1. Neurological Monitoring

2. Outline
EEG
SSEP
MEP
Transcranial Doppler
Cerebral Oximetry

3. 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

4. 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

5. EEG
Electrodes placed so that mapping system relates surface head anatomy to underlying brain cortical regions

6. EEG 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

7. EEG
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)

8. Abnormal EEG

9. 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

10. Anesthetic Agents and EEG
Anesthetic drugs affect frequency and amplitude of EEG waveforms
Subanesthetic doses of IV and inhaled anesthetics (0.3 MAC):
Increases frontal beta activity (low voltage, high frequency)
Light anesthesia (0.5 MAC):
Larger voltage, slower frequency

11. Anesthetic Agents and EEG
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. Anesthetic Agents and EEG
Some agents totally suppress EEG activity (e.g. isoflurane)
Some agents never produce burst suppression or an isoelectric EEG
Incapable (e.g. benzodiazipines)
Toxicity (e.g. halothane) prevents giving large enough dose

13. Anesthetic Agents and EEG
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

14. Anesthetic Agents and EEG
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
Benzodiazepines:
Produce typical EEG pattern
No burst suppression or isoelectric EEG

15. Anesthetic Agents and EEG
Opioids
Slowing of EEG
No burst suppression
High dose – epileptiform activity
Normeperidine
Nitrous oxide
Minor changes, decrease in amplitude and frontal high-frequency activity

16. Anesthetic Agents and EEG
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

17. Anesthetic Agents and EEG
Enflurane
Seizure activity with hyperventilation and high concentrations (>1.5 MAC)
Halothane
3-4 MAC necessary for burst suppression
Cardiovascular collapse

18. Non-anesthetic Factors Affecting EEG Miller et al.
Surgical
Cardiopulmonary bypass
Occlusion of major cerebral vessel (carotid cross-clamping, aneurysm clipping)
Retraction on cerebral cortex
Surgically induced emboli to brain
Pathophysiologic Factors
Hypoxemia
Hypotension
Hypothermia
Hypercarbia and hypocarbia

19. Intraoperative Use of EEG
EEG used to monitor for ischemia
Avoid during critical periods of the case:
Changing anesthetic technique
Changing gas levels
Administering boluses of medications that affect EEG

20. Intraoperative Use of EEG
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)

21. Intraoperative Use of EEG
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

22. Intraoperative Use of EEG
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

23. Intraoperative Use of EEG
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

24. Evoked Potentials
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

25. Sensory Evoked Potential
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

26. Sensory Evoked Potential
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

27. Sensory Evoked Potentials
Signals easily disrupted by background electrical activity (ECG, EMG activity of muscle movement, etc)
Baseline is essential to subsequent interpretation

28. SSEPs 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

29. SSEPs
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

30. Intraoperative SSEPs
Neurologic pathway must be at risk and intervention must be available
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

31. Intraoperative SSEPs Scoliosis surgery – well established
Lessen degree of spine straightening
False-negatives rare, false positives more common
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

32. Intraoperative SSEPs 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

33. Intraoperative SSEPs 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

34. Other SEP’s 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

35. Other SEP’s
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

36. Anesthetic Agents and SEPs
Most anesthetic drugs increase latency and decrease amplitude
Volatile agents: increase latency, decrease amplitude
Barbituates: increase in latency, 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

37. Physiologic Factors and SEP’s
All of these affect SSEPs
Hypotension
Hyperthermia and hypothermia
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)

38. Anesthetic Management Schubert “Clinical Neuroanesthesia”
Stable, constant anesthetic level, especially during critical periods
Response to poor signal
Rule out technical factors:
Electrode impedance, radio frequency interference
Cortical vs. subcortical changes

39. Anesthetic Management Schubert “Clinical Neuroanesthesia”
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

40. Anesthetic Management Schubert “Clinical Neuroanesthesia”
Rule out neurological factors
Brain and spinal cord ischemia
Pneumocephalus
Peripheral n. ischemia and compression

41. 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

42. Motor Evoked Potentials
Evoked responses may be recorded:
Spinal cord, peripheral n., muscle itself

43. 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

44. 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

45. Transcranial Doppler 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
Measure adequacy of CBF during clamping
Technically difficult in ~20%
Useful for detecting embolic events – How much emboli is harmful?

46. Transcranial Doppler CPB Detection of vasospasm (well-established)
Detect air or particulate emboli during cannulation, during bypass, weaning from bypass, decannulation
Significant data pending
Detection of vasospasm (well-established)
Smaller area – increase in velocity (>120cm/s)

47. Cerebral Oximetry (Near infrared spectroscopy)
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
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

48. Cerebral Oximetry (Near infrared spectroscopy)
Concerns:
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?)
High intersubject variability
Low specificity
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

49. 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