Abstract
ObjectivePhantom limb pain (PLP) is notoriously difficult to treat, partly due to an incomplete understanding of PLP‐related disease mechanisms. Noninvasive brain stimulation (NIBS) is used to modulate plasticity in various neuropathological diseases, including chronic pain. Although NIBS can alleviate neuropathic pain (including PLP), both disease and treatment mechanisms remain tenuous. Insight into the mechanisms underlying both PLP and NIBS‐induced PLP relief is needed for future implementation of such treatment and generalization to related conditions.MethodsWe used a within‐participants, double‐blind, and sham‐controlled design to alleviate PLP via task‐concurrent NIBS over the primary sensorimotor missing hand cortex (S1/M1). To specifically influence missing hand signal processing, amputees performed phantom hand movements during anodal transcranial direct current stimulation. Brain activity was monitored using neuroimaging during and after NIBS. PLP ratings were obtained throughout the week after stimulation.ResultsA single session of intervention NIBS significantly relieved PLP, with effects lasting at least 1 week. PLP relief associated with reduced activity in the S1/M1 missing hand cortex after stimulation. Critically, PLP relief and reduced S1/M1 activity correlated with preceding activity changes during stimulation in the mid‐ and posterior insula and secondary somatosensory cortex (S2).InterpretationThe observed correlation between PLP relief and decreased S1/M1 activity confirms our previous findings linking PLP with increased S1/M1 activity. Our results further highlight the driving role of the mid‐ and posterior insula, as well as S2, in modulating PLP. Lastly, our novel PLP intervention using task‐concurrent NIBS opens new avenues for developing treatment for PLP and related pain conditions. ANN NEUROL 2019;85:59–73.
Highlights
Noninvasive brain stimulation (NIBS) Prevents Movement-Induced Phantom limb pain (PLP) Increases Immediately after stimulation offset, PLP significantly increased in the sham condition (1-sample t[13] = 4.81, p < 0.001, d = 1.29), consistent with reports showing that phantom hand movements can increase PLP.[37]
We found that following stimulation, FIGURE 5: Increased insular activity during stimulation is associated with downregulation of sensorimotor phantom hand activity after stimulation. (A) To assess what neural processes during intervention stimulation predicted the subsequent downregulation of sensorimotor cortex activity, we carried out a whole-brain regression analysis
PLP relief correlated with reduced S1/M1 phantom hand activity after intervention stimulation
Summary
Phantom limb pain (PLP) is notoriously difficult to treat, partly due to an incomplete understanding of PLPrelated disease mechanisms. To influence information processing of peripheral missing hand signals (previously associated with PLP), we instructed amputees to execute phantom hand movements during tDCS.[27,29] We applied excitatory tDCS over the S1/M1 missing hand cortex, as previously implemented for related neuropathic pain conditions.[5,11,12] Neuroimaging was used during and after tDCS to evaluate the neural underpinnings of PLP relief
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