Background & Aims
Homeostatic plasticity (HP) prevents excessive neuronal excitability and can be investigated in humans, using two blocks of transcranial direct current stimulation (tDCS). In healthy subjects, an HP response can be demonstrated by reduced motor-evoked potentials after two blocks of excitatory tDCS, reflecting an increased probability of long-term depression (LTD)-like motor system plasticity This HP response is lacking in chronic and experimental pain, and it has been suggested that HP may play a role in pain development or persistence. This study aims to investigate if the cortical nociceptive response by contact heat stimulation (CHEPs) is regulated by HP mechanisms. For this, HP was induced in the primary motor (M1) or sensory cortices (S1) and evaluated with CHEPs. Additionally, a capsaicin-pain model was used to test whether the HP response is impaired by capsaicin-induced pain.
Methods
Ten healthy individuals participated in four tDCS sessions (Anodal-S1, Anodal-M1, Anodal-S1-Capsaicin, and Anodal-S1-Sham ). For every session, a capsaicin or placebo patch was applied to the right hand and the pain intensity was scored on a visual analogue scale (VAS). HP was induced with anodal tDCS to the left M1(C3) or S1 (CP3) by applying 7 min of anodal tDCS (priming, 1 mA), followed by 5 min of anodal tDCS (testing, 1 mA), separated by a 5-min rest. The return electrode was always placed at FP2 (-1mA). The HP response was assessed through CHEPs recorded by 25 electrodes (10-20 system). CHEPs were recorded following heat stimulation at the volar forearm, with a baseline temperature of 35°C and a peak temperature of 60°C. Fifteen CHEPs were analyzed during five time points: baseline, post-patch, post-priming, post-HP, and post-HP+10 min. After data preprocessing, the negative-positive complex (N2P2) was extracted from Cz, C1, and CP1 and normalized to baseline post-patch.
Results
After 30 min post-patch, the capsaicin-induced VAS peak pain remained above 5±1.8 and 1±0.2 for placebo. A two-way repeated measures ANOVA of the N2P2 revealed no interaction, but a main effect of time for Cz (p=0.005). For electrodes CP1 and C1, there was an effect of time (p=0.002, p=0.005) but not significant for group or interaction. The Cz results show a tendency towards an increase of N2P2 at post-priming for the Anodal S1 group, which further decreases in a homeostatic-like behavior at post-HP and post-HP+10 min. This tendency is not observed for the Capsaicin group or the Sham group, where the N2P2 does not change over time. On the contrary, Anodal M1 HP induction seems to decrease the N2P2 at post-priming and continues to decrease it over time.
Conclusions
This is the first study to evaluate homeostatic plasticity regulation of nociceptive evoked potentials. Based on these preliminary findings, there is a tendency for a homeostatic-like behavior at electrode Cz after Anodal S1 HP induction, which is not seen for the Sham group or the Capsaicin group. More subjects are needed to indicate whether an HP response is observed from the nociceptive system and whether this response is impaired by the presence of pain.
References
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Presenting Author
Daniela M. Zolezzi
Poster Authors
Topics
- Mechanisms: Biological-Systems (Physiology/Anatomy)