Isoflurane blunts electroencephalographic and thalamic-reticular formation responses to noxious stimulation in goats

Background: Anesthetics, including isoflurane, depress the electroencephalogram (EEG). Little is known about the quantitative effects of isoflurane on EEG and subcortical electrical activity responses to noxious stimulation. The authors hypothesized that isoflurane would depress the results of EEG and subcortical response to noxious stimulation at concentrations less than those needed to suppress movement. Furthermore, determination of regional differences might aid in elucidation of sites of anesthetic action. Methods: Ten goats were anesthetized with isoflurane, and minimum alveolar concentration (MAC) was determined using a noxions mechanical stimulus. Depth electrodes were inserted into the midbrain reticular formation and thalamus. Needle electrodes placed in the skull periosteum measured bifrontal and bihemispheric EEG. The noxious stimulus was applied at each of four anesthetic concentrations: 0.6, 0.9, 1.1, and 1.4 MAC. Results: At an isoflurane concentration of 0.6 MAC, the noxions stimulus activated the midbrain reticular formation, thalamic, and bifrontal-hemispheric regions, as shown by decreased high-amplitude, low-frequency power. For all channels combined (mean +/- SD), total (-33 +/- 7%), delta (-47 +/- 12%), theta (-23 +/- 12%), and alpha (-21 +/- 6%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 0.9 MAC, total (-35 +/- 5%), delta (-42 +/- 7%), theta (-35 +/- 8%), and alpha (-23 +/- 11%) power decreased after the noxious stimulus CP < 0.001); beta power was unchanged. At 1.1 MAC only one site, and at 1.4 MAC, no site, had decreased power after the noxious stimulus. Conclusions: Isoflurane blunted EEG and midbrain reticular formation-thalamus activation response to noxious stimulation at concentrations (1.1 MAC or greater) necessary to prevent movement that occurred after noxious stimulation, It is unknown whether this is a direct effect or an indirect effect via action in the spinal cord.