• Brian W LeBlanc, Paul M Bowary, Yu-Chieh Chao, Theresa R Lii, and Carl Y Saab.
• aDepartment of Neurosurgery, Rhode Island Hospital, Providence, RI, USA bDepartment of Neuroscience, Brown University, Providence, RI, USA cDepartment of Anesthesiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
• Pain. 2016 Oct 1; 157 (10): 2330-40.

AbstractPain modulates rhythmic neuronal activity recorded by Electroencephalography (EEG) in humans. Our laboratory previously showed that rat models of acute and neuropathic pain manifest increased power in primary somatosensory cortex (S1) recorded by electrocorticography (ECoG). In this study, we hypothesized that pain increases EEG power and corticocortical coherence in different rat models of pain, whereas treatments with clinically effective analgesics reverse these changes. Our results show increased cortical power over S1 and prefrontal cortex (PFC) in awake, freely behaving rat models of acute, inflammatory and neuropathic pain. Coherence between PFC and S1 is increased at a late, but not early, time point during the development of neuropathic pain. Electroencephalography power is not affected by ibuprofen in the acute pain model. However, pregabalin and mexiletine reverse the changes in power and S1-PFC coherence in the inflammatory and neuropathic pain models. These data suggest that quantitative EEG might be a valuable predictor of pain and analgesia in rodents.

29 keywords...

hide…