Botulinum Neurotoxin type-A (BoNT-A) injections are widely used as first-line spasticity treatment in spastic cerebral palsy (SCP). Despite improved clinical outcomes, concerns regarding harmful effects on muscle morphology have been raised. Yet, the risk of initiating BoNT-A to reduce muscle growth remains unclear. This study investigated medial gastrocnemius (MG) morphological muscle growth in children with SCP (n = 26, median age of 5.2 years (3.5)), assessed by 3D-freehand ultrasound prior to and six months post-BoNT-A injections. Post-BoNT-A MG muscle growth of BoNT-A naive children (n = 11) was compared to (a) muscle growth of children who remained BoNT-A naive after six months (n = 11) and (b) post-BoNT-A follow-up data of children with a history of BoNT-A treatment (n = 15). Six months after initiating BoNT-A injection, 17% decrease in mid-belly cross-sectional area normalized to skeletal growth and 5% increase in echo-intensity were illustrated. These muscle outcomes were only significantly altered when compared with children who remained BoNT-A naive (+4% and −3%, respectively, p < 0.01). Muscle length growth persevered over time. This study showed reduced cross-sectional growth post-BoNT-A treatment suggesting that re-injections should be postponed at least beyond six months. Future research should extend follow-up periods investigating muscle recovery in the long-term and should include microscopic analysis.

Only cross-sectional studies have demonstrated muscle deficits in children with spastic cerebral palsy (SCP). The impact of gross motor functional limitations on altered muscle growth remains unclear. This prospective longitudinal study modelled morphological muscle growth in 87 children with SCP (age range 6 months to 11 years, Gross Motor Function Classification System [GMFCS] level I/II/III = 47/22/18). Ultrasound assessments were performed during 2-year follow-up and repeated for a minimal interval of 6 months. Three-dimensional freehand ultrasound was applied to assess medial gastrocnemius muscle volume (MV), mid-belly cross-sectional area (CSA) and muscle belly length (ML). Non-linear mixed models compared trajectories of (normalized) muscle growth between GMFCS-I and GMFCS-II&III. MV and CSA growth trajectories showed a piecewise model with two breakpoints, with the highest growth before 2 years and negative growth rates after 6–9 years. Before 2 years, children with GMFCS-II&III already showed lower growth rates compared to GMFCS-I. From 2 to 9 years, the growth rates did not differ between GMFCS levels. After 9 years, a more pronounced reduction in normalized CSA was observed in GMFCS-II&III. Different trajectories in ML growth were shown between the GMFCS level subgroups. These longitudinal trajectories highlight monitoring of SCP muscle pathology from early ages and related to motor mobility. Treatment planning and goals should stimulate muscle growth.

Our aim was to determine if synergy weights and activations are altered in Duchenne muscular dystrophy (DMD) and if these alterations could be linked to muscle weakness. In 22 children with DMD and 22 typical developing (TD) children of a similar age, surface electromyography (sEMG) of the gluteus medius, rectus femoris (REF), medial hamstrings, tibialis anterior, and medial gastrocnemius (GAS) were recorded during gait. Muscle weakness was assessed with maximal voluntary isometric contractions (MVIC). Synergies were calculated with non-negative matrix factorization. The number of synergies explaining ≥90% of the variance in the sEMG signals (N90), were extracted and grouped with k-means cluster analysis. We verified differences in weights with a Mann-Whitney U test. Statistical non-parametric mapping (Hotelling's T² test and two-tailed t-test) was used to assess group differences in synergy activations. We used Spearman’s rank correlation coefficients and canonical correlation analysis to assess if weakness was related to modifications in weights and activations, respectively. For both groups, average N90 was three. In synergy one, characterized by activity at the beginning of stance, the DMDs showed an increased REF weight (p = 0.001) and decreased GAS weight (p = 0.007). Synergy activations were similar, with only a small difference detected in mid-swing in the combined activations (p<0.001). Weakness was not associated with these differences. Despite the apparent weakness in DMD, synergy weights and activations were similar between the two groups. Our findings are in line with previous research suggesting non-neural alterations have limited influence on muscle synergies.

Children with cerebral palsy (CP) present with a pathological gait pattern due to musculoskeletal impairments, such as muscle weakness and altered bony geometry. However, the effect of these impairments on gait performance is still unknown. Research aim:This study aimed to explore the effect of hip muscle weakness and femoral deformities on the gait performance of CP and typical developing (TD) subjects. 6400 musculoskeletal models were created by weakening the hip extensors, abductors, adductors and flexors from 0% to 75 % and increasing the femoral anteversion angle (FAA) and neck shaft angle (NSA) from 20° to 60° and 120° to 160°, respectively. One TD and five CP gait patterns were imposed to each model and muscle forces were calculated. The effect of weakness and bony deformities on the capability gap (CG) at the hip, i.e. the lack in hip moment generating capacity to perform the gait pattern, was investigated using regression analysis. The CG of apparent equinus, stiff knee gait, TD gait, jump gait and true equinus increased with 0.080, 0.038, 0.015, 0.023 and 0.005 Nm/kg per 10 percent hip abductor weakness increase, with 0.211, 0.130, 0.056, 0.045 and 0.011 Nm/kg per 10 degrees FAA increase and with 0.163, 0.080, 0.036, 0.043 and 0.011 Nm/kg per 10 degrees NSA increase, respectively. Combined weakness and bony deformities explained 96 %, 85 %, 82 %, 65 %, 40 % and 35 % of the variance in the CG of apparent equinus, TD gait, stiff knee gait, jump gait, true equinus and crouch gait, respectively. The results suggest that surgical correction of femoral deformities is more likely to be effective than strength training of hip muscles in enhancing CP gait performance. Jump gait, true equinus and especially crouch were more robust, while apparent equinus and stiff knee gait were limited by hip weakness and femoral deformities.