This document discusses various techniques used to monitor brain function during anesthesia, including: 1. Intracranial pressure monitoring via an intraventricular catheter, which is the gold standard. Normal ICP is 10-15 mmHg in adults and waveforms can indicate increased ICP. 2. Transcranial Doppler measures blood flow velocity in cerebral arteries to monitor for vasospasm. 3. EEG, evoked potentials, brain tissue oxygen monitors, microdialysis, and near infrared spectroscopy provide additional insights into brain activity, oxygenation, and metabolism. EEG changes with anesthesia and can detect ischemia. Bispectral index monitors depth of anesthesia.

1. 
Neuromonitoring in anesthesia

2. Classification of monitoring
techniques:
 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
 Sensory Evoked Potentials
 Visual
 Somatosensory
 Auditory
 Motor Evoked Potentials

3. 
Intracranial pressure monitoring

4. Intra-cranial Pressure
 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.

5. Indications for ICPmonitoring
1. Head Injury
 Sever HI(GCS 3-8) and abnormal CT finding
 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 pres sure < 90 mmHg.
2. Brain Tumors
3. Subarachnoid Heamorrhage
4. Hydrocephalus
5. Neuromedical conditions : stroke, and encephalitis
associated with raised ICP.

6. Techniques of ICP monitoring

7. Intraventricular Catheter : via ventriculostomy
 The gold standard for ICP monitoring.
 The lateral ventricle is cannulated by a frontal, occipital,
parieto-occipital or parasagittal coronal approach.
 The transducer is zeroed at the level of the external
auditory meatus.
Advantages:
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.
“risks of infection and trauma to the brain during
cannulation”

8. ICP waveforms
Flow of 3 upstrokes in one wave.
P1 = (Percussion wave) represents arterial
pulsation
P2 = (Tidal wave) represents intracranial
compliance
P3 = (Dicrotic wave) represents venous
pulsation
In normal ICP waveform P1 should have
highest upstroke, P2 in between and P3
should show lowest upstroke.
On eyeballing the monitor, if P2 is higher
than P1 - it indicates intracranial
hypertension

9. Icp waveform

10. Abnormalities of ICP wave
Earliest sign of ↑ ICP – Changes in pulsatile components
Prominent P1 wave
The systolic BP is too high

11. Diminished P1 wave
• If the systolic BP is too low, P1
decreases and eventually disappears,
leaving only P2.
• P2 and P3 are not changed by this
Prominent P2 wave
The intracranial compliance has decreased
The mass lesion is increasing in volume

12. Diminished P2 and P3 waves
• Hyperventilation
Rounded ICP waveform
• ICP critically high

13. Flat
• EVD clogged / kinked
• Patient expired

14.  A WAVES: plateau waves indicate ICP above
40mmHg and are sustained for 5- 20min.
 Represent severe pathological elevation of ICP caused by
changes in regional cerebral blood volume (CBV)

15.  B WAVES: Amplitude of 20mmHg and
occur at the rate of 1-2/min.
 as warning signs of decreased intracranial
compliance and enhanced risk of intracranial
hypertension.

16. C wave of ICP
 Seen in normal ICP waveform – nonpathological.
 Mean wave < 20 mmhg.
 Represent cyclic variation of SBP.

17. Transcranial Doppler
 Measures the blood flow velocity in major cerebral blood
vessles.
 Examination carried out through the temporal
window, orbital foramen or foramen magnum.
 MCA commonly used.
 Change in velocity is proportional to change in flow
considering the vessel diameter is constant.

18. Interpretation ofwaveforms
Pulsatality Index = (Peak Systolic
Velocity- End Diastolic Velocity) /
Mean Velocity

19. Clinicalapplications ofTCD
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 hyperventilationin patients with
head injury.

20. Intravascular tracercompounds
 Method originally described by Kety and Schmidt.
 Administration of radioactive isotope of xenon-133
 Measurement of radioactivity washout with gamma detectors.
 Disadvantages: 1.Exposure to radioactivity
2.Cumbersome detector equipment
3.Focal areas of hypoperfusion missed
4.Snapshot of CBF not continuous monitor.

21. Monitoring of cerebral oxygenation and
metabloism
 Brain tissue oxygenation
 Jugular bulb venous oximetry monitoring
 Microdialysis catheter
 Near Infrared Spectroscopy (NIRS)

22. Brain tissue oxygen tension monitoring
 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.
 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.
 Currently under clinical investigation

23. Jugular venousoximetry
 Jugular bulb venous oxygen saturation (Sjvo2) measures
the degree of oxygen extraction by the brain and represents
the balance between cerebral oxygen supply and demand.
 The dominant jugular vein (i.e., the right for most patients)
drains predominantly cortical venous blood, whereas the
contralateral jugular vein drains more of the subcortical
regions.
 Any decrease in CBF must be accompanied by a
corresponding decrease in cerebral venous oxygen
saturation if CMRO2 is constant.

24. Jugular venousoximetry
 A catheter placed retrograde
through the internal jugular
vein into the jugular bulb.
 The tip of the catheter must
be placed above the C1-C2
vertebral bodies to avoid
contamination with blood
coming from the facial vein.
 Correct positioning of the
catheter can be confirmed
with a lateral skull x-ray

25. Indices obtained fromSjVO2
1. Jugular venous
oxygen saturation
(SjVO2 )
2. Cerebral arteriovenous
oxygen difference (A-
VDO2 ) (the difference
between arterial and
jugularvenous oxygen
content) and
3. Cerebral oxygen
extraction(CEO2 ) (the
difference between
SaO2 and SjVO2 ).

27. Near Infra-redSpectroscopy NIRS
 Based on the principle of absorption of near-
infrared light by chromophores in the body like
oxyhaemoglobin, deoxyhaemoglobin and
cytochrome aa3.
 Oxygenated hemoglobin, deoxygenated
hemoglobin, and cytochrome aa3 have
different absorption spectra (650-800 nm).
 The main advantage of NIRS is that it is a
noninvasive method for estimating regional
changes in cerebral oxygenation.

28. NIRS limitations
 Its clinical use is limited by an inability
to differentiate between intracranial
and extracranial changes in blood
flow and oxygenation.
 Currently, there are no studies
providing evidence that NIRS use
alone can influence outcomes in adult
neurocritical care.

29. Cerebral Microdialysis
A technique for sampling the extracellular space of a tissue.
This method is based on the diffusion of water-soluble substances
through a semipermeable membrane. Small molecules (<20,000 D)
from the extracellular fluid can diffuse across the membrane and
enter the perfusate. Conversely, substances that have been added
to the perfusate can diffuse across the membrane to gain entry to
the tissue.
The technique of cerebral microdialysis allows continuous and
online monitoring of changes in brain tissue chemistry.

30. • The key substances measured by microdialysis
can be categorized as follows:
1. Energy-related metabolites (glucose, lactate,
pyruvate, adenosine, xanthine)
2. Neurotransmitters (glutamate, aspartate)
3. Markers of tissue damage and inflammation
(glycerol)

31. Markers:
 Increase in Lactate/pyruvate ratio
onset of ischemia.
 High level glycerol inadequate
energy to maintain cellular
integrity membrane
breakdown
 Glutamate neuronal injury

32. Electroencephalograms (EEG)
 Raw EEG
 Computerized Processed EEG: Compressed spectral array, Density spectral
array, Aperiodic analysis, Bispectral analysis (BIS)
Evoked Potential
 Sensory EP:
 Somatosensory EP
 Visual EP
 Brain stem auditory EP
 Motor EP:
- Transcranial magnetic MEP
- Transcranial electric MEP
Function of brain

33. EEG

34. Electroencephalogram – surface recordings of the
summation of excitatory and inhibitory postsynaptic
potentials generated by pyramidal cells in cerebral
cortex
EEG:
 Measures electrical function of brain
 Indirectly measures blood flow
 Measures anesthetic effects
EEG

35. EEG
Three uses perioperatively:
 Identify inadequate blood flow to cerebral cortex
caused by surgical/anesthetic-induced reduction in flow
 Guide reduction of cerebral metabolism prior to
induced reduction of blood flow
 Predict neurologic outcome after brain insult
Other uses: identify consciousness, unconsciousness,
seizure activity, stages of sleep, coma

36. EEG
Electrodes placed so that
mapping system relates
surface head anatomy to
underlying brain cortical
regions
3 parameters of t
Amplitude –size or
voltage of signal
Frequency –number of
times signal oscillates
Time –duration of the
sampling of the signal

37. EEG
EEG Waves :
 Beta: high freq, low amp
(awake state)
 Alpha: med freq, high amp
(eyes closed while awake)
 Theta: Low freq (not
predominant)
 Delta: very low freq high
amp (depressed
functions/deep coma

39. Abnormal EEG
 Regional problems - asymmetry in frequency,
amplitude or unpredicted patterns of such
 Epilepsy – high voltage spike with slow waves
 Ischemia – slowing frequency with preservation of
amplitude or loss of amplitude (severe)
 Global problems – affects entire brain, symmetric
abnormalities
 Anesthetic agents induce global changes similar to global
ischemia or hypoxemia (control of anesthetic technique is
important

40. Anesthetic agents and EEG
Subanesthetic doses of inhaled anesthetics (0.3 MAC):
 Increases frontal beta activity (low voltage, high frequency)
Light anesthesia (0.5 MAC):
 Larger voltage, slower frequency
General anesthesia (1 MAC):
 Irregular slow activity.
Very deep anesthesia (1.6 MAC):
 Burst suppression  eventually isoelectric.
“As the patient loses consciousness with general
anesthesia, the brain waves become larger in amplitude
and slower in frequency”

41. Halothane No

42. Non-anestheticFactorsAffectingEEG
• Surgical
1. Cardiopulmonary bypass
2. Occlusion of major cerebral
vessel (carotid cross-clamping,
aneurysm clipping)
3. Retraction on cerebral cortex
4. Surgically induced emboli to
brain
 Pathophysiol
ogic Factors
1. Hypoxemia
2. Hypotension
3. Hypothermia

43. Uses ofEEG
1. EEG is a gold-standard for monitoring cerebral ischaemia:
during procedures associated with temporary vessel
occlusion and during cardioplumonary bypass procedures.
2. In ICU : 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.
3. To prognosticate the outcome of coma.
4. It is also an ancillary tool for confirmation of brain death.
5. To quantify the depth of anaesthesia. These include
bispectral index and approximate entropy

44. BIS_Bispectral Index

45. Entropy

46. Evoked potential

EVOKED POTENTIALS
 Evoked potentials are the electrical responses
generated in the nervous system in response to
a stimulus.
 The evoked responses are recorded from
surface electrodes placed on scalp, over the
spine or in the epidural space.
 They have much lower amplitude than the
normal EEG activity. Because of their low
amplitude, they are very difficult to record.

47.  Evoked potentials of all types
(sensory or motor) are
described in terms of latency
and amplitude.
 Latency is defined as the time
measured from the application
of the stimulus to the onset or
peak (depending on
convention used) of the
response.
 The amplitude is simply the
voltage of the recorded
response.

48. Clinically significant of evoked potential
 Decreases in amplitude of 50% or more from
baseline associated with a less than 10%
prolongation in latency as clinically significant SER
changes.
 Intraoperative changes in evoked responses, such
as decreased amplitude, increased latency, or
complete loss of the waveform, may result from
surgical misdeed, such as retractor placement or
ischemia. They may also reflect systemic changes,
such as changes in the anesthetic drugs or doses,
temperature, or hypoperfusion.

49. Sensory-Evoked Responses(SERs)
 SERs are electrical CNS responses to electrical,
auditory, or visual stimuli.
 SERs are produced by stimulating a sensory
system and recording the resulting electrical
responses at various sites along the sensory
pathway up to and including the cerebral cortex.
 It include:
 Somatosensory EP
 Visual EP
 Brain stem auditory EP

50. Somatosensory-Evoked Potentials
 SSEPs are recorded after electrical stimulation of a
peripheral mixed nerve.
 Responses may be recorded from electrodes placed on scalp
or over the spine.
 The common sites of stimulation include the median nerve
at the wrist, the common peroneal nerve at the knee, and
the posterior tibial nerve at the ankle.

51.  Dorsal root ganglia
 Posterior dorsal
column
 Medial lemiscus
 Contralateral
thalamus
 Frontoparietal
somatosensory cortex

52. Indications forSSEP
 Indications:
 Scoliosis correction
 Spinal cord decompression and
stabilization after acute injury
 Brachial plexus exploration
 Resection of spinal cord tumor
 Resection of intracranial
lesions involving sensory cortex
 Clipping of intracranial
aneurysms
 Carotid endarterectomy
 Thoracic aortic aneurysm repair

53. Limitations
 Motor tracts not directly monitored
 Posterior spinal arteries supply dorsal columns
(sensory tract)
 Anterior spinal arteries supply anterior (motor tracts) so
injury to anterior spinal arteries goes undetected.
 Possible to have significant motor deficit postoperatively
despite normal SSEPs

54. Brainstem Auditory-Evoked Potentials
 Auditory evoked potentials are
generated in response to
stimulation of the tympanic
membrane by audible clicks.
 Reflects the VIII nerve &
brainstem“well-being”.
 useful for surgical procedures in
the posterior fossa that risk
hearing or structures in the upper
medulla, pons, and midbrain.
 Most resistant to anesthetic
drugs

55. Visual-Evoked Potentials
 Visual evoked potentials are generated in response to
photic stimulation of the retina by flashes of light
from light-emitting diodes.
 VEPs are the least commonly used evoked response
monitoring technique intraoperatively.
 Most useful for testing for optic nerve function.

56. Effect of physiologic variables on evoked potentials
Cerebral Blood Flow: Sensory evoked potentials are normal
upto a CBF value of 20 mL100g–1/min. They start
deteriorating when CBF decreases to 18-13 ml/100g/min.
Evoked potentials cannot be obtained when CBF is below 10-
12 mL100g/min.
Systemic Blood Pressure: Hypotension prolongs the
conduction in the central nervous system thereby increasing
the latencies of various peaks.
Intracranial Pressure : Raised ICP has been shown to result in
an increase in the latency and a decrease in the amplitude

57. Oxygen Tension: Deterioration of evoked potentials
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.

58. Effects of anaesthetics on evoked potentials
 Most anaesthetics decrease the amplitude and increase the
latencies of the various peaks.
 Brainstem and spinal potentials are least affected.
 The effects of anaesthetics on evoked potentials are dose-related.

60. Motor EvokedPotentials
 Evoked responses generated by transcranial stimulation of the
motor cortex.
 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).
 Are often use in conjunction with SSEPs to assess spinal cord
function during surgery.
 While SSEP evaluates the ascending sensory pathway mediated
through the posterior spinal cord (dorsal column), TcMEP
evaluates the anterior portion of the cord or descending motor
pathways

61. • The stimulation may be electric (transcranial
electric motor evoked potentials, tcEMEP) or
magnetic (transcranial magnetic motor evoked
potentials, tcMMEP).
• Anaesthetics may have significant effects on
motor evoked responses. Even low
concentrations of inhalational anaesthetics
may depress CMAP recording

63. References
 Millers anesthesia 8th edition
 Neurological monitoring. Dr. G S Rao IJA
2002;46(4)
 2017 Textbook of Critical Care, 7e 39