The Effect of Intrathecal Baclofen on Muscle co-Contraction in Children with Spasticity of Cerebral Origin

AIM: Investigation of the effect of intrathecal baclofen administration on the time course of electrical patterns of muscle activation in patients with spasticity due to upper motor neuron syndrome. METHODS: Six children with clinical signs of upper motor neuron syndrome resulting from an acquired cerebral hypoxic injury were tested. Simultaneous multichannel acquisition of surface EMG activity from flexor/extensor muscle groups of the upper and lower limbs was recorded. Investigated muscle group pairs included biceps/triceps brachii, wrist flexors/extensors, rectus/biceps femoris and tibialis anterioris/gastrocnemius. Time-frequency analysis of EMG activity at rest and while eliciting a stretch reflex was performed. The non-linear cross-correlation coefficient and time lag estimation were computed between paired channel groups both for baseline and post-intrathecal baclofen injection conditions for epochs consisting of 2 s prior to and 2 s after voluntary contraction. The effect of baclofen was assessed 3 h following single-bolus intrathecal injections of 25 or 50 microg during the baclofen trial and 6 months after baclofen pump implantation. RESULTS: In the baseline condition, the stretch reflex resulted in a synchronous increase in spectral EMG power in both the agonist and the antagonist muscles. The mean correlation coefficient between agonist and antagonist muscles was 0.948 (SD = 0.034), and the mean time lag was 4.64 ms (SD = 1.84 ms). After intrathecal administration of baclofen, a dramatic decrease in the correlation coefficient between agonist and antagonists (mean value = 0.342) during voluntary contraction was observed. This corresponded to a significant reduction of tone and spasticity in all four limbs, and reduction of the Ashworth score by 2 points on average. CONCLUSION: After intrathecal baclofen administration, we observed a significant decrease in the co-contraction pattern typically associated with upper motor neuron spasticity. This was evident clinically and was quantitatively expressed by the significantly decreased degree of coupling in EMG activity of agonist/antagonist muscles. Although a relatively small sample was investigated in this study, we were able to demonstrate the efficacy of this procedure in restoring selective activation of agonists during voluntary contraction. This is one of the prerequisites of an improvement of motor function in patients with spasticity.