Spread of Botulinum Neurotoxin Type A at Standard Doses Is Inherent to the Successful Treatment of Spastic Equinus Foot in Cerebral Palsy: Short-Term Neurophysiological and Clinical Study

SLR - January 2012 - Kristin J. Blanchet

Reference: Frasson, E., Dall’Ora, E., Bordignon, M., Brigo, Francesco B., Tocco, P., Primon, D., Didone, G., Vicentini, S., Fiaschi, A., Bertolasi, L. (2011). Journal of Child Neurology. Epub ahead of print.

Scientific Literature Review

Reviewed by: Kristin J. Blanchet, DPM
Residency Program: Bethesda Memorial Hospital, Boynton Beach, FL

Podiatric Relevance:
Spastic equinus secondary to cerebral palsy is often seen in children. It is important for podiatrists to understand both the etiology of the equinus and the mechanisms of current treatment methods used to treat this spasticity.

Methods:
Eighteen ambulatory hemiplegic children with cerebral palsy between ages 5-7 from the University of Verona were voluntarily enrolled in this prospective study. Pre-injection neurophysiologic studies were performed and 200-400 U of botulinum neurotoxin A were injected to the medial and lateral gastrocnemius muscle at the site of the maximum muscle action potential. The measured neurophysiological outcomes were muscle action potentials of the tibialis anterior (to measure spread of toxin to nearby antagonistic muscles) and the lateral gastrocnemius at day 0, day 10, and day 30. Clinical outcomes were based on passive ankle range of motion at day 0, day 10, and day 30. The Edinburgh Visual Gait Score was also used to assess functional outcomes.

Results:
In all eighteen patients, the areas injected showed significantly decreased muscle action potentials at day 2 and maintenance of these low potentials at day 10 and day 30. Similarly, the Modified Ashworth Scale showed significant decrease in passive ankle joint range of motion at days 10 and 30 on the treated side.  Also, the visual gait scores were significantly decreased in the treated side at days 10 and 30. The control areas showed no significant differences.

Conclusions:
Botulinum toxin A is effective in decreasing muscle action potentials and also clinically improves spastic equinus caused by cerebral palsy. However, the exact mechanism of this functional improvement is unknown since the toxin spreads to nearby antagonistic muscles and has as significant of an effect on these antagonist muscles as it does on the injected muscle. Until the exact mechanism is well understood, botulinum toxin A should be used with caution in children with spastic equinus.