Abstract

Objectives Muscle shortening and spastic cocontraction in ankle plantar flexors may alter gait since early childhood in cerebral palsy (CP). We evaluated gastrosoleus complex (GSC) length, and gastrocnemius medialis (GM) and peroneus longus (PL) activity during swing phase, in very young hemiparetic children with equinovalgus. Methods This was an observational, retrospective, and monocentric outpatient study in a pediatric hospital. Ten very young hemiparetic children (age 3 ± 1 yrs) were enrolled. These CP children were assessed for muscle extensibility (Tardieu scale XV1) in GSC (angle of arrest during slow-speed passive ankle dorsiflexion with the knee extended) and monitored for GM and PL electromyography (EMG) during the swing phase of gait. The swing phase was divided into three periods (T1, T2, and T3), in which we measured a cocontraction index (CCI), ratio of the Root Mean Square EMG (RMS-EMG) from each muscle during that period to the peak 500 ms RMS-EMG obtained from voluntary plantar flexion during standing on tiptoes (from several 5-second series, the highest RMS value was computed over 500 ms around the peak). Results On the paretic side: (i) the mean XV1-GSC was 100° (8°) (median (SD)) versus 106° (3°) on the nonparetic side (p = 0.032, Mann–Whitney); (ii) XV1-GSC diminished with age between ages of 2 and 5 (Spearman, ρ = 0.019); (iii) CCIGM and CCIPL during swing phase were higher than on the nonparetic side (CCIGM, 0.32 (0.20) versus 0.15 (0.09), p < 0.01; CCIPL, 0.52 (0.30) versus 0.24 (0.17), p < 0.01), with an early difference significant for PL from T1 (p = 0.03). Conclusions In very young hemiparetic children, the paretic GSC may rapidly shorten in the first years of life. GM and PL cocontraction during swing phase are excessive, which contributes to dynamic equinovalgus. Muscle extensibility (XV1) may have to be monitored and preserved in the first years of life in children with CP. Additional measurements of cocontraction may further help target treatments with botulinum toxin, especially in peroneus longus.

Highlights

  • In spastic paresis, placing a muscle under tension may increase its cocontraction and the cocontraction of homonymous muscles [1]

  • When considering the whole swing phase, there was a significant difference between the paretic and nonparetic sides for the cocontraction index of both muscles, with CCIs that were about doubled on the paretic side (Wilcoxon: cocontraction indices of GM (CCIGM), 0.30 (0.2) versus 0.15 (0.09), p < 0.01; CCIPL, 0.52 (0.3) versus 0.24 (0.17), p < 0.01) (Figure 4)

  • Statistical analysis for subperiods (T1, T2, and T3) of the swing phase showed an interaction between the side and the period of swing for the cocontraction index in both muscles (Kruskal-Wallis, CCIGM, and CCIPL, p < 0.0001)

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Summary

Introduction

In spastic paresis, placing a muscle under tension may increase its cocontraction (antagonistic recruitment during opposite voluntary effort) and the cocontraction of homonymous muscles [1]. Such tension may arise when stretch is applied on a contractured muscle. There have been suggestions in infant paresis that passive muscle extensibility diminishes with age [2], that this gradual loss of extensibility is the clinical representation of a true histological muscle disease with myofascial thickening [3], and that this muscle disease may represent a more prominent problem than spasticity [2,3,4,5,6].

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