The main objective of my research is to study pain - or nociception- induced central nervous system plasticity. Currently, my studies are focused on characterizing changes in nociceptive pathways that lead or contribute to hyperalgesia, and I am, thereby, particularly interested in the phenomenon of "central sensitization"; the increase responsiveness of nociceptive neurons in the central nervous system that generates widespread hyperalgesia ("secondary hyperalgesia").
After a professional experience in the artistic field I worked as a physiotherapist notably in a chronic pain centre. From 2014-2018, I conducted a PhD at UCLouvain, under the supervision of André Mouraux and Samar Hatem, with the aim of characterizing the relationship and hierarchical organization between brain areas involved in nociceptive processing such as the primary somatosensory cortex and the operculo-insular cortex. I conducted several studies combining neuromodulation techniques (such as repetitive transcranial magnetic (rTMS) or transcranial and spinal direct current stimulation (tDCS)) combined with functional neuroimaging techniques such as electroencephalography (EEG) and functional magnetic resonance imaging (fMRI). I am also collaborating with Emanuel van den Broeke to a research project investigating central and peripheral mechanisms of secondary hyperalgesia. In 2019, I joined the research team of Prof. G.D. Iannetti (UCLondon).
When we feel pain, our brain automatically locates it but also detects, through our vision, what provokes it. Thus it coordinates different sensory modalities: touch and perception of pain to monitor our body, and vision to track our environment. If vision and feeling pain are coordinated by the brain, what happens if one of these two senses is disrupted? Lieve Filbrich tries to answer that question. We want to analyse what happens at the visual level if we suffer chronic pain, and more specifically in the space that surrounds the afflicted limb.
As a neurorehabilitation clinician, I am in charge of a care unit for patients with prolonged disorder of consciousness (i.e. patients with unresponsive wakefulness syndrome or in minimally conscious state). The aim of my research project is to understand how these severely brain injured patients are able to perceive pain using non-invasive methods such as surface EEG recordings. These investigations should also be of interest to develop a novel approach to study the relationship between pain perception and consciousness.
Studies have suggested that Alzheimer's disease (AD) is related to changes in brain function that are present already at very early, pre-clinical stages of the disease. For example, recent functional neuroimaging studies have shown early alterations in brain connectivity, and that these alterations are most prominent in highly-connected cortical "hub areas". These hub areas are also those that are most affected by AD lesions. These findings support the view that AD pathology could, at least in part, result from an activity-dependent degeneration. Initial excessive neural firing in hub areas due to increased excitability or connectivity could lead to later neurodegeneration and disruption of connectivity. Very recently, studies conducted by Prof. JN Octave (UCL) have suggested that AD could be related to a decrease in the expression of the cellular Cl- ion extruder KCC2, leading to an increase in intracellular Cl- and, thereby, an inhibitory-to-excitatory shift of GABAA receptor activity. The aim of the present study is to test whether GABAergic neurotransmission is altered at early pre-clinical and pre-demential stages of AD as compared to matched healthy controls.