I am pleased to announce the defense of my doctoral thesis in Neurosciences, entitled “Individual variability in brain representations of pain control systems: toward personalized neuromodulation treatments.”
It will take place in English on Monday, December 15, 2025,
Abstract
The experience of pain arises from the interaction of sensory, cognitive and affective dimensions, such that one’s emotional state, the anticipation and the memory of pain shape our perception of noxious stimuli and constitute an integral part of the pain experience itself. This thesis aims to investigate the neural correlates of different cognitive and emotional tasks which can have an impact on pain perception, as well as to ascertain the existence of a core neural circuit which mediates this effect.
First, I sought to identify the brain areas more frequently reported as activated and/or deactivated in healthy subjects during contextual pain modulation in the existing literature. My results indicate that the antero-medial frontal cortex, the lateral prefrontal cortex and the anterior insula are often implicated in both contextual hypoalgesia and hyperalgesia. How- ever, different activity profiles could be identified during tasks inducing similar levels of hy- poalgesia: one of them grouped only studies investigating the effects of placebo treatment, another grouped tasks involving an attentional component and a third one was constituted of tasks with a self-referential component. This underscores the notion that pain modulation as a behavioral output can be sustained by very different spatiotemporal combinations of brain activity. In the second part of this thesis, I attempted to develop an fMRI-based multivariate pattern predicting contextual pain modulation in healthy subjects and to verify the existence of distinct brain activity patterns which are specific to cognitive or emotional pain modulation. A global pain modulation pattern (PMP) presented a modest linear predictive performance, with a good forced-choice accuracy to discriminate mainly between pain increase and no change. The cognitive pain modulation pattern (CPMP) presented similar linear predictive performance to the PMP, with implication of visual, sensorimotor and limbic areas, as well as areas in the frontoparietal network. Finally, the affective pain modulation pattern (APMP) presented a better predictive performance than the PMP and CPMP, with implication of sen- sorimotor, limbic and memory-related areas, as well as areas related with self-consciousness.
To sum up, we identified a partially common network of brain regions subtending both cognitive and affective pain modulation, with a partial dissociation of areas predominantly implicated in hypoalgesia and hyperalgesia. This common substrate informed an fMRI-based predictive model with a modest accuracy, but distinct brain activity profiles differentiate hy- poalgesia induced by placebo treatment, attention-related tasks and tasks with a strong self- referential component. Overall, this PhD work unveiled the existence of multiple pathways implicated in contextual pain modulation, which has the potential to inform the development of personalized treatments for chronic pain.