Influence of non-acute musculoskeletal pain on gait analysis biomarkers in individuals with cerebral palsy

Cerebral palsy (CP) is characterized by movement and posture deficiencies, resulting in atypical motor development. This can lead to altered kinematics and selective-motor-control-during-gait (SMCg) [1–3]. Individuals with CP may also experience musculoskeletal (MSK) pain [4], which may cause antalgic gait patterns in an effort to minimize pain [5]. Evidence regarding the influence of MSK pain on gait characteristics of individuals with CP, such as the presence of antalgic gait patterns, is limited. Do gait kinematics and SMCg differ between matched CP cohorts with/without MSK pain? Retrospective treadmill-based gait-analysis data (Motek-GRAIL) for 172 individuals with CP (aged 3-21 years) were screened. Thirty individuals (17%) reported feeling constant non-acute lower-extremity MSK pain during gait, without specifying severity (pain-cohort). From the remaining 142 individuals, a no-pain-cohort (n=30) was individually matched. Matching was performed in order of functional level, unilateral/bilateral-involvement, age, orthopedic intervention history and the use of orthoses/walking aids. All individuals were at least 12-months after their most recent orthopedic intervention. Cohort characteristics are presented in Table 1. Gait kinematics were captured using the human-body-model-2 and evaluated using the Gait-Profile-Score (GPS) [6], whilst spatiotemporal parameters were determined from force plate data. The latter included dimensionless walking speed (dWS), single leg support percentage and step time, which are often altered in antalgic gait patterns [5]. SMCg was assessed using non-negative-matrix-factorisation based on surface electromyography data from seven muscles per leg [1]. The total variance accounted for by one synergy was extracted and transformed to a z-score to calculate the dynamic-motor-control-index (walk-DMC) [7]. The GPS and walk-DMC were calculated using data from a typically developing cohort (n=22, mean age 9.2±2.3 years, 11-males/11-females). Outcome parameters were extracted separately for both legs, and bilaterally, where relevant. Statistical analysis is described in Table 1 (p-value set to ≤0.050). For the pain-cohort, 53% reported pain in their more-involved leg, 7% in the less involved-leg and 40% in both legs, and located primarily at the ankle and foot (57%), knee (50%) and/or hip (33%). Forty-percent had multiple pain locations. No significant differences in outcome measures were found between the cohorts (Table 1). Table 1: Participants characteristics in both groupsDownload : Download high-res image (288KB)Download : Download full-size image whilst secondary analysis revealed no influence of pain location on the results. No significant differences in gait kinematics or SMCg were found, suggesting that the pain-cohort did not exhibit an obvious antalgic gait pattern. This may be a consequence of the already altered gait kinematics and SMCg [1,3]. These findings raise important reflections regarding the assumption that MSK pain plays a significant role in altering gait in individuals with CP. This ongoing study will continue to explore this phenomenon via the use of additional biomarkers, as well as exploration of the impact of location, severity and duration of pain in larger subgroups.