Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 5 uppsatser.

Introduction: Guillain-Barré syndrome (GBS) is a neurological disease caused by an autoimmune attack on the peripheral nerves. The main symptoms are loss of motor and sensory skills in the upper and lower extremities. Autonomic dysfunction also occurs.Aim: To identify which parameters in neurography examination that are showing pathology at three different stages from the onset of symptoms. To practically perform and evaluate different electrode placements at RR-intervals.Materials and methods: The first part of this study was a retrospective study with results from 58 patients which were diagnosed with GBS in 2010-2020 at the University Hospital in Uppsala. The second part of this study included measurement of the heart rate variation with RR-intervals at different electrode placement in ten healthy volunteers. Results: In part 1 of the project, there were no significant differences between the groups at distal latency in the ulnar nerve, F-latency in the tibial nerve and in the conduction velocity in the sural nerve. However, there were significant differences in the amplitude of the radial nerve. In part 2 of the project, there were significant differences between the electrode placements, and most artifacts were found with electrodes placed on the shoulders.Conclusion: Examination with neurography and RR-intervals plays an important role in the diagnosis of GBS. As the amplitude in the radial nerve was the only one that showed significant differences between the groups, the nerve is recommended to be examined bilaterally. With a high presence of artifacts in RR-intervals with electrodes placed on the shoulders and wrists, placement on the chest is to be recommended.

La polyradiculonévrite inflammatoire démyélinisante chronique (PIDC) est une pathologie neurologique auto-immune du système nerveux périphérique dont la physiopathologie est actuellement mal connue, pour laquelle les options thérapeutiques sont peu nombreuses et dont il n’existe pas de modèle animal fiable. Le premier objectif de ce travail était de valider et de caractériser un modèle animal de PIDC par immunisation de rat Lewis avec le peptide P0(180-199) palmitoylé. Les animaux ont développé une pathologie chronique ou à rechute qui a pu être caractérisée aux plans clinique, histologique, électrophysiologique et immunologique. Les résultats sont en faveur d’un modèle fiable et reproductible mimant bien la PIDC humaine. Le deuxième objectif de ce travail était de tester, sur notre modèle, le fingolimod, modulateur des récepteurs à la sphingosine 1-phosphate, comme potentiel traitement de la pathologie. Le fingolimod a permis, dans notre modèle, de diminuer la sévérité et la chronicité de la maladie, d’améliorer les paramètres électrophysiologiques, de diminuer l’infiltration par les cellules inflammatoires et les anomalies immunologiques. / Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an autoimmune pathology of the peripheral nervous system whose pathophysiology is currently poorly understood, for which there are few therapeutic options and no reliable animal model. The first aim of this work was to validate and characterize an animal model of CIDP by immunization of rat Lewis with the palmitoylated peptide P0(180-199). The animals developed a chronic or relapsing pathology that could be characterized clinically, histologically, electrophysiologically and immunologically. The results are in favor of a reliable and reproducible model that mimics the human CIDP. The second aim of this work was to test, on our model, the fingolimod, sphingosine 1-phosphate receptor modulator, as potential treatment of the pathology. In our model, fingolimod has reduced the severity and the chronicity of the disease, improved electrophysiological parameters, reduced infiltration by inflammatory cells and recue immunological abnormalities.