Neonatal motor development transitions from initially spontaneous to later increasingly complex voluntary movements. A delay in transitioning may indicate cerebral palsy (CP). The general movement optimality score (GMOS) evaluates infant movement variety and is used to diagnose CP, but depends on specialized physiotherapists, is time-consuming, and is subject to inter-observer differences. We hypothesised that an objective means of quantifying movements in young infants using motion tracking data may provide a more consistent early diagnosis of CP and reduce the burden on healthcare systems. This study assessed lower limb kinematic and muscle force variances during neonatal infant kicking movements, and determined that movement variances were associated with GMOS scores, and therefore CP. Electromagnetic motion tracking data (Polhemus) was collected from neonatal infants performing kicking movements (min 50° knee extension-flexion, <2 seconds) in the supine position over 7 minutes. Tracking data from lower limb anatomical landmarks (midfoot inferior, lateral malleolus, lateral knee epicondyle, ASIS, sacrum) were applied to subject-scaled musculoskeletal models (Gait2354_simbody, OpenSim). Inverse kinematics and static optimisation were applied to estimate lower limb kinematics (knee flexion, hip flexion, hip adduction) and muscle forces (quadriceps femoris, biceps femoris) for isolated kicks. Functional principal component analysis (fPCA) was carried out to reduce kicking kinematic and muscle force waveforms to PC scores capturing ‘modes’ of variance. GMOS scores (lower scores = reduced variety of movement) were collected in parallel with motion capture by a trained operator and specialised physiotherapist. Pearson's correlations were performed to assess if the standard deviation (SD) of kinematic and muscle force waveform PC scores, representing the intra-subject variance of movement or muscle activation, were associated with the GMOS scores.Abstract
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Focal cartilage defects (FCDs) found in medial and lateral compartments of the knee are accompanied with patient-reported pain and loss of joint function. There is a deficit of evidence to explain why they occur. We hypothesise that aberrant knee joint loading may be partially responsible for FCD pathology, therefore this study aims to use 3-dimensional motion capture (MoCap) analysis methods to investigate differences in gait biomechanics of subjects with symptomatic FCDs. 11 subjects with Outerbridge grade II FCDs of the tibiofemoral joint (5 medial compartment, 6 lateral compartment) and 10 non-pathological controls underwent level-gait MoCap analysis using an infra-red camera (Qualisys) and force-plate (Bertec) passive marker system. 6-degree of freedom models were generated and used to calculate spatio-temporal measures, and frontal and sagittal plane knee, hip and ankle rotation and moment waveforms (Visual 3D). Principle component analysis (PCA) was used to score subjects based on common waveform features, and PC scores were tested for differences using Mann-Whitney tests (SPSS). No group differences were found in BMI, age or spatio-temporal measures. Medial-knee FCD subjects experienced higher (p=0.05) overall knee adduction moments (KAMs) compared to controls. Conversely, lateral-knee FCD subjects found lower (p=0.031) overall KAMs. Knee flexion and extension moments (KFMs/KEMs) were relatively reduced (p=0.013), but only in medial FCD subjects. This was accompanied by a significantly (p=0.019) higher knee flexion angle (KFA) during late-stance. KAMs have been shown to be predictive of frontal plane joint contact forces, and therefore our results may be reflective of FCD subjects overloading their respective diseased knee condyles. The differences in knee sagittal plane knee moments (KFMs/KEMs) and angles (KFA) seen in medial FCD subjects are suggestive of gait adaptations to pain. Overall these results suggest treatments of FCDs should consider offloading the respective affected condyle for better surgical outcomes.
Healthy cartilage is essential for optimal joint function. Although, articular cartilage defects are highly prevalent in the active population and might hamper joint function, the effect of articular cartilage defects on knee contact forces and pressures is not yet documented. Therefore, the present study compared knee contact forces and pressures between patients with a tibiofemoral cartilage defect and healthy controls. This might provide additional insights in movement adaptations and the role of altered loading in the progression from defect to OA. Experimental gait data was collected in 15 patients with isolated articular cartilage defects (8 medial-affected, 7 lateral-affected) and 19 healthy asymptomatic controls and was processed using a musculoskeletal model to calculate contact forces and pressures. Differences between medial-affected, lateral-affected and controls were evaluated using Kruskal-Wallis tests and individually compared using Mann-Whitney-U tests (alpha <0.05). The lateral-affected group walked significantly slower compared to the healthy controls. No adaptations in the movement pattern that resulted in decreased loading on the injured condyle were observed. Additionally, the location of loading was not significantly affected. The current results suggest that isolated cartilage defects do not induce changes in the knee joint loading pattern. Consequently, the involved condyle will be equally loaded, indicating that a similar amount of force should be distributed over the remaining cartilage surrounding the articular cartilage defect and may cause local degenerative changes in the cartilage. This in combination with inflammatory responses might play a key role in the progression from articular cartilage defect to a more severe OA phenotype.
