Neuromonitoring techniques can monitor the brain's function, cerebral blood flow and intracranial pressure, and brain oxygenation and metabolism. Electroencephalography (EEG) measures electrical brain activity and is useful for detecting ischemia. Evoked potentials like somatosensory evoked potentials (SSEPs) monitor sensory pathways from stimulus to cortex. Jugular venous oximetry and near infrared spectroscopy (NIRS) provide noninvasive monitoring of cerebral oxygenation. These techniques guide anesthesia management and detect intraoperative brain injury.

1. 
Neuromonitoring in anesthesia

2. Classification of monitoring techniques:
 The brain can be monitored in terms of:
 Function
 Cerebral blood flow (CBF) & intracranial pressure
(ICP)
 Brain oxygenation and metabolism

3. Monitoring of FUNCTION:
 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
- Direct spinal cord stimulation
 EMG
- Cranial nerve function (V, VII, IX, X, XI, XII)

4. 
EEG

5. EEG
 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

6. 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

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

8. 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

9. 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

10. 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
 Deeper anesthesia (1.25 MAC):
 Alternating activity
 Very deep anesthesia (1.6 MAC):
 Burst suppression  eventually isoelectric

12. Non-anesthetic Factors Affecting EEG
 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
 Pathophysiologic
Factors
1. Hypoxemia
2. Hypotension
3. Hypothermia
4. Hypercarbia and hypocarbia

13. Uses of EEG
1. Carotid endarterectomy
2. Cerebral aneurysm surgery when temporary clipping is
used.
3. Cardiopulmonary bypass procedure
4. Extracranial-intracranial bypass procedure
5. Deliberate metabolic supression for cerebral protection.
 Surgery that place the brain at risk (difficulties: restricted
access)
 Seizure monitoring in ICU

14. Processed EEG
 The gold standard for intra-op EEG monitoring:
continuous visual inspection of a 16- to 32-channel
analog EEG by experienced
electroencephalographer
 “Processed EEG”: methods of converting raw
EEG to a plot showing voltage, frequency, and time
 Monitors fewer channels, less experience required
 Reasonable results obtained.
 The common processing techniques used are time
domain analysis and frequency domain analysis.

15. Time domain analysis
 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.

16. 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 plot by using Fourier
Analysis.
 Compressed Spectral Array
(CSA) and Density Modulated
Spectral Array (DSA)

17. BIS

18. Entropy

19. 
EVOKED POTENTIALS

20. Sensory Evoked Potential
 Definition: electrical activity
generated in response to
sensory or motor stimulus
 Stimulus given, then neural
response is recorded at
different points along
pathway
 Sensory evoked potential
 Latency – time from stimulus
to onset of SER
 Amplitude – voltage of
recorded response

21. SEP
 Sensory evoked potentials
 Somatosensory (SSEP)
 Auditory (BAEP)
 Visual (VEP)
 SSEP – produced by electrically stimulating a
cranial or peripheral nerve
 If peripheral n. stimulated – can record proximally
along entire tract (peripheral n., spinal cord,
brainstem, thalamus, cerebral cortex)
 As opposed to EEG, records subcortically

22. SSEP
 Time-locked, event related,
pathway specific EEG in
respones of peripheral
stimulus
 Monitor integrity of the
pathway from periphery to
the cortex
 Electrical stimulator placed at
median, ulnar, or posterior tibial
nerves

23. Indications for SSEP
 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

24.  Carotid endarterectomy
 Similar sensitivity has been found between SSEP and EEG
 SSEP has advantage of monitoring subcortical ischemia
 SSEP disadvantage do not monitor anterior portions -
frontal or temporal lobes
 Cerebral Aneurysm
 SSEP can gauge adequacy of blood flow to anterior
cerebral circulation
 Evaluate effects of temporary clipping and identify
unintended occlusion of perforating vessels supplying
internal capsule in the aneurysm clip

25. Limitations
 Motor tracts not directly monitored
 Posterior spinal arteries supply dorsal columns
 Anterior spinal arteries supply anterior (motor)
tracts
 Possible to have significant motor deficit
postoperatively despite normal SSEPs
 SSEP’s generally correlate well with spinal
column surgery

26. • Visual Evoked Potential (VEP)
 Using LED goggles to create stimulus
 Difficult to perform
• Brainstem Auditory Evoked Potential (BAEP)
 Repetitive clicks delivered to the ear
 Reflects the VIII nerve & brainstem “well-being”

27. 
AEP

28.  Auditory (BAEP) – rapid clicks elicit responses
 CN VIII, cochlear nucleus, rostral brainstem, inferior
colliculus, auditory cortex
 Procedures near auditory pathway and posterior
fossa
 Decompression of CN VII, resection of acoustic
neuroma, sectioning CNVIII for intractable tinnitus
 Resistant to anesthetic drugs

29. Limitations
 Responds to injury by increased latency, decreased
amplitude, ultimately disappearance
 Problem is response non-specific
 Surgical injury
 Hypoperfusion/ischemia
 Changes in anesthetic drugs
 Temperature changes
 Signals easily disrupted by background electrical activity
(ECG, EMG activity of muscle movement, etc)
 Baseline is essential to subsequent interpretation

30. Anesthetic agents and SEP
 Most anesthetic drugs increase latency and
decrease amplitude
 Exceptions:
 Nitrous oxide: latency stable, decrease
amplitude
 Etomidate: increases latency, increase in
amplitude
 Ketamine: increases amplitude
 Opiods: no clinically significant changes
 Muscle relaxants: no changes

31. Physiologic factors affecting SEP’s
 Hypotension
 Hyperthermia and hypothermia
 Mild hypothermia (35-36 degrees) minimal effect
 Hypoxemia
 Hypercapnia
 Significant anemia (HCT <15%)
 Technical factor: poor electode-to skin-contact
and high electrical impedence (eg
electrocautery)

33. Motor Evoked Potentials
 Motor EP:
- Transcranial magnetic MEP
- Transcranial electric MEP
- Direct spinal cord stimulation

34. Motor Evoked Potentials
 Transcranial electrical
MEP monitoring
 Stimulating electrodes
placed on scalp
overlying motor cortex
 Application of electrical
current produces MEP
 Stimulus propagated
through descending
motor pathways

35. Motor Evoked Potentials
 MEPs very sensitive to
anesthetic agents
 Possibly due to
anesthetic depression of
anterior horn cells in
spinal cord
 Intravenous agents
produce significantly
less depression
 TIVA often used
 No muscle relaxant

36. EMG
 Early detection of surgically
induced nerve damage and
assessment of level of nerve
function intra-operatively.
 Active or passive.
 Uses:
1. Facial nerve monitoring
2. Trigeminal nerve monitoring
3. Spinal Accessory nerve

38. Cerebral blood flow and ICP
monitoring

39. 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.

40. Indications for ICP monitoring
1. Head Injury
2. Brain Tumors
3. Subarachnoid Heamorrhage
4. Hydrocephalus
5. Neuromedical conditions

41. Techniques of ICP monitoring

42. ICP waveforms
 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

43. Abnormalities of ICP waveforms
 A WAVES: plateau waves
indicate ICP above 40mmHg
and are sustained for 5-
20min.
 B WAVES: Amplitude of
20mmHg and occur at the
rate of 1-2/min. Occur
synchronus with cheyne-
stokes breathing
 C WAVES: no pathological
significance

44. Transcranial Doppler
 Measures the blood flow velocity in major cerebral
blood vessles.
 Examination carried out through the temporal
window, orbital foramen or foramen magnum.
 Using 2MHz probe.
 MCA commonly used.
 Change in velocity is proportional to change in flow
considering the vessel diameter is constant.

45. Interpretation of waveforms
Pulsatality Index = (Peak Systolic Velocity
- End
Diastolic Velocity) / Mean Velocity

46. Clinical applications 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.

47. Intravascular tracer compounds
 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.

48. Thermal diffusion cerebral blood flow
monitoring
The rate at which heat dissipates in a
tissue depends on the tissue’s thermal
conductive properties and the blood
flow in that area.
Measurement is automatically
suspended if the passive thermistor
measures a brain temperature of 39.1°
C.
The inability to monitor during a febrile
episode may constitute a true limitation
of the technique

49. Monitoring of cerebral oxygenation
and metabloism

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

51. Jugular venous oximetry :principle
 (A-V)DO2 x CBF = CMRO2
 When CMRO2 is constant, any change in CBF is
associated with a reciprocal change in the cerebral
arteriovenous oxygen difference.
 Based on the principle of reflectance oximetry.

52. Jugular venous oximetry
 Continuous monitoring of
jugular venous oxygen
saturation (SjVO2 ) is carried
out by a catheter placed
retrograde through the
internal jugular vein intothe
jugular bulb.
 For accurate measurement,
the tip of the catheter must
be within 1 cm of the jugular
bulb.

53. Indices obtained from SjVO2
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 ).

54. Interpretation of SjVO2
 Interpretation of jugular venous oxygen saturation (SjvO2)
 Increased values: >90% indicates absolute/relative
hyperemia
 Reduced metabolic need  comatose/brain death
 Excessive flove  sever hypercapnia
 AVM
 Normal Values: 60-70%  focal ischemia?
 Decreased Values: <50%  increased O2 extraction,
indicates a potential risk of ischemia injury
 Increased demand: seizure / fever
 Decreased supply: decreased flow, decreased hematocrit
 As ischemiaprogress to infarction: O2 consumption
decreases

55. Near Infra-red Spectroscopy NIRS
 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. It can
penetrate tissues upto 8 cm.
 Measure regional cerebral blood flow, cerebral
blood volume, cerebral oxygen saturation and
cerebral metabolism.

56. NIRS limitations
 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.
 Measures small portion of frontal cortex, contributions from
non-brain sources
 Temperature changes affect NIR absorption water spectrum
 Degree of contamination of the signal by chromophores in
the skin can be appreciable and are variable
 Not validated – threshold for regional oxygen saturation not
known (20% reduction from baseline?)

57. Tissue partial pressure oxygen
monitoring:
 Based on an oxygen-sensitive electrode originally described by
Clark.
 The diffusion of oxygen molecules through an oxygen-
permeable membrane into an electrolyte solution causes an
electric current that is proportional to Po2.
 The catheter is placed into the brain tissue through a twist
drill hole into the subcortical white matter.
 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

58. Cerebral Microdialysis
 Small catheter inserted with ICP/tissue PO2
monitor
 Artificial cerebrospinal fluid,equilibrates with
extracellular fluid,chemical composition analysis
 Markers:
○ Lactate/pyruvate ratio : onset of ischemia
○ High level glycerol: inadequate energy to maintain
cellular integrity- membrane breakdown
○ Glutamate: neuronal injury and a factor in its
exacerbation

59.  Catheter placement is
usually in ‘high risk’ tissue.
 Uses: 1.Ischemia/trauma
2.epilepsy
3.Tumor chemistry

61. References
 Millers anesthesia 8th edition
 Neurological monitoring. Dr. G S Rao IJA 2002;46(4)
 Advances in neuroanesthesia monitoring Dr.
Pramod Bithal AIIMS new delhi. 2006 ISACON
 GE-Datex Ohmeda Entropy monitor manual
 Coviden BIS monitor users manual

62. 
Thankyou
The end