Center for Neuroplasticity and Pain

Ph.D. Defense by Víctor Doménech García

Víctor Doménech García will defend his Ph.D. thesis “ Modulation of pressure-induced pain distribution due to prolonged experimental pain and prior trauma” On Monday 7 December at 13:00

Last modified: 30.11.2020


13.00 Opening by the Moderator Thomas Graven-Nielsen
13.05 PhD lecture by Víctor Doménech García 
13.50 Break
14.00 Questions and comments from the Committee
          Questions and comments from the audience at the Moderator’s discretion
16.00 Conclusion of the session by the Moderator



The Faculty Council has appointed the following adjudication committee to evaluate the thesis and the associated lecture: 


Professor Deborah Falla, University of Birmingham, United Kingdom

Associate Professor Kristian Bernhard Nilsen, Olso University Hospital, Norway

Associate Professor Søren Schou Olesen, Aalborg University, Denmark

Professor Thomas Graven-Nielsen, Aalborg University, Denmark


Persistent musculoskeletal pain is a consolidated social problem in which underlying mechanisms are not fully understood. Amongst these mechanisms, it is believed that sensitization of the central nervous system has an essential role for the development of persistent pain. Pain sensitization is frequently caused by musculoskeletal trauma and often manifests with specific pain distribution such as expanded pain areas and pain referred to several body regions. Original research demonstrated a tendency of pain to refer to previously painful areas. On the basis of this, it was proposed that prior pain in a specific body region could partially explain pain distribution and its variability. Therefore, investigating the potential effect of prior painful injury on the distribution of pain after injury and pain recovery may help to understand pain mechanisms in general and in particular long-term sensitization. The main objective of the present PhD project was to investigate whether prior pain caused by fracture modulates the distribution of pain induced by mechanical pressure on a muscle in asymptomatic individuals, compared to healthy controls without a history of fracture. Participants were assessed at baseline and 24h after being exposed to eccentric exercise, which produces prolonged muscle pain. The current studies showed that eccentric exercise consistently increases pressure pain thresholds and creates a prolonged pain condition in the exercised muscles of healthy asymptomatic participants, irrespective of having a history of fracture. Furthermore, exercise-induced prolonged pain expands pain areas induced by mechanical pressure in both individuals with a history of fracture and controls, compared to baseline condition. However, under exercise-induced prolonged pain condition, individuals with a history of fracture demonstrated a more expanded distribution of pain areas induced by mechanical pressure, compared to healthy controls and the contralateral non-fractured side. However, despite the differences in pain distribution, the history of fracture did not affect pressure pain thresholds. These results give insight into long-term modifications of pain mechanisms as a consequence of a musculoskeletal trauma.