The clinical effect and molecular mechanism of transcranial direct current stimulation treatment for incomplete cervical spinal cord injury / 中华物理医学与康复杂志

ABSTRACT

Objective:To investigate the clinical effect of transcranial direct current stimulation (tDCS) in treating incomplete cervical spinal cord injury, and to explore the possibility of a relationship between the expression of long chain non-coding RNA (LncRNA) and neurological recovery after such injury.Methods:Forty-six patients suffering from incomplete cervical spinal cord injury were randomly divided into a tDCS group and a control group, each of 23. The American Spinal Cord Injury Association (ASIA) standard, a functional independence scale (FIM) and the modified Barthel index (MBI) were used to evaluate functional changes before and after 8 weeks of treatment. The neurophysiological evaluations of the spinal cord injury were in terms of somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs). The expression of the LncRNA-MALAT1, MIAT, GPNMB, LILRB4 and SCD1 genes was quantified before and after the intervention. The relationship between the expression of LncRNA and MBI was then further explored.Results:The average central motor conduction time (CMCT) of the MEPs and the average central conduction time (CTT) of SEPs in the tDCS group were significantly lower than those before treatment and significantly faster than those of the control group after the treatment. The relative expression levels of LncRNA-MALAT1 and MIAT in the tDCS group were significantly higher than those before treatment and among the control group after the intervention. However, no significant differences were observed in the average expression of the LncRNA-GPNMB, LILRB4 or SCD1 genes. After tDCS the relative expression levels of LncRNA-MALAT1 and MIAT were positively and significantly correlated with MBI scores.Conclusions:tDCS can promote the recovery of motor and sensory functions after incomplete cervical spinal cord injury. The underlying mechanism may lie in the up-regulation of LncRNA-MALAT1 and MIAT expression.