Background & Aims

Spinal Cord Stimulation (SCS) is a successful neuromodulation therapy for chronic pain patients. Traditionally, the mechanisms of action of SCS rely on the gate control theory. Nowadays, the descending inhibitory pathway and other supraspinal structures are thought to be involved. Conditioned Pain Modulation (CPM) can be used to measure the endogenous pain inhibitory capacity. In CPM a first painful stimulus (test stimulus, TS) is inhibited by applying a second painful stimulus (conditioning stimulus, CS). Here we assess how cortical responses elicited by a painful stimulus are affected by CPM in a patient who receives both tonic and burst SCS.

Methods

The patient (40 yo woman) has post spinal surgery syndrome for 5 years and SCS for 2 years. She has a moderate effect of SCS and rates her pain, despite SCS, on average as 5/10. The patient had 2 measurement sessions (burst and tonic SCS) with a 1 week interval in between. We used magneto-encephalography (275-channel CTF MEG) to record evoked cortical responses to the painful TS. TS were generated by a constant current stimulator. The CS consisted of an ice pack (-10 C) on the forearm. CPM recordings consisted of three blocks: painful TS before, during and after application of the CS. The anterior cingulate and primary somatosensory cortices were defined as regions of interest. Averaged evoked responses for each CPM condition per SCS paradigm in each defined region were analyzed.

Results

Ratings of the painful TS were not different between burst and tonic SCS, nor before, during and after Ratings of the painful TS did not vary between burst and tonic SCS, nor before, during and after CPM. In the anterior cingulate cortex, the amplitude of the evoked response was reduced during CPM under both tonic and burst SCS, with the most pronounced reduction occurring under tonic SCS. In the primary somatosensory cortices, the amplitude of the evoked response was reduced during CPM under tonic SCS, while no reduction was observed under burst SCS.

Conclusions

Less efficient CPM in chronic pain patients could be cause or effect of chronic pain, and it is unclear whether CPM can be restored by (effective) SCS. CPM effect is most often measured using pain ratings. In our patient CPM did not decrease the pain rating of the TS, but the amplitude reduction during CPM suggests its inhibitory effects in this patient. During CPM the reduction in amplitude of evoked response in the anterior cingulate cortex was similar under both SCS paradigms, whereas in the primary somatosensory cortices only tonic SCS reduced the evoked response amplitude during CPM.

References

Brock C et al., Brain activity in rectosigmoid pain: Unravelling conditioning pain modulatory pathways. Clinical neurophysiology, 2012; 123(4): 829-837.
2.Cruccu G, Aminoff MJ, Curio G, et al. Recommendations for the clinical use of somatosensory-evoked potentials. Clinical Neurophysiology, 2008; 119(8): 1705-1719.
3.Pickering G, Pereira B et al. Impaired modulation of pain in patients with postherpetic neuralgia. Pain Res Manage, 2014; 19(1): e19-e23.
4.Ramaswamy S and Wodehouse T. Conditioned pain modulation-a comprehensive review. Clinical Neurophysiology, 2021; 51(3): 197-208

Presenting Author

Laurien Reinders

Poster Authors

Laurien Reinders

MSc

Erasmus MC

Lead Author

Frank Huygen

MD

Erasmus MC

Lead Author

Cecile de Vos

MSc

Erasmus MC

Lead Author

Topics

  • Pain Imaging