Background & Aims
No two events are alike, yet humans display a remarkable capacity for generalizing across different situations. Recent theoretical frameworks suggest that this ability stems partly from the formation of latent memory structures that capture the inferred structure of the world. According to this ‘latent cause’ framework, organisms attempt to learn the hidden causes underlying their experiences to make predictions about unobserved or future variables (Gershman & Niv, 2012, Gershman et. al, 2013). In the context of pain, this framework suggests that the brain learns a latent cause model of pain from past experiences, which is then used to make predictions about the likelihood and intensity of future pain. Despite the success of this framework across research fields, it has yet to be applied to placebo analgesia and nocebo hyperalgesia. Our studies aim to address this gap by investigating the role of latent causes in pain modulation.
Methods
We are currently collecting behavioural (n = 96/100) and fMRI (26/55) data. Participants learn associations between visual stimuli (faces, houses) and high/low pain stimuli over multiple trials, to create latent cause representations of stimulus-pain relationships. A morph stimulus equally resembling both categories is then introduced at a 50VAS pain level. In the placebo block, the morph stimulus resembles the 40VAS low pain stimulus more; in the nocebo block, it resembles the 60VAS high pain stimulus more. We expect the identical 50VAS morph stimulus will be integrated into the more similar latent cause, which will shift the pain perception of the mixed stimuli, resembling placebo hypoalgesia or nocebo hyperalgesia respectively.
Results
Preliminary behavioural results show that mixed trial pain ratings indeed shifted towards the associated stimulus of the hypothesized latent state, despite identical stimulation across the nocebo and placebo block (p > 0.001, Cohen‘s d = 0.52). Once data collection is complete, we will fit a non-parametric Bayesian model to infer participants’ latent causes and resulting pain percepts. We will also employ representational similarity analysis to decode specific latent states from activity in the orbitofrontal cortex, fusiform face area, and parahippocampal place area.
Conclusions
Findings would suggest latent causal memory structures encoding prior pain experiences modulate current pain perception through generalization. Such effects could inform clinical leveraging of cues and expectations when treating pain.
References
S. J. Gershman, Y. Niv, Exploring a latent cause theory of classical conditioning. Learning & Behavior 40, 255-268 (2012).
S. J. Gershman, C. E. Jones, K. A. Norman, M.-H. Monfils, Y. Niv, Gradual extinction prevents the return of fear: implications for the discovery of state. Frontiers in Behavioral Neuroscience 7 (2013).
Presenting Author
Alina E. C. Panzel
Poster Authors
Alina Panzel
MSc
University Medical Center Hamburg-Eppendorf
Lead Author
Topics
- Models: Acute Pain