Research Grants for Clinical and Human Experimental Pain Research
These biennial grants totalling € 200,000 from Grünenthal are supporting young scientists early in their career to carry out innovative clinical pain research in any member country of European Pain Federation EFIC®. Individual research grants are valued at up to € 40,000 per project for a duration of up to two years.
Research Grants are intended for clinical and human experimental pain research. Research proposals on animals, computer simulations, cell lines etc. will not be considered. The decision of the awards is made independently by the EFIC® Committee on Scientific Research.
- Encouraging Innovative Pain Research
Long-term commitment to support pain research - Delivering true benefits to patients.
- In a nutshell: About the EGG in less than 3 minutes
Your application has to be made online. Please note that the application and all respective documents must be in English.
Throughout the application forms the fields that have to be filled in are marked with an*. Please note that applications not containing this essential information will not be considered.
Applications for 2018 are open!
- The application is password protected, therefore please click on 'Register for Application'.
- A unique identifier number will be assigned to your application and you will receive a confirmation e-mail.
- In Part I of the application form you state the details on the research project, host institution, budgets as well as personal information (e.g. postgraduate degree).
- Part II of the application form provides you with an Upload Manager. Specific additional documents like Curriculum Vitae, publication list, research plan, research abstract, literature references, can be uploaded (Word Office files and PDF are accepted).
You can log into the application form and add or edit information as often as you like.
- When the application is complete you submit it by pressing the 'final submit' button of the last page of the form. This will terminate your editing option and turns to the view option of the complete application. If in exceptional cases further changes are necessary this can be done via e-mail.
For further information please visit www.e-g-g.info
EFIC® Symposium "New Findings in Clinical Pain Research"
Former E-G-G winners presented their research results during the EFIC® Symposium in Copenhagen. Lively discussions with renowned pain experts enhanced the Symposium which was –chaired by Dr Luis Villanueva, France together with Prof. Katharina Zimmermann, Germany.
Please see here the abstracts of the presentations:
(Photos: Grünenthal/Marko Kovic)
DISRUPTION OF EMOTIONAL MODULATION IN CHRONIC PAIN PATIENTS
Dr Jamila Andoh, PhD
Department of Cognitive and Clinical Neuroscience, Central Institute of Mental Health, Medical Faculty Mannheim / Heidelberg University, Mannheim, Germany
Pain is a multidimensional experience involving sensory, affective and cognitive dimensions. The subjective quality of painful experiences can be modulated by environmental and interpersonal factors such as distraction, attention, as well as positive and negative moods. The mechanisms of such emotional modulation of pain sensations are not well understood and results vary across studies. It is also not clear if emotions can affect the affective dimension of pain. We aimed to examine the modulation of pain perception in healthy controls and in chronic back pain patients.
Participants were presented pictures with either negative, positive or neutral valence, shortly before the application of electrical painful stimuli. We assessed the sensory and affective dimensions of pain using subjective ratings and electrophysiological recordings.
In healthy controls, we found that negative primes increased and positive primes decreased pain unpleasantness. Electrophysiological data showed that the somatosensory evoked-potentials were modulated by the emotional valence of the pictures. Source localization analysis showed that valence was associated with different neural processes during pain at the level of subcortical and cortical structures (somatosensory, frontal). Preliminary analyses on data from chronic pain patients do not show emotional modulation of pain.
We showed that brief presentations of pictures with negative valence increased the affective dimension of pain. This indicates that pain modulatory effects occur very fast, and raise questions regarding long term consequences of negative emotions on pain perception.
This study was supported by a grant from the EFIC-Grünenthal-Grant and the SFB1158/B07.
Brain biomarkers and computational assays of neuroplasticity in Complex Regional Pain Syndrome (CRPS)
Dr Christopher Brown, PhD
Department of Psychological Science at the University of Liverpool, Liverpool, United Kingdom
CRPS is associated with neuroplasticity of the somatotopic cortical representation of the affected limb and attendant loss of tactile spatial resolution. Early detection and treatment can improve symptoms/function and would benefit from specific and clinically practical biomarkers and assays. In this talk I will describe the aims of a project funded by an EFIC-Grunenthal Grant, in which we sought to develop EEG biomarkers of neuroplasticity affecting somatosensory spatial resolution in patients with CRPS. Our starting point was the measurement of somatosensory neural “mismatch” responses, which we hypothesised would provide an objective marker of tactile spatial resolution when mismatch responses are generated from rare changes in the spatial location of an experimental tactile stimulus. I will describe how the project was designed to capture these responses and validate them as markers of between-subject differences in somatosensory resolution, presenting preliminary data from CRPS patients and control participants. Furthermore, neural mismatch responses have been previously investigated as markers of the brain’s sensory “prediction error” processes within the context of a predictive coding framework. I will thus describe a novel approach to our research question that involves applying suitable mathematical models to uncover hidden mechanisms in the brain underlying pain perception and pain-related neuroplasticity, as applied to behavioural and EEG data. For the latter, this involves applying a spatial filter to classify single-trial EEG data according to topographic characteristics, and then a temporal filter to infer hidden predictive coding mechanisms and their evolution over time. In principle, such an approach could provide an objective and clinically practical “computational assay” of somatosensory neuroplasticity in CRPS.
A neurophysiological and psychophysical study showing that Aß-fibres mediate paroxysmal pain in healthy humans
Prof Andrea Truini, MD, PhD
Department of Neurology and Psychiatry, University Sapienza, Rome, Italy
Neuropathic pain manifests with a combination of different symptoms. Although it is generally agreed that most symptoms arise as a consequence of nociceptive fibre damage, some studies suggested that paroxysmal electrical-shock like pain might be selectively mediated by non-nociceptive Aβ-fibres. In this neurophysiological study in humans we aimed at verifying whether a selective activation of intact Aβ-fibres by high-frequency electrical stimulation evokes paroxysmal electrical shock-like pain.
We sought the low-intensity electrical stimulation parameters provoking a painful electrical shocks comparable to the trigeminal pain attacks in ten patients with trigeminal neuralgia. Then we tested perceptions evoked by these stimulation parameters in ten healthy participants; using low- and high-frequency electrical low-intensity stimulation we also recorded scalp potentials. We then verified whether the paroxysmal electrical shock-like pain due to high-frequency, low-intensity electrical stimulation persisted after selective block of nociceptive fibres of the ulnar nerve at the wrist.
We found that electrical stimulation at 100 Hz, 2.5 times the perceptive threshold evoked paroxysmal pain comparable to the trigeminal neuralgia paroxysms in most patients, and an electrical shock-like pain in most healthy participants. Scalp potentials evoked by low- and high-frequency electrical low-intensity stimulation did not differ. The painful perception evoked by high-frequency electrical stimulation did not change after selective block of nociceptive fibres by local anaesthetic.
Our study indicating that a selective activation of Aβ-fibres by a low-intensity, high-frequency stimulation evokes a painful electrical-shock like pain, supports a mechanism-based approach to neuropathic pain, useful in drug trials and in tailoring therapy to the individual patient.