BACKGROUND: Antinociceptive effects of transcranial direct current stimulation (tDCS) over the primary motor cortex (M1) have been extensively studied in the past years. However, M1 does not work in isolation, but it rather interacts within a network, the so-called resting-state motor network.
OBJECTIVE: To explore the anti-nociceptive effects of a new multifocal tDCS approach administered to regions linked to the resting state motor network (network-tDCS) compared to sham tDCS.
METHODS: Healthy individuals were included in this randomized, parallel and double-blinded study comprising two consecutive interventions with 24-hr interval of either active (n = 19) or sham (n = 19) network-tDCS. Prolonged pain was induced by application of topical capsaicin on the dorsum of the hand during a 24-hr period. Assessments of corticomotor excitability (transcranial magnetic stimulation), pain ratings (numerical rating scale, NRS), skin pain sensitivity on the arm (heat and mechanical), temporal summation of pain (TSP) and conditioned pain modulation (CPM) were performed at baseline (Day1-baseline), after 25 min of capsaicin application and before the first tDCS session (Day1-post-cap), and after the second tDCS session (Day2).
RESULTS: Comparing Day2 to Day1-baseline measures, there was reduced corticomotor excitability (p < .05) and impaired CPM-effect (p < .05) after sham but not after active network-tDCS. Pain NRS ratings increased at Day2 compared to Day1-post-cap (p < .01) in both groups whereas no significant changes were found in pain sensitivity and TSP.
CONCLUSIONS: Present findings demonstrate that tDCS applied over regions linked to the resting state motor network reverts the inhibition of corticomotor excitability and CPM impairment both provoked by prolonged experimental pain for 24 hr.
SIGNIFICANCE: These findings highlight that the stimulation of the resting state motor network with multifocal tDCS may represent a potential cortical target to treat chronic pain, particularly in patients exhibiting maladaptive corticomotor excitability and impaired conditioned pain modulation effects.