Central post-stroke pain (CPSP) is a chronic pain resulting from cerebrovascular accidents in somatosensory pathways including thalamus, and clinical findings suggest that the mechanism involves abnormal brain activity and network reorganization due to maladaptive plasticity. Neuromodulation technique, such as repetitive transcranial magnetic stimulation (rTMS) targeting primary motor cortex (M1) have shown promise for the treatment of intractable pain, and high-frequency rTMS (Hf-rTMS) exhibits analgesic effects compared to low-frequency rTMS (Lf-rTMS), while its analgesic mechanism is unknown. Here, we attempted to elucidate this mechanism by evaluating tactile functional magnetic resonance imaging (fMRI) altered by Hf- and Lf-rTMS in our established CPSP model monkey. Consistent to findings from patients, CPSP model monkeys showed an increase in pain threshold after Hf-rTMS, which indicates analgesic effect, but no change after Lf-rTMS. Hf-rTMS, compared to Lf-rTMS, produced enhanced tactile-evoked fMRI signals as well as in M1 but also in somatosensory processing regions such as primary somatosensory and midcingulate cortices. Secondary somatosensory cortex, however, was less active after Hf-rTMS related to Lf-rTMS, suggesting that activation in this region is involved in pain perception and highlighting its involvement in rTMS-induced analgesic mechanisms. Understanding mechanisms of pathophysiology and analgesic following rTMS are critical for optimizing interventions and advancing translational approaches for human CPSP patients.