Altered cognitive-emotional networks in chronic pain: the modulatory role of dopamine
Chronic pain shifts brain processing from nociceptive to cognitive-emotional brain circuits, with altered fronto-striatal functional connectivity as a pathogenetic factor. In addition, the mesolimbic dopamine system is dysfunctional in chronic pain. Considering that dopamine acts not only as a neurotransmitter but also as a neuromodulator, dysfunctional dopamine systems might fuel altered fronto-striatal functional connectivity, augmenting pain chronification. This hypothesis will be tested in two studies with pharmacological functional magnetic resonance imaging, aiming revealing underlying mechanisms of altered cognitive-emotional networks in chronic pain.
Inter-subject variability of the endogenous analgesia expressed by conditioned pain modulation and phenotypical characterization of the nociceptive profile in humans. A cortical-brainstem connectivity study
The conditioned pain modulation (CPM) represents a physiological mechanism to control pain incoming from spinal and trigeminal nociceptive stimulation. In humans, defective functioning of CPM has been demonstrated in several pain conditions, and hypothesized as a possible predictor of pain development, but also as possible target for pain treatment. Several studies suggested a key role of brainstem structures in CPM. However, the exact cortical-brainstem functional connectivity pattern, including the inter-subject variability of CPM, remain undetermined. This fMRI project aims to investigate those aspects of CPM using effective connectivity analysis techniques and temporal summation of pain as test stimulus.
Disentangling pain and fatigue: a clinical and neurocognitive approach
Pain and fatigue are strongly interrelated. Here, I will use a clinical and neurocognitive approach to identify the unique correlates of pain and fatigue. Combining longitudinal data with large clinical databases, I can identify which brain networks independently relate to improvements in pain and fatigue following cognitive behavioural therapy (CBT), which variables (e.g., psychosocial) independently predict improvement in pain and fatigue after CBT, and to what extent pain and fatigue independently relate to cognitive task performance. The results will provide crucial knowledge regarding the need to target both pain and fatigue in pain patients to eventually increase treatment success.
Phantom Motor Execution as treatment of Phantom Limb Pain: Neural correlates
Traumatic events such as amputations or nerve injuries can result in neuropathic pain. One of such pains is Phantom Limb Pain (PLP), which can considerably hinder patients’ quality of life. Dr. Ortiz Catalan developed a novel PLP treatment, namely Phantom Motor Execution (PME). PME relies in decoding phantom motor volition via myoelectric pattern recognition, while providing real-time feedback through virtual and augmented reality. Clinical evaluations have shown PME effective in patients with chronic intractable PLP. In this project, we aim to elucidate underlying mechanisms of chronic pain by performing brain imagining studies on patients undergoing PME and control therapies.
Can training increase reporting accuracy and study power in human pain trials?
Recent findings suggest that training subjects to report their pain more accurately could increase the assay sensitivity of pain trials. The aim of the current project is to confirm our recent findings in an experimental model of an analgesic trial.
Half of study subjects (healthy volunteers) will be trained before enrollment into a double-blind, placebo-controlled, crossover experimental pain trial of ibuprofen. If confirmed and implemented, our training approach could increase the low assay-sensitivity of analgesic trials.
Rheumatoid Arthritis Pain Inhibitory Descending pathways – RAPID
Rheumatoid Arthritis (RA) is a chronic inflammatory disorder affecting primarily small and middle-sized joints. Pain intensity is not well correlated with disease activity and pain may persist even when biological and clinical remission seems achieved, therefore suggesting central pain sensitization mechanisms in RA.
A better analysis of endogenous pain inhibitory pathways in RA patients is needed. Beyond that, understanding how these mechanisms are changing after treatments in responding and non-responding patients may improve pain management in RA patients.