Many studies have investigated the changes of spinal neuronal networks in patients with cortico-subcortical or spinal lesions occurring during adulthood. In contrast, little is known about modifications of transmission within spinal networks implied in motor control for patients suffering from perinatal lesions. In the present series of experiments, we have investigated, in adult patients with cerebral palsy who suffered cerebral damage in the perinatal period, the efficacy of transmission within four spinal networks known for exhibiting pathophysiological changes following a central nervous system lesion occurring in adulthood. These are presynaptic Ia inhibition, post-activation depression, disynaptic reciprocal Ia inhibition and propriospinally-mediated Group I and Group II facilitations. In 28 patients with cerebral palsy and 35 age-matched healthy subjects we were able to show that: (i) disynaptic reciprocal Ia inhibition is intact in patients with cerebral palsy; (ii) both presynaptic Ia inhibition and post-activation depression are impaired in patients with cerebral palsy; and (iii) propriospinally-mediated Group I facilitation is undamaged in patients with cerebral palsy, whereas Group II facilitation is strongly enhanced. Only diminished post-activation depression was highly correlated to the severity of spasticity. Differences in the spinal transmission between patients with cerebral palsy and patients who suffered neuronal damage in adulthood are discussed.

Non-technical summary Transcranial direct current stimulation (tDCS) induces modifications of motor cortex excitability depending on the polarity. However, the impact of tDCS applied to lower limb motor cortex on lumbar spinal network excitability has been unknown up to now. This study was performed in order to assess the effects of anodal tDCS compared to sham stimulation on three lumbar spinal circuits, namely reciprocal Ia inhibition, homonymous recurrent inhibition and presynaptic Ia inhibition, in healthy subjects. The results indicate that anodal tDCS modifies the behaviour of 2 of the 3 spinal circuits studied. Effects of anodal tDCS when applied over lower limb motor cortex should be considered with regard not only to cortical circuits but also to spinal motor circuits. The results also suggest that the effects of anodal tDCS on lumbar spinal circuits are similar to those observed during voluntary muscle co-contractions. AbstractIn recent years, two techniques have become available for the non-invasive stimulation of human motor cortex: transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS). The effects of TMS and tDCS when applied over motor cortex should be considered with regard not only to cortical circuits but also to spinal motor circuits. The different modes of action and specificity of TMS and tDCS suggest that their effects on spinal network excitability may be different from that in the cortex. Until now, the effects of tDCS on lumbar spinal network excitability have never been studied. In this series of experiments, on healthy subjects, we studied the effects of anodal tDCS over the lower limb motor cortex on (i) reciprocal Ia inhibition projecting from the tibialis anterior muscle (TA) to the soleus (SOL), (ii) presynaptic inhibition of SOL Ia terminals, (iii) homonymous SOL recurrent inhibition, and (iv) SOL H-reflex recruitment curves. The results show that anodal tDCS decreases reciprocal Ia inhibition, increases recurrent inhibition and induces no modification of presynaptic inhibition of SOL Ia terminals and of SOL-H reflex recruitment curves. Our results indicate therefore that the effects of tDCS are the opposite of those previously described for TMS on spinal network excitability. They also indicate that anodal tDCS induces effects on spinal network excitability similar to those observed during co-contraction suggesting that anodal tDCS activates descending corticospinal projections mainly involved in co-contractions.

Transcranial direct current stimulation (tDCS) when applied over the motor cortex, modulates excitability dependent on the current polarity. The impact of this cortical modulation on spinal cord network excitability has rarely been studied. In this series of experiments, performed in healthy subjects, we show that anodal tDCS increases disynaptic inhibition directed from extensor carpi radialis (ECR) to flexor carpi radialis (FCR) with no modification of presynaptic inhibition of FCR Ia terminals and FCR H-reflex recruitment curves. We also show that cathodal tDCS does not modify spinal network excitability. Our results suggest that the increase of disynaptic inhibition observed during anodal tDCS relies on an increase of disynaptic interneuron excitability and that tDCS over the motor cortex in human subjects induces effects on spinal network excitability. Our results highlight the fact that the effects of tDCS should be considered in regard to spinal motor circuits and not only to cortical circuits.