The experiments forming the basis for the presentthesis used different methods to induce and assessexperimental pain stimuli in both healthy subjectsand in patients with chronic pancreatitis.Furthermore in attempt to improve the pain models amultimodal and multi-tissue testing approach wassuccessfully applied in these patients. Patients suffering from chronic pancreatitis arethought to have peripheral neural alterations andcentral changes in the pain system. One hypothesis isthat the noxious activity in patients leads toperipheral spinal and supraspinal changes in thepain system. We found generalized hypoalgesia to experimentalvisceral and somatic stimulations but also evidencefor central sensitization and corticalreorganisation. The findings suggest that activationand modulation of central mechanisms is fundamentalin pancreatic pain. This may be related to changes inthe balance between central hyperexcitability andpain modulating pathways. The findings of thepresent thesis may have clinical implications. Drugswhich exert effects on the central nervous system ora combination of different drugs with targets in thecentral nervous system should be tested.
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