Combining muscle morphology and clinical neuro-motor symptoms to explain abnormal gait at the ankle joint in cerebral palsy

Publication date: Available online 4 December 2018

Source: Gait & Posture

Author(s): Simon-Henri Schless, Francesco Cenni, Lynn Bar-On, Britta Hanssen, Marije Goudriaan, Eirini Papageorgiou, Erwin Aertbeliën, Guy Molenaers, Kaat Desloovere

ABSTRACT

Background

Individuals with spastic cerebral palsy (CP) have clinical neuro-motor symptoms contributing towards their pathological gait patterns. However, the role of altered muscle morphology alongside these symptoms is yet to be fully investigated.

Research question: Can a combination of medial gastrocnemius and tibialis anterior volume and echo-intensity, plantar/dorsi-flexion strength and selective motor control, plantarflexion spasticity and passive ankle dorsiflexion explain pathological gait at the ankle.

Method

In thirty children and adolescents with spastic CP (8.6 ± 3.4 y/mo) and ten typically developing peers (9.9 ± 2.4 y/mo), normalised muscle volume and echo-intensity were estimated, along with three-dimensional gait analysis. In the spastic CP participants, plantar/dorsi-flexion strength and selective motor control, plantarflexion spasticity and maximum ankle dorsiflexion were also measured. The combined contribution of these parameters towards the features of gait were evaluated, using backwards multiple regression analyses.

Results

The spastic CP participants cohort had reduced normalised medial gastrocnemius and tibialis anterior volume deficits of 40% and 33%, and increased echo-intensity values of 19% and 16%, respectively. The backwards multiple regression analyses revealed that the combination of reduced ankle dorsiflexion, smaller muscle volume, plantarflexion strength and dorsiflexion selective motor control could explain between 12-62% of the variance in the features of gait.

Significance

The combination of altered muscle morphology and clinical neuro-motor symptoms partly explained pathological gait at the ankle in children and adolescents with spastic CP. Both should be considered as important measures for informed treatment decision-making, but further work is required to better unravel the complex pathophysiology.

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