Mechanical hyperalgesia may develop following tissue inflammation or nerve injury. Basically, peripheral sensitization leads to primary hyperalgesia at the site of injury, whereas secondary hyperalgesia occurs in the surrounding tissue and results from central sensitization. The present study focuses on the cerebral processing of secondary mechanical hyperalgesia. Primary (S1) and secondary (S2) somatosensory cortices and posterior parietal cortex (PPC) are thought to be involved in cerebral processing of noxious mechanical stimuli. However, their response pattern in the presence of mechanical hyperalgesia remains to be elucidated. Therefore, we investigated the cortical processing of secondary mechanical hyperalgesia using magnetoencephalography (MEG). In 12 healthy subjects mechanoinsensitive c-nociceptors were repetitively stimulated using transcutaneously applied high-current electrical stimulation. This procedure resulted in stable areas of secondary mechanical hyperalgesia. Pin-prick stimuli were applied inside and outside the hyperalgesic area. The corresponding cortical activations were detected and quantified using MEG. We found pin-prick-induced sequential activation of contralateral S1, PPC and S2 as well as activation of ipsilateral S2 during both pin-prick hyperalgesia and normal pin-prick pain. During pin-prick hyperalgesia significantly higher activation was detected in contralateral PPC and bilateral S2 but not in S1 compared to normal pin-prick pain. In contrast to PPC, we found a significant correlation between increases of magnetic field strengths within bilateral S2 with the increase of pain ratings during pin-prick hyperalgesia. We conclude that the S2 cortex may be involved for the processing of secondary mechanical hyperalgesia in the human brain. PPC activation may reflect higher attentional processing during mechanical hyperalgesia.