation modelling and a bias-corrected bootstrap approach were applied to examine the indirect effects of the treatment through pretreatment and posttreatment changes in the latent construct reflecting PF. The latent construct consisted of data from the Chronic Pain Acceptance Questionnaire and the Acceptance and Action Questionnaire. The outcomes were pretreatment to follow-up changes in pain interference, anxiety, depression, pain, and mental and physical health. Structural equation modelling analyses revealed that changes in PF significantly mediated pretreatment to follow-up changes in all outcomes in the intervention groups compared with waitlist (standardized estimates ranged from I0.16I to I0.69I). Global model fit yielded modest but acceptable results. Findings are consistent with the theoretical framework behind ACT and contribute to growing evidence, supporting a focus on PF to optimize treatment effects.

  • 28.
    Linnman, Clas
    et al.
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Appel, Lieuwe
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för nuklearmedicin och PET.
    Furmark, Tomas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Söderlund, Anne
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
    Gordh, Torsten
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Långström, Bengt
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för biokemi och organisk kemi.
    Fredrikson, Mats
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Ventromedial prefrontal neurokinin 1 receptor availability is reduced in chronic pain2010Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 149, nr 1, s. 64-70Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Neurokinin 1 (NK1) receptors are involved in pain and anxiety behaviors in animals, but little is known about central alterations in this receptor system in human pain. With positron emission tomography, using a [11]-Carbon labeled NK1 receptor antagonist, we demonstrate attenuated NK1 receptor availability in frontal, insular and cingulate cortex, as well as the hippocampus, amygdala and the periaqueductal gray area in patients with chronic pain. The reduced availability was most pronounced in the ventromedial prefrontal cortex (vmPFC), where attenuations correlated to measures of fear and avoidance of movement. Further, vmPFC NK1 levels also displayed opposing influences in patients as compared to controls on regional cerebral blood flow in the anterior cingulate. We conclude that the central NK1 receptor system is altered in human chronic pain. The results suggest that NK1 receptors in the vmPFC modulate motor inhibition, and contribute to fear and avoidance of movement.

  • 29. Namer, Barbara
    et al.
    Hilliges, Marita
    Ørstavik, Kristin
    Schmidt, Roland
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Klinisk neurofysiologi.
    Torebjörk, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Klinisk neurofysiologi.
    Handwerker, Hermann
    Schmelz, Martin
    Endothelin 1 activates and sensitizes human C-nociceptors2008Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 137, nr 1, s. 41-49Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Microneurography was used to record action potentials from afferent C-fibers in cutaneous fascicles of the peroneal nerve in healthy volunteers. Afferent fibers were classified according to their mechanical responsiveness to von Frey stimulation (75 g) into mechano-responsive and mechano-insensitive nociceptors. Various concentrations of Endothelin1 (ET1) and Histamine were injected into the receptive fields of C-fibers. Activation and heat sensitization were monitored. Axon reflex flare and psychophysical ratings were assessed after injection of ET1 and codeine into the forearms after pre-treatment with an H1 blocker or sodium chloride. 65% of mechanosensitive nociceptors were activated by ET1. One-third showed long lasting responses (>15 min). In contrast, none of thirteen mechano-insensitive fibers were activated. Sensitization to heat was observed in 62% of mechanosensitive and in 46% of mechano-insensitive fibers. Injection of ET1 produced a widespread axon reflex flare, which was suppressed by pre-treatment with an H1 receptor blocker. In addition, pain sensations were induced more often than itching by ET1 in contrast to codeine. No wheal was observed after injection of ET1. Both itching and pain were decreased after H1 blocker treatment. In summary: (1) In humans ET1 activates mechanosensitive, but not mechano-insensitive, nociceptors. (2) Histamine released from mast cells is not responsible for all effects of ET1 on C-nociceptors. (3) ET1 could have a differential role in pain compared to other chemical algogens which activate additionally or even predominantly mechano-insensitive fibers.

  • 30.
    Namer, Barbara
    et al.
    Univ Erlangen Nurnberg, Dept Physiol & Pathophysiol, D-91054 Erlangen, Germany..
    Orstavik, Kristin
    Univ Oslo, Rikshosp, Oslo Univ Hosp, Dept Neurol, N-0027 Oslo, Norway..
    Schmidt, Roland
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Klinisk neurofysiologi.
    Kleggetveit, Inge-Petter
    Univ Oslo, Rikshosp, Oslo Univ Hosp, Dept Neurol, N-0027 Oslo, Norway..
    Weidner, Christian
    Univ Erlangen Nurnberg, Dept Physiol & Pathophysiol, D-91054 Erlangen, Germany..
    Mork, Cato
    Norwegian Univ Sci & Technol, Inst Canc Res & Mol Med, N-7034 Trondheim, Norway..
    Kvernebo, Mari Skylstad
    Oslo Univ Hosp, Dept Rheumatol Skin & Infect Dis, Oslo, Norway..
    Kvernebo, Knut
    Oslo Univ Hosp, Dept Vasc Surg, Oslo, Norway..
    Salter, Hugh
    Karolinska Inst, AstraZeneca Translat Sci Ctr, Dept Clin Neurosci, S-10401 Stockholm, Sweden..
    Carr, Thomas Hedley
    AstraZeneca R&D, Macclesfield, Cheshire, England..
    Segerdahl, Marta
    Karolinska Inst, AstraZeneca Translat Sci Ctr, Dept Clin Neurosci, S-10401 Stockholm, Sweden..
    Quiding, Hans
    Karolinska Inst, AstraZeneca Translat Sci Ctr, Dept Clin Neurosci, S-10401 Stockholm, Sweden..
    Waxman, Stephen George
    Yale Univ, Sch Med, Ctr Neurosci & Regenerat Res, New Haven, CT USA..
    Handwerker, Hermann Otto
    Univ Erlangen Nurnberg, Dept Physiol & Pathophysiol, D-91054 Erlangen, Germany..
    Torebjörk, Hans Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Klinisk neurofysiologi.
    Jorum, Ellen
    Univ Oslo, Rikshosp, Oslo Univ Hosp, Dept Neurol, N-0027 Oslo, Norway..
    Schmelz, Martin
    Heidelberg Univ, Dept Anesthesiol Mannheim, D-68167 Mannheim, Germany..
    Specific changes in conduction velocity recovery cycles of single nociceptors in a patient with erythromelalgia with the I848T gain-of-function mutation of Na(v)1.72015Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 156, nr 9, s. 1637-1646Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Seven patients diagnosed with erythromelalgia (EM) were investigated by microneurography to record from unmyelinated nerve fibers in the peroneal nerve. Two patients had characterized variants of sodium channel Na(v)1.7 (I848T, I228M), whereas no mutations of coding regions of Na(v)s were found in 5 patients with EM. Irrespective of Na(v)1.7 mutations, more than 50% of the silent nociceptors in the patients with EM showed spontaneous activity. In the patient with mutation I848T, all nociceptors, but not sympathetic efferents, displayed enhanced early subnormal conduction in the velocity recovery cycles and the expected late subnormality was reversed to supranormal conduction. The larger hyperpolarizing shift of activation might explain the difference to the I228M mutation. Sympathetic fibers that lack Na(v)1.8 did not show supranormal conduction in the patient carrying the I848T mutation, confirming in human subjects that the presence of Na(v)1.8 crucially modulates conduction in cells expressing EM mutant channels. The characteristic pattern of changes in conduction velocity observed in the patient with the I848T gain-of function mutation in Na(v)1.7 could be explained by axonal depolarization and concomitant inactivation of Na(v)1.7. If this were true, activity-dependent hyperpolarization would reverse inactivation of Na(v)1.7 and account for the supranormal CV. This mechanism might explain normal pain thresholds under resting conditions.

  • 31.
    Peterson, Magnus
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Allmänmedicin och preventivmedicin.
    Svärdsudd, Kurt
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Allmänmedicin och preventivmedicin.
    Appel, Lieuwe
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär medicin.
    Engler, Henry
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk fysiologi.
    Långström, Bengt
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för biokemi och organisk kemi.
    Sörensen, Jens
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk fysiologi.
    PET-scan shows peripherally increased neurokinin 1 receptor availability in chronic tennis elbow: a picture of neurogenic inflammation?2011Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    In response to pain, neurokinin 1 (NK1) receptor availability in the central nervous system is altered in the dorsal horn of the spinal cord as well as in the brain. But the NK1 receptor and its primary agonist, substance P, also play a crucial role in peripheral tissue in response to pain, as part of neurogenic inflammation. However, little is known about alterations in NK1 receptor availability in peripheral tissue in chronic pain conditions and very few studies have been performed on human beings. We therefore performed positron emission tomography (PET) with the NK1 specific radioligand [11C]GR205171 in ten subjects with chronic tennis elbow. We demonstrated increased NK1 receptor availability in the affected arm as compared with the unaffected arm, measured as differences between the arms in number and volume of pixels > 2.5 SD above reference as well as signal intensity of this volume. We conclude that in addition to alteration of the NK1 receptor in the CNS, there is also activation, or up-regulation of the NK1 receptor in the peripheral, painful tissue in a chronic pain condition. We interpret this increased NK1 receptor availability as part of ongoing neurogenic inflammation and suggest that this is part of the cause of chronic tennis elbow.

  • 32. Pérez-Aranda, Adrián
    et al.
    Feliu-Soler, Albert
    Montero-Marín, Jesús
    García-Campayo, Javier
    Andrés-Rodríguez, Laura
    Borràs, Xavier
    Rozadilla-Sacanell, Antoni
    Peñarrubia-Maria, Maria T
    Angarita-Osorio, Natalia
    McCracken, Lance M
    Luciano, Juan V
    A randomized controlled efficacy trial of mindfulness-based stress reduction compared with an active control group and usual care for fibromyalgia: the EUDAIMON study.2019Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Fibromyalgia (FM) syndrome represents a great challenge for clinicians and researchers because the efficacy of currently available treatments is limited. This study examined the efficacy of mindfulness-based stress reduction (MBSR) for reducing functional impairment as well as the role of mindfulness-related constructs as mediators of treatment outcomes for people with FM. Two hundred twenty-five participants with FM were randomized into 3 study arms: MBSR plus treatment-as-usual (TAU), FibroQoL (multicomponent intervention for FM) plus TAU, and TAU alone. The primary endpoint was functional impact (measured with the Fibromyalgia Impact Questionnaire Revised), and secondary outcomes included "fibromyalginess," anxiety and depression, pain catastrophising, perceived stress, and cognitive dysfunction. The differences in outcomes between groups at post-treatment assessment (primary endpoint) and 12-month follow-up were analyzed using linear mixed-effects models and mediational models through path analyses. Mindfulness-based stress reduction was superior to TAU both at post-treatment (large effect sizes) and at follow-up (medium to large effect sizes), and MBSR was also superior to FibroQoL post-treatment (medium to large effect sizes), but in the long term, it was only modestly better (significant differences only in pain catastrophising and fibromyalginess). Immediately post-treatment, the number needed to treat for 20% improvement in MBSR vs TAU and FibroQoL was 4.0 (95% confidence interval [CI] = 2.1-6.5) and 5.0 (95% CI = 2.7-37.3). An unreliable number needed to treat value of 9 (not computable 95% CI) was found for FibroQoL vs TAU. Changes produced by MBSR in functional impact were mediated by psychological inflexibility and the mindfulness facet acting with awareness. These findings are discussed in relation to previous studies of psychological treatments for FM.

  • 33.
    Radojcic, Maja R.
    et al.
    Nord Biosci AS, Nord Biosci Biomarkers & Res, Herlev Hovedgade 205-207, DK-2730 Herlev, Denmark.;Univ Copenhagen, Fac Hlth & Med Sci, Dept Drug Design & Pharmacol, Copenhagen, Denmark..
    Thudium, Christian S.
    Nord Biosci AS, Nord Biosci Biomarkers & Res, Herlev Hovedgade 205-207, DK-2730 Herlev, Denmark..
    Henriksen, Kim
    Nord Biosci AS, Nord Biosci Biomarkers & Res, Herlev Hovedgade 205-207, DK-2730 Herlev, Denmark..
    Tan, Keith
    AstraZeneca, Neurosci Innovat Med & Early Dev, Cambridge, England..
    Karlsten, Rolf
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Dudley, Amanda
    AstraZeneca, Neurosci Innovat Med & Early Dev, Cambridge, England..
    Chessell, Iain
    AstraZeneca, Neurosci Innovat Med & Early Dev, Cambridge, England..
    Karsdal, Morten A.
    Nord Biosci AS, Nord Biosci Biomarkers & Res, Herlev Hovedgade 205-207, DK-2730 Herlev, Denmark..
    Bay-Jensen, Anne-Christine
    Nord Biosci AS, Nord Biosci Biomarkers & Res, Herlev Hovedgade 205-207, DK-2730 Herlev, Denmark..
    Crema, Michel D.
    Boston Univ, Quantitat Imaging Ctr, Sch Med, Dept Radiol, Boston, MA 02215 USA.;Univ Paris 06, Hop St Antoine, Dept Radiol, Paris, France..
    Guermazi, Ali
    Boston Univ, Quantitat Imaging Ctr, Sch Med, Dept Radiol, Boston, MA 02215 USA..
    Biomarker of extracellular matrix remodelling C1M and proinflammatory cytokine interleukin 6 are related to synovitis and pain in end-stage knee osteoarthritis patients2017Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 158, nr 7, s. 1254-1263Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Little is known about local and systemic biomarkers in relation to synovitis and pain in end-stage osteoarthritis (OA) patients. We investigated the associations between the novel extracellular matrix biomarker, C1M, and local and systemic interleukin 6 (IL-6) with synovitis and pain. Serum C1M, plasma, and synovial fluid IL-6 (p-IL-6, sf-IL-6) were measured in 104 end-stage knee OA patients. Contrast-enhanced magnetic resonance imaging was used to semiquantitatively assess an 11-point synovitis score; painwas assessed by theWesternOntario and McMaster Universities Osteoarthritis Index (WOMAC) and the Neuropathic PainQuestionnaire (NPQ). Linear regression was used to investigate associations between biomarkers and synovitis, and biomarkers and pain while controlling for age, sex, and bodymass index. We also testedwhether associations between biomarkers and painwere confounded by synovitis. We found sf-IL-6 was associated with synovitis in the parapatellar subregion (B 5 0.006; 95% confidence interval [ CI] 0.003-0.010), and no association between p-IL-6 and synovitis. We also observed an association betweenC1Mand synovitis in the periligamentous subregion (B50.013; 95% CI 0.003-0.023). Furthermore, sf-IL-6, but not p-IL-6, was significantly associated with pain, WOMAC(B50.022; 95% CI 0.004-0.040), andNPQ(B50.043; 95% CI 0.005-0.082). Therewas no association betweenC1MandWOMACpain, butwe did find an association between C1M and NPQ (B50.229; 95% CI 0.036-0.422). Lastly, synovitis explained both biomarker-NPQassociations, but not the biomarker-WOMAC association. These results suggest that C1M and IL-6 are associated with synovitis and pain, and synovitis is an important confounding variable when studying biomarkers and neuropathic features in OA patients.

  • 34.
    Rogoz, Katarzyna
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Genetisk utvecklingsbiologi.
    Lagerström, Malin C.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Genetisk utvecklingsbiologi.
    Dufour, Sylvie
    Kullander, Klas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Genetisk utvecklingsbiologi.
    VGLUT2-dependent glutamatergic transmission in primary afferents is required for intact nociception in both acute and persistent pain modalities2012Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 153, nr 7, s. 1525-1536Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Glutamate is an essential transmitter in pain pathways. However, its broad usage in the central and peripheral nervous system prevents us from designing efficient glutamate-based pain therapies without causing harmful side effects. The discovery of vesicular glutamate transporters (VGLUT1-3) has been a crucial step in describing specific glutamatergic neuronal subpopulations and glutamate-dependent pain pathways. To assess the role of VGLUT2-mediated glutamatergic contribution to pain transmission from the entire primary sensory population, we crossed our Vglut2(f/f) line with the Ht-Pa-Cre line. Such Vglut2-deficient mice showed significantly decreased, but not completely absent, acute nociceptive responses. The animals were less prone to develop an inflammatory-related state of pain and were, in the partial sciatic nerve ligation chronic pain model, much less hypersensitive to mechanical stimuli and did not develop cold allodynia or heat hyperalgesia. To take advantage of this neuropathic pain-resistant model, we analyzed Vglut2-dependent transcriptional changes in the dorsal spinal cord after nerve injury, which revealed several novel candidate target genes potentially relevant for the development of neuropathic pain therapeutics. Taken together, we conclude that VGLUT2 is a major mediator of nociception in primary afferents, implying that glutamate is the key somatosensory neurotransmitter. 

  • 35.
    Schmidt, Roland
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Klinisk neurofysiologi.
    Kleggetveit, Inge Petter
    Namer, Barbara
    Helås, Tormod
    Obreja, Otilia
    Schmelz, Martin
    Jørum, Ellen
    Double spikes to single electrical stimulation correlates to spontaneous activity of nociceptors in painful neuropathy patients.2012Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 153, nr 2, s. 391-8Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Multiple firing of C nociceptors upon a single electrical stimulus has been suggested to be a possible mechanism contributing to neuropathic pain. Because this phenomenon maybe based on a unidirectional conduction block, it might also be related to neuropathic changes without a direct link to pain. We investigated painful neuropathy patients using microneurography and analysed nociceptors for the occurrence of multiple spiking and spontaneous activity. In 11 of 105 nociceptors, double spiking was found, with 1fibre even showing triple spikes on electrical stimulation. The interval between the main action potential and the multiple spikes ranged from 13 to 100ms. There was a significant association between spontaneous activity and multiple spiking in C nociceptors, with spontaneous activity being present in 9 of 11 fibres with multiple spiking, but only in 21 of 94 nociceptors without multiple spiking (P<.005, Fisher exact test). Among the 75 C nociceptors without spontaneous activity, only 2 nociceptors showed multiple spiking. In 8 neuropathy patients without pain, double spiking was found only in 4 of 90 nociceptors. Multiple spiking of nociceptors coincides with spontaneous activity in nociceptors of painful neuropathy patients. We therefore conclude that rather than being a generic sign of neuropathy, multiple spiking is linked to axonal hyperexcitability and spontaneous activity of nociceptors. It is still unclear whether it also is mechanistically related to the clinical pain level.

  • 36. Scott, Whitney
    et al.
    Calderon Mendoza Del Solar, Maite Garcia
    Kemp, Harriet
    McCracken, Lance M
    de C Williams, Amanda C
    Rice, Andrew Sc
    A qualitative study of the experience and impact of neuropathic pain in people living with HIV.2019Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Painful distal symmetrical polyneuropathy is common in HIV and is associated with reduced quality of life. Research has not explored the experience of neuropathic pain in people with HIV from a person-centred perspective. Therefore, a qualitative interview study was conducted to more deeply understand the experience and impact of neuropathic pain in this population. Semi-structured interviews were conducted with 26 people with HIV and peripheral neuropathic pain symptoms. Interviews explored the impact of pain and participants' pain management strategies. Interviews were transcribed verbatim and analysed using thematic analysis. Four themes and 11 subthemes were identified. Theme one reflects the complex characterisation of neuropathic pain, including the perceived unusual nature of this pain and diagnostic uncertainty. Theme two centred on the interconnected impacts of pain on mood and functioning and includes how pain disrupts relationships and threatens social inclusion. Theme three reflects the struggle for pain relief, including participants' attempts to 'exhaust all options' and limited success in finding lasting relief. The final theme describes how pain management is complicated by living with HIV; this theme includes the influence of HIV stigma on pain communication and pain as an unwanted reminder of HIV. These data support the relevance of investigating and targeting psychosocial factors to manage neuropathic pain in HIV.

  • 37.
    Scott, Whitney
    et al.
    King's College London.
    Williams, Amanda
    University College London.
    Rice, Andrew
    Imperial College London.
    McCracken, Lance
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Psychosocial factors associated with persistent pain in people with HIV: A systematic review with meta-analysis2018Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Chronic pain remains a prevalent and disabling problem for people living with HIV in the current antiretroviral treatment era. Psychosocial treatments may have promise for managing the impact of this pain. However, research is needed to identify psychosocial processes to target through such treatments. The current systematic review and meta-analysis examined the evidence for psychosocial factors associated with pain, disability, and quality of life in people living with HIV and persistent pain. Observational and experimental studies reporting on the association between one or more psychosocial factors and one or more pain-related variables in an adult sample of people living with HIV and pain were eligible. Two reviewers independently conducted eligibility screening, data extraction, and quality assessment. Forty-six studies were included in the review and 37 of these provided data for meta-analyses (12,493 participants). "Some" or "moderate" evidence supported an association between pain outcomes in people with HIV and the following psychosocial factors: depression, psychological distress, posttraumatic stress, drug abuse, sleep disturbance, reduced antiretroviral adherence, health care use, missed HIV clinic visits, unemployment, and protective psychological factors. Surprisingly, few studies examined protective psychological factors or social processes, such as stigma. There were few high-quality studies. These findings can inform future research and psychosocial treatment development in this area. Greater theoretical and empirical focus is needed to examine the role of protective factors and social processes on pain outcomes in this context. The review protocol was registered with PROSPERO (CRD42016036329).

  • 38. Solovieva, Svetlana
    et al.
    Leino-Arjas, P.
    Saarela, J.
    Luoma, Katariina
    Raininko, Raili
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi.
    Riihimäki, Hilkka
    Possible association of interleukin 1 gene locus polymorphisms with low back pain2004Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 109, nr 1-2, s. 8-19Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    Based on a hypothesis that interleukin 1 (IL-1) activity is associated with low back pain (LBP), we investigated relationships between previously described functional IL-1 gene polymorphisms and LBP. The subjects were a subgroup of a Finnish study cohort. The IL-1alpha(C(889)-T), IL-1beta(C(3954)-T) and IL-1 receptor antagonist (IL-1RN)(G(1812)-A, G(1887)-C and T(11100)-C) polymorphisms were genotyped in 131 middle-aged men from three occupational groups (machine drivers, carpenters and office workers). A questionnaire inquired about individual and lifestyle characteristics and the occurrence of LBP, the number of days with pain and days with limitation of daily activities because of pain, and pain intensity, during the past 12 months. Lumbar disc degeneration was determined with magnetic resonance imaging. Carriers of the IL-1RNA(1812) allele had an increased risk of LBP (OR 2.5, 95% CI 1.0-6.0) and carriers of this allele in combination with the IL-1alphaT(889) or IL-1betaT(3954) allele had a higher risk of and more days with LBP than non-carriers. Pain intensity was associated with the simultaneous carriage of the IL-1alphaT(889) and IL-1RNA(1812) alleles (OR 3.7, 95% CI 1.2-11.9). Multiple regression analyses allowing for occupation and disc degeneration showed that carriage of the IL-1RNA(1812) allele was associated with the occurrence of pain, the number of days with pain and days with limitations of daily activities. Carriage of the IL-1betaT(3954) allele was associated with the number of days with pain. The results suggest a possible contribution of the IL-1 gene locus polymorphisms to the pathogenesis of LBP. The possibility of chance findings cannot be excluded due to the small sample size.

  • 39.
    Wicksell, Rikard K.
    et al.
    Karolinska universitetssjukhuset.
    Melin, Lennart
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Lekander, Mats
    Karolinska institutet.
    Olsson, Gunnar L.
    Karolinska institutet.
    Evaluating the effectiveness of exposure and acceptance strategies to improve functioning and quality of life in longstanding pediatric pain: a randomized controlled trial2009Ingår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 141, nr 3, s. 248-257Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Although several studies have illustrated the effectiveness of cognitive behavior therapy (CBT) on adult pain patients, there are few randomized controlled trials on children and adolescents. There is particularly a need for studies on pediatric patients who are severely disabled by longstanding pain syndromes. Acceptance and Commitment Therapy, as an extension of traditional CBT, focuses on improving functioning and quality of life by increasing the patient's ability to act effectively in concordance with personal values also in the presence of pain and distress. Following a pilot study, we sought to evaluate the effectiveness of an ACT-oriented intervention based on exposure and acceptance strategies and to compare this with a multidisciplinary treatment approach including amitriptyline (n=32). The ACT condition underwent a relatively brief treatment protocol of approximately 10 weekly sessions. Assessments were made before and immediately after treatment, as well as at 3.5 and 6.5 months follow-up. Prolonged treatment in the MDT group complicated comparisons between groups at follow-up assessments. Results showed substantial and sustained improvements for the ACT group. When follow-up assessments were included, ACT performed significantly better than MDT on perceived functional ability in relation to pain, pain intensity and to pain-related discomfort (intent-to-treat analyses). At post-treatment, significant differences in favor of the ACT condition were also seen in fear of re/injury or kinesiophobia, pain interference and in quality of life. Thus, results from the present study support previous findings and suggest the effectiveness of this ACT-oriented intervention for pediatric longstanding pain syndromes.

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