AIM: If increased muscle stiffness and contractures in children with cerebral palsy (CP) are related to impaired muscle growth, reduced muscle growth should precede or coincide with increased muscle stiffness during development. Here, we compared the volume of the medial gastrocnemius muscle and the passive (non-neural) stiffness of the triceps surae musculotendinous unit in typically developing children and children with CP from birth until 4 years of age.

METHOD: Forty-one children with CP and 45 typically developing children were included. Freehand three-dimensional ultrasound was used to evaluate the volume of the medial gastrocnemius muscle. Biomechanical and electrophysiological measures were used to determine passive and reflex mediated stiffness of the triceps surae musculotendinous unit.

RESULTS: Medial gastrocnemius muscle volume increased with the same rate in typically developing and children with CP until 12 months of age, when a significant smaller rate of growth was observed in children with CP. Passive stiffness of the triceps surae musculotendinous unit showed a linear increase with age in typically developing children. Children with CP older than 27 months showed a significant increase in passive stiffness. Reflex mediated stiffness was only pathologically increased in four children with CP.

INTERPRETATION: The deviation of medial gastrocnemius muscle volume, earlier than musculotendinous unit stiffness, is consistent with the hypothesis. The data also point out that muscle atrophy and muscle stiffness already develops within the first 1 to 2 years. This emphasizes the necessity of early interventions to promote lower limb muscle growth in this population.

WHAT THIS PAPER ADDS: Medial gastrocnemius muscle growth is reduced in children with cerebral palsy (CP) around 12 months after birth. Triceps surae musculotendinous unit stiffness is increased in children with CP around 27 months after birth. Reflex excitability is rarely increased in children with CP. Reduced muscle growth may be involved in the pathophysiology of contractures.