Background An aspect of pain in chronic diseases is the phenomenon of central sensitization (CS) manifested as pain hypersensitivity with anatomically spread hyperalgesia and enhanced temporal summation of pain after repeated stimulation. CS is a very common phenomena which occurs in OA and it has been clinically characterized using pressure pain stimulation¹. One limitation on research is the subjectivity present in the pain assessment. Functional magnetic resonance imaging (fMRI) is an objective technique that maps neural activity in brain regions and demonstrates considerable anatomical resolution when mapping specific areas involved in pain perception². However, there are little evidences on the study of CS phenomenon in OA by fMRI

Objectives The aim of this study is to show fMRI evidence of pain CS in patients with knee OA compared with control subjects

Methods We designed a cross-sectional, single blind study and compared OA patients following clinical and radiological ACR criteria vs healthy controls. All participants were recruited in the OA Unit at the Hospital del Mar during one year and a half. Clinical CS was assessed using extended version of the ArendtNielsen peripatellar map¹(number of tender points, minimal pressure needed to suffer pain) and increased pain response to repeated stimulation (temporal summation). We used a three-step strategy: (1) identifying brain response to direct pulsed pressure stimulation on the painful knee (interline), (2) identifying brain response to pulsed pressure stimulation on a non-arthritic hyperalgesic area (anterior surface of the tibia) and (3) identifying brain response to painful contact heat stimulation on a healthy skin area (volar forearm).

Results We included 60 OA patients and 30 controls (66.7+/ 7.8yrs and 62.8 +/ 7.7yrs, respectively). A total of 33 patients showed some evidence of CS which 19 met all criteria of CS. At interline test, there was no difference on fMRI outcomes. At tibial test we found significant differences on brain activity which involved greater activation, in sensitized patients, in primary somatosensory area, supramarginal gyrus, sensorymotor cortex and basal ganglia. Correlation between brain response and clinical CS assessment was significant on somatosensory cortex, suppramarginal gyrus, anterior cingulated cortex and ventral putamen nucleus, bilaterally. Finally, we found no significant differences on brain activation between groups on the painful heat stimulation

Conclusions CS phenomenon is frequent in knee OA patients. Pressure on tibial bone looked adequate to discriminate between sensitized and non sensitized patients, unlike pressure on interline. The correlation maps involving fronto-subcortical activation could suggest that CS is related to learning and associative processes like associations between pain and daily activities

References

1. Arendt-Nielsen L, Nie H, Laursen MB, Laursen BS, Madeleine P, Simonsen OH, Graven-Nielsen T. Sensitization in patients with painful knee osteoarthritis. Pain 2010;149:573–581.

2. Schweinhardt P, Lee M, Tracey I. Imaging pain in patients: is it meaningful? Curr Opin Neurol 19 2006 392-400.

Disclosure of Interest None declared