Effectiveness of transcranial direct current stimulation for the management of neuropathic pain after spinal cord injury: a meta-analysis

Abstract

Objectives: To conduct a systematic review and meta-analysis to examine the effect of transcranial direct current stimulation (tDCS) on reducing neuropathic pain intensity in individuals with spinal cord injury (SCI). Methods: Medline, CINAHL, EMBASE and PsycINFO databases were searched for all relevant articles published from 1980 to November 2014. Trials were included if (i) tDCS intervention group and a placebo control group were present; (ii) at least 50% of participants in the study had an SCI and there were at least three participants; (iii) participants were aged 18 years or older; and (iv) persistent pain for at least 3 months. Studies were excluded if: (i) the tDCS intervention group was compared with an active treatment group; (ii) there was insufficient reporting detail to enable pooling of data; and (iii) it was a nonclinical trial (that is, reviews, epidemiology, basic sciences). A standardized mean difference (SMD) ± s.e. and 95% confidence interval (CI) was calculated for each outcome of interest and the results were pooled using a fixed or random effects model, as appropriate. Effect sizes were interpreted as: small 40.2, moderate 40.5, large 40.8. Results: Five studies met inclusion criteria of which four were randomized controlled trials and one was a prospective controlled trial. The pooled analysis found a significant effect of tDCS on reducing neuropathic pain after SCI post treatment (SMD = 0.510 ± 0.202; 95% CI, 0.114-0.906; Po0.012); however, this effect was not maintained at follow-up (SMD = 0.353 ± 0.272; 95% CI, − 0.179 to 0.886; Po0.194). A reduction of 1.33 units on a 10-item scale was observed post treatment. No significant adverse events were reported. Conclusion: Meta-analytic results indicate a moderate effect of tDCS in reducing neuropathic pain among individuals with SCI; however, the effect was not maintained at follow-up. A mean pooled decrease of 1.33 units on a 10-item scale was found post treatment. Several factors were implicated in the effectiveness of tDCS in reducing pain. Due to the limited number of studies and lack of follow-up, more evidence is required before treatment recommendations can be made. Spinal Cord (2015) 53, 780-785; doi:10.1038/sc.2015.118; published online 21 July 2015 INTRODUCTIONChronic neuropathic pain (NP) can occur following lesions in the somatosensory nervous system 1 and incidence rates range from~50 2,3 to 75-81%. 4,5 Several treatments have been proposed and used to manage NP, particularly pharmacological methods (for example, antidepressants, anticonvulsants, opioids). 6,7 Despite multiple pharmacological options for pain, the majority of individuals fail to find relief; the refractory nature of NP is what makes it such a difficult condition to treat and to endure. Studies have shown that refractory NP is common post SCI 8 and that few (4-6%) obtain relief over the long-term. 9 This situation has created interest in alternative neuromodulary stimulation approaches such as cranial electrotherapy stimulation, transcutaneous electrical nerve ...

Addition of transcranial direct current stimulation to quadriceps strengthening exercise in knee osteoarthritis: A pilot randomised controlled trial

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Brain Stimulation Therapy for Central Post-Stroke Pain from a Perspective of Interhemispheric Neural Network Remodeling

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Top-Down Effect of Direct Current Stimulation on the Nociceptive Response of Rats

“…Evidence suggests that anodal tDCS increases the excitability of the underlying motor cortex, whereas cathodal tDCS diminishes cortical excitability [ 12 , 29 , 30 ]. Anodal tDCS over M1 produces long-lasting therapeutic effects in chronic pain conditions, including fibromyalgia [ 31 – 33 ], central pain [ 34 , 35 ], and phantom limb pain [ 36 ]. Experimental anodal direct current stimulation (DCS) in rats has been shown to induce thermal antinociceptive effects [ 37 ] and to reverse inflammatory chronic pain [ 38 ] and chronic stress-induced pain via the inhibition of hippocampal TNFα and spinal BDNF levels [ 39 , 40 ].…”