scholarly journals Do Genetic Predictors of Pain Sensitivity Associate with Persistent Widespread Pain?

2009 ◽  
Vol 5 ◽  
pp. 1744-8069-5-56 ◽  
Author(s):  
Kate L Holliday ◽  
Barbara I Nicholl ◽  
Gary J Macfarlane ◽  
Wendy Thomson ◽  
Kelly A Davies ◽  
...  
2010 ◽  
Vol 69 (11) ◽  
pp. 2009-2012 ◽  
Author(s):  
Barbara I Nicholl ◽  
Kate L Holliday ◽  
Gary J Macfarlane ◽  
Wendy Thomson ◽  
Kelly A Davies ◽  
...  

ObjectivesThe aim of this study was to investigate the association between the catechol-O-methyltransferase (COMT) ‘pain sensitivity’ haplotypes and chronic widespread pain (CWP) in two distinct cohorts.MethodsCases of CWP and controls free of pain were selected from two population-based studies: the Epidemiology of Functional Disorders study (EPIFUND) (UK) and the European Male Ageing Study (European). The number of cases and controls were 164 and 172, and 204 and 935, respectively. Identical American College of Rheumatology criteria were used in both studies to ascertain CWP status. The EPIFUND study had three time points and cases were classified as subjects with CWP at two or three time points and controls as those free of pain at all three time points. Four single nucleotide polymorphisms (SNP): rs6269, rs4633, rs4818 and rs4680 (V158M) were genotyped using Sequenom technology. Allele and genotype frequencies were compared and haplotype analysis was conducted using PLINK software.ResultsNo differences in allele or genotype frequencies for any of the four SNP were observed between cases and controls for either cohort. Haplotype analysis also showed no difference in the frequency of haplotypes between cases and controls.ConclusionsThere was no evidence of association between the COMT ‘pain sensitivity’ haplotypes and CWP in two population-based cohorts.


2019 ◽  
Vol Volume 12 ◽  
pp. 1743-1755 ◽  
Author(s):  
Helene van Ettinger-Veenstra ◽  
Peter Lundberg ◽  
Péter Alföldi ◽  
Martin Södermark ◽  
Thomas Graven-Nielsen ◽  
...  

Author(s):  
Jennifer Pierce ◽  
Afton L Hassett ◽  
Chad M Brummett ◽  
Jenna McAfee ◽  
Christine Sieberg ◽  
...  

Abstract Background Childhood trauma and adversity have been linked to chronic pain and pain sensitivity, particularly centralized pain. Yet, there remain numerous gaps in our understanding of this link. Purpose We explored the association between nonviolent and violent childhood trauma and a component of centralized pain (i.e., generalized sensory sensitivity) and pain sensitivity using self-report measures of centralized pain and quantitative sensory testing (QST). Methods Patients scheduled for a total knee arthroplasty (n = 129) completed questionnaires and QST prior to surgery. Results We found that self-report measures of centralized pain (i.e., widespread pain, somatic awareness, and sensory sensitivity) displayed a graded relationship across trauma groups, with patients with a history of violent trauma reporting the highest scores. Univariable multinomial logistic regression analyses showed that higher sensory sensitivity was associated with increased risk of being in the nonviolent trauma group compared to the no trauma group. Furthermore, higher widespread pain, higher somatic awareness, and higher sensory sensitivity distinguished the violent trauma group from the no trauma group. In multivariable analyses, sensory sensitivity is uniquely distinguished between the violent trauma group and the no trauma group. QST did not distinguish between groups. Conclusions The findings highlight the need for future research and interventions that reduce sensory sensitivity for chronic pain patients with a history of violent childhood trauma.


Author(s):  
George D. Pappas ◽  
Jacqueline Sagen

We have been interested in the use of neural transplants mainly as a local source of neuroactive substances, rather than as a replacement for damaged neural circuities. In particular, we have been exploring the possibilities of reducing pain by transplants of opioid peptide producing cells, and reducing depression by transplants of monoamine-producing cells. For the past several years, work in our laboratory has demonstrated in both acute and chronic pain models that transplantation of adrenal medullary tissue or isolated chromaffin cells into CNS pain modulatory regions can reduce pain sensitivity in rodents. Chromaffin cells were chosen as donor source since they produce high levels of both opioid peptides and catecholamines, substances which independently, and probably synergistically, reduce pain sensitivity when injected locally into the spinal cord. The analgesia produced by these transplants most likely results from the release of both opioid peptides and catecholamines, since it can be blocked or attenuated by opiate or adrenergic antagonists, respectively. Furthermore, CSF levels of met-enkephalin and catecholamines are increased by the transplants.


2001 ◽  
Vol 120 (5) ◽  
pp. A7-A7
Author(s):  
S ROSS ◽  
S MASCHERETTI ◽  
H HINRICHSEN ◽  
P BUGGISCH ◽  
U FOELSCH ◽  
...  

2009 ◽  
Vol 23 (3) ◽  
pp. 104-112 ◽  
Author(s):  
Stefan Duschek ◽  
Heike Heiss ◽  
Boriana Buechner ◽  
Rainer Schandry

Recent studies have revealed evidence for increased pain sensitivity in individuals with chronically low blood pressure. The present trial explored whether pain sensitivity can be reduced by pharmacological elevation of blood pressure. Effects of the sympathomimetic midodrine on threshold and tolerance to heat pain were examined in 52 hypotensive persons (mean blood pressure 96/61 mmHg) based on a randomized, placebo-controlled, double-blind design. Heat stimuli were applied to the forearm via a contact thermode. Confounding of drug effects on pain perception with changes in skin temperature, temperature sensitivity, and mood were statistically controlled for. Compared to placebo, higher pain threshold and tolerance, increased blood pressure, as well as reduced heart rate were observed under the sympathomimetic condition. Increases in systolic blood pressure between points of measurement correlated positively with increases in pain threshold and tolerance, and decreases in heart rate were associated with increases in pain threshold. The findings underline the causal role of hypotension in the augmented pain sensitivity related to this condition. Pain reduction as a function of heart rate decrease suggests involvement of a baroreceptor-related mechanism in the pain attrition. The increased proneness of persons with chronic hypotension toward clinical pain is discussed.


2010 ◽  
Author(s):  
Suzanne G. Helfer ◽  
Ashley D. Bugeja ◽  
Sarah E. Jackson ◽  
Elizabeth Woltja

Sign in / Sign up

Export Citation Format

Share Document