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Trial Lecture – time and place
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- First opponent: Professor Håkan Olausson, Linköping University, Sweden
- Second opponent: Associate Professor Sissel Løseth, UiT The Arctic University of Norway
- Third member and chair of the evaluation committee: Professor Iver Arne Langmoen, University of Oslo
Chair of the Defence
Professor Jon Berg-Johnsen, University of Oslo
Professor II Ellen Jørum, University of Oslo
Neurophysiological mechanisms in patients with neuropathic pain and pain insensitivity due to gene mutations
This thesis includes three different papers and discusses neuropathic pain mechanisms from a clinical neurophysiological perspective.
The aim was to study peripheral mechanisms involving nociceptive C-fibers that may lead to neuropathic pain by approaching patients with pain and pain insensitivity syndromes due to gene mutations. A better understanding of peripheral neuropathic mechanisms may lead to better pain treatments.
The methods used include clinical examination, sensory testing protocols and routine laboratory methods like neurography. We also assess small fiber function by using thermal threshold testing (QST) and microneurography (single fiber recordings). Further we examine electrophysiological properties using the patch clamp technique.
The three different papers render different types of results, however the main finding is that the electrophysiological behavior, mainly the excitability, of the nociceptive C-fibers is hard to predict and it does not always correlate with what one would expect based on genotype and phenotype. We also observe that the evoked sensory protocols used in our studies do not predict underlying genotypes or mechanisms in our patients.
In conclusion the peripheral mechanisms involving nociceptive function can be hard to predict even when the etiology of the pain condition can be narrowed down to a single gene mutation, however excitability of the peripheral nociceptive neuron is likely a key component. One may view neuropathic pain as a result of an active complex neuroplastic process that in some patients may change and develop in accordance with disease and etiology. Thus neuropathic pain could be considered a disease in its own right, and not a secondary symptom to another disease. This interpretation suggests that single-mechanism based drugs may not be the most effective when treating or developing treatments for neuropathic pain.
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