Aim The aim of this article was to compare medial gastrocnemius muscle volume, physiological cross-sectional area (PCSA), muscle length, fascicle length, and pennation angle in children aged 2 to 5 years with spastic cerebral palsy (CP) and in typically developing children.
Method Fifteen children with spastic CP (11 males, four females; mean age 45mo [SD 15mo]; five with hemiplega; 10 with diplega; 10 classified at Gross Motor Function Classification System (GMFCS) level I, five at GMFCS level II) and 20 typically developing children (11 males, nine females; mean age 48mo [SD 14mo]) participated in the study. Individuals with spastic CP were included if they had a minimum range of motion of 0° ankle dorsiflexion with the knee extended and were excluded if they had had previous botulinum toxin treatment to the calf muscles or previous calf surgery. Typically developing children were included if they were able to walk independently and were excluded if there was a history of previous lower leg injury or other developmental disorder affecting the lower limb. Freehand two-dimensional and three-dimensional ultrasound was used to assess muscle properties of the relaxed medial gastrocnemius muscle at three ankle joint angles: maximum dorsiflexion, neutral and maximum plantarflexion. PCSA was calculated as a function of muscle volume and muscle fascicle length and pennation angle was recorded at the neutral ankle joint angle.
Results Medial gastrocnemius muscle volume was 22% lower in the group with spastic CP than in the typically developing group, which in the absence of significant group differences in neutral fascicle length gave rise to an equivalent reduction in PCSA for the group with spastic CP. Significant positive correlations were found between muscle volume and age (r=0.63–0.65) and between muscle length and age (r=0.72–0.81) in both groups. Maximum ankle dorsiflexion angle was also reduced in the group with spastic CP (8°) compared with the typically developing group (26°).
Interpretation The observed reduction in muscle PCSA in the group with spastic CP would be expected to contribute to the clinically observed muscle weakness in spastic CP and suggests the need for early intervention in order to minimize loss of muscle PCSA in spastic CP.