Richard Lauer, PhD,
Samuel Pierce, PT, PhD, NCS;
The treatment of spasticity is often a primary goal for therapeutic interventions for children with cerebral palsy (CP). Spasticity is defined as a “velocity dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex”.1 Many interventions are currently employed to treat spasticity associated with CP. For example, surgical procedures, such as tendon lengthening, and serial casting are used in the clinical setting to correct for reduced range of motion around a given joint due to spasticity. Botulinum toxin injections, intrathecal baclofen, or oral antispasmodic medications may be administered in an attempt to improve function by weakening spastic muscles or reduce co-contraction of antagonistic muscle pairs.
While the efficacy of the above mentioned treatments have been reported, their success has been based upon changes in impairments and functional parameters. For example, the assessment of botulinum toxin injections in the child with CP is through measurements of muscle spasticity using the Modified Ashworth Scale, kinematic analysis of ankle or knee range of motion during walking, or looking at the levels of co-contraction in antagonistic muscle pairs using surface electromyography (sEMG) during walking. Little effort has been directed to the understanding the neurological and muscular changes that occur in the child with CP as a result of the injection. The understanding of neurological and muscular plasticity, both the magnitude and the time course, as a result of the botulinum toxin injection could provide valuable and meaningful insights necessary to better direct and advance clinical treatment.
We have recently completed a pilot study, with the support of the Cerebral Palsy International Research Foundation, to examine these changes. In a small sample of children, we not only examined the changes in the kinematics of the ankle and knee in response to the botulinum toxin treatment, but we also examined changes in the brain through the use of functional magnetic resonance imaging, changes at the spinal cord level through H-reflex testing, changes at the neuromuscular junction using time-frequency analyses of the sEMG signal during gait, and the reflexive and non-reflexive components of spasticity. Early results seem to indicate the possibility of long term improvements in brain and spinal activity that persist even after the treatment has worn off. However, the return to the poor gait kinematics after the botulinum toxin injection has worn off appears to be based on poor muscle re-education during the effective period of the botulinum toxin injection. This results in even poorer muscle activation patterns than were present at baseline. These results would seem to indicate that during the effective period of the botulinum toxin treatment, other therapies are needed to help re-educate the muscle in response to the positive changes in the brain and spinal cord. This could ensure a better “carry over” effect, leading to better gait for the children undergoing this therapy. This will be pursued in future studies in our lab.
[1] Lance JW. The control of muscle tone, reflexes, and movement: Robert Wartenberg Lecture. Neurology 1980;30:1303-1313.