|Ph.D Student||Moont Ruth|
|Subject||'Pain Inhibits Pain' Mechanism: is Pain Modulation Simply|
Due to Distraction?
|Department||Department of Medicine||Supervisors||Professor David Yarnitsky|
|Dr. Dorit Pud|
|Full Thesis text|
The human ability to endogenously inhibit pain via supraspinal descending networks can be revealed by the 'pain inhibits pain' test paradigms when applying two concomitant remote noxious stimuli; ‘conditioned pain modulation’ (CPM). One issue that has been inadequately addressed in CPM studies is whether this phenomenon is due to a distraction effect. We hypothesized the CPM is an independent process from cognitive distraction.
Firstly, we recorded psychophysical responses to phasic noxious heat stimuli, the test pain, under visual cognitive distraction tasks and conditioning hot-water pain (CPM), both individually and simultaneously. Our findings from 1) healthy male and females and 2) healthy males expressing CPM showed that both CPM and distraction reduced subjective pain scores to a similar extent. Combining CPM and distraction further reduced pain ratings compared to CPM or distraction alone.
CPM involves spinal-bulbar-spinal neuronal loops to effect pain modulation. Nevertheless, there is some top-down control from the cortex. Secondly, we aimed to investigate the interplay of areas involved in the perception of pain and those involved in controlling descending inhibition. This was the first study to observe temporal and spatial changes in cortical activations under CPM. We examined brief consecutive time windows using EEG-based sLORETA in male healthy subjects capable of expressing CPM, to determine dynamic changes in localized cortical potentials evoked by the test pain under CPM. We found a CPM effect characterized by an initial increased activation in the OFC and amygdala followed by reduced activations in pain network areas associated with perception and processing. The increases in brain activity were specifically associated with greater reductions in the subjective pain scores under CPM. This suggests that the OFC increases its activity in parallel with subjective pain analgesia under CPM and that this increased activity occurs prior to reductions in activations of pain sensory and processing areas. We conclude that the OFC is likely to play a key role in inhibition of pain under CPM.
Thirdly, we compared the dynamic cortical activation pattern seen under CPM directly with that under distraction. Distraction caused a different extent of cortical activation compared to CPM; greater early activation of frontal areas, yet lesser reduction in pain sensory and processing areas. Based on the additive effect of CPM and distraction on pain inhibition, the cases of no distraction despite CPM, and the different patterns of cortical activity changes under the two manipulations, we suggest that CPM acts independently from distraction.