Fentanyl-induced seizures activate subcortical brain metabolism

Neurophysiologic studies have demonstrated epileptoid activity during high-dose narcotic anesthesia. The authors utilized the 14C-2-deoxyglucose method to evaluate the local cerebral glucose metabolism (1-CMRg) during high-dose fentanyl-induced epileptoid discharges as evaluated by electroencephalography (EEG) in ventilated rats. Fentanyl was administered intravenously at two dose levels (200 μg·kg-1, n = 5; and 400 μg·kg-1, n = 8). Seven unanesthetized animals served as controls. During fentanyl administration, the EEG was characterized by the appearance of isolated high voltage (>100 μV) spike and polyspike and wave complexes at a frequency of one every 1-4 s, superimposed on a baseline of reduced frequency and voltage. Isolated ictal discharges (spike or sharp waves at a frequency of 12-20/s) rarely were superimposed upon the spike and polyspike activity. As a general trend, fentanyl administration induced a significant (P <0.05) decrease of the 1-CMRg in the majority of the 37 brain structures surveyed. A clear relationship between 1-CMRg and epileptoid activity appeared when the anatomic areas were grouped into functional systems. Cerebral metabolism was globally decreased in the visual and sensorimotor systems (53-78%), in the white matter structures (76-78%), and reticular formation (59-69%) with both fentanyl treatments. The largest deviation from this trend appeared in the limbic system. Here with both treatments, the 1-CMRg in the claustrum, septal nucleus, amygdala, and ventral areas of CA1 and CA3 of the hippocampus remained at control values. At the higher fentanyl dosage, there was a more widespread depression of 1-CMRg in the rest of the brain, while in the limbic system this effect was reversed, with the 1-CMRg returning to control values in the hippocampus (CA1), denate gyrus, and interpeduncular nucleus.