Abstract
Spinal cord stimulation via epidurally implanted electrodes is a common treatment for medically intractable neuropathic pain of different origins. Because tonic electrical stimulation evokes paresthesias over the painful area, this method has never been proven scientifically to be superior to placebo. Recently, burst stimulation (in which closely spaced, high-frequency stimuli are delivered to the spinal cord) has been developed, which does not generate paresthesias.
A randomized placebo controlled trail in which we compared three stimulation paradigms (burst, tonic, and placebo) was performed on 15 consecutive pain patients. In contrast to tonic stimulation, burst stimulation was able to provide pain relief without the generation of paresthesias, permitting us to use a double-blinded placebo controlled approach. Primary outcome measures were visual analog scale pain scores for back pain, limb pain, and general pain. Secondary outcome measures included the pain vigilance and awareness questionnaire, which is used to measure attention to pain and pain changes, and visual analog scale of the worst, least, and momentary pain. In a subgroup of five patients, a source-localized electroencephalogram was performed under four conditions: baseline, tonic, burst, and placebo stimulation.
Burst stimulation was able to improve back, limb, and general pain by 51%, 53%, and 55% and tonic stimulation by 30%, 52%, and 31%, respectively. Pain now, least, and worst pain were improved by 50%, 73%, and 36% by burst stimulation, respectively, and 26%, 46%, and 13% by tonic stimulation. In comparison with placebo, burst, corrected for multiple comparisons, was significantly better for all measurements. However, the greatest differences were obtained in the pain vigilance and awareness questionnaire measurements: burst improved the attention to pain and pain changes, whereas tonic and placebo worsened these measurements. The analysis via encephalogram demonstrates burst stimulation activates the dorsal anterior cingulate and right dorsolateral prefrontal cortex more than tonic stimulation.
The differences between tonic and burst stimulation are likely attributable to a more-selective modulation of the medial pain pathways by burst stimulation, as shown by the activation of the dorsal anterior cingulate cortex.