Electromechanical delay and reflex response in spastic cerebral palsy.

OBJECTIVE: Electromechanical delay (EMD) and reflex response in patients with spastic cerebral palsy (CP) were quantified and compared with those in normally developing individuals. It was hypothesized that the increased muscle stiffness associated with spasticity must make EMD shorter than the EMD of normally functioning muscles. DESIGN: Electromechanical reflex behavior was assessed in a case-control study. SETTING: Motion Analysis and Motor Performance Laboratory, University of Virginia, a tertiary clinical referral center and research facility. PARTICIPANTS: A volunteer sample of 12 children diagnosed with spastic CP and 12 age-matched, normally developing children recruited from the local community and clinical services. RESULTS: EMD in the patients with spasticity was significantly shorter than in the normally developing subjects, 40.5 msec and 54.7 msec, respectively. The spastic group also had greater reflex activity, rate of force development, and antagonistic muscle activation. Knee flexion angle did not influence EMD in either group. CONCLUSIONS: Increased biomechanical stiffness in spastic muscle results in abnormally reduced EMD. Reciprocal excitation of antagonistic cocontraction was uniquely observed in the spastic group, but did not explain the reduced EMD.

Quantification of cocontraction in spastic cerebral palsy.

Antagonist cocontraction was hypothesized to limit net moment production in children with spastic diplegic cerebral palsy (CP). A second hypothesis was that concontraction would vary with joint angle. To test these hypotheses, surface EMG activity and moment data from the quadriceps and hamstrings muscle groups were obtained from children with CP and compared with normally developing children during isometric flexion and extension exertions. A biomechanical model was developed to predict individual moments produced by the agonist and antagonist muscle groups. Concontraction was defined as the percentage of the net moment that was negated by the antagonist moment. The model performed well in predicting the measured moment as illustrated by high R2 correlation coefficients and low prediction errors. The mean maximum moment produced was greater in normally developing children than children with CP in both flexion and extension. Antagonist cocontraction during extension was greater in children with CP (12.2 +/- 14.4%) than in normally developing children (4.9 +/- 3.8%), implying that antagonist cocontraction is one explanation for the observed extension weakness in children with CP. However, during flexion, cocontraction was not significantly different between the two groups. Cocontraction differed significantly with joint angle in both groups during flexion and in the normally developing children during extension. Although quantifying coactivation based on EMG activity alone produced similar results, it underestimated the effect of the antagonist. The quantification of cocontraction has potential applications for characterizing spastic muscle dysfunction and thereby improving clinical outcomes in children with CP.