Temporal summation of second pain (TSSP) is a phenomenon that has clinical relevance but insights into its functioning are limited. Lately, 'affective touch' (AT) has been shown to have pain relieving properties but only one study has investigated its effects on TSSP and the neural underpinnings of such interaction are unknown. In the present EEG study, thirty-six healthy participants went through three conditions where a TSSP protocol was applied in concomitance with no touch (NoT), discriminative touch (DT) and AT. A fourth no-pain no-touch condition acted as a baseline. Measures of attention during the four conditions and of pleasantness during the touch conditions were also recorded. Pain ratings were significantly lower only during the AT condition. The neural response during NoT, compared to the baseline, brought about a temporal decrease in power at delta and theta frequencies and a fronto-central increase mainly in the alpha rhythm. Adding AT to TSSP yielded, compared to NoT, a decrease in delta, theta and beta bands in midline regions at both central (Cz) and parietal (Pz) and also of gamma at Pz. Notably, DT was not associated with significant changes compared to pain alone (NoT), but a specific marked difference was found between AT and DT with the former showing a significant decrease in beta frequencies localized at Pz. While TSSP seems to be characterized by a modulation mostly of the lower frequencies, adding AT to TSSP brings a clear depression of all the major frequency bands. Additionally, the parietal beta reduction may be a biomarker of AT. Future studies can examine if such brain response can help finding a suitable intervention for TSSP-related chronic pain conditions. PERSPECTIVE: This study consolidates the idea that AT can lower pain in a TSSP paradigm and shows what are the brain (EEG) responses associated with both TSSP and TSSP modulation by AT. Given that TSSP is linked to central sensitization and that it can be used as an experimental model for chronic pain, our results pave the way for further studies into the neural mechanisms of AT-led analgesia, which can lead to future effective treatments.