Transcript neurologicalMonitoring

Neurological Monitoring
Outline
EEG
 SSEP
 MEP
 Transcranial Doppler
 Cerebral Oximetry

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
EEG
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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
EEG

Electrodes placed so
that mapping system
relates surface head
anatomy to
underlying brain
cortical regions
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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

Normal EEG:
characteristic
frequency (beta, then
alpha) with
symmetrical signals
EEG
EEG
Abnormal EEG:
 Regional problems - asymmetry in frequency,
amplitude or unpredicted patterns of such
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– Epilepsy – high voltage spike with slow waves
– Ischemia – slowing frequency with preservation of
amplitude or loss of amplitude (severe)
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Global problems – affects entire brain,
symmetric abnormalities
– Anesthetic agents induce global changes similar to
global ischemia or hypoxemia (control of anesthetic
technique is important)
Abnormal EEG
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
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– Monitors fewer channels, less experience
required
– Reasonable results obtained
Anesthetic Agents and EEG
Anesthetic drugs affect frequency and
amplitude of EEG waveforms
 Subanesthetic doses of IV and inhaled
anesthetics (0.3 MAC):
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– Increases frontal beta activity (low voltage,
high frequency)
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Light anesthesia (0.5 MAC):
– Larger voltage, slower frequency
Anesthetic Agents and EEG
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General anesthesia (1 MAC):
– Irregular slow activity
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Deeper anesthesia (1.25 MAC):
– Alternating activity
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Very deep anesthesia (1.6 MAC):
– Burst suppression  eventually isoelectric
Anesthetic Agents and EEG
Some agents totally suppress EEG activity
(e.g. isoflurane)
 Some agents never produce burst
suppression or an isoelectric EEG
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– Incapable (e.g. benzodiazipines)
– Toxicity (e.g. halothane) prevents giving large
enough dose
Anesthetic Agents and EEG
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Barbiturates, propofol, etomidate:
– Initial activation, then dose-related
depression, results in EEG silence
– Thiopental – increasing doses will reduce
oxygen requirements from neuronal activity
 Basal requirements (metabolic activity) reduced by
hypothermia
– Epileptiform activity with methohexital and
etomidate in subhypnotic doses
Anesthetic Agents and EEG
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Ketamine:
– Activates EEG at low doses (1mg/kg), slowing
at higher doses
– Cannot achieve electrocortical silence
– Also associated with epileptiform activity in
patients with epilepsy
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Benzodiazepines:
– Produce typical EEG pattern
– No burst suppression or isoelectric EEG
Anesthetic Agents and EEG
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Opioids
–
–
–
–
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Slowing of EEG
No burst suppression
High dose – epileptiform activity
Normeperidine
Nitrous oxide
– Minor changes, decrease in amplitude
and frontal high-frequency activity
– No burst suppression
Anesthetic Agents and EEG
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Isoflurane, sevoflurane, desflurane:
– EEG activation at low concentrations; slowing,
eventually electrical silence at higher
concentrations
– Isoflurane
 Periods of suppression at 1.5 MAC
 Electrical silence at 2 – 2.5 MAC
Anesthetic Agents and EEG
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Enflurane
– Seizure activity with hyperventilation and high
concentrations (>1.5 MAC)
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Halothane
– 3-4 MAC necessary for burst suppression
 Cardiovascular collapse
Non-anesthetic Factors Affecting
EEG
Miller et al.
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Surgical
Cardiopulmonary bypass
 Occlusion of major
cerebral vessel (carotid
cross-clamping, aneurysm
clipping)
 Retraction on cerebral
cortex
 Surgically induced emboli
to brain
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Pathophysiologic
Factors
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Hypoxemia
Hypotension
Hypothermia
Hypercarbia and
hypocarbia
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Intraoperative Use of EEG
EEG used to monitor for ischemia
 Avoid during critical periods of the case:
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– Changing anesthetic technique
– Changing gas levels
– Administering boluses of medications that
affect EEG
Intraoperative Use of EEG
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Cardiopulmonary bypass
– Theoretically beneficial
 Embolic events with cannulation
 Increased risk in patients with carotid disease
– Difficult to interpret EEG changes
 Alteration of arterial carbon dioxide tension
 Changes in blood pressure
 Hypothermia
 Hemodilution (anemia)
Intraoperative Use of EEG
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Carotid endarterectomy
– Well-established
– 20% of patients with major EEG
changes awaken with neurological
deficits
– Normal cerebral blood flow
50mL/100g/min
– Cellular survival threatened
12mL/100g/min
– EEG changes seen at 20mL/100g/min
 With isoflurane EEG changes not seen until
10mL/100g/min
– If EEG changes noted, intervene
 Shunting
 Increase CBF
Intraoperative Use of EEG
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Limitations to EEG for CEA
– Need for experienced technician to monitor
– Strokes still occur despite normal intra-op EEG
 Subcortical events not monitored by EEG
– Not proven to reduce incidence of stroke
– False positives
Intraoperative Use of EEG
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What to do if EEG technician indicates a
possible problem?
– Check to see if anesthetic milieu is stable
– Rule out hypoxemia, hypotension,
hypothermia, hypercarbia and hypocarbia
 Raise the MAP, obtain ABG
– See if there is a surgical reason
Evoked Potentials
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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
Sensory Evoked Potential
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Sensory evoked potentials
– Somatosensory (SSEP)
– Auditory (BAEP)
– Visual (VEP)
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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)
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As opposed to EEG, records subcortically
Sensory Evoked Potential
Responds to injury by increased latency,
decreased amplitude, ultimately
disappearance
 Problem is response non-specific
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 Surgical injury
 Hypoperfusion/ischemia
 Changes in anesthetic drugs
 Temperature changes
Sensory Evoked Potentials
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Signals easily disrupted by background
electrical activity (ECG, EMG activity of
muscle movement, etc)
– Baseline is essential to subsequent
interpretation
SSEPs
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Stimulation with fine
needle electrodes
Stimulate median nerve –
signal travels anterograde
causing muscle twitch,
also travels retrograde up
sensory pathways along
dorsal columns all the
way to brain cortex
SSEPs
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Can measure the
electrophysiologic
response to nerve
stimulation all the way up
this pathway
Monitor many waves
(representing different
nerves along pathway)
and localization of where
the neural pathway is
interrupted is possible
Intraoperative SSEPs
Neurologic pathway must be at risk and
intervention must be available
 Indications:
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– 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
Intraoperative SSEPs
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Scoliosis surgery – well established
– Lessen degree of spine straightening
– False-negatives rare, false positives more common
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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
 Poor correlation in thoracic aortic surgery
Intraoperative SSEPs
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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
Intraoperative SSEPs
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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
Other SEP’s
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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
Other SEP’s
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VEP – flash stimulation of retina assess
pathway from optic n. to occipital cortex
– Procedures near optic chiasm
– Very sensitive to anesthetic drugs and
variable signals - unreliable
Anesthetic Agents and SEPs
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Most anesthetic drugs increase latency and
decrease amplitude
– Volatile agents: increase latency, decrease amplitude
– Barbituates: increase in latency, decrease amplitude
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Exceptions:
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–
–
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Nitrous oxide: latency stable, decrease amplitude
Etomidate: increases latency, increase in amplitude
Ketamine: increases amplitude
Opiods: no clinically significant changes
Muscle relaxants: no changes
Physiologic Factors and SEP’s
All of these affect SSEPs
 Hypotension
 Hyperthermia and hypothermia
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– Mild hypothermia (35-36 degrees) minimal effect
Hypoxemia
 Hypercapnea
 Significant anemia (HCT <15%)
 Technical factor: poor electode-to skin-contact
and high electrical impedence (eg
electrocautery)
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Anesthetic Management
Schubert “Clinical Neuroanesthesia”
Stable, constant anesthetic level,
especially during critical periods
 Response to poor signal
 Rule out technical factors:
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– Electrode impedance, radio frequency
interference
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Cortical vs. subcortical changes
Anesthetic Management
Schubert “Clinical Neuroanesthesia”
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Rule out systemic factors:
– KEY: improve neural tissue blood flow and nutrient
delivery
– Intravascular volume and cardiac performance
optimized (crystalloid/colloid or blood) to increase
oxygen-carrying capacity – optimal HCT 30% or
higher
– Elevate MAP
– Blood gas – assure oxygenation, normocarbia to help
improve collateral blood supply if hypocarbic
– Consider steroids (shown to work with traumatic
spinal cord injury)
– Mannitol – improve microcirculatory flow and
reducing interstitial cord edema
Anesthetic Management
Schubert “Clinical Neuroanesthesia”
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Rule out neurological factors
– Brain and spinal cord ischemia
– Pneumocephalus
– Peripheral n. ischemia and compression
Motor Evoked Potentials
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Transcranial electrical
MEP monitoring
– Stimulating electrodes
placed on scalp
overlying motor cortex
– Application of electrical
current produces MEP
– Stimulus propagated
through descending
motor pathways
Motor Evoked Potentials
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Evoked responses
may be recorded:
– Spinal cord, peripheral
n., muscle itself
Motor Evoked Potentials
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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
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Transcranial Doppler
Direct, noninvasive
measurement of CBF
 Sound waves
transmitted through
thin temporal bone,
contact blood, are
reflected, and
detected
 Most easily monitor
middle cerebral artery
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Transcranial Doppler
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Does not measure actual blood flow but velocity
– Velocity often closely related to flow but two are not
equivalent
Surgical field may limit probe placement and
maintenance of proper position
 Carotid endarterectomy
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– Measure adequacy of CBF during clamping
 Technically difficult in ~20%
– Useful for detecting embolic events – How much
emboli is harmful?
Transcranial Doppler
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CPB
– Detect air or particulate emboli during
cannulation, during bypass, weaning from
bypass, decannulation
– Significant data pending
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Detection of vasospasm (well-established)
– Smaller area – increase in velocity
(>120cm/s)
Cerebral Oximetry (Near infrared
spectroscopy)
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Measures oxygen saturation in the vascular bed of the
cerebral cortex
Interrogates arterial, venous, capillary blood within field
– Derived saturation represents a tissue oxygen saturation
measured from these three compartments
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Unlike pulse oximetry (requires pulsatile blood), NIRS
assess the hemoglobin saturation of venous blood, which
along with capillary blood, composes approximately 90%
of the blood volume in tissues
Believed to reflect the oxygen saturation of hemoglobin
in the post extraction compartment of any particular
tissue
Measures tissue oxygen saturation
Cerebral Oximetry (Near infrared
spectroscopy)
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Concerns:
– Measures small portion of frontal cortex, contributions from nonbrain 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?)
– High intersubject variability
– Low specificity
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Rigamonti et al.
(J Clin Anesth 2005;17:426)
– Compared EEG to rSO2 in CEA in terms of predicting need to
place shunt 44% sens 84% spec
Conclusion
EEG is a useful modality for measuring
intraoperative cerebral perfusion
 SSEP offers the additional advantage of
measuring subcortical adverse events
 New techniques for neurological
monitoring are being developed which
need to be further evaluated and validated
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