Ph.D. Defense by Lea Tøttrup

Lea Tøttrup will defend hers Ph.D. thesis “Functional cortical changes in an animal model of neuropathic pain”


26.02.2021 kl. 13.00 - 16.00



13.00 Opening by the Moderator Prof. Winnie Jensen
13.05 PhD lecture by Lea Tøttrup
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:


Prof. Dr. Ulrich G. Hofmann, Freiburg Institute for Advanced Studies, Albert-Ludwigs-Universität Freiburg, Germany

Prof. Dr. Markus Ploner, Munich Center fro Neurosciences - Brains & mind, Ludwig-Maximilians-Universität München, Germany


Associate Professor Erika Spaich, HST, Aalborg Universitet


Professor Winnie Jensen, HST, Aalborg Universitet



Despite being a global issue and subject to enormous research interest, chronic pain still remains poorly understood due to its inherent complexity, the heterogeneity in symptom development among patients, and lack of objective measures to evaluate. With animal models of chronic pain conditions, it is possible to study specific mechanisms in a highly controlled environment. Several of these models have shown that functional cortical changes are already present days or weeks after an intervention, which suggests that the change must happen before this point of recording. With the aim of investigating functional cortical changes in the processing of cortical activity and interactions after a chronic injury to the nervous system, an animal model of neuropathic pain was used.

This thesis is based on three original scientific studies. In Study I, changes in the characteristics of electrically evoked cortical potentials following the spared nerve injury model was investigated. The results showed changes in both amplitude and latency of the accumulated spiking activity in primary sensory cortex and anterior cingulate cortex. Study II consisted of measuring the functional connectivity between primary sensory cortex and anterior cingulate cortex during electrical stimulation, and how these interactions changed following the same animal model of pain. This study demonstrated early cortical changes in the hours following injury. The interaction from primary sensory cortex to anterior cingulate cortex was increased as shown previously, although it has not been shown or even investigated in an acute time frame as done here. In Study III, spontaneous cortical activity was analyzed before and after intervention with the pain model. The results showed that the model of pain led to a decreased spontaneous information flow between anterior cingulate cortex and primary sensory cortex.

The overall conclusion of this thesis is that cortical functionality is affected as early as a few hours after a peripheral nerve injury. The evoked activity seems to change in a way similar to hyperalgesia and allodynia mechanisms–such as seen in human neuropathic patients–with an increased response to both noxious and non-noxious stimuli. The spontaneous cortical functionality changes in a complete opposite direction (decreasing), indicating that other mechanisms or cortical areas takes over after injury.


Department of Health Science and Technology


Ph.D. Defense take place via Zoom.

Registration Deadline

24.02.2021 kl. 12.00

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