Central pain processing in chronic low back pain: Evidence for reduced pain inhibition
Schmerz, ISSN: 0932-433X, Vol: 20, Issue: 5, Page: 411-417
2006
- 34Citations
- 87Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations34
- Citation Indexes34
- 34
- CrossRef22
- Captures87
- Readers87
- 66
- 14
Article Description
Introduction. A study of patients with low back pain (LBP) had revealed altered central pain processing. At an equal pain level LBP patients had considerably more neuronal activation in the somatosensory cortices than controls. In a new analysis of this dataset, we further investigated the differences in central pain processing between LBP patients and controls, looking for possible pathogenic mechanisms. Methods. Central pain processing was studied by functional magnetic resonance imaging (fMRI), using equally painful pressure stimuli in a block paradigm. In this study, we reanalyzed the fMRI data to statistically compare pain-elicited neuronal activation of both groups. Results. Equally painful pressure stimulation resulted in a significantly lower increase of regional cerebral blood flow (rCBF) in the periaqueductal gray (PAG) of the LBP patients. The analysis further revealed a significantly higher increase of rCBF in LBP than in HC in the primary and secondary somatosensory cortex and the lateral orbitofrontal cortex (LOFK), elicited by these same stimuli. Conclusions. These findings support a dysfunction of the inhibitory systems controlled by the PAG as a possible pathogenic mechanism in chronic low back pain. © 2006 Springer Medizin Verlag.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=33749145841&origin=inward; http://dx.doi.org/10.1007/s00482-006-0473-8; http://www.ncbi.nlm.nih.gov/pubmed/16586062; http://link.springer.com/10.1007/s00482-006-0473-8; http://www.springerlink.com/index/10.1007/s00482-006-0473-8; http://www.springerlink.com/index/pdf/10.1007/s00482-006-0473-8; https://dx.doi.org/10.1007/s00482-006-0473-8; https://link.springer.com/article/10.1007/s00482-006-0473-8
Springer Science and Business Media LLC
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