INTRODUCTION

Chronic pain after total knee arthroplasty (TKA) affects approx. 15%-20% of patients undergoing surgery. It is largely unexplained why some patients develop chronic pain after TKA, but several factors, e.g., central pain mechanisms and psychosocial factors, have been suggested. This study assessed central pain mechanisms and psychosocial factors in patients with chronic pain after TKA, receiving neuromuscular exercise and pain neuroscience education (PNE) as treatment.

METHODS

This is the secondary analysis of a randomised controlled trial. Sixty-nine patients with chronic pain at least one-year post-TKA, experiencing an average daily pain intensity of ≥ 4 on a numerical rating scale, were recruited. Participants were randomised to receive either 12 weeks of group-based neuromuscular exercise and two sessions of group-based PNE or two sessions of group-based PNE alone. Outcomes measured included temporal summation of pain (TSP) and pressure pain thresholds at the index knee and forearm, conditioned pain modulation, PainDETECT scores, fear-avoidance beliefs and pain catastrophizing.

RESULTS

The study found a significant between-group difference in change from baseline to 12 months for TSP at the index knee, favouring the neuromuscular exercise and PNE group (-1.45, 95% CI -2.48 to -0.42, p = 0.006). This indicates less facilitated TSP in the neuromuscular exercise and PNE group after intervention. No significant between-group differences were observed for the remaining outcomes.

CONCLUSION

The results indicated that neuromuscular exercise combined with PNE significantly reduced TSP at the index knee, suggesting a reduction in central pain amplification. The clinical importance of this exploratory finding should be further investigated.

SIGNIFICANCE STATEMENT

This trial showed that neuromuscular exercises in combination with pain neuroscience education resulted on decreased pain sensitization, measured as temporal summation of pain, in patients with chronic pain after total knee arthroplasty. The clinical relevance of central amplification of pain remains unclear but point at improved pain processing, i.e., reduced pain amplification.