Modulation of spinal and cortical neuronal excitability by transcutaneous spinal direct current stimulation in restless legs syndrome.

STUDY

OBJECTIVES

This study explored the changes in cortical and spinal excitability in patients with restless legs syndrome (RLS) induced by transcutaneous spinal cord direct current stimulation (tsDCS), thereby revealing the neural electrophysiological mechanism underlying tsDCS-mediated improvements in RLS symptoms.

METHODS

Thirty patients with RLS were randomly assigned to active RLS-tsDCS group or sham stimulation group for 2 consecutive weeks. Symptom severity and sleep quality were assessed using the International Restless Legs Syndrome Rating Scale (IRLS-RS) and the Pittsburgh Sleep Quality Index (PSQI). Electrophysiological parameters, including the H-reflex from the gastrocnemius muscle and transcranial magnetic stimulation-induced motor evoked potentials (TMS-MEP), were performed to assess changes in cortical and spinal excitability before and after treatment.

RESULTS

The main analysis showed that the improvement in IRLS-RS score in the RLS-tsDCS group (Δ = 12.20 ± 5.68) was significantly greater than that in the sham stimulation group (Δ = 1.20 ± 3.59, t = 6.337, p = 0.000). PSQI score improvement was greater in the RLS-tsDCS group (Δ = 4.60 ± 2.72) compared to the sham stimulation group (Δ = 0.40 ± 2.26; t = 4.598, p < 0.001). After 14 days tsDCS treatments, the RLS-tsDCS group exhibited a significantly prolonged cortical silent period, a significant increase in MEP amplitude after 15min rest during movement tasks, and a significant reduction in the paired H-reflex ratio (H2/H1) in the lower limbs compared to baseline. No significant changes were observed in any neurophysiological parameters in the sham stimulation group.

CONCLUSION

Our research results indicated that anodal tsDCS can significantly improve the clinical symptoms of RLS patients and reduce the IRLS-RS and PSQI scores. This may be achieved through tsDCS enhancing the cortical inhibitory function and thereby reducing spinal neuronal excitability.