Indian

304 J. Anaesth. 2002; 46 (4) : 304-314 INDIAN JOURNAL OF ANAESTHESIA, AUGUST 2002
304

NEUROLOGICAL MONITORING
Dr. G. S. Umamaheswara Rao1

Specialised monitoring is essential in neurological Intracranial pressure

patients in the operating rooms and intensive care units
to prevent ischaemic and mechanical injury to the nervous
system. The systems currently available for the purpose
may be broadly classified into those that monitor
intracranial pressure and blood flow dynamics and those
that monitor brain electrical activity. The current review
aims to present the principles and clinical applications
of some of the monitoring systems. The role of some of
these systems still remains ill-defined. Many of them
are expensive. Interpretation of the data from these
monitors depends on a thorough knowledge of the clinical
and technical aspects of the modality in use. A list of
monitors that are clinically available at present is given
in Table 1.
Table 1. Neurological Monitors
Monitors of Intracranial Pressure and Blood Flow Dynamics
Intracranial Pressure Monitor
Jugular Venous Oximetry
Transcranial Doppler Sonography
Brain Tissue Oxygen Tension Monitor
Near-infrared Spectroscopy
Monitors of Brain Electrical Activity
Electroencephalography
Evoked Potentials
Normal Intracranial Pressure (ICP) is defined as
the pressure inside the lateral ventricles/lumbar
subarachnoid space in supine position. The normal value
of ICP is 10-15 mm Hg in adults. It is around 2-4 mmHg
in neonates and infants. ICP is a reflection of the relation
between intracranial contents and the available intracranial
volume. Normal intracranial contents include brain (80%),
cerebrospinal fluid (CSF) (10%) and intracranial blood
volume (10%). Any increase in the volume of intracranial
contents (tumours, haematomas, oedema, hyperaemia,
hydrocephalus) within the confines of rigid skull increases
the ICP. As the volume of intracranial contents increases,
displacement of intracranial blood volume and CSF tends
to prevent an increase in ICP. With increasing ICP, the
rate of CSF reabsorption increases. The rate of CSF
formation decreases very little until ICP approaches arterial
pressure. Exhaustion of intracranial reserve leads to rapid
rise in ICP. The purpose of ICP monitoring is to identify
such increase in ICP and treat it before it causes cerebral
ischaemia or herniation of the brain structures.
Indications for ICP monitoring
Head trauma provided the largest volume of
experience with ICP monitoring, though it has also been
used in various other neurological conditions.
Recommendations for ICP monitoring in some of the
common neurological conditions are as follows:

Sensory Evoked Potentials Head injury

Visual About two thirds of patients with severe head injury
Somatosensory have intracranial hypertension (ICP>20 mmHg).
Auditory
Aggressive maintenance of ICP at less than 15 mmHg has
Motor Evoked Potentials
been suggested to improve the outcome1 though this is
contested by some recent evidence.2 The recommendations
of the Brain Trauma Foundation and American Association
of Neurological Surgeons, for ICP monitoring, in head
trauma are as follows3:
Correspond to :
1. Professor, Department of Neuroanaesthesia 1. ICP monitoring is appropriate in patients with severe
National Institute of Mental Health and Neurosciences
head injury (GCS 3-8 after cardiopulmonary
Bangalore 560 029.
Tel : 91-80-699 5415 / 699 5416, resuscitation) with an abnormal admission CT scan.
Fax : 91-80-656 4830 An abnormal CT scan of the head is one that reveals
Email : gsuma@nimhans.kar.nic.in haematomas, contusions, oedema, or compressed
gsuma123@yahoo.com
basal cisterns.
UMAMAHESWARA RAO : NEUROLOGICAL MONITORING
2. ICP monitoring is appropriate in patients with severe
head injury with a normal CT scan if two or more
of the following features are noted at admission:
age over 40 years, unilateral or bilateral motor
posturing, systolic blood pressure < 90 mmHg.
3. ICP monitoring is not routinely indicated in patients
with mild or moderate head injury. However, a
physician may choose to monitor ICP in certain
conscious patients with traumatic mass lesions such
as haematomas and contusions.
Augmentation of CPP helps to avoid both global
and regional ischaemia in brain trauma. The Brain Trauma
Foundation suggests a CPP > 70 mmHg as an option in
the management of severe head injury.4 This can be
effectively achieved only by concurrent measurement of
ICP and systemic blood pressure.
Brain tumours
The indications for ICP monitoring in patients with
brain tumours are not clearly defined. Postoperative ICP
monitoring is employed in patients with massive
intraoperative brain swelling requiring aggressive
treatments such as mechanical ventilation, barbiturate
therapy etc. ICP monitoring is also helpful to diagnose
postoperative haematoma in patients at enhanced risk
(e.g., intraventricular tumours).
Subarachnoid haemorrhage
In patients with aneurysmal subarachnoid
haemorrhage, ICP monitoring helps to diagnose occurrence
of hydrocephalus and brain oedema due to cerebral
vasospasm. In patients undergoing surgical or
interventional neuroradological procedures for
arteriovenous malformations, ICP monitoring aids in early
detection of normal perfusion pressure breakthrough
oedema, a complication that follows acute ablation of a
high flow AVM.
Hydrocephalus
ICP monitoring establishes the need for CSF
diversion procedures in patients with hydrocephalus when
the indication for such an intervention is equivocal
(e.g., tuberculous meningitis).
Neuromedical conditions
ICP monitoring has also been used in Rye’s
syndrome, stroke, and encephalitis associated with raised
ICP though the indications are not clearly mentioned.
Techniques of ICP monitoring
The credit for systematic monitoring of ICP goes
to Lundberg who performed CSF pressure measurements
in 1960s. Currently there are a number of devices for
monitoring the ICP (Fig 1).
305
Figure 1. Techniques of intracranial pressure monitoring : 1.Intraventricular
Catheter, 2. Intraparenchymal fiberoptic device, 3. Subdural bolt, 4. Epidural
Device, 5. Subdural catheter.
Intraventricular Catheter : Percutaneous
intraventricular pressure monitoring is the gold standard
against which all other ICP monitors are evaluated. The
lateral ventricle is cannulated by a frontal, occipital,
parieto-occipital or parasagittal coronal approach and the
cannula is connected to a pressure transducer through a
fluid column. The transducer is zeroed at the level of the
external auditory meatus. The advantages of
intraventricular monitoring are: a) it is reliable, b) it can
be used for measurement of intracranial compliance, c)
ventricular catheter can also be used for draining CSF to
decrease the ICP. However, it is an invasive procedure
associated with definite risks of infection and trauma to
the brain during cannulation. Ventricular collapse in
patients with brain oedema may render placement of the
catheter difficult and also interfere with actual pressure
recordings, even if the catheter is in place.
Subdural Bolt : It is a hollow bolt threaded through
a twist drill hole into the skull and duramater until the
inner surface of the bolt lies flush with the arachnoid
membrane. The bolt is connected to a pressure transducer
via a saline column. The pressure transmitted to the
arachnoid membrane is conducted through the fluid column
to the pressure transducer. The advantage of this system
is that it does not involve injury to the brain. Its
disadvantages include inability to draw CSF, infection,
and malfunction if the bolt becomes loose or the brain
matter protrudes into the hollow of the bolt.
Fiberoptic Devices : Miniature fiberoptic catheters
are presently available, which can be placed in the
ventricles, epidural or subdural space or even in the brain
parenchyma. Since it is a self enclosed electronic system,
problems associated with fluid filled systems such as
leaking, drift and infection are minimised. The level of
the transducer is of no concern because the transducer is
at the tip of the catheter.
306
Gaeltec Transducer Tipped Catheter : This is a
device containing a small strain gauze at the tip of a
flexible 5 F double lumen tube. Any deformation of the
diaphragm of the strain gauze caused by raised ICP
changes its resistance. The measured change in resistance
is used to calibrate the ICP. The device has a provision
for calibration in situ.
Anterior Fontanel Monitor : The device is applied
to the anterior fontanel in infants. A pneumoelectric switch
inside the device closes when external pressure is applied.
It activates a pneumatic system that pressurises the device.
The switch opens when the external and internal pressures
on the device are equal. The internal pressure of the device,
at this stage, is taken as being representative of the ICP.
Ventricular pressure measurement is the reference
standard for ICP monitoring. Fluid-coupled epidural or
subarachnoid devices are less accurate than ventricular
pressure monitors. Devices with transducer tipped catheters
have been found to be comparable to ventricular pressure
monitors.
Abnormalities of ICP waveform
Under physiological conditions ICP shows a
pulsatile recording with slow respiratory component
superimposed on a biphasic recording synchronous with
cardiac cycle. Normally, respiratory oscillations are greater
than the cardiac oscillations, but when ICP increases,
arterial pulsations also assume greater amplitude. In
addition to these two types of physiological fluctuations,
three other pathological wave forms have been described
in patients with raised ICP - Lundberg ‘A’ (plateau), ‘B’
and ‘C’ waves.
Figure 2. Pathological ICP Fluctuations : A) ‘A’ waves (Plateau Waves),
B) ‘B’ Waves occurring synchronous with Cheyne-Stoke’s breathing
INDIAN JOURNAL OF ANAESTHESIA, AUGUST 2002
‘A’ waves, also called as plateau waves, represent
severe pathological elevation of ICP caused by changes
in regional cerebral blood volume (CBV). During these
episodes, ICP rises to above 40 mmHg and is sustained
at that level for 5-20 min (Fig 2). Initially, ICP returns
to baseline level between two successive plateau waves,
but progressively the baseline ICP also tends to increase.
Occurrence of plateau waves is associated with clinical
deterioration of the patient. The patient may complain of
headache, loss of consciousness, or exhibit abnormal motor
responses, breathing patterns and pupillary signs during
these episodes.
‘B’ waves have an amplitude of about 20 mm Hg
and occur at a rate of 1-2 per min. They are of less
dramatic importance than ‘A’ waves, but act as warning
signs of decreased intracranial compliance and enhanced
risk of intracranial hypertension. ‘B’ waves, most often,
occur synchronous with Cheyne-Stoke’s breathing
(Fig 2).
‘C’ waves are not of any major pathological
significance.
A change in ICP in response to a change in the
volume of intracranial contents is a measure of intracranial
elastance. The reciprocal of elastance is called compliance.
The ICP change caused by addition of 1 ml of saline into
the CSF space is a parameter that quantifies intracranial
compliance and is referred to as Volume Pressure Ratio
(VPR). A VPR of 4 mmHgml–1 or more indicates a gross
decrease in intracranial compliance. Pressure Volume Index
(PVI) is another measure of intracranial compliance. PVI
is calculated by the following formula:
PVI = dV / Log (Pf/Pi)
In the above equation, dV is the change in the
volume of the intracranial contents, Pi is the initial ICP
and Pf is the ICP after addition or withdrawal of a known
volume of CSF. A PVI less than 10 ml is associated with
a poor outcome.
Transcranial doppler
Transcranial Doppler sonography is used to measure
the blood flow velocity in the major cerebral blood vessels.
Normal skull offers barrier for ultrasonic beam. An
examination carried out through the temporal window,
orbital foramen or foramen magnum by using a 2 MHz
probe has been found to provide clinically useful
information that has a good correlation with the cerebral
blood flow (CBF) changes.5 Middle cerebral artery is
commonly chosen for examination as it can be easily
insolated and 75-80% of ipsilateral carotid blood flow,
flows through MCA.
UMAMAHESWARA RAO : NEUROLOGICAL MONITORING
Figure 3. Normal transcranial Doppler flow velocity waveform
The morphology of a normal flow velocity
waveform from MCA is shown in figure 3. The velocities
that are measured are the peak systolic velocity, end-
diastolic velocity and mean velocity. Pulsatality index
(PI) is a derived parameter calculated from the measured
velocities.
Pulsatality Index = (Peak Systolic Velocity - End
Diastolic Velocity) / Mean Velocity
Interpretation of TCD data requires an understanding
of the relationship between CBF and cerebral blood flow
velocity (CBFV). Provided the vessel diameter is constant,
a change in velocity is proportional to the change in flow.
In other words, an increase or decrease of CBFV represents
a similar change of CBF. When the insolated vessel diameter
is not constant, a change in the velocity has no predictable
relation to the CBF; it merely signifies a change in the
diameter of the vessel. For example, in a patient with
cerebral vasospasm, an increase in CBFV indicates
aggravation of vasospasm. From the foregoing discussion,
it follows that an increase in MCA blood flow velocity
may indicate cerebral hyperemia or cerebral vasospasm.
The distinction between the two can be made by hemispheric
index, which is calculated as follows :
Hemispheric Index = VMCA/VICA
VMCA is the MCA flow velocity and VICA is the
ipsilateral extracranial internal carotid artery (ICA) flow
velocity. A value greater than 3 is a definite indicator of
cerebral vasospasm.
A progressive increase in ICP and decrease in CPP
are associated with characteristic changes in the
morphology of flow velocity waveform (Fig 4). As the
ICP increases, diastolic velocity decreases and the
pulsatality increases. When the ICP is higher than the
diastolic blood pressure but lower than the systolic blood
pressure, a biphasic wave pattern results, followed later,
by a total disappearance of the wave form when intracranial
circulatory arrest occurs.6 A good correlation exists
between PI and ICP in head trauma.7
307
Figure 4. Changes in TCD flow velocity waveform
associated with a progressive increase in ICP
Some of the important clinical applications of TCD
are as follows:
1. It is useful as a noninvasive monitor of CBF.
2. It is helpful to diagnose cerebral vasospasm and
monitor response to therapy in patients with
subarachnoid haemorrhage and head injury.
3. It is used to study autoregulation of CBF and cerebral
vascular response to carbon dioxide.
4. It can be used to assess intracranial circulatory status
in raised ICP.
5. It can be a useful tool to identify intraoperative
cerebral embolisation during surgery on carotid artery
and cardiopulmonary bypass procedures.
6. It can be used to optimise CPP and hyperventilation
in patients with head injury.
Jugular venous oximetry
Monitoring cerebral venous oxygen saturation as a
measure of adequacy of CBF is based on the premise that
the product of CBF and arteriovenous oxygen difference
gives the cerebral metabolic rate of oxygen.
(A-V)DO2 x CBF = CMRO2
From the above, it can be deduced that when
CMRO2 is constant, any change in CBF is associated with
a reciprocal change in the cerebral arteriovenous oxygen
difference. Since arterial oxygen content varies very little
over time in an individual with normal cardiorespiratory
function, any decrease in CBF must be accompanied by
a corresponding decrease in cerebral venous oxygen
saturation if CMRO2 is constant.
308
Continuous monitoring of jugular venous
oxygen saturation (SjVO2) is carried out by a catheter
placed retrograde through the internal jugular vein into
the jugular bulb. For accurate measurement, the tip of
the catheter must be within 1 cm of the jugular bulb.
Improper placement of the tip of the catheter may lead to
erroneous values because of the contamination of the
blood sample with venous drainage from extracranial
veins. Once the catheter is in place, blood samples
may be obtained intermittently and subjected to gas
analysis. Alternatively, commercially available oximetric
catheters may be used for continuous online measurement
of SjVO2.
With the help of a jugular catheter it is possible to
obtain at least three indices that are helpful in assessing
the adequacy of CBF: 1) jugular venous oxygen saturation
(SjVO2), 2) cerebral arteriovenous oxygen difference
(A-VDO2) (the difference between arterial and jugular
venous oxygen content) and 3) cerebral oxygen extraction
(CEO2) (the difference between SaO2 and SjVO2). Normal
and abnormal values for these indices are given in table
2. A low SjVO2, a high (A-V)DO2 or a high CEO2
indicates increased extraction of oxygen, which could be
an early sign of cerebral ischaemia.
Table 2 : Indices of adequacy of cerebral blood flow
derived from SjVO2 monitoring
1. SjVO2 : Normal - 60-80%
: Hyperaemia > 90%
: Low flow < 50%
2. (A-V)DO2 : Normal - 5 - 7.5 vol %
(CMRO2/CBF) : Hyperaemia < 5 vol %
: Low flow > 7.5 vol %
3. CEO2 : Normal - 24-40%
: Hyperaemia < 24%
: Low flow > 40%
SjVO2 = Jugular venous oxygen saturation; (A-V)DO2 = Cerebral
arteriovenous oxygen difference
CEO2 = Cerebral oxygen extraction
Clinical applications of SjVO2 monitoring
SjVO2 monitoring has been used to detect cerebral
ischaemia during vascular neurosurgical and
cardiopulmonary bypass procedures. Episodes of cerebral
oxygen desaturation have been documented in about a
third of patients with even normal CPP during craniotomy.8
In head injured patients, cerebral oxygen desaturation to
less than 50% has been correlated with unfavorable
outcome.9 SjVO2 monitoring can also be utilised to optimise
the levels of CPP and hyperventilation in patients with
cerebral pathology.
INDIAN JOURNAL OF ANAESTHESIA, AUGUST 2002
The major limitation of SjVO2 monitoring is that
it provides only a global estimate of the adequacy of CBF
and focal ischaemic events may not be detected by this
technique. A recent study showed a good correlation
between SjVO2 and direct brain tissue oxygen tension
only in the normal areas of brain and not in areas with
focal injury.10
Brain tissue oxygen tension monitoring
Direct brain tissue oxygen tension (PbtO 2)
monitoring is currently under clinical investigation. The
technology uses a miniature Clarke’s electrode
incorporated into the tip of a catheter. The catheter is
placed into the brain tissue through a twist drill hole.
Early clinical studies indicate its usefulness in brain
injury. Normal values for brain tissue oxygen tension
are 20-40 mmHg. In patients with cerebral ischaemia
the values are 10 ± 5 mmHg as against 37 ± 12 mmHg
in normal individuals.11 Valadka et al showed that
in patients with severe head injury, the risk of
death increased significantly with the duration of
PbtO2 values less than 15 mmHg and any occurrence
of PbtO2 less than 6 mmHg.12 An SjVO2 value of
50% has been shown to correlate with a PbtO2 of
8.5 mmHg.13
Near-infrared spectroscopy
This system of monitoring used for quantification
of cerebral blood flow, cerebral blood volume, regional
cerebral oxygen saturation and cerebral metabolism, is
based on the principle of absorption of near-infrared light
by chromophores in the body like oxyhaemoglobin,
deoxyhaemoglobin and cytochrome aa3. Light in the
near-infrared region (70-1000 nm) is very minimally
absorbed by body tissues. As a result, it can penetrate
tissues upto 8 cm. By using light with different wave
lengths, it is possible to simultaneously and continuously
measure the changes in oxyhaemoglobin, deoxyhaemoglobin
and cytochrome aa3 in brain from where equations can
be derived to measure regional cerebral blood flow,
cerebral blood volume, cerebral oxygen saturation and
cerebral metabolism.14 There are a number of problems
that need to be resolved with this technology before it can
be recommended for routine clinical use. Important among
them is the inability to assess the contribution of
extracranial tissue to the signal changes. Presence of
intracranial blood in the form of haematomas and
contusions can interfere with the measurements. In adults,
the currently available equipment seems to significantly
underestimate CBF and CBV.
UMAMAHESWARA RAO : NEUROLOGICAL MONITORING 309

Electroencephalography
Electroencephalogram represents the electrical
A
activity of the cerebral cortex. It is a random electrical
activity, which represents the summation of the inhibitory
and excitatory electrical potentials on the pyramidal cells.

Figure 5. Placement of electrodes for EEG recording: 21 electrode

positions are defined by 10% or 20% of three measurements: Nasion-Inion
distance (NI), Preauricular distance (AA’) and hemicircumference (XX’)

Technique of Recording: Surface or needle

electrodes are used to record the electrical activity. The
electrode placement for EEG recording is shown in fig 5.
The electrical potentials are recorded between any two
chosen electrodes. Differential amplifiers are used to
eliminate artifacts due to electrocardiogram and other
physiological electrical activity. For monitoring purposes
recordings are made from multiple channels.
Interpretation of EEG
The amplitude of the normal EEG is 10-100 mV.
Clinically, the EEG activity can be divided into four
frequency bands: a - 8-13 Hz, b - 13-20 Hz, q - 4-8 Hz
and d - 2-4 Hz. An isoelectric EEG represents total
abolition of cortical electrical activity.
Manual interpretation of EEG consists of
eliminating the artifacts followed by appreciation of the
predominant frequencies and the amplitudes of the sine
waves in the recording. The record is also examined for
abnormal patterns such as spikes. Since this form of
analysis is cumbersome during the course of continuous
monitoring, the signal is normally subjected to computer
processing and the interpretation is carried out based on
some of the measures obtained from the processed EEG.
The common processing techniques used are time domain
analysis and frequency domain analysis.
Figure 6. Techniques of Time-Domain Analysis: A) Zero-crossing
Frequency, B) Aperiodic Analysis and C) Burst Suppression ratio
In time domain analysis, the raw EEG is split into
small epochs of a given duration, usually about 1-4 sec.
The frequency and/or amplitude information contained in
each epoch is depicted graphically. A change in the value
of the variables derived form this display is expected to
represent a change in the raw EEG. Some of the techniques
of time domain analysis are depicted in figure 6. Some
variables derived form these forms of analysis are defined
below:
Average signal amplitude: This is calculated as the
mean of the amplitudes of all the sine waves in a given
epoch. This is a measure of the amplitude content of the
raw EEG.
Zero Crossing Frequency: This is the average of
all the time intervals between sequential points of EEG
crossing the zero voltage line in the epoch. This is a
measure of the frequency content of the raw EEG.
Aperiodic Analysis: In this form of analysis, each
sine wave in the epoch is plotted as a bar depicting
amplitude and frequency. One look at a plot of successive
epochs over time gives an idea about any changes in the
predominant frequency and amplitude with time.
310
Burst Suppression Ratio: This parameter represents
the percentage of time the EEG is suppressed (isoelectric)
in a given epoch.
Figure 7. Compressed Spectral Array: Note shift of EEG power
from high to low frequencies over time
In frequency domain analysis, the EEG is split
into small epochs. Each epoch is further resolved into its
component sine waves and reconstructed as frequency Vs
power (square of amplitude) plot by using Fourier
Analysis. Successive epochs is displayed in a number of
ways. Two common forms of display are Compressed
Spectral Array (CSA) and Density Modulated Spectral
Array (DSA). CSA displays frequency Vs power plots of
successive epochs as lines one over the other (fig 7). In
DSA, power in various frequency bands of each epoch is
represented by dots, the density of which is proportional
to the power; successive epochs are plotted one above the
other. Some of the measures derived from the power
spectrum that are clinically used are Peak Power
Frequency, the frequency with maximum power in an
epoch, Mean Power Frequency, the frequency that divides
the power spectrum of the epoch into equal halves and
Spectral Edge Frequency, the frequency below which 95%
of the power in the epoch is contained (fig 8).
Figure 8. Power Spectral Variables : PPF: Peak Power Frequency,
MF: Median Frequency, SEF: Spectral Edge Frequency
Effects of anaesthetic agents on EEG
An understanding of the effects of anaesthetics on
EEG is necessary to be able to distinguish them from
the pathological changes that may occur intraoperatively.
INDIAN JOURNAL OF ANAESTHESIA, AUGUST 2002
Though anaesthetic agents have been documented to have
variable effects on the EEG, there exists a general pattern
which is characterised by an initial excitation resulting in
a high frequency low amplitude activity followed by a
progressive decrease in the frequency and increase in the
amplitude, and finally, a decrease in both frequency and
amplitude until an isoelectric trace occurs at high doses.
Inhalational Anaesthetics: During induction,
halothane,15 enflurane,16 isoflurane,17 sevoflurane18 and
desflurane19 cause loss of occipital activity and genesis
of frontal synchronised to b activity. In surgical planes
of anaesthesia, the anaesthetics differ in their effects on
EEG. Isoflurane 20 and desflurane, 19 at1.2 MAC
concentration, cause burst suppression without any further
slowing in the frequency of the EEG activity in the bursts.
Enflurane causes spike and wave complexes/seizure-like
activity at 1.5 MAC (R15). Halothane causes linear slowing
of frequency without burst suppression in clinical
concentrations.21
When used alone, nitrous oxide, in subanaesthetic
concentrations, causes fast rhythmic activity in frontal
region with a peak frequency of 34 Hz.22 When combined
with volatile agents, it has been shown to antagonise or
potentiate the EEG effects of volatile agents. In some
studies, nitrous oxide decreased the amplitude and
increased the frequency of the volatile agent-induced fast
activity and decreased the duration of burst suppression
suggesting antagonism between nitrous oxide and volatile
agents.23 In other studies, nitrous oxide increased the
delta activity and decreased the alpha to beta activity at
non-burst suppressing doses of volatile agents suggesting
a potentiation of the two agents.24
Intravenous Anaesthetics: Barbiturates, in small
doses cause drug-induced fast activity. In higher doses
they cause EEG suppression. Very high doses cause
burst suppression.25 Methohexital enhances interictal
epileptiform activity in patients with seizure disorders.26
Etomidate and propofol cause myoclonic activity at
induction.27 Etomidate increases interictal epileptiform
activity when used in small doses28 and causes burst
suppression at high doses.29 Propofol in anaesthetic doses
may increase30 or decrease31 interictal epileptiform
activity. High doses of propofol cause burst suppression.
Ketamine causes high amplitude theta activity and a
significant increase in beta activity. Seizures may be
caused in epileptic patients.32
EEG changes during cerebral ishaemia
Under stable anaesthetic conditions, any change
in EEG may represent cerebral ischaemia and hypoxia.
UMAMAHESWARA RAO : NEUROLOGICAL MONITORING
Slowing and flattening of EEG progressing to isoelectricity
are the characteristic changes seen during ischaemia.
Loss of slow activity may be one of the earliest signs
of ischaemia. Seizure activity could be another
manifestation of cerebral ischaemia. Intraoperatively, the
CBF threshold for signs of cerebral ischaemia depends on
the background anaesthetic; ischaemic changes occur at a
CBF of 10mL 100gm–1.min–1 under isoflurane anaesthesia
and 15-20 mL 100gm–1.min–1 under halothane anaesthesia.
Clinical applications of EEG
1. EEG is a gold-standard for monitoring cerebral
ischaemia. A 16-channel EEG has been shown to be
as sensitive as direct CBF measurement
intraoperatively during carotid endarterectomy.
2. Intraoperative EEG monitoring could be helpful to
identify cerebral ischaemia during procedures
associated with temporary vessel occlusion and during
cardioplumonary bypass procedures
3. In the intensive care unit, EEG monitoring may be
helpful to monitor seizure activity in patients with
status epilepticus under the effect of muscle relaxants.
Subclinical seizures causing neurological deterioration
may also be diagnosed by EEG.
4. EEG has also been used to prognosticate the outcome
of coma. It is also an ancillary tool for confirmation
of brain death.
5. Various mathematical measures derived from EEG
have been investigated for their potential to quantify
the depth of anaesthesia. These include median
frequency, spectral edge frequency, bispectral index
and approximate entropy.
Evoked potentials
Evoked potentials are the electrical responses
generated in the nervous system in response to a
stimulus. After appropriate stimulation, the evoked
responses are recorded from surface electrodes placed
on scalp, over the spine or in the epidural space depending
on the modality of the evoked potential used and the
clinical requirement. Unlike EEG, which is a random
electrical activity, evoked potentials are event-related.
They are pathway-specific. They have much lower
amplitude than the normal EEG activity. Because of
their low amplitude, they are very difficult to record
and require computer averaging techniques to eliminate
noise from the signal. There are two broad categories
of evoked potentials in clinical use currently: 1. Sensory
evoked potentials and 2. Motor evoked potentials.
311
Sensory evoked potentials
Sensory evoked potentials are the electrical
potentials generated in response to stimulation of a
peripheral sensory nerve. The individual modalities of
evoked potentials are named after the sensory fibres
stimulated: somatosensory evoked potentials (SSEP) are
obtained by stimulation of somatic sensory nerve fibres,
visual evoked potentials (VEP) by stimulation of visual
pathways, and auditory evoked potentials (AEP) by
auditory pathway stimulation. Once the nerves are
stimulated, the responses are generally recorded from the
scalp by surface electrodes; they may also be recorded
from any point along the pathway of transmission of the
nerve impulse.
Figure 9 : Interpretation of an Evoked Potential Record: Measurements
include amplitudes of the peaks, and absolute and inter-peak latencies.
Interpretation of an evoked potential recording
consists of identification of specific peaks representing
specific neural originators and quantification of the
latencies and amplitudes of the individual peaks (Fig 9).
Changes in the amplitudes and latencies of specific
peaks indicate injury to their corresponding neural
originators.
The electrical potentials in a given record are
arbitrarily classified into three categories based on their
latencies: potentials occurring up to 10-40 msec after
stimulus are called Short Latency Potentials; those
occurring from 20 to 120 msec are termed Intermediate
Latency Potentials and potentials occurring after 120 msec
are referred to as Long Latency potentials. Short latency
potentials arise from subcortical structures while the
intermediate and long latency potentials arise from cerebral
cortex. The practical implication of this is that short latency
potentials are used to monitor structures such as cranial
or peripheral nerves, spinal cord and brain stem while
long and intermediate latency potentials are used to monitor
cerebral cortex. A typical auditory evoked potential record
with all its cortical and subcortical peaks is depicted in
figure 10.
312
Figure 10 : A typical Auditory Evoked Potential record with its
subcortical and cortical components
Somatosensory Evoked Potentials : These
potentials are obtained by applying electrical stimulus to
the ulnar, median or posterior tibial nerves. Responses
may be recorded from electrodes placed on scalp or over
the spine. Sterile epidural electrodes are used during spinal
surgery.
Visual Evoked Potentials: Visual evoked potentials
are generated in response to photic stimulation of the
retina by flashes of light from light-emitting diodes.
Auditory Evoked Potentials: Auditory evoked
potentials are generated in response to stimulation of the
tympanic membrane by audible clicks.
Effect of physiologic variables on evoked potentials
A number of physiological parameters can affect
the latencies and the amplitudes of the various peaks in
evoked potential recordings. It is essential to ensure that
these parameters do not fluctuate widely during the course
of evoked potential monitoring in order to obtain reliable
information on intraoperative neurological injury. Some
of the important parameters that influence evoked responses
are as follows:
Cerebral Blood Flow: Sensory evoked potentials
are normal upto a CBF value of 20 mL100g–1min–1.
They start deteriorating when CBF decreases to 18-13
mL100g–1min–1. Evoked potentials cannot be obtained when
CBF is below 10-12 mL100g–1min–1.
Systemic Blood Pressure: Hypotension prolongs the
conduction in the central nervous system thereby increasing
the latencies of various peaks. Central conduction time in
SSEP has been shown to be prolonged by hypotension.
Intracranial Pressure : Raised ICP has been shown
to result in an increase in the latency and a decrease in
the amplitude of cortical potentials of VEP, AEP, and
SSEP.
INDIAN JOURNAL OF ANAESTHESIA, AUGUST 2002
Oxygen Tension: Deterioration of evoked potentials
occurs when PaO2 decreases to less than 40 mmHg.
Haematocrit: Latencies of VEP and SSEP are
increased at a haematoctrit of 10-15%. Their amplitude is
decreased when the haematoctrit is less than 10%.
Carbon Dioxide Tension: Extreme hypocapnia
(PaCO2 < 25 mmHg) causes deterioration of evoked
potentials.
Temperature: Hypothermia increases the latency.
No reliable evoked potential recording is possible at
temperatures below 180C.
Effects of anaesthetics on evoked potentials
Most anaesthetics decrease the amplitude and
increase the latencies of the various peaks. Cortical
potentials (long and intermediate latency potentials) are
affected more than the subcortical potentials (short latency
potentials). Brainstem and spinal potentials are least
affected. The effects of anaesthetics on evoked potentials
are dose-related; low concentrations of anaesthetics are
compatible with reliable evoked potential recording.
Irrespective of the anaesthetic agent used, the important
requirement during evoked potential recording is the
maintenance of a steady state anaesthesia.
Inhalational anaesthetics vary in their potential to
depress evoked potentials in the following order: N2O >
Isoflurane > halothane. Among the intravenous agents,
thiopentone has no effect on brainstem potentials; however
it depresses the cortical potentials which recover in
15-20 min. Etomidate has no effect on brainstem potentials
while it enhances the cortical potentials. Propofol has no
effect on spinal potentials. It depresses cortical components
of auditory and somatosensory evoked potentials; the
depression, however, recovers very rapidly. Opioids and
ketamine have no effect while benzodiazepines may exert
a mild effect.33
Motor evoked potentials
Monitoring the motor tracts is very important during
spinal procedures. Evoked responses generated by
transcranial stimulation of the motor cortex have been
used for this purpose. The stimulation may be electric
(transcranial electric motor evoked potentials, tcEMEP)
or magnetic (transcranial magnetic motor evoked potentials,
tcMMEP). The wave of depolarisation generated by the
stimulation of corticospinal neurons descends through the
corticospinal tracts and causes compound muscle action
potentials. Responses to transcranial stimulation can be
recorded in the epidural space, over the peripheral nerves
or from evoked muscle activity (compound muscle action
potentials, CAMP).
UMAMAHESWARA RAO : NEUROLOGICAL MONITORING
Anaesthetics may have significant effects on
motor evoked responses. Even low concentrations of
inhalational anaesthetics may depress CMAP recording,34
while epidural recording is not affected by even high
concentrations of inhalational anaesthetics.35 Thiopentone
and midazolam produce CMAP depression that lasts
for as long as 45 min after a bolus injection, making
these agents less desirable.36 Propofol has been
successfully used for epidural recording while CMAP
recordings were depressed.37 Etomidate, ketamine and
opioids seem to be the popular agents for CMAP
recording.38 Muscle relaxants may be helpful to reduce
muscle artifact during epidural recording. However, tight
control of muscle relaxation is necessary during recording
of CMAP.
Clinical applications of evoked potentials
Evoked potentials are the only objective quantifiable
measures of neurological function. Apart from their role
in diagnosis of neurological conditions such as acoustic
neuromas (brainstem auditory evoked responses, BAER)
and multiple sclerosis (VEP), they have been used to
assess the integrity of neural tracts when clinical
examination is not feasible because of unconsciousness.
SSEP and BAER have been extensively investigated in
head injured patients to monitor for neurological
deterioration, to assess the efficacy of therapeutic
interventions, to determine prognosis and to diagnose brain
death. SSEP have been used extensively in prognostication
of spinal injuries. Complete absence of SSEP is reliably
followed by no recovery of function.37
Intraoperative evoked potential monitoring has been
successfully used in many neurosurgical operations. Some
of the common conditions in which they are employed
are shown in table 3.
Table 3 : Surgical Procedures Utilising Evoked Potential
Monitoring
Brain Stem Lesions (SSEP, BAER)
Cerebellopontine Lesions (SSEP, BAER)
Posterior Circulation Aneurysms (SSEP, BAER)
Pituitary Lesions (VEP)
Carotid Endarterectomy (SSEP, VEP)
Cardiopulmonary Bypass (SSEP, VEP)
Spinal Arteriovenous Malformations (SSEP)
Scoliosis Surgery (SSEP)
Stabilisation of Spinal Fractures (SSEP)
Spinal Tumours (SSEP)
Syringomyelia (SSEP)
313
Facial nerve monitoring
Frequent involvement of facial nerve in
cerebellopontine tumours has necessitated development of
techniques for intraoperative monitoring of facial nerve
function. Initial efforts to monitor facial nerve involved
stimulation of the nerve in the operative field and
mechanical detection of the facial muscle activity. Current
methods use recording of electromyogram of specific
muscles such as orbicularis oculi after stimulating the
nerve in the operative filed. The signal is displayed on an
oscilloscope and an audible confirmation of EMG is also
provided. Several studies reported improved outcome in
posterior fossa surgery with this monitor.
References
1. Marshall LF, Smith RW, Shapiro HM: The outcome with
aggressive treatment in severe head injuries Part I. Significance
of intracranial pressure monitoring. J Neurosurg 1979;50:20-25
2. Resnick DK, Marion DW, Carlier P: Outcome analysis of
patients with severe head injury and prolonged intracranial
hypertension. J Trauma 1997; 42: 1108-1111
3. The Brain Trauma Foundation. The American Association of
Neurological Surgeons. The joint section on neurotrauma and
critical care: Indications for intracranial pressure monitoring.
J Neurotrauma 2000; 17:479-491
4. The Brain Trauma Foundation. The American Association of
Neurological Surgeons. The joint section on neurotrauma and
critical care: Guidelines for cerebral perfusion pressure.
J Neurotrauma 2000; 17:507-511
5. Aaslid R, Markwalder TM, Nornes H. Noninvasive transcranial
Doppler ultrasound recording of flow velocity in basal cerebral
arteries. J Neurosurg 1982; 58:769-774
6. Hassler W, Steinmetz H, Gawlowski J: Transcranial Doppler
ultrasonography in raised intracranial pressure and in
intracranial circulatory arrest. Neurosurgery 1988;68:745-751
7. Muttaqin Z, Vozumi T, Kuwabara S, Arita K, Ohba S, Kohno
H, Ogasawara H, Ohatani H, Mikami T: Hyperemia prior to
acute cerebral swelling in severe head injuries: The role of
transcranial Doppler monitoring. Acta Neurochir 1993; 123:
76-81
8. Matta BF, Lam AM, Mayberg TS, Shapira Y, Win HR: A
critique of the introperative use of jugular venous bulb
catheters during neurosurgical procedures. Anesth Analg.
1994, 79: 7450-50.
9. Gopinath SP, Robertson CS, Constant CF, Hayes C, Feldman
Z, Narayan RK, Grossman RG: Jugular venous desaturation
and outcome after head injury. J Neurosurg Psychiatry 1994,
57: 717-23.
10. Gupta AK, Hutchinson PJ, Al-Rawi P, Gupta S, Swart M,
Kirkpatrick PJ, Menon DK, Datta AK: Measuring brain tissue
oxygenation compared with jugular venous oxygen saturation
for monitoring cerebral oxygenation after traumatic brain
injury. Anesth Analg 1999; 88:549-553
314
11. Hoffman WE, Charbel FT, Edelman G: Brain tissue oxygen,
carbon dioxide, and pH in neurosurgical patients at risk for
ischemia, Anesth Analg:1996;83:582-586
12. Valadka A, Gopinath SP, Contant CF, Uzura M, Robertson
CS: Relationship of brain tissue PO2 to outcome after severe
head injury. Crit Car Med 26:1998; 1576-1581
13. Kiening KL, Unterberg AW, Bardt TF, Shneider GH, Lanksch
WR: Monitoring of cerebral oxygenation in patients with
severe head injuries: Brain tissue PO2 vs. jugular vein oxygen
saturation, J Neurosurg 85:1996;751-757
14. Owen-Reece H, Smith M, Elwell CE, Goldstone JC: Near-
infrared spectroscopy. Brit J Anaesth 1999; 82:418-426
15. Oshima E, Shingu K, Mori K: EEG activity during halothane
anesthesia in man. Br J Anesth 1981; 53:65-72
16. Neigh JL, Garman JK, Harp JR: The electroencephalographic
pattern during anesthsia with Ethrane: Effects of depth of
anesthesia, PaCO 2 , and nitrous oxide. Anesthesiology
1971;35:482-487
17. Eger EI II, Stevens WC, Cromwel TH: The electroencephalogrm
in man anesthetized with Forane. Anesthesio;ogy 1971; 35:
504-508
18. Scheller MS, Tateishi A, Drummond JC, Zornow MH: The
effects of sevoflurane on cerebral blood flow, cerebral
metabolic rate for oxygen, intracranial pressure, and the
electroencephalogram are similar to those of isoflurane in the
rabbit. Anesthesiology 1988; 68:548-551.
19. Rampil IJ, Lockhart SH, Eger EI II, Yasuda N, Weiskopf RB,
Cahalan MK: The electroencephalographic effects of
desflurane in humans. Anesthesiology 1991; 74:434-439
20. Rampil IJ, Weiskopf RB, Brown JG, Eger EI II, Johnson BH,
Holmes MA, Donegan JH: I-653 and isoflurane produce
similar dose-related changes in the electroencephalogram of
pigs. Anesthesiology 1988; 69:298-302
21. Yli-Hankala A, Eskola H, Kaukinen S: EEG spectral power
during halothane anesthesia. A comparison of the spectral
bands in the monitoring of anesthesia level. Acta Anesthesiol
Scand 1989; 33:304-308.
22. Yamamura T, Fukuda M, Takeya H, Goto Y, Fukuwara K:
Fast oscillatory EEG activity induced by analgesic concentrations
of nitrous oxide in man. Anesth Analg 1981;60:283-288
23. Kaieda R, Todd MM, Warner DS: The effects of anesthetics
and PaCO 2 on the cerebrovascular, metabolic and
electroencephalographic response to nitrous oxide in the rabbit.
Anesth Analg 1989; 68:135-143
24. Avramov MN, Shnigu K, Mori K: Progressive changes in
electroencephalographic responses to nitrous oxide in humans:
INDIAN JOURNAL OF ANAESTHESIA, AUGUST 2002
A possible acute drug tolerance. Anesth Analg 1990; 70:
369-374
25. Clark DL, Rosner BS: Neurophysiologic effects of general
anesthetics. I. The electroencephalogram and sensory evoked
responses in man. Anesthesiology 1973; 38:564-582.
26. Paul R, Harris R: A comparison of Methohexitone in
electrocorticography. J Neurol Neurosurg Psychiatry
1973;33:100-104
27. Reddy RV, Moorthy SS, Dierdorf SF, Deitch RD Jr, Link L:
Excitatory effects and elecroencephalographic correlation of
etomidate, thiopental, methohexital, and propofol. Anesth
Analg 1993; 77:1008-1011
28. Ebrahim ZY, De Boer GE, Luders H, Hahn JF, Lesser RP:
Effect of etomidate on the electroencephalogram of patients
with epilepsy. Anesth Analg 1986; 65:1004-1006
29. Milde LN, Milde JH, Michenfelder JD: Cerebral functional,
metabolic and hemodynamic effects of etomidate in dogs.
Anesthesiology 1985; 63:371-377
30. Samra SK, Sneyd JR, Ross DA, Henry TR: Effects of propofol
sedation on seizures and intracanially recorded epileptiform
activity in patients with partial epilepsy. Anesthesiology 1995;
82:843-851
31. Rampil IJ, Lopez CE, Laxer KD, Barbaro NM: Propofol
sedation may disrupt interictal epileptiform activity from a
seizure focus. Anesth Analg 1993; 77:1071-1073
32. Modica PA, Tempelhoff R, White PF: Pro- and anti-convulsant
effects of anesthetics (Part II). Anesth Analg1990; 80:433-444
33. Sloan TB. Evoked potentials. In: Text Book of
Neuroanaesthesia, Albin MS (Ed), New-York, McGraw Hill
Companies, 1997 pp:221-276
34. Hicks RG, Woodforth IJ, Crawford MR: Some effects of
isoflurane on I-waves of the motor evoked potentials. Br J
Anaesth 1992; 69:130-136
35. Zentner J, Albrecht T, Heuser D: Influence of halothane,
enflurane and isoflurane on motor evoked potentials.
Neurosurgry 1992; 32:298-305
36. Glassman SD, Shields CB, Linden RD: Anesthetic effects on
motor evoked potentials in dogs. Spine 1993; 18:1083-1089.
37. Kalkman CJ, Drummond JC, Ribberink AA: Effects of
propofol, etomidate, midazolam, and fentanyl on motor evoked
responses to trascranial electrical or magnetic stimulation in
humans. Anesthesiology 1992;76:502-509.
38. Sloan TB. Evoked potentials. In: Anesthesia and Neurosurgery,
Cottrell JE, Smith DS (Eds), St. Louis, Mosby 2001, pp:
183-200