WINNERS OF THE EFIC-GRÜNENTHAL GRANT 2012
Nociceptive nerve endings as a target for autoantibodies.
The objective of this project is to investigate the presence of autoantibodies against the contacting-associated protein 2 (CASPR2), a subtype of voltagegated potassium channel (VGKC) which has been recently reported in patients with idiopathic small fiber neuropathy. This potential use makes skin biopsy a promising tool to help on the etiology of SFN that now remains unknown for most patients. Also, the identification of immunomediated damage could give support to specficic treatment for patients suffering of neuropathic pain.
A longitudinal study on chronic pain, anxiety and depression
Pain frequently co-occurs with anxiety and depression, but it is largely unknown why this is the case. In this study, I aim to investigate how these conditions develop over time, at the level of subclinical symptomatology rather than endpoint diagnoses. In addition, I will use latent class analysis to test whether different symptom profiles are associated with a different course of development of these conditions. Investigating how symptoms develop over time and how they cluster in individuals will shed more light on the mechanisms underlying the comorbidity of pain, anxiety and depression.Fear generalization as a pathway to chronic widespread pain
Increasing evidence indicates that pain-related fear plays a pivotal role in the transition from acute to chronic disabling pain. Fear generalization however has been largely neglected in pain research so far. This project aims to examine how fear and avoidance spread to other movements/activities, and whether fear generalization fosters pain sensitivity. We will investigate fear generalization 1) in chronic pain versus healthy controls, 2) in relation to the spreading of pain itself, 3) based on functional equivalence, and 4) and the effects of individual differences and inhibitory control.
Imaging grey and white matter pathology in central post-stroke pain with MRI.
Central post-stroke pain (CPSP) is characterized by severe hemibody pain following stroke. In this project, we aim at studying the somatosensory profile (QST), subcortical and cortical structure as well as structural and functional connectivity of CPSP patients, stroke patients without pain and healthy subjects using MRI. These studies will shed light on the framework of brain areas and mechanisms of brain plasticity involved in the generation of CPSP. The study will further help to understand how sensory symptoms and brain structure / function relate to each other.‘Pain engrams’: psychophysiologic investigations of memory traces of nociceptive information
Electroencephalography (EEG) responses triggered by nociceptive stimuli are thought to reflect the salience (bottom-up capture of attention) and relevance (top-down attentional control) of the sensory event. However, little is known on how the encoding and maintenance of nociceptive somatosensory information is represented by EEG activity. The present project aims to study (i) EEG correlates of nociceptive sensory memory (encoding) as reflected by the evoked mismatch negativity, and (ii) nociceptive working memory (maintenance) as reflected by nociceptive-related EEG oscillatory activity during a memory task. The studies will contribute to elucidate the brain processes associated to short-term memory traces formation and manipulation of nociceptive somatosensory information.
Defining peripheral and central pathophysiology and heritable susceptibility factors of ciguatera-associated cold allodynia
Cold allodynia is a major and dreadful symptom of many neuropathic pain states and it is a hallmark symptom of Ciguatera, a disease caused by intoxication with the fish poison ciguatoxin, which meanwhile represents a major global public health concern. Identification of the pain pathways activated by ciguatoxin as well as analysis of heritable susceptibility factors will help understand the mechanism and the interindividual variability of Ciguatera symptomatology and eventually the pathogenesis of painful cold hypersensitivity.