BackgroundTraditionally, chronic pain in OA is considered to be a classical model of nociceptive pain. Nociceptive mechanism can’t explain the presence: referred pain, secondary hyperalgesia and other sensitive phenomena[.1 Recent studies has shown that besides nociceptive pain there is another mechanism that takes place in chronic pain OA –central sensitisation[.2 Expolore of chronic pain OA can be reached only by a complex approach in examining patients with chronic knee OA that includes not only a rheumatological examination, but examination of the neurological sphere and algometria. At the moment there are only few studies dedicated to neurophysiological changes in pain OA[3
Objectivesto assess pain system with neurophysiological examination in chronic pain OAMethods46 chronic knee pain OA and 23 healthy group control women, 45–65 years old, were included. The study included clinical rheumatologic, neurological examinations, neuropathic pain scales (DN4 and Pain DETECT). Knee X-ray and ultrasound studies. Neurophysiological examination included algometria with algometer and wind-up fenomena observed by Neuropen. Five test sites in the peripatellar region and one control site on tibialis anterior (5 cm distal to the tibial tuberosity) were located and marked for examinationResultsNeuropathic pain scales demonstrated neuropathic descriptors present in OA patients. Neurological examination revealed no somatosensory deficit. But examination of the sensitive sphere indicated hyperalgesia: primary hyperalgesia (increased sensitivity to pain in the damaged joint) and secondary hyperalgesia. Algometria revealed low pressure pain threshold(PPT) above injured knee and intact region compared with healthy group. (tab.1) PPT in intact region was compared between OA patients and control group by ROC-analysis. Max of PPT in intact region in patient with OA was −14,70, min – 1,80, mean value – 7,34. Mean value of PPT in contral group was 15,18. Area under curve was- 0888. Sensitivity – 70%. Specificity – 83%. ROC-analysis demonstrasted that low PPT in OA patints is a specific feature of central sensitisation (figure 1) Wind-up fenomena examination in intact region revealed significant difference of data in OA patients with reffered pain and control group (4,3±2,1 vs 2,44±1,3 p=0,003)and OA patients without reffered pain and control group (3,67±1,43 vs 2,44±1,3 p=0,011).PPT dataOA patients n=46Control group n=23P
V17,04±2,9215,13±5,080000V28,41±4,3914,86±4,50001V37,75±3,4516,08±4,970000V44,57±2,211,27±4,980000V54,41±2,110,7±4,80000V67,34±3,6615,18±5,070000Figure 1 Diagonal segments are produced by ties.ConclusionsChronic OA is a complex of mechanisms and includes nociceptive and central sensitisation. Neurophysiological changes: low ppt in demaged area and even intact region and wind-up fenomena were revealed in all OA patients and charectrerises central sensitisation. Mechanism-oriented treatment should also target CNS, including anticonvulsant, and antidepressant agents.References[1] Schaible HG, Ebersberger A, von Banchet G...
