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We aimed to disentangle the proportional contributions of upper and lower motor neuron dysfunction to motor impairment in children with spina bifida. We enrolled 42 children (mean age, 11.2 years; standard deviation, 2.8 years) with spina bifida and 36 control children (mean age, 11.4 years; standard deviation, 2.6 years). Motor impairment was graded to severity scales in children with spina bifida. We recorded motor evoked potentials after transcranial and lumbosacral magnetic stimulation and compound muscle action potentials after electric nerve stimulation. Regarding lower motor neuron function, severely impaired children with spina bifida demonstrated smaller compound muscle action potential areas and lumbosacral motor evoked potential areas than control children; mildly impaired children hardly differed from control children. Compound muscle action potential latencies and lumbosacral motor evoked potential latencies did not differ between children with spina bifida and control children. Regarding upper motor neuron function, children with spina bifida demonstrated smaller transcranial motor evoked potential areas and longer central motor conduction times than control children. The smallest motor evoked potential areas and longest central motor conduction times were observed in severely impaired children. In children with spina bifida, the contribution of upper motor neuron dysfunction to motor impairment is more considerable than expected from clinical neurologic examination., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Searching for a tool to quantify motor impairment in spina bifida, transcranial and lumbar magnetic stimulation were applied in affected newborn infants. Lumbar magnetic stimulation resulted in motor evoked potentials in both the quadriceps muscle and the tibialis anterior muscle in most (11/13) subjects. However, transcranial magnetic stimulation did not lead to any response at all. A strong left-to-right correlation existed for amplitude and for latency. Lumbar magnetic stimulation proved to be applicable in newborn infants with spina bifida. Although current concepts regarding spina bifida suppose lower motor neuron dysfunction, the results of this study suggest that lower motor neuron integrity is at least partly preserved after birth. Transcranial magnetic stimulation does not lead to responses in healthy newborn infants because of insufficient synaptogenesis, myelinogenesis, and axon thickness. Therefore, conclusions on upper motor neuron function in spina bifida cannot be drawn. To what extent the method used here can achieve the aim of quantifying motor impairment is a matter of further study.