Epilepsy may cause increased pain sensitivity: Evidence from absence epileptic WAG/Rij rats
Epilepsy and Behavior, cilt.75, ss.146-150, 2017 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 75
- Basım Tarihi: 2017
- Doi Numarası: 10.1016/j.yebeh.2017.07.007
- Dergi Adı: Epilepsy and Behavior
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.146-150
- Anahtar Kelimeler: Epilepsy, Pain, Genetic absence epilepsy, WAG/Rij rats, Pain threshold
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
Objective The comorbidity of epilepsy and pain disorders as well as effectiveness of certain therapeutic approaches in both conditions attracted attention to epilepsy–pain interactions. This lead to the discovery of significantly shared pathophysiological mechanisms although many aspects remain largely unknown. To test the hypothesis that epilepsy may be associated with altered pain sensitivity, we analyzed interictal pain sensitivity using epilepsy prone WAG/Rij rats, a genetic model exhibiting age-related-onset absence epilepsy. Methods Two series of experiments were conducted. In experiment I, pain sensitivity of symptomatic WAG/Rij rats were compared with age-matched control Wistar rats. In experiment II, pain sensitivity of WAG/Rij rats were monitored longitudinally when they were presymptomatic (at 2 months) and symptomatic (after maturation, at 8 months), and compared with age-matched control Wistar rats. Pain sensitivity was assessed by applying heat stimuli to hind paws and measuring the paw-withdrawal latency using thermal plantar analgesia meter in awake and freely moving animals. All pain measurements were made during the interictal period, confirmed by simultaneous electroencephalography through intracranially implanted electrodes. Results In experiment I, the interictal pain withdrawal latency of symptomatic WAG/Rij rats was significantly shorter than control Wistar rats (P < 0.01). In experiment II, WAG/Rij rats had significantly shorter latency of withdrawal response than control Wistar rats, both at presymptomatic (P < 0.05) and symptomatic stage (P < 0.0001). Matured (8 months old) control Wistar rats demonstrated significantly increased withdrawal latency compared to the 2 months animals (P < 0.01), but the WAG/Rij rats did not (P > 0.5). Conclusion Epileptic WAG/Rij rats present significantly increased pain sensitivity when compared to control Wistar rats, suggesting comorbidity of epilepsy and pain.