Abstracts

Rationale: The physiological process that constitute the characteristic spontaneous seizures of epilepsy is due to lowering of excitability threshold of the neurons often without any obvious cause. The pathophysiological mechanisms that leads to the sudden onset of excess neuronal electrical discharge is still not fully understood. It is conceivable that these neurons that seems silent during interictal period are actually different than normal neurons. Headaches and painful syndromes are common co-morbidities with epilepsy. The reasons for these co-morbidities are still not known. On the other hand there is no study addressing interictal pain sensitivity in epilepsy. If the epileptic experimental animals has an altered pain sensitivity, it can be proposed that there could be a change in normally silent cortico-thalamic circuits causing deflection of some physiological responses. In this study it was aimed to investigate the interictal pain sensitivity in epilepsy by using genetic absence epilepsy rats in comparison with the controls. Methods: Experiments were approved by the animal ethics committee of Karadeniz Technical University. Two experimental groups were formed. Independent group was consisted of 8 male epileptic 8 month WAG/Rij rats while 8-age and gender-matched Wistar without epilepsy served as control. In the dependent group, experiments were started before epileptic seizure manifestation when the rats were 2 months old and the measurements were repeated when they were epileptic at (8 months old). In the dependent group there were 12 male WAG/Rij and 11 age and gender-matched control Wistar rats. Permanent cortical electrodes, 2 active EEG electrodes to left frontal and the reference electrode to mid-line cerebellum was implanted under general anesthesia using stereotaxic frame and interictal pain threshold measurements were performed following 10 days recovery from electrode surgery. Interictal, as confirmed by synchronized video EEG monitorization, pain threshold measurements were performed when the animals were awake and freely moving. In vivo pain threshold values were determined by using thermal plantar analgesiameter. Pain threshold values were determined by averaging the 2 measurements from right and left hind-paw by 15 minutes intervals. Results: The pain latency values of 8 month-old epileptic rats in the independent group significantly lower than their respective controls [3,0 vs 4,5 sec (P=0,001), respectively]. In the dependent group of rats, pain threshold values of WAG/Rij rats were significantly lower than controls at both when they were non-epileptic at 2 months [epileptic vs. control: 2,7 and 3,1 sec (P=0,036) ] and at 8 months when they were epileptic [[epileptic vs. control, 2,8 and 3,9 sec (P=0.00014)]. Conclusions: These results are of importance to demonstrate that pain sensitivity of genetic absence epileptic rats is higher. Funding: This study was supported by T܂ITAK (The Scientific and Technological Research Council of Turkey) with 1001- Scientific and Technological Research Projects Funding Program. Project No: 214S/206.