British Journal of Anaesthesia, 2002, Vol. 89, No. 3 382-388
© 2002 The Board of Management and Trustees of the British Journal of Anaesthesia
Clinical Investigations |
Effect of propofol anaesthesia on the event-related potential mismatch negativity and the auditory-evoked potential N1
1 Department of Anaesthesia and 2 Department of Neurophysiology Frenchay Hospital, Frenchay Park Road, Bristol BS16 1LE, UK. 3 The Burden Neurological Institute, Stoke Lane, Bristol BS16 1QT, UK*Corresponding author
Background. Studies on the effects of anaesthesia on event-related potentials and long latency auditory-evoked potentials (AEP) are sparse. Both provide information on cortical processing and may have potential as monitors of awareness. We studied the effect of propofol on the event-related potential mismatch negativity (MMN) and the long-latency AEP N1.
Methods. Twenty-one patients received 1 µg ml–1 stepped increases in the target concentration of propofol using DiprifusorTM until a maximum of 6 µg ml–1 was achieved or the patient had lost consciousness. Neurophysiological responses (MMN and N1) and the patients’ level of consciousness were recorded before the administration of propofol and at a target effector site concentration of propofol of 1, 2, 3, 4, and 6 µg ml–1. Grand average evoked potentials were computed at baseline, before the administration of propofol (A); at the highest propofol concentration at which each patient was responsive (B); and at the concentration of propofol at which the patient became unconscious (C).
Results. Patients lost consciousness at different target concentrations of propofol, all being unresponsive by 4 µg ml–1. The response to the deviant stimuli used to elicit duration-shift MMN was significantly more negative than to the standard stimuli at A (mean difference 2.58 µV, P=0.0011) but this difference was virtually abolished at point B, before the patients lost consciousness (mean difference 0.63 µV, P=ns). The amplitude of N1 evoked by standard stimuli was negative compared with electrical baseline at both point A (mean amplitude –3.81 µV, P<0.001) and at point B (mean amplitude –2.2 µV, P=0.002), but was no longer significantly different to baseline at point C (mean amplitude 0.51 µV, P=ns). The change in the mean amplitude of N1 from last awake (point B) to first unconscious (point C) was also significant (mean difference in amplitude 1.69 µV, P=0.02).
Conclusions. MMN is unlikely to be a clinically useful tool to detect awareness in surgical patients. In contrast, the loss of N1 may identify the transition from consciousness to unconsciousness and deserves further study.
Br J Anaesth 2002; 89: 382–8
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