EEG measures the electrical activity of the brain through electrodes placed on the scalp. It can detect different wave patterns associated with different brain states. Evoked potentials involve stimulating a sensory pathway and measuring the electrical response along the pathway. This allows localization of lesions. Somatosensory evoked potentials involve stimulating a peripheral nerve like the median nerve and measuring the response along the pathway to detect spinal cord or brain injuries. Auditory evoked potentials involve measuring the brainstem response to a click stimulus to detect acoustic neuromas or other posterior fossa lesions. Both evoked potentials and EMG monitoring are used during surgery to detect injuries.

1. EEG and Evoked Potentials
Speaker : Dr. Tushar kumar

2. What is EEG
It is the study , observation and recording
of brain, which are measureable expression
of electrical activity of brain.
It could be Unipolar or bipolar
Unipolar : where reference point is fixed
Bipolare : voltage recorded lies near to
scalp or brain.

3. EEG
Standard EEG:
has 10 – 20 standardized placement system.
Electrodes placed on anatomic location.
8 – 20 wave lines are graphed.

4. EEG signals
There are 3 basic parameters that are recorded
in EEG waves:
1. Amplitude : measurement of electrical
height. Ranges from 0 -200 μV.
2. Frequency : it is no of times per second the
wave touches the zero voltage line. It is the
degree of activity of cerebral cortex.
3. Time : plotted on x axis

5. Type of waves
1. Alpha waves: 8 – 13 Hz
occurs during awake and quiet resting state.
2. Beta waves: > 13 Hz
excited and specific mental activity.
3. Theta waves: 4 -8 Hz
4. Delta waves: 0 – 4 Hz
occurs during deep sleep, infancy, organic
brain disease.

6. EEG ! How does it look like?

7. EEG interpretations
• Sudden development of delta waves
coincident with surgical manuver  injury
warning
• In penumbra region, EEG poorly predict
brain damage
• Anesthetics & hypothermia causes EEG
changes  multifactorial interpretation

8. Uses of EEG
1. Monitoring the functional integrity of neural
structures that may be at risk.
2. Identification of specific structures
3. Monitoring the effects of specific agents and
other drugs that affect nervous system
4. Diagnosis and monitoring of
pathophysiological conditions.

9. Anaesthesia and EEG
a. Ketamine : rhythmic theta activity…. 4 -8
Hz increased epileptiform activity.
b. Opioid : dose related decrease in frequency.
but if further doses are not given then
there is return of higher wave occurs.
Epileptiform waves occur with large doses
of opioid such as during fentanyl induction.
c. Nitrous oxide : when used in combination
with other anaesthetic agents it depresses
EEG pattern.

10. Anaesthesia and EEG….
d. Isoflurane: depression in EEG pattern with
increase in depth of anaesthesia. Electrical
silence at 2 – 2.5 MAC.
e. Halothane: smaller degree of EEG
suppression. At 3 – 4 MAC EEG suppression
occurs to greater extent but cardiac depression
also occurs.
f. Sevoflurane: smaller degree of EEG
suppression but greater epileptiform activity.

11. Surgery and EEG
1. No change in anaesthetic technique should be
made during critical period of monitoring.
for eg. Induced hypotension, carotid
clamping, aneurysm clipping.
2. Avoid major changes in anaesthetic gas level/
bolus opioid or benzodiazepines near time of
increases ischemic risk.
3. If drug must be given then monitor it with
Evoked Potential.

12. Why Evoked potentials…
The EEG machine records tiny electrical
voltages from the brain, representing the
averaged electrical activity of millions of
neurons. ……… non specific.
But evoked potentials are triggered.
They are very specific.

13. Evoked potentials
What are evoked potentials:
• The electrical potentials produced after
stimulation of specific neural tracts.
• The recorded plot of voltage versus time
Initial artifact representing the stimulation
of the tract followed by the neuronal
response, which is recorded as a series of
peaks and valleys

14. Evoked potentials
Many times signals are small  an amplifier
reduces the electrical noise by subtracting
the signal at a referenceelectrode from the
recording electrode.
• Filtering of this signal we focus on the
evoked response of interest.

15. Evoked potentials
• The evoked response always occurs at a set
time after stimulation.
• Summating all those responses increases
the time-locked response, whereas the
background activity acts as a random signal
and averages out to zero.
• So we get only the evoked potential
response.

16. CLASIFICATION OF EVOKED POTENTIALS
SENSORY
EVOKED
POTENTIALS
MOTOR
EVOKED
POTENTIALS
EVENT
RELATED
POTENTIALS
VISUAL
EVOKED
POTENTIAL
AUDITORY
EVOKED
POTENTIAL
SOMATOSENSORY
EVOKED
POTENTIAL
EVOKED POTENTIALS

17. Visual Evoked potential:

18. Visual evoked potential:

19. Visual evoked potential:
Primary visual system is arranged to emphasize
the edges and movements so shifting patterns with
multiple edges and contrasts are the most
appropriate method to assess visual function.
Flash VEP
• Greater variability of response with multiple
positive and negative peaks
• Primarily use when an individual cannot
cooperate or for gross determination of visual
pathway. Ex in infants / comatose patients

20. VEP response:

21. Clinical application of VEP:
VEPs can be used to monitor:
• the anterior visual pathways during
a. craniofacial procedures,
b. pituitary surgery,
c. surgery in the retrochiasmatic visual
tracts and occipital cortex.
Their specificity ranges from 95% to > 99%

22. Clinical application of VEP:
Other medical applications:
1. Multiple sclerosis
2. Demylinating disorders
3. Axonal loss disorders
4. Migraine headaches

23. VEP

24. Limitations of VEP
Less useful in surgical monitoring.
Do not measure the pathways of useful
clinical vision
The large, bulky “goggles” usually used for
stimulation pose technical problems,
The bilateral nature of the response may
obscure focal changes,
Anaesthetic sensitivity makes recording
difficult.

25. Somatosensory evoked
potentials (SSEP) :

26. SSEP :
• Evoked potentials of sensory nerves in the
peripheral & central nervous system
• Used to diagnose nerve damage or
degeneration in the spinal cord
• Can distinguish central Vs peripheral nerve
lesion

27. Anatomical & Physiological basis
of SSEP
SENSE ORGANS – PACINIAN AND GOLGI COMPLEXES
IN JOINTS, MUSCLES AND TENDONS
DORSAL ROOT GANGLIA
TYPE A FIBRES
GRACILE AND CUNEATE Nu. IN MEDULLA
Nu POSTEROLATERALIS OF THALAMUS
MEDIAL LEMNISCUS
SENSORY CORTEX
THALAMOPARIETAL
RADIATYIONS

28. Dorsal column pathways:
They carry sensory inputs to
brain for vibration and
proprioception.
First synapse near
the nucleus cuneatus and nucleus
gracilis and then decussates near
the cervicomedullary junction,
ascending via the contralateral
medial lemniscus.
Second synapse occurs in the
ventroposterolateral nucleus of
the thalamus, from which it
projects to the contralateral
sensory cortex

29. SSEP:
Peripheral sensory nerves are stimulated
electrically and the response is measured
along the sensory pathway.
The large, mixed motor and sensory nerves
are usually monitored:
1. Median (C6-T1),
2. ulnar (C8-T1),
3. Common peroneal (L4-S1),
4. posterior tibial (L4-S2) nerves.

30. SSEP
Median SEP:
Recording electrodes are placed at the
following locations:
• Erb’s point on each side (EP)
• Over the second or fifth cervical spine
process (C2S or C5S)
• Scalp over the contralateral cortex (CPc)
and ipsilateral cortex (CPi)
• Noncephalic electrode (Ref)

32. SSEP
Stimulation activates predominantly the large-
diameter nerve fibers.
 Anatomically, peripheral nerve stimulation
produces both orthodromic and antidromic
neural transmission.
The orthodromic motor stimulation elicits a
muscle response, which is seen as a twitch
(verifying stimulation), and the orthodromic
sensory stimulation produces the SSEP.

33. SSEP:
• STIMULUS: Electrical – square wave pulse by
surface or needle electrode
• DURATION: 100 – 200 msec at a rate of 3 – 7
/ sec
• INTENSITY: for producing observable
muscle twitch or 2.5 – 3 times the threshold for
sensory stimulus.
Unilateral stimulation for localization
Bilateral stimulation for intra-operative
monitoring

34. Stimulus is given as vibration that ascends via
ipsilateral dorsal column.

35. Monitoring of SSEP:
Monitoring is estimated to reduce the
morbidity in spinal surgery by 50% to 80%.
sensitivity of 52% and a specificity of 100%
 Blood flow: clinical functional neurologic
findings become abnormal at a cortical blood
flow of about 25 mL/min/100 g, but the SSEP
remains normal until cortical blood flow is
reduced to about 20 mL/min/100 g. SSEP
responses are lost at a local blood flow of
between 15 and 18 mL/min/100 g.

36. 1. Monitoring during temporary clipping in
aneurysm surgery has shown that a very
prompt loss of cortical SSEP response (less
than 1 minute after clipping) is associated
with development of permanent neurologic
deficit.
2. SSEP in spinal surgeries has become standard
care of monitoring.
3.Monitoring during carotid endarterectomy.
Intraoperative SSEP changes are used as an
indication for shunt placement and to predict
postoperative morbidity.
Clinical application of
SSEP

37. SSEP

38. Auditory evoked potentials

39. AUDITORY BRAINSTEM RESPONSES
I. organ of Corti and extracranial cranial nerve VII; II. cochlear
nucleus; III. superior olivary complex; IV. lateral
lemniscus; V. inferior colliculus; VI. medial geniculate body;
VII. auditory radiation.

40. • Breif electrical pulse “ click”
• Intensity – 65 – 70 dB above threshold
• Rate – 10 – 50 clicks / sec
• Averaging of 1000 – 4000 Hz range
• Read after first 10 msec of stimulus
AUDITORY BRAINSTEM RESPONSES

41. Findings:
• Absolute waveform latencies
• Interpeak latencies ( I – III, I – V & III – V )
• Amplitude ratio of wave V / I
In general I – V peak are preserved then hearing
is preserved.
AUDITORY BRAINSTEM RESPONSES

42. Clinical utility of AER:
1. Acoustic neurinoma
2. Vertebral-basilar aneurysm
3. Cerebellar vascular malformations
4. Other posterior fossa procedure , eg. during
microvascular decompression for relief of
hemifacial spasm or trigeminal neuralgia.

43. Clinical utility of AER:

44. Electromyographic monitoring
• EMG: Muscle responses to monitor neural
tracts
• Two types of EMG monitoring :
1. recording spontaneous activity
2. recording responses subsequent to stimulation
of the motor nerves or motor pathways

45. Clinical utility: EMG
All cranial nerves with a motor component
are monitored from their EMG activity in
their respectively innervated muscles.
1. Facial nerve monitoring: most common
cranial nerve monitored (e.g., acoustic
neuroma)
2. Cranial nerves IX and X : in head & neck
surgeries  when injured produces
cardiovascular changes.

46. Continue….
3. Cranial nerve XI: harmful head movement due
to trapezius and sternocleidomastoid ms.
4. Vagus nerve (CN X) monitoring by vocal cord
EMG is for skull base (large brainstem tumors)
and anterior neck procedures.
Monitoring of the recurrent laryngeal and
superior laryngeal branches is done with
electrodes in the cricothyroid or vocalis muscles
or contact electrodes mounted on an ET Tube.

47. Cont…
ET tube with
electrodes

48. Motor evoked potentials
More sensitive to ischemic vascular insults.
MEP monitoring has become important during
surgery for:
1. Correction of axial skeletal deformity,
2. Intramedullary spinal cord tumors,
3. Intracranial tumors,
4. Vascular lesions.
5. Assessment of outcome in stroke and spinal
cord function during thoracoabdominal

49. • The MEP allows rapid detection of ischemia
because the gray matter, with its higher
metabolic rate, is more sensitive to
hypoperfusion.
During middle and anterior cerebral aneurysm
clipping several neural structures in the motor
pathway are at risk for hypoperfusion.
The sensitivity and specificity of MEP is 100%
and 97.4%
Motor evoked potentials

50. MEPs can :
1. Identify vasospasm
2. Incorrect placement of the aneurysm clip,
3. Inadequate clip placement.
KINDLING: Inherent risk with MEP.
it is cortical thermal injury.
Motor evoked potentials

51. Evoked potentials & Anaesthesia
Monitoring of EP: The anesthesiologist must
consider the various effects of anaesthesia
management on the different modalities used.
In general, the inhalational anaesthetic agents
which have drug effects at multiple synaptic
receptor types appear to have the most
profound effect on monitoring.
A. SSEP: Volatile anaesthetics produce an increase
in latency and a decrease in amplitude of cortical
sensory responses.

52. Continue…
B. MEP: No synapses are involved in the
production of the D wave, so recordings of the
D wave in the epidural space are altered little
by anaesthetics.
I waves are generated by synaptic mechanisms,
so they are progressively reduced by increasing
doses of anaesthetic agents.

53. Nitrous oxide (N2O) also produces amplitude
reduction and latency increases in cortical
sensory responses or MEP responses when
used alone or when combined with
halogenated inhalational agents or opioid
agents.
Opioids cause only mild depression of all
responses, with loss of late sensory evoked
response peaks. ( at sedative dose)
Continue…

54. Ketamine : subcortical and peripheral responses
are also minimal.
Preferred drug for monitoring responses that are
usually difficult to record during anaesthesia
and in children.
Use of ketamine with propofol reduces the
depressant effect of propofol while providing
an enhancement effect on responses.
Continue…

55. Barbiturates and benzodiazepines:
• Thiopental and midazolam produce mild
depression of cortical sensory responses but
long-lasting depression of MEPs.
• Hence not good for MEP monitoring.
• The ABR is virtually unaffected by doses of
phenobarbital that produce coma, and the
SSEP is unaffected at doses that produce a
silent EEG.
• so to monitor with SSEP is best.
Continue…

56. • Etomidate Produces an amplitude
increase of cortical sensory components
following injection, with no changes in
subcortical and peripheral sensory
responses. As consistent with myoclonus.
• SSEP recording commonly done but not
MEP monitoring.
Continue…

57. Propofol Most commonly used sedative
component of total intravenous anesthesia
when SSEPs and MEPs are monitored.
• Induction produces amplitude depression
in cortical SSEPs, with rapid recovery after
termination of infusion.
• Recordings in the epidural space are
unaffected, consistent with the site of
anaesthetic action of propofol in the cerebral
cortex.
Continue…

58. Droperidol and Dexmedetomidine
• Have minimal effects on responses
Dexmedetomidine has been successfully
used with MEP.
Continue…

59. Impairs or prevents MEP and EMG
monitoring.
Muscle relaxants are generally thought to have
no effect on the SSEPs
Partial NMB reduces the amplitude of motor
unit potentials and might therefore change the
ability to detect impending axonal injury from
nerve irritation.
Effect of neuromuscular blocking
agents

60. Cont….
It is preferred to avoid NMB after
anaesthesia induction and during EMG
and MEP monitoring.

61. Cont…
Effect of isoflurane on VEP

62. Effects on SSEP

63. Conclusion:
Evoked potential monitoring require
training, financial obligations and not 100
percent full proof in minimizing
complications.
Have risk involved.
On the other hand they have been shown to
be cost effective and have become part of
routine management.
For many surgeons and anesthesiologists,
these methods have become an indispensable
intraoperative diagnostic tool.

64. THANK
YOU