Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society
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J Clin Neurophysiol · Jun 2012
Randomized Controlled TrialAdvanced pharmaco-EEG reveals morphine induced changes in the brain's pain network.
By using a novel brain source modeling approach, where the evoked potential (EP) signal was decomposed with multichannel matching pursuit (MMP) before source localization, we investigated brain generators of EPs after a pain stimulus in the esophagus before and after administration of placebo/morphine. We showed that this new approach of pharmaco-electroencephalogram (EEG) analysis can shed light on subtle changes, which cannot be foreseen from conventional analysis (amplitude/latency/topography). ⋯ Decomposing the EPs into the original brain generators showed that morphine mainly changes the low frequency electrical activity in the frontal brain area. This method can be used to increase the basic understanding of the opioid effect on the brain's processing of pain and eventually identify biomarkers of analgesia in experimental pain models.
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Standardized research terminology critical to the establishment of a multicenter intensive care unit (ICU) electroencephalogram (EEG) database was originally proposed in 2005 and has been modified many times since. However, interrater agreement (IRA) of the revised terminology has not been investigated. ⋯ Main terms 1 and 2 have high IRA and are reasonable for use in multicenter research. There is a suggestion that assessment of amplitude has good reliability, while assessment of frequency may have less reliability. The fast and rhythmic "plus" modifiers have moderate IRA, while sharp/spike modifier has only slight IRA implying that further refinement and assessment of terminology modifiers may be necessary.
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There is evidence for comorbidity of migraine and epilepsy. We used transcranial magnetic stimulation (TMS) to assess cortical excitability in migraine compared with control subjects and patients with epilepsy. ⋯ Cortical excitability increases in migraine suggesting the involvement of intracortical inhibitory circuits. This may be a common feature underlying some of the similarities observed in migraine and epilepsy.