Journal
BMC NEUROLOGY
Volume 13, Issue -, Pages -Publisher
BIOMED CENTRAL LTD
DOI: 10.1186/1471-2377-13-14
Keywords
Complex regional pain syndrome; Macrovascular changes; Intima-media thickness; Inflammatory alterations
Categories
Funding
- Ruhr University Bochum [F634-2008, K046-10]
- Sonosite (Nurnberg, Germany)
- GE Healthcare (Solingen, Germany)
- Esaote (Cologne, Germany)
- BK Medical (Pinneberg, Germany)
- Pajunk (Geisingen, Germany)
- B. Braun (Melsungen, Germany)
- German Federal Ministry of Education and Research (BMBF) [01EM0107, 01EM0502]
- Pfizer
- MSD
- Mundipharma
- Grunenthal
- Astellas
- Lilly
- Sanofi Aventis
- Wyeth
- Eli Lilly
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Background: Although intima-media thickness (IMT) was increased in several inflammatory diseases, studies investigating whether the inflammatory processes lead to macrovascular alteration with increased IMT in complex regional pain syndrome (CRPS) lack. Methods: Using ultrasound (high-resolution B-mode), we compared bilaterally the IMT of the common carotid artery (CCA-IMT), the radial artery (RA-IMT), the brachial artery (BRA-IMT) and the quotient Q(RA/CCA), in CRPS type I (n=17), peripheral nerve injury (PNI, n=17) and pain-free controls (PFC, n=22, matched to CRPS by gender, age and traditional cardiovascular risk factors). Statistics: Spearman's correlation, paired t-test, ANOVA (p<0.05). Results: Compared to PFC, RA-IMT were significantly increased in both patient groups bilaterally (mean +/- standard deviation, CRPS affected side vs. PFC dominant side: 0.32 +/- 0.08 mm vs. 0.19 +/- 0.08 mm, p<0.001; PNI affected side vs. PFC dominant side: 0.27 +/- 0.09 mm vs. 0.19 +/- 0.08 mm, p<0.05; CRPS non-affected side vs. PFC non-dominant side: 0.30 +/- 0.10 mm vs. 0.19 +/- 0.09 mm, p<0.001; PNI non-affected side vs. PFC non-dominant side: 0.25 +/- 0.10 mm vs. 0.19 +/- 0.09 mm, p<0.05) and Q(RA/CCA) (CRPS affected-side vs. PFC dominant side: 0.49 +/- 0.12 vs. 0.30 +/- 0.11, p<0.001; PNI affected side vs. PFC dominant side: 0.41 +/- 0.10 vs. 0.30 +/- 0.11, p<0.05; CRPS non-affected side vs. PFC non-dominant side: 0.43 +/- 0.19 vs. 0.30 +/- 0.13, p<0.001; PNI non-affected side vs. PFC non-dominant side: 0.39 +/- 0.14 vs. 0.30 +/- 0.13, p<0.05), and BRA-IMT - only on the affected side in CRPS (CRPS: 0.42 +/- 0.06 mm vs. PFC: 0.35 +/- 0.08 mm; p<0.05). In CRPS, Q(RA/CCA) was significantly higher on the affected side compared to PNI (p<0.05). However, only CRPS displayed within-group side-to-side differences with a significantly increased RA-IMT and Q(RA/CCA) on the affected side (p<0.05). The CCA-IMT was comparable between all groups and sides. Conclusions: The increased IMT of peripheral arteries in CRPS suggests ongoing inflammatory process. Until now, only endothelial dysfunction has been reported. The presented morphological macrovascular alterations might explain the treatment resistance of some CRPS patients.
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