Modulation of Pain-Related Somatosensory Evoked Potentials by General Anesthesia

Abstract

The aim of the present study was to assess if late somatosensory evoked cerebral potentials (SEPs) in response to painful electrical stimuli are a sensitive indicator for analgesic treatment during general anesthesia. For this purpose, a pain model developed for the quantification of drug-induced analgesia in awake volunteers was used in 10 patients scheduled for elective abdominal hysterectomy. Before induction of anesthesia, stimuli were adjusted to two and three times the pain threshold for each individual. Late auditory evoked potentials (AEPs, 30 dB hearing level) and spontaneous electroencephalogram were also evaluated. After control recordings, anesthetic treatments were varied in the following sequences: (a) 0.8% (end-tidal) halothane with 70% nitrous oxide (HN); (b) 0.8% halothane in oxygen (H1); (c) same anesthetic condition as in H1, but the SEP and AEP stimulus intensities were increased to 15 times pain threshold and to 70 dB hearing level, respectively (H2); and (d) fentanyl (0.25 mg) was given with 0.8% halothane in oxygen with no further change in stimulus intensities (HF). In treatments HN and H1, blood pressure and heart rate increases to pain stimuli were abolished, and SEPs and AEPs were both suppressed. Increasing the somatosensory stimulus intensity (treatment H2) stimulated heart rate and arterial pressure responses and again elicited the SEPs. However, AEP components remained suppressed with increased auditory stimulus intensity. Addition of fentanyl (HF) suppressed SEP amplitudes and stimulus-induced hemodynamic responses. Our results suggest that late SEPs in response to painful stimuli change with different analgesic levels.