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 (l-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 micrograms X kg-1, n = 5; and 400 micrograms X kg-1, n = 8). Seven unanesthetized animals served as controls. During fentanyl administration, the EEG was characterized by the appearance of isolated high voltage (greater than 100 microV) 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 less than 0.05) decrease of the l-CMRg in the majority of the 37 brain structures surveyed. A clear relationship between l-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 l-CMRg in the claustrum, septal nucleus, amygdala, and ventral areas of CA1 and CA3 of the hippocampus remained at control values.(ABSTRACT TRUNCATED AT 250 WORDS)