Introduction Chronic pain is an increasing problem in terms of prevalence and disease-related costs. Due to its complexity, it is difficult to treat. Spinal cord stimulation (SCS) is a neurostimulation therapy with a relatively good success rate for patients with severe, intractable chronic pain. The mechanisms of action (MOAs) of SCS are considered to rely on spinal and supraspinal mechanisms. It has been suggested that newer SCS paradigms, such as burst SCS, may act through different MOAs than the traditional tonic SCS paradigm. Tonic and burst SCS are both postulated to act on the lateral pain pathway, which is associated with the location and character of a stimulus, whereas burst SCS is postulated to additionally act on the medial pain pathway, which is associated with the emotional/attentional processing of a stimulus. Somatosensory evoked responses (SERs) can be used to evaluate the processing of somatosensory stimuli and may aid in the unraveling of the MOAs of SCS. Aim The aim of this thesis is to assess how burst and tonic SCS affect the supraspinal SERs elicited by non-painful transcutaneous electrical stimulation of the tibial nerve as well as of the median nerve. The two distinct SERs are evaluated using magnetoencephalography (MEG). Methods 26 chronic pain patients treated with SCS underwent MEG sessions after receiving tonic and burst SCS for one week. Four of these patients additionally underwent a MEG session before SCS treatment. During each session, approximately 200 non-painful electrical stimuli were applied to the median nerve as well as to the tibial nerve to elicit SERs. The SERs were compared in various cortical and subcortical regions of interest (ROIs). The following comparisons were made: 1) SERs in chronic pain patients before SCS implantation versus SERs in the same individuals during SCS, 2) SERs elicited by tibial nerve stimulation versus SERs elicited by median nerve stimulation, 3) SERs during tonic SCS versus SERs during burst SCS, and 4) the SERs in four case studies of two good and two poor responders to the tonic and/or burst SCS paradigms. Results 22 patients were included for analysis. The number of patients varied among comparisons to facilitate within-patient comparisons. The results suggested an inhibitory effect of SCS on the SER elicited by tibial nerve stimulation, whereas the amplitude of the SER elicited by median nerve stimulation tended to increase during SCS. For both the SERs elicited by tibial nerve and by median nerve stimulation, the SER amplitudes were predominantly higher during burst SCS compared to tonic SCS. Differences in SER amplitude that were observed in the case studies did not correlate with pain relief. Conclusion The results suggested a spinal MOA of SCS on the SER, however, supraspinal MOAs likely play a role as well. The results did not suggest that burst SCS additionally acts on the emotional/attentional processing compared to tonic SCS. No evidence was found to support a correlation between the effect of SCS on the SER and the effect of SCS on the pain, underscoring the complexity of the relationship between somatosensory processing and pain perception in the context of SCS.