Neurological Monitoring

1. Neurological Monitoring Augusto Torres, MD Department of Anesthesiology MetroHealth Medical Center April 2009 www.anaesthesia.co.inanaesthesia.co.in@gmail.com

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 • No burst suppression

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. 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 Non-anesthetic Factors Affecting EEG Miller et al.

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 ManagementSchubert “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 ManagementSchubert “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 ManagementSchubert “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 • 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 www.anaesthesia.co.inanaesthesia.co.in@gmail.com