Table 1_Transspinal direct current stimulation as targeted therapy to increase motor neuron output and restore inhibition in human spinal cord injury.docx

IntroductionIn this clinical trial, we evaluated changes in the output of motoneurons and spinal inhibitory mechanisms across multiple spinal segments before and after a series of transspinal direct current stimulation (tsDCS) sessions in humans with and without spinal cord injury (SCI).
MethodsTen people with chronic SCI and ten healthy participants received daily tsDCS over the low thoracic area while supine with an average stimulation intensity of 2.28 ± 0.02 mA for one hour. Participants with SCI and healthy subjects participated in an average of 15 sessions and 10 sessions, respectively. One day before and 1–2 days after cessation of stimulation sessions, we evaluated the recruitment input–output curves of transspinal evoked potentials (TEPs) and TEPs homosynaptic and postactivation depression in response to low frequency and paired transspinal stimuli.
ResultsWe found significant changes in the spinal motor output for 10/16 muscles in the American Spinal Injury Association (ASIA) Impairment Scale (AIS) A-B injury, 8/16 muscles in the AIS D, and 10/16 muscles in healthy subjects with facilitation or inhibition to be muscle-dependent. Facilitation was exerted mostly to distal muscles and inhibition to proximal hip muscles. TEPs homosynaptic depression at baseline was similar across subject groups, while TEPs postactivation depression was of lesser strength in the right soleus and medial gastrocnemius in AIS A-B compared to healthy subjects. tsDCS potentiated TEPs postactivation depression of the right soleus and left peroneus longus muscles in AIS A-B but remained unchanged in AIS D and healthy subjects. TEPs homosynaptic depression remained unchanged in all subject groups.
DiscussionThis study showed that tsDCS alters the net motor output across multiple spinal segments, potentiates postactivation depression in AIS A-B, and does not affect homosynaptic inhibition in AIS D and healthy subjects. These results provide the first systematic support for tsDCS as a therapeutic intervention in SCI.