|
 |
EEG and AEP monitoring during surgery
Dr. Gerhard Schneider, MD
Klinik für Anaesthesiologie,
Klinikum Rechts der Isar Technische Universität
Munich, Germany
Article also available in
PDF:
47 KB
Presented at the 9th ESA Annual Meeting, Gothenburg,
Sweden: April 7-10, 2001.
For many years, neurological signs have been used to
quantify the effect of anesthetics on the brain. When balanced general
anesthesia with a combination of drugs became popular, Guedel’s
traditional classification of stages of general anesthesia [1] was not
useful, as it was based on patients’ neurological signs.
Today, monitoring the target organ of general anesthesia
can be accomplished using spontaneous and evoked electrical responses
of the brain. This abstract focuses on the use of EEG and auditory evoked
potentials (AEP) during general anesthesia and surgery.
Spontaneous EEG
The conventional EEG is recorded from scalp electrodes,
and shows cortical electrical activity. This includes cortical manifestation
of the sub cortical regions (projection pathways, thalamus, reticular
formation, mesencephalon).
Recording electrodes
Standard placement of scalp electrodes follows the international 10-20
system. This allows for the anatomic localization of the signal. In order
to obtain good signal quality, recording electrode impedance should be
kept below 5kOhms, with only little differences between the electrodes.
If the electrode impedance increases, background noise and artifacts may
obscure the EEG signal. As a consequence, the signal to noise ratio would
then decrease.
Characteristics
of the EEG signal
The EEG signal can be described by three basic parameters:
- Amplitude (20-250 µV)
- Frequency (0.5-70 Hz)
- Time (continuous in raw EEG, epoch in processed EEG).
Processed EEG
Since the interpretation of the standard raw EEG is time consuming and
requires much experience, different EEG processing methods have been developed
to facilitate interpretation. Typically, raw EEG can be described as a
sum of superimposed sine waves. The Fast Fourier analysis is a method
to decompose the signal into sine waves, and this
analysis results in the power spectrum of the EEG. According to predefined
frequencies, the spectrum can be divided into spectral bands: delta (0.5-4
Hz), theta (4-8 Hz), alpha (8-13 Hz) and beta (over 13 Hz). Further analysis
can be applied to calculate single numerical parameters, such as spectral
edge frequency (SEF) and median frequency (MF) [2]. Lately, scientific
papers have appeared suggesting non-linear analysis as a target for future
EEG research [3-5].
As the EEG reflects the functional status of the brain,
it can be used to monitor its functional integrity. However, changes in
EEG are not necessarily specific to underlying mechanisms. For example,
slowing of EEG may reflect either changes in anesthetic concentrations
or cerebral ischemia.
Auditory Evoked Potentials
Audio evoked potentials (AEP) reflect the function
of the auditory pathway [6]. AEP can be evoked by repeated clicks of short
duration (100-500 ms) given into an ear piece. Trigger-synchronized averaging
of a defined number of EEG-segments is used to extract the AEP by reduction
of the underlying EEG signal (background noise). The reduction in background
noise is proportional to the square root of the number of averaged segments;
the more averaged segments, the better the quality of the AEP. However,
increasing number of segments, results in prolonged duration of measurement
and delays display of results. Then, the system becomes less responsive
to rapid changes.
The extracted AEP signal consists of a number of waves.
Conventional analysis of the AEP response measures latencies and amplitudes
of particular peaks. Three main groups of peaks can be distinguished and
they can be correlated to the anatomical structures [7]:
- Brainstem AEP (BAEP) with latencies shorter than
10 milliseconds. Anatomical structures: cochlea, acoustic nerve (BAEP
wave I, II), brainstem (BAEP wave III-V)
- Middle latency AEP (MLAEP) with latencies of 10-50
milliseconds. Anatomical structures: medial geniculate and primary auditory
cortex (temporal lobe).
- Late cortical waves with latencies over 50 milliseconds.
Anatomical structures: frontal cortex, association fields.
Sophisticated research level methods of AEP analysis include wavelet-transformation
[8], and the use of an autoregressive model with exogenous input (ARX
model) [9].
Some factors which
may influence AEP
Variations in the auditory stimulus influence the AEP waveform. The increased
volume of the auditory stimulus increases amplitudes and decreases latencies.
If binaural stimulation is used, it can increase AEP amplitudes and decreases
latencies.
Some physiological variables may also influence AEP. These include hypothermia
(increasing latencies, decreasing amplitudes) and hyperthermia (producing
the opposite effect). In addition, psycho-physiological factors like habituation,
vigilance, and attention (with influence on late cortical waves) may have
an impact. As an example, sleep and arousal leads to dramatic changes
on MLAEP (wave peak Pa), up to complete loss of wave peaks Pb and P1 [6].
Pathophysiological factors may also influence AEP signals.
That list includes conductive and sensory neural hearing disorders, demyelinating
diseases (multiple sclerosis), ischemia, coma, and tumors.
Clinical Applications
Application of
AEP
In anesthesia, clinical applications of AEP include use of BAEP (hardly
influenced by anesthetics) in acoustic neurinoma (vestibulocochlear nerve)
and posterior fossa surgery. Anesthetic drugs may influence MLAEP (Wave
Peaks Pa, Nb). Scientific papers have appeared suggesting use of that
information to quantify anesthesia [10].
Application of
EEG in anesthesia and surgery
Although anesthetic drugs often cause drug-specific EEG changes, a general
pattern of change in anesthesia can be observed. Most anesthetic drugs
(not ketamine) lead to a decrease of frequencies and an increase of amplitudes.
Specific applications of the EEG include mapping of
brain electrical activity for seizure surgery [11]. Epileptic discharges
can be detected in the spontaneous EEG, which may not only be useful in
epileptic patients, but also with the use of some inhalation
agents (enflurane, sevoflurane) [12-15]. In epileptic patients, not only
seizure detectioncontrol of therapeutic measures (i.e. medications) can
be accomplished by EEG [16].
Detection of brain
ischemia
Before irreversible damage, global ischemia can be detected by a slowing
of the EEG, followed by burst suppression and electrical silence. The
electric failure precedes membrane failure [17].
The decrease of cerebral perfusion (40-50 ml min-1
100 g-1 brain tissue) results in progressive EEG changes (increase of
polymorph slow waves, i.e. theta and delta) (16-20 ml min-1 100 g-1 brain
tissue), loss of evoked brainstem potentials (12-15 ml min-1 100 g-1 brain
tissue) before irreversible neuronal death occurs (<6 ml min-1 100
g-1 brain tissue).
The influence of mean arterial pressure, body temperature,
arterial O2, and Hct can be assessed directly, as EEG provides functional
monitoring. Focal changes can be judged in clinical context as e.g. provoked
by a subdural hematoma, resulting in depression of amplitudes.
During surgery of the carotid artery, ischemia can
be detected by observing differences between brain hemispheres. Characteristic
changes include increase of polymorph slow waves (theta and delta) or
changes of processed parameters, like spectral edge frequency (SEF). The
changes usually occur within 60 seconds following ischemia [18-19].
In addition to detection of critical cerebral perfusion,
the effect of therapy can directly be assessed. The effects of measures
for cerebral protection (e.g. induction of total electrical suppression)
can also be monitored [20].
Summary
The advantages of EEG and AEP monitoring outweigh their
limitations, in spite of some complexity and multifactorial influences
that need to be understood. Hence, monitoring of these signals has not
been routine practice. However, their measurement would enable observation
of functional integrity and changes, where clinical symptoms could not
be reliably observed. The introduction of computerized signal analysis
makes it easier for the non-expert to interpret the EEG and AEP signals
in daily clinical work.
References
- Guedel, A.E.: Third Stage Ether Anesthesia: A Sub-Classification Regarding
the Significance of the Position and Movement of the Eyeball. American
Journal of Surgery, Quarterly Supplement of Anesthesia and Analgesia,
1920. 34(4): p. 53-7.
- Drummond, J.C., et al.: A comparison of median frequency, spectral
edge frequency, a frequency band power ratio, total power, and dominance
shift in the determination of depth of anesthesia. Acta Anaesthesiologica
Scandinavica, 1991. 35(8): p. 693-9.
- Viertiö-Oja, H.E., et al.: New Method to Determine Depth of Anesthesia
From EEG Measurements. Abstracts of The Annual Meeting of the Society
for Technology in Anesthesia www.anestech.org/publications/Annual_2000/Viertio-Oja.html,
2000.
- Bruhn, J., H. Röpcke, and A. Hoeft: Approximate entropy as an
electroencephalographic measure of anesthetic drug effect during desflurane
anesthesia. Anesthesiology, 2000. 92(3): p. 715-26.
- Abke, J., et al.: Detection of Inadequate Anesthesia by EEG Power
and Bispectral Analysis. Anesthesiology, 1996. 85(3A): A477.
- Thornton, C. and R.M. Sharpe: Evoked responses in anaesthesia. British
Journal of Anaesthesia, 1998. 81(5): p. 771-81.
- Picton, T.W., et al.: Human auditory evoked potentials. I. Evaluation
of components. Electroencephalography & Clinical Neurophysiology,
1974. 36(2): p. 179-90.
- Stockmanns, G., et al.: Wavelet-Analyse akustisch evozierter Potentiale
wahrend wiederholter Propofol-Sedierung. Biomedizinische Technik, 1997.
42(S): p. 373-4.
- Jensen, E.W., P. Lindholm, and S.W. Henneberg: Autoregressive modeling
with exogenous input of middle-latency auditory-evoked potentials to
measure rapid changes in depth of anesthesia. Methods of Information
in Medicine, 1996. 35(3): p. 256-60.
- Schneider, G. and P.S. Sebel: Monitoring depth of anaesthesia. European
Journal of Anaesthesiology, 1997. 15(S): p. 21-8.
- MacDonald, D.B. and N. Pillay: Intraoperative electrocorticography
in temporal lobe epilepsy surgery. Canadian Journal of Neurological
Sciences, 2000. 27(S 1): p. S85-91.
- Woodforth, I.J., et al.: Electroencephalographic evidence of seizure
activity under deep sevoflurane anesthesia in a nonepileptic patient.
Anesthesiology,1997. 87(6): p. 1579-82.
- Yli-Hankala, A., et al.: Epileptiform electroencephalogram during
mask induction of anesthesia with sevoflurane. Anesthesiology, 1999.
91(6): p. 1596-603.
- Kaisti, K.K., et al.: Epileptiform discharges during 2 MAC sevoflurane
anesthesia in two healthy volunteers. Anesthesiology, 1999. 91(6): p.
1952-5.
- Hilty, C.A. and J.C. Drummond: Seizure-like activity on emergence
from sevoflurane anesthesia. Anesthesiology, 2000. 93(5): p. 1357-9.
- Van Ness, P.C.: Pentobarbital and EEG burst suppression in treatment
of status epilepticus refractory to benzodiazepines and phenytoin. Epilepsia,
1990. 31(1): p. 61-7.
- Drummond, J.C. and Patel P.J.: Cerebral physiology and the effects
of anesthetics and techniques. In: Miller R.D. (ed) Anesthesia. Churchill
Livingstone, New York, 2000: p. 695-733.
- Rampil, I.J., et al.: Prognostic value of computerized EEG analysis
during carotid endarterectomy. Anesthesia & Analgesia, 1983. 62(2):
p. 186-92.
- Minicucci, F., et al.: Computer-assisted EEG monitoring during carotid
endarterectomy. Journal of Clinical Neurophysiology, 2000. 17(1): p.
101-7.
- Doyle, P.W. and B.F. Matta: Burst suppression or isoelectric encephalogram
for cerebral protection: evidence from metabolic suppression studies.
British Journal of Anaesthesia, 1999. 83(4): p. 580-4.
Last
updated: 1 June 2001Created |
 |
| Legal
notice |
© GE
Healthcare 2008
ISSN 1795-6269 (Web)
ISSN 1795-6277 (CD) |
Webmaster |
|
 |
|