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Spinal Sensitization to Nociception Assessed with Cortical Somotosensory Evoked Potentials (CSEPs) and Spinal Microdialysis

Wednesday, 21 December, 2005 - 17:00
Campus: Brussels Health Campus
Faculty: Medicine and Pharmacy
auditorium R. Vanden Driessche
Lin Shi
phd defence

Adequate pain treatment in medical care is often
not reality as pain may depend on a myriad of
factors. Also the optimal strategy to treat pain is not
known. Part of this is due to the lack of an objective
individual measurement tool for pain quantification.
This work first focuses on different methods to
objectify transmission of nociceptive signals and the
sensitization phenomenon at the level of the spinal
cord in freely moving rats. The first method involved
includes the use of cortical somatosensory evoked
potentials to measure central sensitization of the
spinal cord. Data from this method suggested to
incorporate non-steroidal inflammatory agents to
treat pain induced by inflammation. The second
method used spinal microdialysis with two different
anatomic approaches: a dorsal horn and an
intrathecal approach. Both methods to study pain
were submitted to two different peripheral
inflammations models. The response to
inflammation, and afterwards to different pain
treatments, was assessed by dosing glutamate and
prostaglandin E2 levels in cerebrospinal fluid and by
comparing it with behavioral changes. During the
investigations particular attention was given to the
involvement of spinal cylooxygenases (COX) in
spinal pain sensitization. Later on, the impact of
treatment with selective COX-1 and COX-2-
inhibitors was investigated. Though both inhibitors
prevented pain development, an enhanced
efficacy was observed with early COX-2 selective
inhibitor treatment. The contribution of humoral
signals to spinal nociceptive transmission was then
further explored by IL1β administration in the
microdialysis model. Giving IL1β coincided with
increased pain parameters and suggested that IL-
1β activated the COX-2 enzyme in the spinal cord.