1Department of Neurosurgery and 2Department of Anaesthetics, Frenchay Hospital, Bristol, UK*Corresponding author: Department of Neurosurgery, The Radcliffe Infirmary, Woodstock Road, Oxford OX2 1HE, UK
Accepted for publication: November 17, 2000
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Abstract |
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Br J Anaesth 2001; 86: 51922
Keywords: anaesthesia, depth; equipment, piezoelectric strain gauge; anaesthetics i.v., propofol
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Introduction |
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Ocular microtremor (OMT) is a small high frequency tremor of the eyes present in all individuals. This tremor is caused by high frequency extra-ocular muscle stimulation which originates in the oculomotor area of the brainstem.2 The oculomotor neurons are embedded in the reticular formation of the brainstem.3 However, neural activity from other areas outside of the brainstem impinge on the oculomotor nuclei. These include the frontal eye fields (areas 6 and 8),4 the inferior parietal cortex (area 7)5 and the cerebellum.6 The OMT signal appears as an irregular oscillatory movement with intermittent burst-like components. The peak-to-peak rotation involves a displacement of the surface of the eye of between about 150 and 2000 nm.7 The mean OMT peak count frequency in the normal population is 84 Hz (SD 6).8
The initial interest in OMT was stimulated by its purported role in the visual process, as part of the dynamic theories of vision.9 More recently, the appreciation of OMT as a primarily neurological phenomenon has stimulated interest in its clinical applications.1 Several studies have already shown that the frequency of this tremor is reduced in patients whose level of consciousness has been affected by head injury or anaesthesia.1 1012 Both Coakley13 and Bolger12 studied the effect of thiopental on OMT activity. Both studies showed a reduction in the high frequency components of OMT activity with a shift of the spectrum to the left, although the number of subjects studied was small. However, in the case of Coakley,13 a number of agents were used including neuromuscular block.
It would therefore seem possible that OMT recordings could be used to determine depth of anaesthesia. The present study was undertaken to show the effect of general anaesthesia induced with propofol on OMT. Assessment of the changes in OMT in the awake and unconscious state was also studied independent of the dose of propofol.
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Methods |
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Recording session
OMT recordings were taken pre-operatively on the ward at admission using the piezoelectric strain gauge technique (baseline recording).14 This technique has been described in detail elsewhere7 and provides a reliable estimate of OMT activity.15 Briefly, the piezoelectric transducer is mounted in a Perspex rod and the protruding end is coated with rubber. The subject lies supine looking straight ahead wearing a headset. During anaesthesia this eye position may change but studies by Bolger12 have shown there is no significant overall variation in OMT mean peak count frequency with eye deviation. The subjects eyelids are taped apart and the scleral surface is anaesthetized with 0.5% hydroxymethacaine hydrochloride. The piezoelectric probe is mounted in the headset and lowered so the rubber tip is just touching the scleral surface. Probe placement is judged by visual inspection and by listening to the signal being recorded using audiocassette headphones. The signal is processed in a conditioning unit and then recorded on an audiocassette recorder. A recording of between 30 and 60 s was taken.15 Analysis is performed on an IBM compatible PC with a special OMT processing package. An example of a normal OMT recording from an alert individual is shown in Figure 1.
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However, the model assumes immediate mixing in blood and takes no account of the delay required to achieve equilibration in the brain. Thus, a delay occurs between the time when a DiprifusorTM system indicates a target concentration has been reached and the time of maximum pharmacodynamic effect. Using a computer simulated model based on the Marsh pharmacokinetic parameters, it was clear that a period of 5 min would be long enough to allow steady state conditions to occur between the blood and effector site compartments.
The TCI infusion was started at a concentration of 1 µg ml1 predicted blood propofol concentration and after a period of 5 min, allowing for equilibration, OMT activity was recorded and then the patients level of consciousness was assessed. They were deemed to have lost consciousness if there was loss of response to verbal command and no eyelash reflex present.
The reading taken before this point, at the lower predicted blood propofol concentration, was termed the last awake recording. The process was then repeated at predicted blood propofol concentrations of 2, 3 and 5 µg ml1. When all the required recordings had been made either the patients trachea was intubated or a laryngeal mask inserted and anaesthesia maintained appropriate for the intended surgery.
Analysis of records
Each subject had a baseline OMT record and then between two and four further recordings at each different predicted plasma propofol concentration. OMT recording was difficult in some subjects at different levels of awareness because of coughing or sneezing. Records were analysed using peak count analysis of dominant frequency. Comparison of peak count variables was performed using the Wilcoxon matched-pairs signed-ranks test.
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Results |
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Discussion |
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Anaesthetic agents appear to have a predilection for the reticular activating system even if they do also act more diffusely in the brain. Recent studies by Rampil and colleagues20 in rats support the hypothesis that anaesthetics have a primary action within the midbrain or lower. OMT is a high frequency tremor caused by impulses emanating from the oculomotor area in the brain stem. The oculomotor neurons are embedded in the reticular activating system.3 Therefore, we would expect that agents affecting this area would also influence OMT activity.
This study confirms that ocular microtremor activity is affected by propofol. Previous studies by Coakley13 and Bolger12 also showed that OMT activity is affected by thiopental. In the study by Coakley13 a number of agents were used, including neuromuscular block, and in all but two cases recordings were made with a closed eye transducer. The report by Bolger12 studied only five patients. However, neither study gave details of induction times or assessment of levels of awareness.
This study has shown that the mean OMT peak count frequency is reduced progressively at predicted plasma propofol concentrations of 1 and 2 µg ml1 and then plateaued between 3 and 5 µg ml1. Significantly, in this study no subject was conscious at predicted plasma concentrations of 3 µg ml1 and at these concentrations none of the subjects had a peak count frequency above 55 Hz. After loss of consciousness, OMT activity remained below this level (55 Hz). There was no significant difference between mean peak count frequency at loss of consciousness and readings taken thereafter, even at increasing predicted plasma propofol concentrations. There is a significant difference between the last awake OMT recording and the first recording taken at loss of consciousness (P<0.001). The actual frequency at which subjects lost consciousness, however, was very variableranging from 27 to 55 Hz. It may be that a better predictor of the actual mean peak count frequency at which there was loss of consciousness in each subject would be to calculate a percentage of the baseline frequency for each subject. In this study, if we set a value of 45% of the baseline frequency for each subject, then 17 out of the 21 subjects had lost consciousness at this predicted OMT frequency (81%).
These results are encouraging and indicate that in the subjects studied OMT activity varies with awareness. With regards to depth of anaesthesia, we could postulate that any increase in OMT above the mean peak count frequency noted at loss of consciousness could indicate lightening of anaesthetic depth. It is interesting that studies of the effect of propofol on the auditory evoked response have shown no significant effect on the amplitude and latency of the brain stem waves.21 In our study there is a clear effect on OMT, which has been shown to be an indicator of brain stem function.1 However, if this is to be used in the clinical setting, more information is required on the effect of other agents on OMT activity such as opiates, neuromuscular block agents and, in particular, surgical stimulus. For continuous monitoring during anaesthesia, recordings will need to be made through the closed eyelid. These points are currently being investigated.
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Acknowledgements |
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References |
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