Abstract
Neurophysiological changes that involve activity-dependent neuroplasticity mechanisms via repeated stimulation and locomotor training are not commonly employed in research even though combination of interventions is a common clinical practice. In this randomized clinical trial, we established neurophysiological changes when transcranial magnetic stimulation (TMS) of the motor cortex was paired with transcutaneous thoracolumbar spinal (transspinal) stimulation in human spinal cord injury (SCI) delivered during locomotor training. We hypothesized that TMS delivered before transspinal (TMS-transspinal) stimulation promotes functional reorganization of spinal networks during stepping. In this protocol, TMS-induced corticospinal volleys arrive at the spinal cord at a sufficient time to interact with transspinal stimulation induced depolarization of alpha motoneurons over multiple spinal segments. We further hypothesized that TMS delivered after transspinal (transspinal-TMS) stimulation induces less pronounced effects. In this protocol, transspinal stimulation is delivered at time that allows transspinal stimulation induced action potentials to arrive at the motor cortex and affect descending motor volleys at the site of their origin. Fourteen individuals with motor incomplete and complete SCI participated in at least 25 sessions. Both stimulation protocols were delivered during the stance phase of the less impaired leg. Each training session consisted of 240 paired stimuli delivered over 10-min blocks. In transspinal-TMS, the left soleus H-reflex increased during the stance-phase and the right soleus H-reflex decreased at mid-swing. In TMS-transspinal no significant changes were found. When soleus H-reflexes were grouped based on the TMS-targeted limb, transspinal-TMS and locomotor training promoted H-reflex depression at swing phase, while TMS-transspinal and locomotor training resulted in facilitation of the soleus H-reflex at stance phase of the step cycle. Furthermore, both transspinal-TMS and TMS-transspinal paired-associative stimulation (PAS) and locomotor training promoted a more physiological modulation of motor activity and thus depolarization of motoneurons during assisted stepping. Our findings support that targeted non-invasive stimulation of corticospinal and spinal neuronal pathways coupled with locomotor training produce neurophysiological changes beneficial to stepping in humans with varying deficits of sensorimotor function after SCI.
Highlights
The pathological reorganization of spinal networks and disruption of supraspinal inputs after spinal cord injury (SCI) impairs modulation of muscle spindle reflexes which are partly responsible for the coordinated muscle activity during walking [1,2,3,4,5,6]
Fourteen individuals (3 females, 11 males) between the ages of 21 and 71 years of age with chronic (>12 months) SCI participated in this study (Table 1)
The level of injury ranged from C4 to T11 and based on the Association Impairment Scale (AIS) scale, 5 individuals had a neurological deficit classified as AIS D, 6 were AIS C, 1 was AIS B, and 2 were AIS A (Table 1)
Summary
The pathological reorganization of spinal networks and disruption of supraspinal inputs after spinal cord injury (SCI) impairs modulation of muscle spindle reflexes which are partly responsible for the coordinated muscle activity during walking [1,2,3,4,5,6]. Paired associative stimulation (PAS) of two different neural sites such as transcranial magnetic stimulation (TMS) of motor cortices (M1) or TMS of M1 paired with peripheral electrical nerve stimulation produces significant neuroplasticity [16, 17] This plasticity shares similar neuronal mechanisms to that of motor learning and exercise [18,19,20]. We have recently shown that TEPs summate with the homonymous MEPs and soleus H-reflex in the surface electromyogram (EMG) [26, 27] Based on these findings we theorize that transspinal stimulation can activate dormant spinal networks and increase their sensitivity to residual supraspinal and sensory inputs enabling neuronal integration of signals after SCI in humans similar to that shown in anesthetized neurologically intact monkeys [28]
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