Abstract
Background and Aims: Pain modulation can be evaluated psychophysically in different dimensions; conditioned pain modulation (CPM) expressing spatial filtering, and offset analgesia (OA) expressing temporal filtering. We examined the inter-relations and possible accumulation effect between these paradigms, asking whether they are sub-served by a single mechanism.
Methods: 29 healthy subjects (14 women) underwent 4 series of thermal stimuli, in random order: OA evoked by three-temperature stimulus train (T1 = 49, T2 = 50, T3 = 49°C; 5s, 5s, 20s respectively), 30 s constant 49°C stimulus (‘control train’) and two CPM paradigms (30 s of OA or constant 49°C stimulus given alone and simultaneously with immersion of the other hand in hot water). Differences in pain rating between (i) T1 and T3 in the OA train, and (ii) before and during immersion for the CPM paradigms, both versus the ‘control train’, were taken as OA and CPM effects, respectively.
Results: A correlation was found between OA and CPM (r = 0.59, P = 0.000) at the maximum OA effect. For simultaneous activation of OA+CPM a nearly significant additive effect was found (P = 0.056).
Conclusions: Correlation between OA and CPM suggests similar mechanism for the two. However, accumulation of the magnitude of pain inhibition implies some differences. It might be that while both activate brainstem analgesia centers, the spino-bulbar-spinal tonic pain inhibition evoked via CPM, is further improved by the short offset stimulus possibly evoking a phasic activity in the cerebral pain gate-keepers amygdala and accumbens. The ability to augment pain inhibition by simple means of stimulus manipulation is of importance in future pain treatment.
Methods: 29 healthy subjects (14 women) underwent 4 series of thermal stimuli, in random order: OA evoked by three-temperature stimulus train (T1 = 49, T2 = 50, T3 = 49°C; 5s, 5s, 20s respectively), 30 s constant 49°C stimulus (‘control train’) and two CPM paradigms (30 s of OA or constant 49°C stimulus given alone and simultaneously with immersion of the other hand in hot water). Differences in pain rating between (i) T1 and T3 in the OA train, and (ii) before and during immersion for the CPM paradigms, both versus the ‘control train’, were taken as OA and CPM effects, respectively.
Results: A correlation was found between OA and CPM (r = 0.59, P = 0.000) at the maximum OA effect. For simultaneous activation of OA+CPM a nearly significant additive effect was found (P = 0.056).
Conclusions: Correlation between OA and CPM suggests similar mechanism for the two. However, accumulation of the magnitude of pain inhibition implies some differences. It might be that while both activate brainstem analgesia centers, the spino-bulbar-spinal tonic pain inhibition evoked via CPM, is further improved by the short offset stimulus possibly evoking a phasic activity in the cerebral pain gate-keepers amygdala and accumbens. The ability to augment pain inhibition by simple means of stimulus manipulation is of importance in future pain treatment.
| Original language | English |
|---|---|
| Pages | 200-200 |
| Number of pages | 1 |
| DOIs | |
| State | Published - 2011 |