Department of Anaesthesia, Imperial College School of Anaesthesia at Northwick Park Hospital, Watford Road, Harrow, Middlesex HA1 3AJ, UK*Corresponding author
Accepted for publication: August 21, 2000
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Abstract |
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Br J Anaesth 2001; 86: 5962
Keywords: anaesthetics volatile, desflurane; anaesthetics volatile, sevoflurane; brain, evoked responses
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Introduction |
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Patients and methods |
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Patients were randomized to receive five sequential concentrations of sevoflurane or desflurane. To correct for possible time trends and to ensure adequate equilibration at each anaesthetic level patients were also randomized to receive the agent in an ascending or descending order. The levels were set at approximately 0.5 MAC intervals, and each end-tidal concentration was maintained for at least 10 min to allow equilibration prior to data collection. At the end of data collection the patients were transferred to the operating theatre and the operation started.
Data collection
The median nerve was stimulated at the wrist with an electrical pulse delivered at a rate of 2.2 s1 and at an intensity adjusted to just above the motor threshold (1113 mA). The SER was derived from the electroencephalogram, and recorded using silver/silver chloride electrodes attached at Fz and C3. SER data were collected over the last 2.6 min of each agent concentration period (356 EEG sweeps) on a system developed in our unit.10 These were averaged and analysed offline. The amplitudes P15-N20, N20-P25 and P25-N35 were measured at each anaesthetic concentration.
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Results |
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Discussion |
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Increases in P15-N20 amplitude after bolus doses of etomidate have been reported,1315 during surgery with non standardized and varied doses of anaesthetic agents. This may represent the same phenomenon but the presence of other agents and variable surgical stimuli may be confounding. The technique was recommended to augment SER signals during surgery. Jantti and colleagues also reported an increase in this amplitude during sevoflurane anaesthesia.16 They recorded data at burst suppression (1.52.5 MAC sevoflurane) rather than at specific anaesthetic end-tidal concentrations and found similar potentiation of this amplitude, but did not report amplitude changes over a range of concentrations in each subject.
There are several plausible reasons for this increase. The site of increased activity cannot be localized anatomically from these data, because the amplitude represents the activity attributable to the median nerve stimulus at the stated time after stimulation rather than at a known site in the midbrain. However, it is widely held that the generators of the P15-N20 amplitude are in the pontothalamic area.
Increasing electrical activity in the midbrain could be caused by a direct, anaesthetic mediated increase in inhibitory postsynaptic potential (IPSP) generation, or a more generalized interruption of intercellular communication. One interesting possibility involves recent in vitro work by Traub, Whittington and others, which shows that anaesthetic and analgesic drugs disrupt gamma frequency oscillations originating in the hippocampus and midbrain.17 18 These high-frequency signals are thought to represent the co-ordination of sensory input analysis between anatomically discrete areas of the brain. When disrupted, the gamma frequency output increases. This is thought to be due to anaesthetic and analgesic drugs decreasing gamma-aminobutyric acid (GABA) type A receptor mediated inhibition of excitatory and inhibitory interneurons.19 This increase in gamma signal could explain the increased electrical activity in the midbrain seen up to the point where direct pathway effects (burst suppression of the EEG) are seen, causing the fall in voltage at higher anaesthetic concentrations. It also may explain the increasing sensory detachment leading to and including the state of anaesthesia. However there is no human in vivo evidence to support or refute this at present.
The peak values at the points of inflexion of sevoflurane and desflurane differ significantly when compared using MAC values. These data must be interpreted carefully as the desflurane group peak value is not central in the data points measured. However, MAC is primarily a motor descriptor and the SER relies on a purely sensory pathway. Thus, in the same way as different volatile anaesthetics may have different vasodilator effects at equal MAC concentrations, their effects on neuronal transmission may differ.
In conclusion, we have found that the subcortical SER does not respond in a uniform way to increasing anaesthetic concentration. The N20-P25 and P25-N35 amplitudes decrease with increasing anaesthetic concentration, but the P15-N20 wave is potentiated at clinically relevant end tidal sevoflurane and desflurane concentrations.
Further work is needed to more closely analyse the anatomical site, if any, of this increased signal.
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References |
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