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Miller: Miller's Anesthesia, 7th ed. Copyright © 2009 Churchill Livingstone, An Imprint of Elsevier << Previous | Next >> 46 – Neurologic Monitoring Christoph N. Seubert, Michael E. Mahla Key Points

1.

There are four key principles of intraoperative neurologic monitoring.

2.

The pathway at risk during the surgical procedure must be amenable to monitoring.

3.

If evidence of injury to the pathway is detected, there must be some intervention possible.

4.

If changes in the neurologic monitor are detected, and no intervention is possible, although the monitor may be of prognostic value, it does not have the potential to provide direct benefit to the patient from early detection of impending neurologic injury.

5.

The monitor must provide reliable and reproducible data.

6.

There are few randomized prospective studies evaluating the efficacy of neurologic monitoring modalities.

7.

Based on clinical experience and nonrandomized studies, practice patterns for use of neurologic monitoring have emerged.

8.

There are procedures for which monitoring is recommended and used by most centers

9.

There are procedures for which monitoring is used frequently in some centers, but not in others.

10. There are procedures for which there is no clear clinical experience or evidence indicating that monitoring is useful at all (experimental use). 11. There are procedures in which monitoring is used selectively for patients believed to be at higherthan-usual risk for intraoperative neurologic injury. Neurologic monitoring in the context of anesthesia care for a patient spans a wide spectrum of techniques, diverse procedures, and various intraoperative or even postoperative settings. Techniques for monitoring fall into two broad categories: techniques to assess metabolic integrity of the nervous system, which typically entail either global or regional determinations of blood flow or oxygenation, or techniques to assess functional integrity, which likewise may be global or focused on specific anatomic components of the nervous system. The procedures and settings in which neurologic monitoring is typically applied all share the characteristic that changes in the monitored parameters can be corrected or minimized by either modifying the surgical approach or manipulating parameters under the control of the anesthesiologist. Monitored procedures range from procedures where monitoring dictates the surgical approach, such as localization of the motor strip during tumor surgery or the neurologic examination during an “awake” craniotomy, to procedures that by their nature put parts of the nervous system at increased risk. In many procedures that require neurologic monitoring, the surgical target overlaps with the site of action


of drugs a patient receives. The anesthesiologist and the surgeon need to be aware not only of limitations inherent in individual monitoring techniques, but also of nonsurgical factors that influence the monitoring results. The monitoring approach ideally should anticipate nonsurgical factors by providing a degree of redundancy that helps distinguish a localized surgical trespass from a systemic event. For some procedures, neurologic monitoring is a marker of the quality of care and is routinely employed because outcome data support its use. Examples include correction of scoliosis and resection of vestibular schwannomas. More frequently, the approach to monitoring is based on local conventions and surgical expectations. In this latter case, monitoring utility depends even more on a good understanding of the technique's capabilities and limitations by anesthesiologists and surgeons and on their mutual collaboration to allow corrective action in the face of changing signals or to prevent false alarms that disrupt surgery. This chapter first discusses individual monitoring modalities in isolation so that the clinician can appreciate the inherent strengths and weaknesses of each. Subsequent sections apply this information by describing suitable approaches to various clinical settings that combine and integrate individual techniques to optimize neurologic outcome for patients. The chapter ends with a brief discussion of how neurologic monitoring is believed to be useful today, and where more work is needed to determine whether monitoring has a role in surgical patients in the future. Monitoring Modalities Monitors of Adequacy of Nervous System Blood Flow

Adequacy of cerebral blood flow (CBF) can be monitored by two principal methods. The first method assesses blood flow itself with the implicit assumption that “normal” flow provides adequately for the metabolic needs of the brain. The second approach assesses oxygen delivery either locally or globally with the implicit assumption that “normal” values at the site of measurement are reflective of adequate blood supply throughout the central nervous system (CNS). To illustrate the limitations imposed by such implicit assumptions, let us examine global or hemispheric CBF in the context of a patient's disease process. In normal brain, values of hemispheric CBF of approximately 50 mL/100 g/min reflect adequate oxygen delivery for maintaining structural integrity and function. Values of less than 20 to 25 mL/100 g/min are associated first with failure of function and on further decrease with structural damage. [1] In neurosurgical patients, structural integrity and function may be altered by disease processes and anesthetics, which have an impact on the interpretation of measured CBF. A CBF of 40 mL/100 g/min in a patient in barbiturate coma after resection of an arteriovenous malformation may represent hyperemia (because metabolic demand is very low), whereas the same CBF in a patient with a mass lesion may reflect a modest decrease in cerebral perfusion pressure secondary to increasing intracranial pressure. Global Blood Flow Monitoring Techniques (Noninvasive) Intravascular Tracer Compounds.

Direct measurement of CBF is possible by determining kinetics of washin or washout, or both, of an inert tracer compound, a method originally described by Kety and Schmidt. [2] The most widely used measurement technique involves administration of a radioactive isotope of xenon ( 133 Xe), followed by measurement of the radioactivity washout with gamma detectors placed over specific areas of the brain. Depending on the number of detectors, this method can provide a spatial resolution of 4 cm. In normal brain, flow at different depths may be inferred from the early washout, which should reflect high-perfusion cortical gray matter, and late washout from low-perfusion deeper white matter. Drawbacks of the method are the patient's exposure to radioactive compounds and the need for externally


placed and potentially cumbersome detector equipment, which may interfere with surgery itself in the case of intracranial surgery. Focal areas of hypoperfusion may be missed because of underlying or overlying adequate flow, a phenomenon described as “look-through.” [3] Despite these shortcomings, 133 Xe washout has been used at a few major centers for intraoperative monitoring during operations such as carotid endarterectomy. [4] [5] [6] [7] [8] Modern variations of the same concept are mean transit time determinations of intravascular contrast agents during neuroimaging for determining locoregional blood flow [7] [8] or a double-indicator technique for determining global CBF. [9] All these techniques share the limitation of providing a snapshot of CBF in time instead of continuous monitoring. Transcranial Doppler Ultrasound.

Transcranial Doppler (TCD) ultrasound is a technique that infers CBF from measurements of the blood flow velocity in the large conducting arteries of the brain. The TCD probe transmits pulses of sound waves through the thin temporal bone in a variation of the pulsed wave Doppler technique with which anesthesiologists may be familiar from echocardiography. When these sound waves are reflected off the red blood cells back toward the TCD probe, the velocity of the reflected sound waves is changed because the blood cells themselves are in motion toward or away from the probe. This phenomenon is known as the “Doppler shift,” and is directly related to flow velocity and flow direction of the blood cells. Blood flow is faster during systole and in the center of a vessel and slower in diastole and near the vessel wall. TCD records a spectrum of flow velocities, whose outline resembles an arterial waveform tracing. These concepts are illustrated in Figure 46-1 .

Figure 46-1 A, Transcranial Doppler monitoring is done by insonating the arteries at the base of the brain through a thin part of the temporal bone. B, If this is done with an imaging probe, some intracranial structures, such as the cerebral peduncles ( white triangles ) or the sella complex ( white triangle labeled “S”), can be visualized. The Doppler signals originate from the right middle, right anterior, and left anterior cerebral arteries. C, Normal Doppler spectrum obtained from the middle cerebral artery. D, Doppler profile of the bifurcation of the terminal internal carotid artery as it branches into the middle cerebral artery (flowing toward the transducer) and the anterior cerebral artery (flowing away). This flow signal can be obtained if the transducer is focused as shown in A. E-G, Examples of three clinical applications of transcranial Doppler. E, Emboli are highly echogenic and show up as high-energy transient signals (HITS). On the audible output, these emboli are easily noticed as brief beeps or chirps. F, Doppler profile of a middle cerebral artery in a patient with severe vasospasm after an aneurysmal subarachnoid hemorrhage (compare with C). G, Transcranial Doppler examination consistent with intracranial circulatory arrest. There is a brief systolic inflow followed by retrograde flow during diastole.

Intraoperatively, TCD measurements are most commonly and easily made by continuous monitoring of the middle cerebral artery for the purpose of detecting either significant changes in flow velocity or the presence of particulate emboli. As a diagnostic study, in addition to the middle cerebral artery, the anterior cerebral, anterior communicating, posterior cerebral, and posterior communicating arteries can be examined through the temporal bone window. The basilar, ophthalmic, and internal carotid arteries also can be insonated through the foramen magnum (TCD probe at the back of the flexed neck) (basilar artery), the closed eyelid (with reduced sound energy) (ophthalmic artery), and near the angle of the jaw (internal carotid artery). An important limitation of TCD results from the fact that most of the examination is done through the temporal bone, which may be thick enough to preclude an adequate examination in 10% to 20% of patients. [10] [11] Two assumptions that are intuitive and plausible, but ultimately unproven, must be made for TCDmeasured blood flow velocity to have a direct relationship to CBF. First, blood flow velocity is directly related to blood flow only if the diameter of the artery where the flow velocity is measured and the measurement angle of the Doppler probe remain constant. In practical terms, the difficulty with this assumption lies in finding a means to affix the TCD probe in a way that prevents dislodgment or movement during monitoring. The second assumption requires that CBF in the basal arteries of the brain is directly related to cortical CBF. Because TCD monitoring is typically done mainly using the middle cerebral artery, this assumption may be invalid if collateral blood flow by leptomeningeal collaterals from anterior and


posterior cerebral artery territories is adequate. Although these two assumptions constrain the utility of TCD as a stand-alone monitor of CBF, the changes in flow velocity seen in typical applications (discussed subsequently) are large enough to provide useful clinical information. More importantly, TCD is the only continuous neurologic monitoring technique that provides early warning for hyperperfusion and for the number of emboli delivered to the brain during various phases of an operation. Because of their high echogenicity, emboli show up in the TCD spectrum as high-intensity transient signals (HITSs) (see Fig. 46-1 ) and are easily identified as brief beeps or chirps within the background of the Doppler sounds. Jugular Bulb Venous Oxygen Saturation.

The degree of oxygen extraction by an organ can be monitored by following the oxygen saturation of the mixed venous blood that drains that organ. In the case of the brain, jugular bulb venous oxygen saturation (SjVO 2 ) is believed to measure the degree of oxygen extraction and to represent the balance between cerebral oxygen supply and demand. To monitor Sj VO 2 , a fiberoptic catheter is placed in a retrograde fashion into the jugular bulb through the internal jugular vein under fluoroscopic guidance. The fiberoptic bundle emits near-infrared light and records light reflected back to the catheter, a technique known as “reflectance oximetry.” Because near-infrared light can travel several centimeters in tissue and is mostly absorbed by hemoglobin, it is possible to determine the oxygen saturation of the surrounding tissue (i.e., the jugular venous blood). Correct tip placement is crucial to minimize admixture of extracranial venous blood. To decrease the risk of complications, usually only one side is monitored. Several theoretical limitations of the technique must be borne in mind to interpret Sj VO 2 values and trends properly. Although nearly all blood from the brain drains via the jugular veins, intracranial mixing of venous blood is incomplete and may result in differences between right-sided and left-sided measurements. The dominant jugular vein (i.e., the right for most patients) drains predominantly cortical venous blood, whereas the contralateral jugular vein drains more of the subcortical regions. [12] Despite such regional differences, Sj VO 2 must be considered a monitor of global cerebral oxygenation because inadequate perfusion to a focal brain region may not decrease Sj VO 2 values below the normal range of 55% to 75%. Because Sj VO 2 represents the balance between supply and demand, interpretation of the absolute value of Sj VO 2 must take the clinical circumstances into account. Cerebral Oximetry.

Cerebral oximetry is a noninvasive technique that, similar to Sj VO 2 monitoring, uses reflectance oximetry to measure the oxygen saturation of the tissues underneath the sensor. Typically, two sensors are applied to both sides of the forehead. The light passes not only through parts of the frontal brain, but also through the overlying skull and scalp. Contamination of the oximetry signal by extracranial blood sources is a serious concern, although the use of two sensing diodes with different distances from the light source within one sensor patch and adjustments of the algorithm of the oximeter may minimize this problem. [13] [14] Because two thirds to four fifths of the cerebral blood volume is venous blood, cerebral oximetry determines predominantly “local venous oxygen saturation.” [15] It can be expected that in the face of cerebral ischemia, oximetry values decrease as a result of increased oxygen extraction, well before function fails, or permanent neuronal damage ensues. The simplicity of its use and the familiarity with the principles of treating decreases in systemic mixed venous oxygen saturation have made cerebral oximetry a popular trend monitor in operations that potentially cause decreases in blood flow to the vessels of the head. There are some significant limitations, however, of the use of cerebral oximetry during such procedures. First, adequacy of global cerebral perfusion is inferred from measurements over the frontopolar brain. Second, normative data on normal values or expected changes for cerebral oximetry are largely absent, but


preoperative application of the sensors allows the start of a trend in conjunction with a neurologic baseline examination. An example of how these limitations play out is provided by a study of the use of cerebral oximetry during 100 carotid endarterectomies in awake patients. [16] Cerebral oximetry was able to identify 97.4% of patients with adequate CBF as indicated by the absence of clinical symptoms. The monitor frequently indicated inadequate CBF, defined as a 20% decrease in cerebral oxygen saturation from the preclamp baseline, although the patient had no clinical symptoms of inadequate CBF. The false-positive rate of 66.7% may simply illustrate the fact that oxygen extraction increases before function fails. The real problem is that the lower limit for acceptable regional oxygen saturation is unknown in a large population of patients. [17] The value may be different from patient to patient, and addition of anesthetic drugs that influence cerebral metabolism may confuse the picture further. Tissue-Level Blood Flow Monitoring Techniques (Invasive)

Tissue-level monitoring for the brain is by definition invasive. All monitors in current clinical or research use are implanted through a burr hole, extend either into the white matter or ventricular system, and typically use a bolt for stabilization. They all share a 1% to 2% risk of bleeding, infection, or ischemia owing to the implantation procedure. [18] A second shared feature is their limited spatial resolution (i.e., each monitoring probe monitors only a limited area of brain surrounding the probe). When these monitors were first developed, there was considerable debate regarding the optimal placement of the device given such limited spatial resolution. Based on today's appreciation for the impact of secondary neurologic insults on the ultimate outcome, there is growing agreement that tissue-level monitoring is best performed in morphologically and functionally normal tissue that is part of the penumbra or vulnerable zone of interest. [19] [20] [21] Placing a blood flow monitor into the brain tissue supplied by an aneurysm-carrying artery in the setting of a subarachnoid hemorrhage maximizes, but does not ensure, the chances of early detection of vasospasm. Of the tissue-level monitors, two have undergone sufficient refinement to be in wider clinical use. They represent the two principal modes of assessing adequate blood flow—assessing CBF through thermal diffusion monitoring or assessing oxygen delivery through tissue partial pressure of oxygen (PO2 ) monitoring. Thermal Diffusion Cerebral Blood Flow Monitoring.

Thermal diffusion CBF monitoring is based on the idea that the rate at which heat dissipates in a tissue depends on the tissue's thermal conductive properties and the blood flow in that area. Because thermal conduction properties remain constant, changes in heat dissipation reflect changes in blood flow and can be expressed quantitatively in the conventional units of CBF as mL/100 g/min. In practice, the probe consists of a thin catheter with two thermistors placed 5 mm apart ( Fig. 46-2 ). When inserted, both thermistors are located in subcortical white matter. The proximal or passive thermistor measures brain temperature, whereas the distal or active thermistor is heated to 2°C above the temperature measured by the passive thermistor. The power required to sustain the 2°C temperature difference is directly proportional to CBF. The initial rate of propagation of the thermal field is used to establish the fixed conductive component of heat transfer.

Figure 46-2 Thermal diffusion measurement of cerebral blood flow. The probe is placed in the subcortical white matter. It contains a passive thermistor (T 1) that measures brain temperature and is located outside of the area influenced by the active thermistor. The active thermistor (T 2) is heated to 2°C above brain temperature. The energy required to maintain that increase in temperature is proportional to cerebral blood flow.


The acute performance of this technology has been validated against stable xenon computed tomography (CT) in patients with head injury and performed well across a wide range of CBF values in a sheep model of hypercarbia, hyperventilation, and cardiac arrest. [22] In continuous clinical use, the probe shows some drift and recalibrates at regular intervals. [23] To avoid thermal tissue injury, measurement is automatically suspended if the passive thermistor measures a brain temperature of 39.1째C. Because fever is a frequent complication, particularly in patients with severe brain disease, the inability to monitor during a febrile episode may constitute a true limitation of the technique. Tissue Partial Pressure of Oxygen Monitoring.

Localized monitoring of tissue PO2 is based on an oxygen-sensitive electrode originally described by Clark. [24] The diffusion of oxygen molecules through an oxygen-permeable membrane into an electrolyte solution causes an electric current that is proportional to PO2 . Currently available catheter-based electrodes provide stable recording conditions over long periods. Similar to regional CBF probes, they are placed into the subcortical white matter. Most of the data on brain tissue oxygen levels (PBr O2 ) comes from studies in patients with head trauma. Comparison with stable xenon CT for assessment of CBF shows good correlation between PBr O2 and CBF. [25] [26] Similarly, the time course of changes in PBr O2 after traumatic brain injury resembles that of CBF. [27] [28] Critics of the technique argue that PBr O2 values are highly influenced by the partial pressure of arterial oxygen (Pa O2 ) and are merely an elaborate indicator of the quality of patient ventilation. This view is supported by the observation that increasing the fraction of inspired oxygen (F IO2 ) increases PBr O2 , but likely represents an oversimplification. [29] Concurrent microdialysis studies have shown that increasing F IO2 not only increases PBr O2 , but also decreases tissue lactate levels, suggesting a true improvement in the metabolic milieu of the brain tissue itself. [30] [31] Monitors of Nervous System Function

The most commonly used monitors of function are the electroencephalogram (EEG), sensory evoked responses (SERs), motor evoked responses, and the electromyogram (EMG). The EEG is a surface recording of the summation of excitatory and inhibitory postsynaptic potentials spontaneously generated by the pyramidal cells in the cerebral cortex. The signals are very small, and each recording electrode records only information generated directly beneath the electrode. Monitoring the EEG is usually directed toward one or more of four perioperative uses. First, the EEG is used to help identify inadequate blood flow to the cerebral cortex caused by either a surgically induced or anesthetic-induced reduction in blood flow or retraction on cerebral tissue. Second, the EEG may be used to guide an anesthetic-induced reduction of cerebral metabolism either in anticipation of a loss of CBF or in the treatment of high intracranial pressure, when a reduction in CBF and blood volume is desired. Third, the EEG may be used to predict neurologic outcome after a brain insult. Finally, the EEG may be used to gauge the depth of the hypnotic state of the patient under general anesthesia (see Chapter 39 ). More than 50 years of experience monitoring the EEG has led to many known correlations of EEG patterns with clinical states of the normal and pathologic cerebral cortex. The electroencephalographer can accurately identify consciousness, unconsciousness, seizure activity, stages of sleep, and coma. In the absence of significant changes in anesthetic technique, the electroencephalographer also can accurately identify inadequate oxygen delivery to the brain (from either hypoxemia or ischemia). By using high-speed computerized EEG analysis and statistical methods, EEG patterns in the continuum from awake to deeply anesthetized are becoming, with few exceptions, much better understood. In addition, computer advances have made possible high-speed mathematic manipulation of the EEG signal to present the data in a manner more suitable to continuous trends for use during surgical or anesthetic monitoring.


Evoked potentials are electric activity generated in response to either a sensory or a motor stimulus. Measurements of evoked responses may be made at multiple points along an involved nervous system pathway. The evoked responses are generally smaller than other electric activity generated in nearby tissue (muscle or brain) and are readily obscured by these other biologic signals. In the case of SERs, repeated sampling and sophisticated electronic summation and averaging techniques are needed to extract the desired evoked potential signal from background biologic signals. Motor evoked responses are generally larger and commonly do not require averaging. SERs are the most common type of evoked potentials monitored intraoperatively. During the last 2 decades, much research has been done on the use of intraoperative motor evoked potentials (MEPs). Although routine use of MEP monitoring is still not widespread, it is becoming more so. There are three basic types of sensory evoked responses: somatosensory evoked potentials (SSEPs), brainstem auditory evoked potentials (BAEPs), and visual evoked potentials (VEPs). The SSEP is produced by electrically stimulating a peripheral (or rarely cranial) nerve. Responses may be recorded proximally over the stimulated nerve, the spinal cord, and the cerebral cortex. The recorded responses assess the function of the peripheral nerve, the posterior and lateral aspects of the spinal cord, a small portion of the brainstem, the ventral posterolateral nucleus of the thalamus, the thalamocortical radiation, and a portion of the sensory cortex. The BAEP is usually produced by a series of rapid, loud clicks applied directly to the external auditory canal. Responses are most commonly recorded from electrodes applied to the scalp, although more invasive direct recordings from auditory structures and nerves may also be made. BAEPs assess function of the auditory apparatus itself; cranial nerve VIII; the cochlear nucleus; and a small area of the rostral brainstem, the inferior colliculus, and the auditory cortex. The VEP is produced by flash stimulation of the retina. Recordings are made from cortically placed electrodes and assess visual pathways from the optic nerve to the occipital cortex. MEP responses are generated most commonly by the application of a transcranial train of electric stimuli, and responses are recorded at various points along the spinal column, peripheral nerve, and innervated muscle. Electric stimuli to activate motor tracts also may be applied at the level of the spinal cord, but this method of stimulation is controversial (see later), with research suggesting that the response, as it is currently recorded, is at best a mixed response and at worst primarily a sensory response. Magnetic stimuli also may be applied transcranially or at the level of the spinal cord, but use of magnetic stimulation is much less common than electric stimulation, primarily for technical reasons involving fixation of the magnet to the patient to avoid shifts in magnetic field application, which would significantly alter responses. MEPs assess the integrity of the descending motor pathway through the internal capsule, the brainstem, the spinal cord, the peripheral nerve, and finally the muscle itself. The ability to record MEPs from some patients with cerebral palsy indicates that normal functional organization of the motor cortex cannot be inferred from MEPs. Electroencephalogram Basic Unprocessed Electroencephalogram Concepts.

The EEG is produced by a summation of excitatory and inhibitory postsynaptic potentials produced in cortical gray matter. Because the EEG signal is generated only by postsynaptic potentials and is much smaller than action potentials recorded over nerves or from the heart, extreme care must be taken when placing electrodes to ensure proper placement and excellent contact with the skin to avoid significant signal loss. Alternatively, subdermal needle electrodes may be used, particularly when sterile application of an electrode close to a surgical field is necessary. When electrodes are applied directly to the surface of the brain, impedance is minimized by close electrode contact and saturation of the area with an electrolyte solution.


EEG electrodes generally are placed according to a mapping system that relates surface head anatomy to underlying brain cortical regions. The placement pattern of recording electrodes is called a montage. Use of a standard recording montage permits anatomic localization of signals produced by the brain and allows development of normative EEG patterns and comparison of EEG recordings made at different times. The standard EEG “map” is called the 10-20 system for EEG electrode placement ( Fig. 46-3 ). This system is a symmetric array of scalp electrodes placed systematically based on the distance from the nasion to the inion and from the pretragal bony indentations associated with both temporomandibular joints. Based on 10% or 20% of these distances, recording electrodes are placed systematically over the frontal (F), parietal (P), temporal (T), and occipital (O) regions at increasing distances from the midline. Left-sided electrodes are given odd number subscripts, and right-sided electrodes are given even number subscripts. Increasing numbers indicate an increasing distance from the midline. Midline electrodes are designated with a “z” subscript. The standard diagnostic EEG uses at least 16 channels of information, [32] but intraoperative recordings have been reported using 1 to 32 discreet channels.

Figure 46-3 International 10-20 system of electrode placement for recording electroencephalogram and sensory evoked responses. (From Hughes JR: EEG in Clinical Practice, 2nd ed. Newton, MA, ButterworthHeinemann, 1994.)

The intraoperative EEG is most commonly recorded from electrodes placed on the scalp. Recordings also may be made from electrodes placed on the surface of the brain (electrocorticography), or from microelectrodes placed transcortically to record from individual neurons (e.g., during surgery for Parkinson's disease). [33] [34] The EEG signal is described using three basic parameters: amplitude, frequency, and time. Amplitude is the size, or voltage, of the recorded signal and ranges commonly from 5 to 500 µV (versus 1 to 2 mV for the electrocardiogram signal). Because neurons are irreversibly lost during the normal aging process, EEG amplitude decreases with age. Frequency can be thought of simply as the number of times per second the signal oscillates or crosses the zero voltage line. Time is the duration of the sampling of the signal; this is continuous and real time in the standard paper or digital EEG, but is a sampling epoch in the processed EEG (see later). Normal Electroencephalogram.

Normal patterns seen on the EEG vary among normal individuals, but are consistent enough to allow for accurate recognition of normal and pathologic patterns. The usual base frequency in an awake patient is the beta range (>13 Hz). This high-frequency and usually low-amplitude signal is common from an alert attentive brain and may be recorded from all regions. With eye closure, higher amplitude signals in the alpha frequency range (8 to 13 Hz) seen best in the occipital region appear ( Fig. 46-4 ). This “eyes closed” resting pattern is the baseline awake pattern used when anesthetic effects on the EEG are described. When events that lead the brain to produce higher frequencies and larger amplitudes occur, the EEG is described as “activated,” and when slower frequencies are produced (theta = 4 to 7 Hz, and delta = <4 Hz), the EEG is said to be “depressed.” The EEG in a sleeping patient may contain all of these frequencies at various times. The slower frequencies occur during deep natural sleep with “sleep spindles” ( Fig. 46-5 ), but during light sleep or rapid eye movement (REM) sleep, the EEG becomes activated, and the eye muscle EMG appears on the EEG.

Figure 46-4 The loss and return of α activity as the eyes open and close can be seen. The large spikes are muscle artifact.


Figure 46-5 Characteristic sleep spindles in normal sleep are shown in the center.

In the normal EEG in awake and asleep patients, patterns recorded from corresponding electrodes on each hemisphere are symmetric in terms of frequency and amplitude, the patterns are predictable if clinical states are known, and spike (epileptic) waveforms are absent. In most cases, normal EEG patterns are associated with normal underlying brain function in awake and anesthetized patients. Abnormal Electroencephalogram.

General characteristics of the “abnormal” EEG include asymmetry with respect to frequency, amplitude, or both, recorded from corresponding electrodes on each hemisphere, and patterns of amplitude and frequency that are unpredictable or unexpected in the normal recording. These abnormal patterns reflect either anatomic or metabolic alterations in the underlying brain. Regional asymmetry can be seen with tumors, epilepsy, and cerebral ischemia or infarction. Epilepsy may be recognized by high-voltage spike and slow waves, whereas cerebral ischemia manifests first with EEG slowing with preservation of voltage. Further slowing and loss of voltage occurs as ischemia becomes more severe. Factors affecting the entire brain may produce symmetric abnormalities of the signal. Identifying pathologic abnormal patterns in the global EEG signal is very important, although sometimes quite difficult, in the clinical situation. Many of the normal global pattern changes produced by anesthetic drugs are similar to pathologic patterns produced by ischemia or hypoxemia. Control of anesthetic technique is very important when the EEG is being used for clinical monitoring of the nervous system. Processed Electroencephalogram Concepts.

Interpretation of the standard paper EEG tracing is a science and an art. Until the last quarter of the 20th century, the paper EEG was used during intraoperative monitoring with the technologist relying on memory of the baseline and on experience to determine when significant EEG changes occurred. This qualitative approach was used simply because the waveforms could not be described mathematically in a time frame that would make such information of any practical use. Computer hardware has dramatically improved in speed and size, and real-time signal processing is now possible and commonly used. Numerous limitations are introduced when moving from the raw EEG domain to the processed EEG domain. First, artifact is processed in many cases along with desired signal leading to a perfectly believable processed EEG display that is materially incorrect. Second, the standard 16-channel EEG montage provides more information than can be practically analyzed or displayed by most processed EEG monitors and perhaps more than is needed for routine intraoperative use. Most available processed EEG devices used by anesthesiology personnel use four or fewer channels of information—translating to at most two channels per hemisphere. Processed EEG devices generally monitor less cerebral territory than a standard 16-channel EEG. Third, some intraoperative changes are unilateral (e.g., regional ischemia owing to carotid clamping), and some are bilateral (e.g., EEG depression by bolus administration of an anesthetic). Display of the activity of both hemispheres is necessary to delineate unilateral from bilateral changes. An appropriate number of leads over both hemispheres is needed. Most early studies validating intraoperative EEG monitoring used continuous visual inspection of a 16- to 32-channel analog EEG by an experienced electroencephalographer—such monitoring was considered the gold standard. [35] [36] Adequate studies comparing the processed EEG with fewer channels with this gold standard across multiple uses and operations have not been done, although limited data using processed EEG monitoring during carotid surgery suggest that two- or four-channel instruments would detect most significant changes, [37] [38] provided that the electrodes are appropriately placed over watershed areas of blood supply. Devices.


Two basic forms of EEG processing are used currently: power analysis and bispectral analysis. Power analysis uses Fourier transformation to convert the digitized raw EEG signal into component sine waves of identifiable frequency and amplitude. The raw EEG data, which is a plot of voltage versus time, is converted to a plot of frequency and amplitude versus time. Many commercially available processed EEG machines display power (voltage or amplitude squared) as a function of frequency and time. These monitors display the data in two general forms, either compressed spectral array or density spectral array. In compressed spectral array, frequency is displayed along the x axis, and power is displayed along the y axis with height of the waveform equal to the power at that frequency. Time is displayed along the z axis. Tracings overlap each other, with the most recent information in front ( Fig. 46-6 ). Density spectral array also displays frequency along the x axis; time is displayed along the y axis, and power is reflected by the density of the dots at each frequency. Each display format provides the same data, and choice depends on the preference of the user.

Figure 46-6 Diagram of technique used to generate compressed spectral array. Example at the bottom of the figure shows compressed spectra of the Îą rhythm from a normal subject. (From Stockard JJ, Bickford RG: The neurophysiology of anaesthesia. In Gordon E [ed]: A Basis and Practice of Neuroanesthesia. New York, Elsevier, 1981, p 3.)

Many changes that occur during anesthesia and surgery are reflected as changes in amplitude, frequency, or both. These changes can be clearly seen in these displays if adequate and appropriate channels are monitored. Power analysis has been used clinically for many years as a diagnostic tool during procedures with risk for intraoperative cerebral ischemia, such as carotid endarterectomy and cardiopulmonary bypass (CPB). Power analysis has proven to be a sensitive and reliable monitor in the hands of experienced operators using an adequate number of channels. In addition, parameters obtained from power analysis have been investigated as monitors for depth of anesthesia. [39] [40] [41] [42] Although earlier attempts to use parameters derived from power analysis for assessment of anesthetic depth were largely unsuccessful, these same parameters are now used to varying degrees with much more success as a part of different algorithms (including BIS [Bispectral Index Score] and PSI [Patient State Index]) to measure hypnotic states. Data Acquisition Period.

An important consideration in the processed EEG is time. The standard paper or digital EEG is continuous in real time. The processed EEG samples data over a given time period (epoch), processes the data, and then displays information in various formats. There is a relationship between epoch length and spectral resolution. If a long epoch length is chosen, the waveform can be described precisely, but the time required for data processing is long and not real time. If a short length of data is sampled, analysis may be done in near real time, but the epoch chosen for analysis may not be representative of the overall waveform (i.e., the condition of the patient). There also may be insufficient data points for meaningful Fourier transformation. This issue, as related to the use of intraoperative EEG for analysis of anesthetic depth, has been studied by Levy. [43] A longer epoch may produce less epoch-to-epoch variability and allow more precise description of frequency and power; however, the longer epoch increases the delay before new information is processed and displayed, reducing the amount and timeliness of information available for clinical decision making. In studying EEG epochs of 2 to 32 seconds, Levy [43] concluded that 2-second epochs are appropriate during general anesthesia. Many commercially available devices have used 2-second epoch lengths, updated at varying user-selected intervals. With better and faster computers, continuous monitoring of 2-second epochs and now even longer epochs is possible. Evoked Potentials Basic Concepts Common to All Modalities.


EEG signals provide information about cortical function, but little to no information about subcortical neural pathways crucial to normal neurologic function. Intraoperative monitoring of SERs has gained increasing popularity over the last 25 years because it provides the ability to monitor the functional integrity of sensory pathways in an anesthetized patient undergoing surgical procedures placing these pathways at risk. Because motor pathways are often adjacent anatomically to these sensory pathways or supplied by the same blood vessels, or both, function of motor pathways may be inferred, albeit imperfectly, from the function of these sensory pathways. Today, MEPs are ideally monitored together with SERs to provide direct information about function of motor pathways. Sensory Evoked Responses.

SERs are electric CNS responses to electric, auditory, or visual stimuli. SERs are produced by stimulating a sensory system and recording the resulting electric responses at various sites along the sensory pathway up to and including the cerebral cortex. Because of the very low amplitude of SERs (0.1 to 10 µV), it is often impossible to distinguish SERs from other background biologic signals, such as the EEG or EMG, which may be considered in this case undesirable “noise.” To extract the SER from the background noise, the recorded signal is digitized, and signal averaging is applied. With this technique, signal recording is time-locked to the application of the sensory stimulus. During intraoperative median nerve SER monitoring, after nerve stimulation at the wrist, only signal information occurring less than 50 msec after the stimulus is recorded. The SER occurs at a constant time after the stimulus application; other electric activity, such as spontaneous EEG, occurs at random intervals after the sensory stimulus. The averaging technique improves the SER signal-to-noise ratio by eliminating random elements and enhancing the SER. This enhancing effect increases directly with the square root of the number of responses added into the averaged response. SER recordings are of two general types determined by the distance of the recording electrode from the neural generator of the evoked response. SERs recorded from electrodes close to the neural generators (within approximately 3 to 4 cm in the average adult) are termed “near-field potentials.” [44] Near-field potentials are recorded from electrodes placed very close to the actual signal generator site, [45] and the morphology is directly affected by electrode location. [44] Far-field potentials are recorded from electrodes located a greater distance from the neural generator and are conducted to the recording electrode through a volume conductor (brain, cerebrospinal fluid, and membranes). As a result, it is more difficult to locate the source of the recorded signal (the current spreads diffusely throughout the conducting medium), and the electrode position has little effect on the morphology of the recorded evoked potential. [44] [45] As the distance between the recording electrode and the neural generator increases, the recorded SER becomes smaller. More responses have to be averaged to record far-field potentials (several thousand) than nearfield potentials (50 to 100). [44] [45] SERs also may be described as cortical or subcortical in origin. Cortical SERs are generated by the arrival at the cortex of the volley of action potentials generated by stimulating the sensory system. Because they are recorded as a near-field potential, they are typically easy to identify by elapsed time, waveform morphology, and amplitude. Subcortical responses may arise from many different structures depending on the type of response, including peripheral nerves, spinal cord, brainstem, thalamus, cranial nerves, and others. Cortical SERs are usually recorded from scalp electrodes placed according to the standard 10-20 system for EEG recordings (see Fig. 46-3 ). Subcortical evoked responses also may be recorded as far-field potentials from scalp electrodes or, as appropriate, from electrodes placed over the spinal column or peripheral nerve. Evoked potentials of all types (sensory or motor) are described in terms of latency and amplitude ( Fig. 467 ). Latency is defined as the time measured from the application of the stimulus to the onset or peak (depending on convention used) of the response. The amplitude is simply the voltage of the recorded response. According to convention, deflections below the baseline are labeled “positive (P),” and deflections above the baseline are labeled “negative (N).” Because amplitude and latency change with recording circumstances, normal values must be established for each neurologic monitoring laboratory, and may differ


from values recorded in other laboratories.

Figure 46-7 Sensory evoked responses are described in terms of latency and amplitude. Interpeak latency is the measured time between two peaks. Interpeak latency may be measured between two peaks in the same channel or between peaks in different channels (shown in figure). Note that the polarity of peaks is displayed contrary to standard convention (see text).

SERs used for intraoperative monitoring include SSEPs, BAEPs, and rarely VEPs. For all these techniques, cortical recording electrodes are placed on the scalp, using the same standard 10-20 system as for recording the EEG, whereas recordings for subcortical and peripheral signals are placed in various standardized anatomic locations. The surgical incision and the need for sterility may necessitate nonstandard electrode placements. Such deviations must be considered when interpreting baseline and subsequent SERs. In the case of MEPs, stimulating electrodes also are placed according to the 10-20 system of electrode placement, but over motor cortex instead. Recording electrodes may be placed over the spinal column, peripheral nerve, and (most commonly) innervated muscle. Intraoperative changes in evoked responses, such as decreased amplitude, increased latency, or complete loss of the waveform, may result from surgical trespass, such as retractor placement or ischemia, or they may reflect systemic changes, such as changes in anesthetic drug administration, temperature changes, or hypoperfusion. When these changes are detected and considered to be significant, the surgeon or anesthesiologist can make changes to relieve or lessen the insult to the monitored pathway (and presumably surrounding neural structures). Interventions by the anesthesiologist are directed at improving perfusion to the nervous tissue at risk and include increasing arterial blood pressure, especially if induced hypotension is used, or if the patient's pressure has decreased to below the preoperative level; transfusion, if significant anemia is present; volume expansion; augmentation of cardiac output; and normalization of arterial blood gas tensions if indicated. Changes in evoked potentials after retractor placement during a craniotomy or after compression of the blood supply to the spinal cord from spinal column distraction promptly allow the surgeon and the anesthesiologist to make appropriate changes to the operative procedure and anesthetic management that may prevent or minimize any postoperative neurologic deficit ( Fig. 46-8 ).

Figure 46-8 Somatosensory evoked potentials during an aneurysm clipping. Responses generated by the cortex at risk are indicated by arrows. Baseline, after retractor placement, after retractor removal, and recovery traces are shown. The initial evoked response change occurred 4 minutes after retractor placement. Note loss of voltage of cortical evoked response caused by inadvertent compression of the middle cerebral artery.

Tolerance limits for degree of change in evoked response signals or duration of complete loss of waveform before permanent neurologic dysfunction occurs are not clearly defined, and this problem is especially true for transcranial MEPs. Such ambiguity is common among intraoperative monitors. Although we do know that increased frequency and duration of ST segment depression during coronary bypass surgery is associated with an increased risk of perioperative infarction, exact limits for degree and duration of ST segment depression for surgery do not exist, and likely vary significantly from patient to patient. The same problem may be exhibited with neurologic monitors. Many centers using intraoperative SER monitoring define decreases in amplitude of 50% or more from baseline associated with a less than 10% prolongation in latency as clinically significant SER changes. Uncorrected, such changes are associated in clinical series and in case reports with onset of new postoperative neurologic deficits. As a result, such changes are immediately investigated. In practice, any


SER changes directly associated with a surgical event are considered clinically significant, however, even if the magnitude of change is less than just described. Changes in SER that do not progress to complete loss of the waveform are less likely to be associated with a major new postoperative neurologic deficit. Complete loss of the SER waveform intraoperatively without recovery is highly likely to be associated with a major new deficit. If the SER recovers either spontaneously or after intraoperative interventions, the likelihood of neurologic injury depends on the procedure, the duration of the SER loss, and on whether the SER is mainly used to judge integrity of adjacent unmonitored structures. In one study of aortic vascular surgery in which SSEPs were monitored, loss of the SSEP waveform for less than 15 minutes was not associated with a new permanent neurologic deficit, whereas complete loss of the SSEP for longer periods was increasingly likely to reflect permanent neurologic injury, even if the response recovered completely to its intraoperative baseline during surgery. [46] One of the most important principles of recording SERs intraoperatively is that reproducible, reliable tracings must be obtained at baseline before any intervention likely to cause changes in the evoked response. If good quality tracings with identifiable waveforms cannot be recorded and reproduced at baseline, evoked response monitoring would be of little use in monitoring the integrity of the CNS intraoperatively. If significant variability exists, or waveforms are difficult to identify, it would be impossible intraoperatively to distinguish SER changes that are clinically significant from a preexisting baseline variability of waveforms. When good, reproducible responses cannot be recorded at baseline, monitoring should not be used for clinical decision making. Somatosensory Evoked Potentials.

SSEPs are recorded after electric stimulation of a peripheral mixed nerve. Stimulation is provided most commonly with surface electrodes (e.g., electrocardiogram electrodes) placed on the skin above the nerve or with fine needle electrodes. A square wave stimulus of 50 to 250 Âľsec duration is delivered to the peripheral nerve, and the intensity is adjusted to produce a minimal muscle contraction. Increasing the stimulus intensity beyond the sum of the motor and sensory threshold does not influence the amplitude or latency of the recorded evoked potential. On a practical basis, however, many laboratories do not establish SSEP monitoring until after the patient is already anesthetized and paralyzed. In these cases, stimulus intensity is increased until no further increase in response size occurs at any recording site, typically constant current stimulation of 20 to 50 mA. For comparison, consider supramaximal stimulation used for the neuromuscular blockade monitor, commonly 80 mA. The rate of stimulation varies from 1 to 6 Hz. The common sites of stimulation include the median nerve at the wrist, the common peroneal nerve at the knee, and the posterior tibial nerve at the ankle. [47] SSEP responses consist of short-latency and long-latency waveforms. Cortical short-latency SSEPs are most commonly recorded intraoperatively because they are less influenced by changes in anesthetic drug levels. The pathways involved in the generation of upper extremity short-latency SSEPs include large-fiber sensory nerves with their cell bodies in the dorsal root ganglia and central processes traveling rostrally in the ipsilateral posterior column of the spinal cord synapsing in the dorsal column nuclei at the cervicomedullary junction (first-order fibers), second-order fibers crossing and traveling to the contralateral thalamus via the medial lemniscus, and third-order fibers from the thalamus to the frontoparietal sensorimotor cortex. These primary cortical evoked responses, which are recordable with most anesthetic techniques, result from the earliest electric activity generated by the cortical neurons and are thought to arise from the postcentral sulcus parietal neurons. The longer latency secondary cortical waves are thought to arise in the association cortex. These responses have much greater variability in an awake patient, [45] habituate rapidly on repetitive stimulation, [44] and are only poorly reproducible during general anesthesia. Cortical SSEPs other than the primary cortical response are not monitored or interpreted intraoperatively because they are severely altered by general anesthesia. [44] Although most evidence indicates that upper extremity evoked potentials are conducted rostrally in the spinal cord via dorsal column pathways, much data suggest that lower extremity SSEPs are conducted


substantially by the lateral funiculus. [48] Stimulation of the posterior tibial nerve or common peroneal nerve at or above motor threshold activates group I fibers that synapse and travel rostrally through the dorsal spinocerebellar tract. After synapsing in nucleus Z at the spinomedullary junction, the pathway crosses and projects onto the ventral posterolateral thalamic nucleus. [49] Studies with dogs, cats, and monkeys support the concept that lower extremity SERs are conducted in all quadrants of the spinal cord, but primarily in the dorsal lateral funiculus. [50] [51] This pathway difference is important because the dorsal lateral funiculus is supplied primarily by the anterior spinal artery, the artery that also supplies the descending motor pathway and neurons in the spinal cord. Manipulations, such as distraction of the spinal column to correct scoliosis, which may secondarily compress or distort radicular blood supply to the anterior spinal cord, should cause changes in the SSEP in the event blood supply is reduced to critical levels. This hypothesis is verified by the very low, but not zero, incidence of postoperative paraplegia on awakening without any intraoperative changes in SSEPs. For SSEP recordings with median nerve stimulation, recording electrodes (usually electrocardiogram pads) are first placed at Erb's point, just above the midpoint of the clavicle. This point overlies the brachial plexus, and signals recorded here assure the clinician that the stimulus is actually being delivered properly to the patient. The next electrode (either an electrocardiogram pad or a gold cup electrode) is placed midline posteriorly over the neck at level of the second cervical vertebra, relatively near the dorsal column nuclei. Signals recorded here ensure proper transmission of the response from the peripheral nervous system into the spinal cord and rostral along the spinal cord to the lower medulla. The final electrodes (gold cup electrodes or needle electrodes) are placed on the scalp overlying the sensory (parietal) cortex contralateral to the stimulated limb. Signals recorded here ensure the integrity of the pathway through the brainstem, thalamus, and internal capsule, and may assess adequacy of CBF in this area of the cortex. [52] [53] [54] [55] [56]

To record SSEPs after posterior tibial nerve stimulation, electrodes (electrocardiogram pads) are placed first over the popliteal fossa to ensure proper stimulus delivery to the nervous system. Electrodes also may be placed over the lower lumbar spine to ensure proper transmission of the signal into the spinal cord itself, but this site is not commonly used because of the proximity of sterile surgical incisions. Cervical spine and scalp recording electrodes are placed in a similar fashion as described previously, although different locations may be used as required by the placement of the surgical incision. More invasive recording methods, such as epidural electrodes, also may be used intraoperatively. Purported generators for short-latency SSEPs are listed in Table 46-1 and shown in Figure 46-9 . [44] [47] Induction of anesthesia and use of different recording electrode locations (montage), necessitated by the surgical incision, may significantly alter the appearance of the SSEP. In these cases, attribution of a particular generator to a given wave on the tracing may be quite difficult. During neurologic monitoring, such precision is not needed, and recorded waveforms are compared with tracings obtained at baseline and during earlier portions of the surgical procedure. After lower limb stimulation, absolute latencies are increased because of the greater distance the response to stimulation must travel along the peripheral sensory nerve and spinal cord. Interpeak latencies (see Fig. 46-7 ) also are evaluated to assess specific conduction times, such as N9 to N14 conduction time, reflecting transmission time from the brachial plexus to brainstem, or N14 to N19 conduction time, reflecting transmission time between the dorsal column nuclei and the primary sensory cortex. [57] Table 46-1 -- Generators of Somatosensory Evoked Potentials after Median Nerve Stimulation Peak Generators N9 (EP) Brachial plexus * N11

Posterior columns or spinal roots

N13/P13 Dorsal column nuclei * N14, 15 Brainstem or thalamus N19/P22 Parietal sensory cortex *


* Indicates sites commonly recorded during surgery. All other waveforms indicated are not commonly monitored.

Figure 46-9 Short-latency somatosensory evoked potentials produced by stimulation of the median nerve at the wrist. The ability to identify each of the labeled peaks shown in the tracing from the awake patient is compromised by the anesthetic state and use of different recording electrode locations (A to C). Corresponding tracings are labeled with the same letter. (From Chiappa KH, Ropper AH: Evoked potentials in clinical medicine. N Engl J Med 306:1205, 1982.)

Brainstem Auditory Evoked Potentials.

BAEPs are produced in the diagnostic laboratory by delivering repetitive clicks or tones via headphones. Headphones are not practical for surgical monitoring of neurosurgical procedures, and click stimuli are delivered using foam ear inserts attached to stimulus transducers ( Fig. 46-10 ). Stimulus intensity is usually set at 60 to 70 dB above the patient's click-hearing threshold, although, practically speaking, many intraoperative laboratories establish monitoring after induction of anesthesia and instead begin with a stimulus intensity of 90 dB nHL (normal hearing level). The duration of the click is approximately 100 µsec, and the stimulus is given usually 10 to 15 times per second. Clicks are delivered using different “polarities”—that is, the click may cause initial movement of the tympanic membrane away from the transducer (rarefaction) or toward the transducer (condensation). Use of these two different methods commonly produces very different waveforms, amplitudes, and latencies in individual patients, and the method that produces the largest reproducible response is chosen. If stimulus artifact is a serious problem, clicks of alternating polarity may be used to decrease the artifact, but the waveforms produced are an average of those produced by either stimulating technique alone and may be more difficult to monitor.

Figure 46-10 Schematic of brainstem auditory evoked potential stimulating apparatus. Loud click stimuli are delivered directly to the eardrum through the ear insert.

Rate and intensity of stimulus delivery affect BAEPs. [44] [58] Unilateral stimulation is used because responses from the other ear, which may remain normal during surgery, may obscure any abnormal responses from the monitored ear. Recording electrodes (usually gold cup electrodes) are placed on the lobe of the stimulated ear and on the top of the head (vertex). [58] White noise commonly may be delivered to the contralateral ear to prevent bone conduction from stimulation of the monitored ear from producing an evoked response from the contralateral ear. On average, 500 to 2000 repetitions are required because BAEPs recorded from the scalp are far-field potentials and extremely small (often <0.3 µV). [44] [58] Peaks in recordings of BAEPs are labeled I through VII; the purported neural generators for these peaks and the auditory pathway are shown in Figure 46-11 . The anatomic auditory pathway would predict that BAEP monitoring would be most useful for surgical procedures in the posterior fossa that risk hearing or structures in the upper medulla, pons, and midbrain. As with other SERs, amplitude, absolute latencies, and interpeak latencies are evaluated to assess integrity of the auditory system, localize the functional defect when it occurs, and assess peripheral and central conduction times. Because waves VI and VII are inconsistent and variable, they are not routinely monitored, [58] and most articles reporting use of BAEP for surgical monitoring in the operating room monitor waves only up to wave V. [59] [60] [61]

Figure 46-11 Schematic of auditory neural pathway. The brainstem auditory evoked potential is initiated by stimulation of the cochlea with a broadband click stimulus given via an ear insert in the external auditory


canal. Neural generators of the brainstem auditory evoked potential peaks are shown.

Visual Evoked Potentials.

VEPs are recorded after monocular stimulation with recording electrodes over the occipital, parietal, and central scalp. [60] Flash stimulation of the retina using light-emitting diodes embedded in soft plastic goggles through closed eyelids or as needed via contact lenses with built-in light-emitting diodes is provided. VEPs are cortical SERs, which vary with the type of stimulus, part of the retina stimulated, degree of pupil dilation, and patient's attention level. [44] Because some of these factors change commonly and even constantly during the course of every anesthetic, VEPs would be expected to be highly variable during surgery even when no surgical trespass on the visual system occurs. VEPs are the least commonly used evoked response monitoring technique intraoperatively. Motor Evoked Potentials.

MEPs are generated most commonly by the application of a transcranial train of electric stimuli, and responses are recorded at various points along the spinal column, peripheral nerve, and innervated muscle. TRANSCRANIAL MOTOR EVOKED POTENTIALS.

Monitoring of the integrity of the motor tracts within the spinal cord is a technique with great potential benefit, and even during the relative short history of MEP monitoring, there are reported cases of loss of MEPs with preservation of the SSEP. [62] [63] [64] [65] [66] [67] This technique has potential applications in spinal surgery, in which transmission across the operative field can be assessed, and in aortic surgery, with the potential for impairment of the blood supply to the vulnerable anterior spinal cord. Relative to SER monitoring, MEP monitoring is quite invasive and, in the case of transcranial stimulation, uses much higher stimulus intensity (â&#x2030;Ľ400 V). Several variants of MEP monitoring exist. The first method involves transcranial stimulation, either electric or magnetic. During transcranial electric MEP monitoring, stimulating electrodes (usually small, metallic screw-type electrodes similar to those used in fetal monitoring) are placed into the scalp overlying the motor cortex, and a train of electric stimuli (usually around 400 to 500 V) is applied to the scalp. This stimulation definitely activates muscles of mastication, and bite-blocks must be placed to prevent serious damage to the tongue during stimulation. During magnetic stimulation, a powerful magnetic stimulator is placed on the scalp over the motor cortex. Magnetic stimulation is more difficult for two reasons. First, the magnetic stimulator must be fixed to the head to prevent movement because even a slight movement of the stimulator can substantially alter the stimulus applied to the motor cortex. Second, the stimulator is quite large and cannot practically be used intraoperatively if a craniotomy is performed. Brief repetitive applications of electric current or a strong magnetic field induce current in the motor cortex and produce an MEP. These transcranial stimulating methods also may activate surrounding cortical structures and subcortical white matter pathways (sensory and motor). Distal antidromic propagation of the transcranially applied stimulus is blocked by synapses in all of the ascending sensory pathways. The stimulus is propagated easily orthodromically via descending motor pathways. The evoked responses may be recorded over the spinal cord, the peripheral nerve, and, most commonly, the muscle itself. To enhance the MEP, these responses may be averaged in the same manner as SERs, but averaging is almost always unnecessary. SPINAL MOTOR EVOKED POTENTIALS.

Another method of producing the MEP involves electric stimulation of the spinal cord itself above the area of


the cord at risk during surgery. Responses may be recorded over the distal spinal cord, peripheral nerve, and muscle. [68] [69] [70] Responses are recorded distally, usually over the peripheral nerve, and profound surgical muscle relaxation is used to prevent gross movement during surgery. This type of MEP is called a “neurogenic” MEP. Initially, investigators believed that this response, recorded over a peripheral nerve in the lower extremity (typically the tibial nerve in the popliteal fossa), was generated by stimulation of the descending motor tracts, activation of the anterior horn cells, and propagation of the nerve action potential via the peripheral nerve. Multiple clinical trials were conducted using this technique and comparing results of MEP monitoring with the SSEP with good results. [68] [69] [70] These responses also have the advantage that they do not show the same sensitivity to anesthetics that SSEPs do and may be recorded with any anesthetic technique. Subsequent studies in animals and humans [71] have shown that neurogenic MEPs are, at best, mixed responses with a significant component of an antidromically conducted response along the sensory pathway. Stimulation of the dorsal column results in an antidromically conducted recordable signal peripherally because the somesthetic system does not synapse in the dorsal root ganglion, and fibers pass directly from the dorsal column through the cell body in the ganglion into the peripheral nerve. Because of this problem, use of neurogenic MEP monitoring has decreased significantly, replaced by the more invasive transcranial stimulation techniques, which produce responses that are exclusively produced by activation of the motor system. Electromyography.

Intraoperative monitoring of EMG responses generated by cranial and peripheral motor nerves allows early detection of surgically induced nerve damage and assessment of level of nerve function intraoperatively. In these cases, the ability of a nerve to produce a response in the innervated muscle is used to assess the health of a cranial or peripheral nerve at risk during surgery. Recordings are made from either surface (electrocardiogram or gold cup) electrodes or needle electrodes placed directly in the innervated muscle of interest. The most experience with this monitoring modality has been obtained during facial nerve monitoring. EMG monitoring may be either active or passive. During active monitoring, a cranial or peripheral nerve is stimulated electrically, and the evoked EMG (compound muscle action potential) response from the muscle is recorded. Stimulation of the nerve proximal to the operative area or tumor can be used to assess functional integrity of the nerve. [72] Nerve function also may be assessed by noting the intensity of nerve stimulus needed to evoke a muscle response and by the morphology of the compound muscle action potential. Nerve function may be monitored passively during surgery with continuous recording of all generated responses from innervated muscle groups. “Popcorn” EMG discharges are produced by simple, benign contact with the monitored nerve. Response trains are produced with more significant nerve irritation. Neurotonic discharges are produced by significant nerve irritation or damage or both ( Fig. 46-12 ). [72] These EMG responses, when they reach a certain voltage threshold, are usually converted into audible signals that provide immediate feedback to the surgeon and warn of impending nerve damage in real time. Real-time feedback is key because density and frequency of neurotonic discharges may correlate with degree of postoperative nerve dysfunction, as shown by data obtained from patients undergoing resection of acoustic tumors. [73]

Figure 46-12 Schematic of facial nerve monitoring and typical responses seen during surgery.

Intraoperative monitoring of the motor component of other cranial nerves also has been successfully performed. EMG monitoring of the trigeminal nerve can be accomplished with electrodes placed over or in the temporalis or masseter muscles. Trigeminal nerve motor monitoring has been used during nerve section


for tic douloureux to ensure preservation of the motor branch of the trigeminal nerve and in combination with facial nerve monitoring during resection of large posterior fossa lesions. [72] Using recording electrodes placed in or over the trapezius or sternocleidomastoid muscles, the spinal accessory nerve has been successfully monitored during resection of large meningiomas, glomus jugulare tumors, and neck carcinomas. [72] EMG monitoring of the hypoglossal nerve with needle electrodes placed in the tongue has been infrequently used for large posterior fossa lesions and clivus tumors. [72] Although EMG monitoring of the eye muscles can be performed using tiny hook wires for recording, it is rarely used. Monitoring of peripheral motor nerves has been performed by placing needle electrodes in or over the muscles innervated by nerves that traverse the operative area and are at risk from the planned surgical procedure. Auditory feedback from EMG monitoring can warn the surgeon of unexpected surgical trespass of the nerve, help locate a nerve within the field (e.g., during untethering of the spinal cord), and localize the level of any conduction block or delay. Because radiculopathies have been reported to occur after spine surgery, EMG monitoring of peripheral nerves has been used in patients undergoing spine surgery to decrease the risk of nerve root injury during the procedure. [72] Clinical Applications of Neurologic Monitoring Neurovascular Surgery (also see Chapter 63 ) Extracranial Neurovascular Surgery: Carotid Vascular Surgery (Monitors: EEG, SSEPs, TCD, Cerebral Oximetry) Electroencephalogram.

The use of the EEG as a monitor of the adequacy of CBF during carotid endarterectomy has been established for many years. In a large series of patients undergoing carotid endarterectomy at the Mayo Clinic, [36] the EEG was compared with regional CBF using the 133 Xe washout method. This study validated the EEG as an indicator of the adequacy of regional CBF. Normal CBF in gray and white matter averages 50 mL/100 g/min. With most anesthetic techniques, the EEG begins to become abnormal when CBF decreases to 20 mL/100 g/min. The threshold for EEG changes apparently is much lower (8 to 10 mL/100 g/min), however, when isoflurane is used. [74] Cellular survival is not threatened until CBF decreases to 12 mL/100 g/min (lower with isoflurane). The difference in blood flow between when the EEG becomes abnormal and the blood flow at which cellular damage begins to occur provides a rational basis for monitoring the EEG during carotid surgery. In many cases, prompt detection of EEG changes may allow intervention (e.g., shunting, increasing cerebral perfusion pressure) to restore CBF before onset of permanent neurologic damage. Standard hemodynamic monitoring provides no direct information about the adequacy of CBF. Blood pressure is not a specific indicator of the adequacy of CBF. Significant hypotension is not predictably associated with EEG evidence of cerebral ischemia. Severe anemia and decreases in oxygen saturation also decrease oxygen delivery. EEG activity becomes abnormal when increased blood flow cannot compensate for decreased arterial oxygen content. Serious intraoperative reduction in cerebral oxygen supply may result from surgical factors (e.g., carotid cross-clamping) that are usually beyond the anesthesiologist's control, and from factors that the anesthesiologist can correct. Reduction in CBF produced by hyperventilation, hypotension, or temporary occlusion of major blood vessels may be corrected by reducing ventilation, by restoring normal blood pressure, or, in the case of temporary vessel occlusion, by increasing blood pressure above normal. Because the EEG may readily detect cerebral ischemia, continuous EEG monitoring may be used to evaluate the effectiveness of therapy instituted to correct ischemia. If monitoring of the EEG could be proved scientifically to reduce the incidence of stroke during carotid vascular surgery, EEG monitoring would be established as a standard of care. Definitive data showing stroke reduction do not yet exist, however, and given the number of patients required to power a trial that would


show a reduction in stroke rate from 2% to 1%, such studies are unlikely to be funded or forthcoming. What data are available do not provide a basis to recommend universal use of EEG monitoring during carotid surgery. In a large series of patients undergoing carotid endarterectomy with selective shunting who were monitored with 16-channel unprocessed EEG, no patient awakened with a new neurologic deficit that was not predicted by EEG. [75] Transient, correctable EEG changes were not associated with stroke. Persistent changes were associated with stroke. This study had no comparison group, however, analyzing stroke rate when EEG monitoring was not used during surgery. In the North American Symptomatic Carotid Endarterectomy Trial and the European Carotid Surgery Trial, retrospective comparison of patients receiving EEG monitoring and patients not receiving EEG monitoring failed to show a significant difference in outcome. [76] [77] Because the EEG detects reductions in CBF that would not otherwise be apparent in unmonitored patients, and permits intervention that may correct the problem (usually placing a shunt or increasing blood pressure), EEG monitoring should logically be useful in reducing the incidence of stroke when selective shunting is used. Data available from studies at this time bring us no closer to resolving this question, however, than we were 30 years ago. Advocates of monitoring and individuals who believe monitoring is of no value can cite multiple studies supporting each viewpoint. Even more difficult to prove is that EEG monitoring is useful when all patients are shunted during carotid clamping. Such monitoring has detected correctable shunt malfunction, and investigators have described hypotension-related EEG changes in patients with critical stenoses and poor collateral circulation. [78] Advocates of selective shunting based on EEG (or other monitoring) criteria claim that inserting a shunt unnecessarily through a region of diseased vessel would surely increase embolization. A multicenter study of 1495 carotid endarterectomies provides some evidence that shunting of patients without evidence of decreased cerebral perfusion increases the incidence of stroke more than sixfold. [79] Although this study and other more recent studies [80] [81] [82] advocate that selective shunting using some form of monitoring of the adequacy of CBF should improve perioperative stroke rate, an analysis by the Cochrane Stroke Group [83] failed to show sufficient evidence to advocate for routine shunting, selective shunting, or even no shunting at all. Until compelling studies addressing this issue are done, it is unlikely that EEG monitoring during carotid vascular surgery would become a standard method. Processed EEG also has been used during carotid vascular surgery. Two issues affect the efficacy and reliability of processed EEG as a monitor for cerebral ischemia. First, what is the minimum number of channels (or areas of the brain) to be monitored? The 16-channel unprocessed EEG is a reliable and sensitive monitor for intraoperative cerebral ischemia during carotid endarterectomy. In a series of more than 2000 patients monitored with 16-channel EEG at the Mayo Clinic, there were no false-negative EEGs [75] ; in other words, no patient had undetected intraoperative cerebral injury. In operating rooms where carotid surgery is performed, however, 16-channel EEG monitored by a dedicated technician is unavailable. Processed EEG using less than 16 channels is used much more commonly. Clinical experience and clinical investigations suggest that four channels (two per side) are the minimum number of channels for adequate sensitivity and specificity. [37] When a limited number of channels were compared with 16channel EEG monitoring, 100% sensitivity and specificity were obtained using 2 channels per hemisphere, provided that those channels monitored the middle cerebral artery territory. These results were obtained with a frontoparietal channel combined with a frontotemporal channel. [37] The second issue is the experience level of the observer monitoring the processed EEG. Is a dedicated, experienced technician or electroencephalographer needed? In a study addressing this question, the 16channel unprocessed EEG monitored by a dedicated technician was compared with a processed EEG reviewed by three anesthesiologists of differing levels of experience with processed EEG. [38] The three anesthesiologists interpreted the tracings without knowledge of the case. They were presented only with the written trace with an indication of the point at which the carotid artery was clamped. In these cases, the most important interpretation pitfall to avoid is the â&#x20AC;&#x153;false-negativeâ&#x20AC;? pattern. If the clinician interprets the EEG as showing adequate CBF when in fact it does not, the surgeon may fail to shunt an ischemic patient. A false-positive result may be less of a problem because that patient is not ischemic but is given a


shunt anyway. In this case, only the risk of emboli from the “unnecessary” shunt is incurred. The positive predictive value of the anesthesiologist correctly interpreting the trace as unchanged after clamping was 91% to 98%, which indicates that the device can be used by novice interpreters with fair accuracy to determine the presence of cerebral ischemia at the time of carotid occlusion. In this study, the review by the anesthesiologist was not done during the course of the procedure, but rather “off line,” and does not address the issue of whether an anesthesiologist providing the intraoperative anesthetic management of the patient can provide adequate monitoring of the processed EEG simultaneously. EEG monitoring has limitations. Despite the data available from the Mayo Clinic, immediately evident postoperative strokes have been reported in patients without any evidence of EEG changes intraoperatively. In our experience, such strokes result from emboli via the lenticulostriate arteries to subcortical structures that do not generate or affect the EEG, but are critically involved in the descending motor pathway. Overall, such events are rare. Should the patient undergoing carotid endarterectomy have EEG monitoring? That question cannot be answered based on any available data. EEG monitoring provides information about CBF that would not otherwise be available. The clinician has an opportunity to intervene to increase inadequate blood flow when it occurs. Anecdotally, many clinicians have found such monitoring useful and use it routinely. Population studies do not support routine use, and it is up to the clinician to decide whether to use it. Somatosensory Evoked Potentials.

SSEP monitoring also has been used to gauge adequacy of CBF to the cerebral cortex and subcortical pathways during carotid vascular surgery. [56] [84] [85] SSEPs have been found in the laboratory to have a similar but slightly lower threshold for failure compared with the EEG. SSEPs are generally intact until the cortical blood flow decreases to less than 15 mL/100 g/min. [54] In a few comparison studies with the EEG, a similar sensitivity and specificity for postoperative neurologic function was found. These studies involved few patients, however, and are inadequate to support the hypothesis that SSEP monitoring may substitute for EEG monitoring of the adequacy of CBF. [84] [85] [86] Logic also would suggest that changes in SSEP are unlikely, for example, with ischemia involving the anterior portions of either the frontal or temporal lobe, which could readily be detected by an appropriately placed EEG electrode. Finally, a more recent metaanalysis does not support the use of SSEPs during carotid vascular surgery as a sole monitor of neurologic function. [87] There is even less outcome evidence to support the use of SSEPs during carotid surgery than there is for the EEG, but the authors and others have found SSEPs to be useful as a simultaneous monitor with EEG to detect subcortical ischemia. Transcranial Doppler.

TCD monitoring during carotid vascular surgery is based on measurement of two primary parameters—blood flow velocity in major conducting arteries leading to the cerebral cortex (most commonly middle cerebral artery) and the number of emboli detected in the same artery. The hypothesis justifying the use of this monitoring during carotid vascular surgery has two components: blood flow velocity correlates with CBF, and increasing numbers of emboli increase the likelihood of emboli related cerebral ischemia or stroke. The first component has not been well tested and shows variable results. An early study in a small group of patients undergoing carotid surgery did not show good correlation between CBF and blood flow velocity. [88] Subsequent studies in patients with varying intracranial pathology have yielded mixed results. [89] [90] [91] [92]

The correlation between CBF and TCD-measured blood flow velocity remains good over time only when the artery being insonated does not change diameter, and when cortical blood flow in the distribution of the measured artery does not have significant collateral sources of blood flow. The relationship between emboli count and stroke is better established with multiple studies conducted in the preoperative, intraoperative, and postoperative periods indicating that higher emboli counts are associated with higher stroke risk and


warrant intervention. [93] [94] [95] [96] [97] [98] [99] Intraoperative use of TCD has not been widely adopted for many reasons. As previously noted, good TCD signals cannot be obtained in many individuals who could benefit from monitoring. Also, TCD probe motion during surgery causes major problems with loss of signal or with angle of insonance–induced changes in the relationship between blood flow velocity and blood flow. Nonetheless, multiple series of carotid endarterectomies with TCD monitoring have been reported with good success, quoting a critical blood flow velocity reduction around 50% as indicative of inadequate CBF requiring intervention (shunt or increased blood pressure or both). [93] [94] [95] [96] [97] [98] [99] There are no good outcome data supporting TCD use intraoperatively, but data regarding emboli count and risk of stroke suggest that if technical issues with probe attachment to the patient can be overcome, TCD may be useful as a predictor of impending stroke in the preoperative, postoperative, and perhaps intraoperative periods. Cerebral Oximetry (Near-Infrared Spectroscopy).

Near-infrared spectroscopy (NIRS) is an attractive monitor because of its ease of application and lack of training required for interpretation. The hypothesis governing its use is very simple: As oxygen delivery to the brain decreases, oxygen extraction from arterial blood increases, and the oxygen saturation in cerebral venous blood decreases. NIRS applied to cerebral monitoring measures the oxygen saturation in the cerebral venous blood in the prefrontal cortex and promptly detects increases in oxygen extraction resulting from decreased oxygen delivery. Multiple case reports and series document the use of cerebral oximetry during neurovascular surgery, but several major questions surrounding use of NIRS during carotid surgery remain unanswered. The first and most important question is what degree of decrease in oxygen saturation can be tolerated before intervention is necessary. Because most interventions involve some risk (e.g., shunt emboli, increased BP myocardial ischemia), the answer to this question is important. The answer does not yet exist, however, and may vary from patient to patient. Two more recent studies showed that in awake patients, the saturation value at which any patient would develop symptoms varied from patient to patient, [100] [101] and an absolute value that required shunting could not be determined. Another study showed that cerebral oxygen saturation decreased before the EEG developed changes, and the authors used this observation to claim superiority for NIRS monitoring of the brain during carotid surgery. [102] This finding should not be surprising, however, because function of the brain (in this case, electric function) does not fail until increased extraction of oxygen no longer meets metabolic demands for the tissue. If metabolic demands are being met by increased extraction, it is unclear that intervention is needed. Finally, a study by Friedell and colleagues [103] compared NIRS with EEG and SSEP monitoring during carotid surgery. In 24 of 323 patients, significant differences were observed between NIRS and monitors of electric function. Seventeen patients showed no changes in electric function with significant decreases in cerebral oxygen saturation. In seven patients, no change in cerebral oxygen saturation occurred despite significant change in the EEG and SSEP. These data in combination with the data from studies in awake patients suggest that use of NIRS alone during carotid vascular surgery may be inappropriate. Intracranial Neurovascular Surgery (Monitors: SSEPs) Somatosensory Evoked Potentials.

SSEPs have been extensively studied during cerebral aneurysm surgery. During these procedures, the surgical incision and brain retraction precludes placement of scalp or brain surface electrodes that could detect cerebral ischemia in at-risk cortex. Recording electrodes placed on the surface of the brain have been used successfully, but they are commonly considered “in the way” by neurosurgeons. Scalp electrodes may be placed easily for SSEP monitoring, although the recording montage is frequently not the same as that used in an awake patient.


For aneurysms involving the anterior cerebral circulation, SSEP monitoring has an excellent, but not perfect, record for predicting postoperative neurologic function. Most patients without surgically induced SSEP changes during surgery awaken with an unchanged neurologic examination. Patients with significant SSEP changes that do not revert to normal awaken with a new neurologic deficit. Patients with SSEP changes that return to normal after a significant intraoperative change may show at least a transient postoperative deficit, with the severity and duration increasing as the duration of the SSEP change increases. Many authors have reported significant utility of SSEP monitoring in detecting improper aneurysm clip placement (see Fig. 46-8 ) and in guiding intraoperative blood pressure management, particularly in patients already showing or at significant risk for vasospasm after subarachnoid hemorrhage. [55] [104] [105] [106] [107] [108] [109] The same success cannot be reported, however, for posterior circulation aneurysms. In these cases, many areas of the cortex and subcortical structures are at risk for damage that cannot be monitored at all by somatosensory pathway function. A significant false-negative monitoring pattern exists for these patients, but changes can still be detected when a surgical insult is sufficiently severe to involve large portions of the brain. [110] [111] [112] [113] Supratentorial Intracranial Nonvascular Surgery (Monitors: Awake Patient, EEG, SSEPs)

During supratentorial procedures, neurologic monitoring can contribute to the precise localization of structures that need to be preserved or conversely supplement the anatomic information provided by imaging with functional data. Three techniques fall under this category: (1) Awake craniotomy can be a suitable approach for the resection of tumors and seizure foci. (2) Intraoperative electrocorticography (i.e., the recording from strategically placed subdural electrodes) is used to target more closely the resection of seizure foci. (3) Localization of the central sulcus and by extension the precentral motor cortex is sometimes helpful, if these structures have been displaced by a tumor. The most comprehensive approach to the problem of functional localization of brain structures that need to be preserved to achieve a good outcome is to perform entire segments of a supratentorial craniotomy in an awake patient, who is undergoing repeated neurologic examinations targeted to assess the eloquent area at risk. Such procedures are typically divided into exposure, mapping, and resection phases, and can be done with the patient entirely awake or awake only during periods when the neurologic examination needs to be assessed. [114] Common to all these approaches is the need for meticulous locoregional anesthesia of the scalp at the craniotomy site and the pin sites of the head holder. [115] A second requirement is a patient who is well informed about the awake parts of the procedure and willing and able to cooperate. Dexmedetomidine, propofol, and remifentanil are the agents most frequently incorporated into the anesthetic regimens for awake craniotomy. [116] Complications of awake craniotomy include nausea and vomiting, respiratory problems, and â&#x20AC;&#x153;tightâ&#x20AC;? brain, but are typically mild and occur in less than 10% of cases in experienced centers. Seizures triggered by cortical stimulation can be stopped by the application of iced saline to the exposed cortex or a small amount of barbiturate or propofol. Seizure Focus Localization Surgery

Patients with epilepsy who have seizures that generalize from an anatomically distinct focus may benefit greatly from the surgical resection of that seizure focus. [117] Precise localization of a seizure focus is important for achieving the therapeutic objective of seizure control and for minimizing complications from the resection. With sensitive magnetic resonance tomography techniques, neuronavigation, and recordings of typical seizure activity in the awake patient after placement of subdural and depth electrodes, the anatomic location and the appropriate extent of the resection frequently can be determined preoperatively. [118] These developments have diminished the role of intraoperative recordings from the epileptogenic zone using electrocorticography. [119] Neurologic monitoring during such a resection is performed using two different techniques. First, activity of the seizure focus can be recorded through electrocorticography. Second, eloquent brain areas next to the


seizure focus can be monitored during an awake craniotomy as described in the previous section. Electrocorticography is done by placing a grid of subdural electrodes onto the exposed brain surface and recording spontaneous electric activity. Electrocorticography is constrained by several limitations. The time for such recordings is limited to a few minutes; recordings are limited to interictal discharges, which may not correlate with the epileptogenic focus; and recordings need to be obtained from a brain that is under the effects of general anesthetic agents, which alter the EEG. To provide good conditions during the recording, the level of anesthesia is lightened (e.g., by use of a strict nitrous-narcotic technique or low concentrations of volatile agents). Provocative techniques, such as hyperventilation or administration of a small dose of methohexital, may be useful to activate the seizure focus. Intraoperative seizure mapping requires the involvement of an expert electroencephalographer familiar with this technique. Motor Strip Localization

Electrophysiologic monitoring of the somatosensory system in anesthetized patients can provide a simple anatomic guide to the location of the rolandic fissure, which separates the parietal primary sensory and frontal primary motor cortex. The fissure is located by recording cortical SSEPs from a subdural strip electrode that is placed perpendicular to the presumed location of the fissure. The exact location of the fissure is characterized by a reversal in the polarity of the primary cortical response between the electrodes straddling the fissure, as illustrated in the clinical example in Figure 46-13 .

Figure 46-13 Intraoperative localization of the rolandic fissure separating the primary sensory and motor cortex. The clinical example is from a patient with a large parietal tumor shown in the scan. Two of the recordings made from a four-contact subdural electrode strip are shown. The relative positions of the strip electrode are labeled B and A. In recording A, the primary cortical response from the electrodes anterior to the rolandic fissure shows an upward deflection, whereas the response from electrodes posterior to the fissure shows a downward deflection. Moving the strip electrode anterior (recording B) moves this â&#x20AC;&#x153;phase reversalâ&#x20AC;? between electrodes 3 and 4.

Posterior Fossa Surgery (Monitors: BAEPs, Cranial Nerve Monitoring, SSEPs, MEPs)

Beside the cerebellum, the posterior fossa contains within the narrow space of the brainstem many crucial neural structures, including ascending and descending sensorimotor pathways; cranial nerve nuclei; cardiorespiratory centers; the reticular activating system; and the neural networks that underlie crucial protective reflexes, such as eye blink, swallowing, gag, and cough. Posterior fossa surgery is not undertaken lightly, and even small injuries can leave significant neurologic deficits. Although some of these neural structures, such as the sensory or auditory pathway, can be monitored consistently, intraoperative integrity of other neural structures is frequently only inferred from the well-being of neighboring structures amenable to monitoring. Microvascular Decompression of Cranial Nerves V, VII, and IX

Microvascular decompression is done most frequently for trigeminal neuralgia (cranial nerve V) in patients who present acceptable medical risks for a posterior fossa craniotomy. More rarely, the same approach is used to treat hemifacial spasm or neurovascular compromise of lower cranial nerves. The surgery entails dissecting along the intracranial portion of the nerve, identifying offending blood vessels that encroach on the nerve, and placing an insulating Teflon pad between vessel and nerve. The surgery risks ischemic damage to perforating vessels coming off the offending arteries and cerebellar retractionâ&#x20AC;&#x201C;related damage to cranial nerves. The facial and vestibulocochlear nerves are at particular risk for stretch-induced injury caused by medial retraction of the cerebellum. Retraction-induced stretch produces a prolongation of the interpeak latency between peaks I and V of the BAEP waveform, ultimately leading to a complete loss of all


waves beyond wave I ( Fig. 46-14 ). Failure to release retraction in a timely manner results in postoperative hearing loss. Such monitoring increases the chances for preserved hearing after microvascular decompression. [120] [121] [122] [123] [124]

Figure 46-14 Intraoperative monitoring of brainstem auditory evoked responses during microvascular decompression. The baseline recording shows the typical five waves of the brainstem auditory evoked potential response. Intraoperative events are designated to the right of each trace. Placement of the retractor causes a severe increase in latency of wave V even after adjustment of retraction. During placement of the sponge, all waves subsequent to wave I, which originates in the inner ear, are nearly completely lost. Removal of the retractor causes brainstem auditory evoked potentials to revert toward baseline.

Vestibular Nerve Schwannoma

Vestibular nerve schwannomas are the most common tumors located in the cerebellopontine angle. Because of the common origin of the cochlear component of cranial nerve VIII and the essentially identical intracranial trajectory of the facial nerve, hearing loss and facial nerve palsy are concerns during surgical resection of these tumors. Size and preoperative auditory function are the best predictors of postoperative hearing. [125] For tumors up to about 2 to 3 cm in size, monitoring of BAEPs can increase the chances of preserving hearing. [126] In addition to BAEPs, the facial nerve is monitored through spontaneous and stimulated EMG. Prospective trials have shown a higher percentage of patients with a functional facial nerve 1 year after surgery if facial nerve monitoring was used as previously described. Tonic discharges warn of impending damage caused by stretch or heat (bovie). Sharp section of the nerve may elicit no discharge, and neuromuscular blockade may eliminate the ability to monitor. If the course of the nerve is displaced by the tumor, the surgeon can map its course with a hand-held stimulator and real-time auditory feedback. Other Posterior Fossa Neoplasms

Monitoring for operations on other neoplasms located in the brainstem typically is individualized to each particular case or to the particular surgical approach. EMG may be recorded not only from the territory of the facial nerve, but also from the tongue to monitor the hypoglossal nerve, and from the glottis through electrodes embedded into a specialized endotracheal tube to monitor the vagus nerve. Such a setup can be used to map the floor of the fourth ventricle functionally, if it is distorted by a tumor. [127] Such monitoring may be insufficient to preserve vital reflexes because only the efferent limb of these reflexes is monitored by recording EMG from innervated muscle. Use of neurologic monitoring for brainstem ischemia, although done in some centers, is not well documented or supported by clinical studies. Global well-being of the brainstem may be monitored by combining multiple modalities of evoked potentials, such as BAEPs, SSEPs, and MEPs. Each modality monitors a function whose integrity would be considered important in its own right for the functional outcome of an individual patient. As illustrated in Figure 46-15 , the cross-section monitored by combining all these modalities still leaves out crucial areas. Given that perfusion occurs through perforating vessels, it is easy to see that monitoring may indicate that all is well or, more likely, that a therapeutic intervention was helpful in restoring function, when clinically the patient is still left with a significant deficit. This occurrence invalidates neither monitoring nor the therapeutic intervention, but indicates only that the monitored pathway was not located in an area at risk from the surgical procedure. Because of such obligatory â&#x20AC;&#x153;false-negatives,â&#x20AC;? few studies address the utility of such monitoring. Because each individual monitoring modality comes with its own constraints, such an approach typically requires a dedicated neurophysiologist for interpretation and troubleshooting.

Figure 46-15 Monitoring of the brainstem with evoked potentials. Evoked potentials monitor specific tracts that encompass defined areas in the brainstem. This is shown in three transverse sections approximately at the levels indicated in the drawings. The areas directly monitored by a given modality are indicated in blue


and labeled M (motor), S (somatosensory), and A (auditory). Conclusions about the well-being of the remainder of the brainstem are made by inference from the monitored areas.

Spinal Column and Spinal Cord Surgery (Monitors: SSEPs, MEPs, EMG)

Intraoperative monitoring of SSEPs has been used most extensively in patients undergoing surgical procedures involving the spinal column or spinal cord, or both. Extensive experience has been gained in patients who have decompressive laminectomies or who have undergone corrective procedures for scoliosis. Intraoperative changes in SSEPs have been noted in 2.5% to 65% of patients undergoing surgical procedures on the spine or spinal cord. [128] [129] [130] [131] When these changes are promptly reversed either spontaneously or with interventions by the surgeon or anesthesiologist (e.g., lessening the degree of spine straightening in scoliosis surgery or increasing arterial blood pressure), the patients most often have preserved neurologic function postoperatively. When these changes persisted, however, the patients most often awakened with worsened neurologic function. False-negative (rare) and false-positive (common) results have been reported with SSEP monitoring during spine surgery. Patients with intact SSEPs throughout the procedure have awakened with a new significant neurologic deficit, but the total reported incidence of this finding is far less than 1% of all cases monitored. Patients with no postoperative neurologic deficit commonly experience significant changes in intraoperative SSEPs. [131] This monitoring pattern is most commonly caused by failure to control for other, nonpathologic factors that may alter the SSEP. Overall, the reliability of properly performed SSEP monitoring to predict the postoperative sensory and motor function has been reported to be excellent. [44] [130] [132] Motor tracts are not directly monitored by SSEPs, however. In addition, the blood supply to the dorsal columns of the spinal cord, which carries all of the upper extremity SSEPs and at least a portion of the lower extremity SSEPs, is derived primarily from the posterior spinal arteries. The blood supply to motor tracts and neurons is derived primarily from the anterior spinal artery. It is possible for a significant motor deficit to develop postoperatively in patients with intact SSEPs throughout the operative course. Such events have been reported. [133] [134] In operations on the spinal column and after acute spinal cord injury, the sensory and motor changes generally correlate well [44] ; however, in patients with neurologic dysfunction after thoracic aortic vascular surgery, frequently posterior spinal cord function (proprioception, vibration, light touch) is left intact when motor and other sensory functions (pain, temperature) are impaired. This result occurred in 32% of patients with neurologic injury after aortic aneurysm repair in one series, [135] with similar results in many other series. Intraoperative SSEP monitoring in these patients carries a significant risk for false-negative results, and as a result, such monitoring is not widely used. Multiple anecdotal reports and an increasing number of case series suggest that MEP monitoring during surgery on the spine or its blood supply is useful. Several series have reported significant changes in MEPs without changes in SSEPs. These series suggest that combined use of SSEP monitoring and MEP monitoring may eliminate false-negative monitoring patterns during spine surgery. [136] [137] [138] [139] [140] [141] In the case of monitoring paraplegia risk during thoracoabdominal aneurysm surgery, the literature shows mixed but improving support for the use of MEP monitoring. Two earlier studies suggested that MEPs may not be as effective as hoped. The first study recorded MEPs from the lumbar spinal cord in dogs produced by transcranial electric stimulation. [135] Elmore and associates [142] found that these spinally recorded potentials did not accurately predict postoperative motor function. In a second study, Reuter and colleagues [143] recorded MEPs at the spinal cord and the peripheral nerve level in dogs produced by transcranial electric stimulation. They also found that the spinally recorded responses were inaccurate in predicting motor function postoperatively. The peripheral nerve responses disappeared in all animals and were not present 24 hours later regardless of whether the animal could move its lower extremities.


These studies suggest that the spinally recorded MEP likely represents a response generated by the descending corticospinal tract. This white matter pathway is resistant to ischemia compared with the more metabolically active anterior horn cells (gray matter). Recovery of this white matterâ&#x20AC;&#x201C;generated MEP response could occur after reperfusion of the cord, whereas the gray matter might not recover. Responses recorded from the peripheral nerve would reflect postsynaptic anterior horn cell function, but lower extremity ischemia occurring after aortic cross-clamping may preclude recording this or the response from muscles during surgery. More recent clinical series have shown much greater success with MEP monitoring during aortic vascular surgery in correctly detecting inadequate spinal cord blood flow and in improving operative outcome. The technique has proven useful, particularly when operative strategies such as reimplantation of crucial intercostal vessels based on results of MEP monitoring, alteration of spinal cord perfusion pressure (blood pressure increase or cerebrospinal fluid drainage or both), spinal cord cooling, and other methods are used. [144] [145] [146] [147] [148] [149] [150] [151] [152] [153] Although this monitoring technique holds promise in aortic surgery, much more clinical work is needed before MEP monitoring during aortic surgery becomes widely accepted and used. Peripheral Nerve Surgery (Monitors: EMG, Nerve Action Potential)

Neurologic monitoring for surgeries involving peripheral nerves can be done in two different settings. In the first, the peripheral nerve is intact, but threatened by the surgery. Examples would be an intrinsic nerve tumor, such as a schwannoma or an extensive soft tissue tumor, particularly if it displaces the normal anatomic course of a nerve. Monitoring of spontaneous and stimulated muscle responses from muscle groups innervated by the nerve in question can be used to guide the resection. Spontaneous EMG discharges can be generated by stretch or compression of the nerve, by local heating from electrocautery, or from ischemia. Two caveats apply to the monitoring of spontaneous EMG. First, the neuromuscular junction is part of the monitored pathway, and muscle relaxation decreases/abolishes the sensitivity of monitoring in a dose-dependent manner. Second, sharp section of the nerve may not result in a noticeable discharge. To search out the course of the nerve intraoperatively, the surgeon may stimulate the wound area with a hand-held probe and listen for stimulated EMG or palpate for muscle contraction. The underlying concept should be familiar to anesthesiologists from the use of nerve stimulators in regional anesthesia. A variation of this technique of monitoring that is gaining popularity is monitoring of pedicle screw placement during spinal instrumentation with the aim of avoiding nerve root injuries owing to malpositioned pedicle screws. [154] [155] Typically, the shank of an implanted pedicle screw is stimulated repetitively with increasing current to determine the threshold for eliciting a dermatomal compound muscle potential. Because thresholds vary among cervical, thoracic, and lumbar spine, and between healthy and diseased nerve roots, this technique is currently not universally regarded as useful, but shows some promise. [156] A second setting where monitoring of peripheral nerves is used is in patients with prolonged weakness and sensory loss after nerve injury undergoing nerve exploration. [157] The aim is to determine whether nerve reconstruction may improve outcome. The area of the lesion is determined by preoperative nerve conduction studies. Intraoperatively, the nerve is first stimulated proximal to the lesion, and a recording of the nerve action potential is made directly from the nerve distal to the lesion, as illustrated in Figure 46-16 . If there is nerve conduction across the lesion, lysis of scar is performed, and the incision is closed. Natural recovery by means of axonal regrowth produces the best outcome. If conduction does not occur across the lesion, resection of the damaged nerve and nerve cable grafting is performed. [158] [159] [160]

Figure 46-16 Recording a nerve action potential during a brachial plexus exploration. The site of the injury on the lateral fascicle is indicated in red. As shown in the inset, the surgeon places hook electrodes on either side of the exposed part of the nerve. If the injury is limited to an axonotmesis, proximal stimulation will result in a distal nerve action potential similar to the ones shown in the recording to the right. The delay in


the response in the third tracing is simply due to a change in technical settings.

Non-neurologic Surgery That Risks Damage to the Central Nervous System (Monitors: EEG, TCD, Cerebral Oximetry, SjVO2 ) Cardiopulmonary Bypass Electroencephalogram.

In humans, changes that occur with the institution of cardiopulmonary bypass (CPB) may alter the EEG via multiple different mechanisms. Plasma and brain levels of anesthetic drugs may be altered by CPB or by anesthetic drugs commonly given at the institution of CPB, alterations in arterial carbon dioxide tension and blood pressure may occur, and hemodilution with hypothermic perfusate nearly always occurs. These effects, all of which may produce EEG changes similar to pathologic changes seen with ischemia, make it difficult to interpret EEG changes occurring around the time of institution of CPB. Levy and others [161] [162] have tried to distinguish the normal effects of hypothermia from other events occurring at the institution of and conclusion of CPB. Initially, Levy concluded that only a qualitative relationship could be determined, but later, with the use of a much more sophisticated EEG analysis technique (approximate entropy), EEG changes associated with changes in temperature could be quantified. Chabot and colleagues in Boston [163] and Edmonds and colleagues in Louisville [164] have attempted to use quantitative (processed, multiple-channel) EEG during CPB to detect cerebral hypoperfusion and relate these changes to postoperative neurologic function. In addition, some minimal work has been done with intervention after detection of cerebral hypoperfusion using quantitative EEG. Such monitoring techniques have not been widely adopted because although the data seem promising, only a few patients have been studied, and there are very few corroborating studies. In addition, this type of monitoring is extremely costly in time, personnel, and equipment costs, and given the lack of convincing outcome data, the cost-tobenefit ratio is unclear at best. Some other investigators failed to show any convincing relationship between intraoperative EEG parameters and postoperative neurologic function, especially in small infants and children. [165] [166] Much work remains to be done studying use of the processed, quantitative EEG to provide information for clinical management of patients during CPB. None of the currently available studies and recommendations would support an evidence-based justification for their routine application. Transcranial Doppler.

TCD also has been used to monitor the cerebral circulation during CPB. Anecdotal reports and case series document the use of TCD for determining adequacy of CBF, detection of emboli, and detection of improper cannula placement. [167] Only very limited outcome data exist, and use of TCD during CPB does not stand up to evidence-based examination, primarily because of lack of information. Probe placement instability and inability to obtain signals in some patients also have limited the use of this monitor intraoperatively. Cerebral Oximetry and Jugular Venous Oxygen Saturation.

As is the case with EEG monitoring during CPB, there are multiple case reports and several series that advocate the use of NIRS or Sj VO 2 as indicators of adequate perfusion of the brain during CPB. [168] [169] Incorrect placement of CPB cannulas has been detected clinically and in laboratory studies. One more recent series of patients undergoing CPB for coronary bypass surgery showed a higher incidence of major organ system dysfunction and longer hospital stays in patients with lower baseline and intraoperative cerebral oxygen saturation values. [170] The same questions exist for this application of NIRS, however, as do for the use of NIRS during carotid vascular surgery. Use of NIRS during CPB, although it provides information that would not otherwise be available, does not stand up to evidence-based examination, and


much more work is needed before NIRS can be recommended as a standard of care during CPB. Sj VO 2 is very invasive. Although data from case reports and studies suggest that Sj VO 2 may have utility in detecting inadequate CBF, lack of outcome data, lack of clearly defined critical values at different temperatures during CPB, and availability of more noninvasive modalities (EEG, cerebral oximetry) have resulted in only limited use of this monitoring method during CPB. Based on current information, no neurologic monitoring techniques either alone or in combination are clearly useful in improving outcome during surgery requiring CPB. Further research is needed before the cost in personnel and in equipment of neurologic monitoring during CPB can be justified. Intensive Care Applications of Neurologic Monitoring (Monitors: EEG, Evoked Potentials, TCD, SjVO2 )

Secondary injury to the CNS has been recognized in past decades as a major modifiable risk factor in patients with CNS disease. Aneurysmal subarachnoid hemorrhage, stroke, and traumatic brain injury are examples of CNS insults in which secondary injury has important implications for the ultimate functional outcome. [171] [172] [173] The same diseases frequently result in a primary insult to the CNS that severely constrains the utility of the clinical neurologic examination because of the need for mechanical ventilation and sedation. Many techniques of neurologic monitoring discussed earlier also have been used in the intensive care unit. Generally, however, techniques that require continued presence of skilled technologists, such as monitoring of evoked potentials, are prohibitively expensive and of less practical value than techniques that can be performed as a daily examination, or techniques that provide data easily integrated into the intensive care frame of mind. Along with monitoring, some of the techniques discussed previously also can provide important prognostic information in comatose patients and guide decision making. Cerebral Ischemia

Cerebral ischemia is an important cause of secondary injury to the CNS. It can be difficult to detect in patients who are either comatose or sedated, but can occur even in the face of an adequate cerebral perfusion pressure. [174] [175] Three techniques may provide intensivists with additional information about cerebral perfusion. None of the monitors is considered â&#x20AC;&#x153;standard of care.â&#x20AC;? As with all monitors, the impact of the monitor on outcome depends on the quality of the therapeutic interventions that result from integration of the additional data into the clinical management of a given patient. Sj VO 2 monitoring is used most extensively in the intensive care unit to monitor patients with traumatic brain injury. The data have been used to guide blood pressure and ventilatory management to optimize blood flow. Sj VO 2 monitoring has had a major effect on ventilatory management of head-injured patients and has significantly reduced the routine use of hyperventilation in neurosurgical patients. [176] [177] [178] [179] [180] Sj VO 2 values of less than 50% generally indicate cerebral ischemia. Increases in Sj VO 2 may occur in response to therapy, or may be an ominous sign if the increase is caused by falling demand because of neuronal death. Similar to Sj VO 2 monitoring, monitoring of PBr O2 and blood flow is used most frequently in patients with traumatic brain injury. PBr O2 performs well in clinical practice. Decreases to less than 10 to 15 mm Hg are associated with worsening outcome, [27] [180] whereas PBr O2 -targeted treatment strategies may improve outcome. [181] The data for thermal diffusion CBF are not as comprehensive, perhaps reflecting the slightly less robust technology. [182] Nonetheless, in the setting of subarachnoid hemorrhage, thermal diffusion CBF less than 15 mL/100 g/min showed a sensitivity of 90% and a specificity of 75% for detecting symptomatic vasospasm. [19] TCD is widely used in the intensive care unit to document the presence and severity of cerebral vasospasm


after subarachnoid hemorrhage. As the major cerebral arteries narrow, flow velocity within the lumen must increase if blood flow is to be maintained. Such narrowing occurs 12 to 24 hours before the onset of clinical symptoms, allowing therapy to be initiated before the onset of clinical symptoms. [183] [184] [185] [186] [187] Mean flow velocities of more than 120 cm/sec seem to correlate well with angiographic vasospasm, [188] [189] although intracranial pressure and concurrent therapy with hypertensive hypervolemic hemodilution modify the flow velocity. The latter two factors result in characteristic changes of the TCD waveform, however, preserving the utility of the examination. Prognosis in Coma and Determination of Brain Death.

EEG monitoring may help to assess the clinical course and the prognosis of comatose patients. Assessment of prognosis must be separated from the insult that precipitated the coma by more than 24 hours. If not, the EEG may reflect predominantly the effect of the insult and may not predict prognosis. More than 24 hours after the insult, spontaneous sustained burst suppression correlates strongly with severe irreversible brain injury. [190] Absence of EEG variability portends a high likelihood of persistent vegetative state or death, [190] [191] whereas spontaneous variability, reactivity to external stimuli, and typical sleep patterns are associated with more favorable outcomes. [192] [193] [194] A specific indication for EEG monitoring is the therapeutic induction of a coma by barbiturate administration. Because neither blood nor cerebrospinal fluid concentrations of barbiturates reliably predict burst suppression and near-maximal reduction in cerebral metabolic rate of oxygen consumption, [195] and because barbiturate administration usually requires an increase in cardiovascular support, documentation of a burst suppression pattern on EEG allows the use of the minimal effective dose of barbiturate. Similar to EEG, evoked potential studies have a place in predicting prognosis in comatose patients. The presence of normal SSEPs bilaterally is an excellent prognostic sign, whereas the absence of any SSEP cortical response is a poor prognostic indicator. The degree of bad outcome can be predicted by BAEPs. Intact and normal BAEPs with absent cortical SSEPs predict a best outcome of a chronic vegetative state. Outcome may be worse, however, because BAEPs commonly deteriorate later with rostral-to-caudal deterioration. Absent BAEP responses beyond wave I predict a high likelihood of brain death. Present but abnormal SSEPs are associated with outcomes intermediate between good/high function and a chronic vegetative state. [196] [197] [198] [199] [200] [201] [202] [203] [204] [205] TCD also has been used in the intensive care unit as an aid to the diagnosis of brain death. As intracranial pressure increases, the pulsatility of the TCD waveform increases, accentuating the systolic peak and diminishing flow during diastole. With further increases in intracranial pressure, a characteristic to-and-fro pattern of flow is established, which is consistent with clinical brain death. [206] TCD studies are easily performed at the bedside and can minimize the need for unnecessary transports of the patient for definitive radiologic studies. Nonsurgical Factors Influencing Monitoring Results Anesthesia and the Electroencephalogram

Anesthetic drugs affect the frequency and amplitude of EEG waveforms. Although each drug class and each specific drug has some specific, dose-related EEG effects ( Table 46-2 ), some basic anesthesia-related EEG patterns may be described. Subanesthetic doses of intravenous and inhaled anesthetics usually produce an increase in frontal beta activity and abolish the alpha activity normally seen in the occipital leads in an awake, relaxed patient with the eyes closed. As the patient actually goes to sleep with general anesthesia, the brain waves become larger in amplitude and slower in frequency. In the frontal areas, small beta activity seen in an awake patient slows to the alpha range and increases in size. In combination with the loss of the occipital alpha activity, this phenomenon produces the appearance of a â&#x20AC;&#x153;shiftâ&#x20AC;? of the alpha activity from the posterior cortex to the anterior cortex. Further increases in the dose of the inhalation or


intravenous agent produce further slowing of the EEG, and some agents have the capability to suppress EEG activity totally (see Table 46-2 ). Other agents never produce burst suppression or an isoelectric EEG, despite increasing dose, either because they are incapable of completely suppressing the EEG (e.g., opioids, benzodiazepines) or because cardiovascular toxicity of the drug (e.g., halothane) prevents administration of a large enough dose. Table 46-2 -- Anesthetic Drugs and Electroencephalogram (EEG) Effect on EEG Drug Effect on EEG Frequency Amplitude Isoflurane

Burst Suppression? Yes, >1.5 MAC

Subanesthetic

Loss of alpha, ↑ frontal beta

Anesthetic

Frontal 4-13 Hz activity

Increasing dose >1.5 MAC

Diffuse theta and delta suppression silence

burst

Desflurane

Similar to equi-MAC dose of isoflurane Similar to equi-MAC dose of isoflurane

Yes, >1.5 MAC

Sevoflurane

Similar to equi-MAC dose of isoflurane Similar to equi-MAC dose of isoflurane

Yes, >1.5 MAC

Nitrous oxide (alone)

Frontal fast oscillatory activity (>30 Hz)

0

↑, especially with inspired concentration >50%

Enflurane

Yes, >1.5 MAC

Subanesthetic

Loss of alpha, ↑ frontal beta

Anesthetic

↑ frontal 7-12 Hz activity

Spikes/spike and slow waves burst suppression; hypocapnia seizures

↑↑

Increasing dose >1.5 MAC

0 Not seen in clinically useful dosage range

Halothane Subanesthetic

↑ frontal 10-20 Hz activity

Anesthetic

↑ frontal 10-15 Hz activity

Diffuse theta, slowing with increasing dose

Increasing dose >1.5 MAC Barbiturates

Yes, with high doses

Low dose

Fast frontal beta activity

Slight ↑

Moderate dose

Frontal alpha frequency spindles

Diffuse delta silence

↑↑↑

Increasing high dose

burst suppression

0

Etomidate

Yes, with high doses

Low dose

Fast frontal beta activity

Moderate dose

Frontal alpha frequency spindles

Diffuse delta silence

↑↑

Increasing high dose

burst suppression

Propofol Low dose

No

0 Yes, with high doses

Loss of alpha, ↑ frontal beta


Moderate dose Increasing high dose

Frontal delta, waxing/waning alpha

Diffuse delta silence

↑↑

burst suppression

0

Ketamine

No

Low dose

Loss of alpha, ↑ variability

↑↓

Moderate dose

Frontal rhythmic delta

High dose

Polymorphic delta, some beta

↑↑ (beta is low amplitude)

Benzodiazepines

No

Low dose

Loss of alpha, increased frontal beta activity

High dose

Frontally dominant delta and theta

Opiates

No

Low dose

Loss of beta, alpha slows

↔↑

Moderate dose

Diffuse theta, some delta

High dose

Delta, often synchronized

↑↑

Dexmedetomidine Moderate slowing, prominent spindles

↑↑

No

MAC, minimum alveolar concentration. *delta =<4 Hz frequency; theta = 4-7 Hz frequency; alpha = 8-13 Hz frequency; beta =>13 Hz frequency.

Intravenous Anesthetic Drugs Barbiturates, Propofol, and Etomidate.

Despite widely varying potencies and durations of action, barbiturates, propofol, and etomidate produce similar EEG patterns ( Fig. 46-17 shows EEG effects of thiopental). These drugs all follow the basic anesthesia-related EEG pattern described previously with initial EEG activation (see Fig. 46-17A ), followed by dose-related depression. As the patient loses consciousness, characteristic frontal spindles are seen (see Fig. 46-17B ), which are replaced by polymorphic 1- to 3-Hz activity (see Fig. 46-17C ) as the drug dose is increased. Further increases in dose result in lengthening periods of suppression interspersed with periods of activity (burst suppression). With a very high dose, EEG silence results. All of these drugs have been reported to cause epileptiform activity in humans, but epileptiform activity is clinically significant only after methohexital and etomidate when given in subhypnotic doses.

Figure 46-17 Electroencephalogram effects of intravenous administration of thiopental in humans. A, Rapid activity. B, Barbiturate spindles. C, Slow waves. D, Burst suppression. (From Clark DL, Rosner BS: Neurophysiologic effects of general anesthetics. Anesthesiology 38:564, 1973.)

Ketamine.


Ketamine does not follow the basic anesthesia-related EEG pattern. Anesthesia with ketamine is characterized by frontally dominant rhythmic, high-amplitude theta activity. Increasing doses produce intermittent polymorphic delta activity of very large amplitude interspersed with low-amplitude beta activity. [207] Electrocortical silence cannot be produced with ketamine. EEG activity may be very disorganized and variable at all doses. This disorganization of the EEG with ketamine is responsible for the failure of the bispectral index to be useful in looking at the effect of ketamine on consciousness. Recovery of normal EEG activity even after a single bolus dose of ketamine is slow compared with barbiturates. There is no information available about the relationship between emergence reactions after ketamine and the EEG. Ketamine also has been associated with increased epileptiform activity. [207] Benzodiazepines.

Despite varying potencies and durations of action, benzodiazepines also follow the basic anesthesia-related EEG pattern. As a class, however, these drugs are incapable of producing burst suppression or an isoelectric EEG. Opioids.

As a class, opioids do not follow the basic anesthesia-related EEG pattern. Opioids generally produce a dose-related decrease in frequency and increase in amplitude of the EEG. If no further doses of opiates are given, alpha and beta activity return as drug redistribution occurs. The rapidity of return depends on the initial dose and on the drug. Remifentanil is associated with the most rapid return to normal. [208] Complete suppression of the EEG cannot be obtained with opioids. Epileptiform activity occurs in humans and in animals receiving large to supraclinical doses of opioids. Sharp wave activity is common after induction of anesthesia with fentanyl, with 20% of patients showing this phenomenon after 30 µg/kg; 60%, after 50 µg/kg; 58%, after 60 µg/kg; and 80%, after 70 µg/kg. Alfentanil bolus has been used clinically to activate seizure foci during epilepsy surgery. [209] This epileptiform activity is mainly noted in the frontotemporal region. [210] Dexmedetomidine.

Dexmedetomidine is being increasingly used for sedation in the operating room and in the intensive care unit. EEG studies of patients undergoing sedation with dexmedetomidine alone show patterns similar to those seen in normal human sleep with increased slow-wave activity and sleep spindles prominent. [211] Burst suppression or an isoelectric EEG pattern cannot be produced even with high doses of the drug. Level of sedation with dexmedetomidine can be effectively monitored using processed EEG parameters and has been reported using bispectral index and entropy techniques. [212] Inhaled Anesthetics Nitrous Oxide.

Used alone, nitrous oxide causes a decrease in amplitude and frequency of the dominant occipital alpha rhythm. With the onset of analgesia and depressed consciousness, frontally dominant fast oscillatory activity (>30 Hz) is frequently seen. [213] This activity may persist to some extent for 50 minutes after discontinuation of nitrous oxide. When nitrous oxide is used in combination with other agents, it increases the effects that would be associated with the agent alone clinically and with respect to the EEG pattern seen. Isoflurane, Sevoflurane, Enflurane, Halothane, and Desflurane.

Potent inhaled anesthetics follow the basic anesthesia-related EEG pattern. Isoflurane initially causes an


activation of the EEG followed by a slowing of the EEG activity that is more marked with increasing dose. Isoflurane begins to produce periods of EEG suppression at 1.5 minimum alveolar concentration (MAC), which become longer with increasing dose until electric silence is produced at 2 to 2.5 MAC. Isolated epileptiform patterns sometimes can be seen during intersuppression activity at 1.5 to 2 MAC isoflurane. [214] Sevoflurane causes similar dose-dependent EEG effects. Equi-MAC concentrations of sevoflurane and isoflurane cause similar EEG changes. [215] Epileptiform activity has been induced by administration of sevoflurane in patients without epilepsy, and seizure activity on EEG, but not clinical seizure activity, has been reported in pediatric patients with a history of epilepsy during induction of anesthesia with sevoflurane. [216] [217] Despite these observations, sevoflurane, similar to other inhalation agents, is not suitable for use during electrocorticography for localization of seizure foci. [218] EEG patterns seen with enflurane are similar to the patterns seen with isoflurane except that epileptiform activity is considerably more prominent. At 2 to 3 MAC, burst suppression is seen, but virtually all intersuppression activity consists of large spike/wave pattern discharges. Hyperventilation with high concentrations of enflurane increases the length of suppression, decreases the duration of bursts, but increases the amplitude and main frequency component of the intersuppression epileptiform activity. Frank EEG seizures also may occur with enflurane that produce the same cerebral metabolic effects as pentylenetetrazol, a known convulsant. Halothane also produces EEG patterns similar to those of isoflurane, but dosages of halothane that would produce burst suppression in the EEG (3 to 4 MAC) are associated with profound cardiovascular toxicity. Desflurane produces EEG changes similar in nature to equi-MAC concentrations of isoflurane. In limited clinical studies, there has been no evidence of epileptiform activity with desflurane, despite hyperventilation and 1.6 MAC dosage, [219] and desflurane has been used as a treatment of refractory status epilepticus. [220] Clinical studies have shown that the EEG effects of inhalational anesthetic agents are influenced by age and baseline EEG characteristics. Older patients and patients with EEG slowing at baseline were more sensitive to the EEG effects of isoflurane and desflurane. As anesthesia was deepened, similar EEG pattern changes were noted, but these changes occurred at lower end-tidal anesthetic concentrations. [221] Anesthesia and Sensory Evoked Responses Volatile Anesthetics

Multiple drugs used in the perioperative period can influence the ability to monitor SERs accurately ( Table 46-3 ). A more recent review provides the interested clinician with a detailed analysis of all drug effects on SERs, [222] which is beyond the scope of this chapter. Table 46-3 does not quantify drug effects, but rather lists whether an individual drug is capable of producing a change in any part of an evoked response that could be mistaken for a surgically induced change. A “no” designation in this table does not mean that there are no effects of a given drug on SERs. The “no” designation indicates that any effects that do occur would not be called clinically significant by clinicians experienced in intraoperative monitoring. Several general concepts ( Table 46-4 ) help the clinician who is trying to determine the best choice of drugs for use during monitored cases. Table 46-3 -- Ability of an Individual Anesthetic Drug to Produce a Change in Sensory and Motor Evoked Potentials That Could Be Mistaken for a Surgically Induced Change SSEPs BAEPs VEPs Transcranial MEPs Drug LAT AMP LAT AMP LAT AMP LAT AMP Isoflurane Yes Yes No No Yes Yes Yes Yes Enflurane

Yes Yes

No

No

Yes Yes

Yes

Yes

Halothane

Yes Yes

No

No

Yes Yes

Yes

Yes

Nitrous oxide *

Yes Yes

No

No

Yes Yes

Yes

Yes


Barbiturates

Yes Yes

No

No

Yes Yes

Yes

Yes

Etomidate

No

No

No

Yes Yes

No

No

Propofol

Yes Yes

No

No

Yes Yes

Yes

Yes

Droperidol

No

No

No

Yes

Yes

Diazepam

Yes Yes

No

No

Yes Yes

Yes

Yes

Midazolam

Yes Yes

No

No

Yes Yes

Yes

Yes

Ketamine

No

No

No

No

Yes Yes

No

No

Opiates

No

No

No

No

No

No

No

No

Dexmedetomidine No

No

No

No

No

ND

ND

No

No No

Note : This table is not quantitative in any way. “Yes” or “no” designations indicate whether an individual drug is capable of producing an effect on any portion of the evoked response that could be mistaken for a surgically induced change. (p): Use of this drug and any dose may render this type of monitoring impossible for a signifieant period of time. AMP, amplitude; BAEPs, brainstem auditory evoked potentials; LAT, latency; MEPs, motor evoked potentials; ND, no data available from the literature; SSEPs, somatosensory evoked potentials; VEPs, visual evoked potentials. * Increases the effect of the agent(s) with which it is used.

Table 46-4 -- Guidelines for Choosing Anesthetic Techniques During Procedures in Which Sensory Evoked Responses Are Monitored 1.

Intravenous agents have significantly less effect than “equipotent” doses of inhaled anesthetics

2.

Combinations of drugs generally produce “additive” effects

3.

Subcortical (spinal or brainstem) sensory evoked responses are very resistant to the effects of anesthetic drugs. If subcortical responses provide sufficient information for the surgical procedure, anesthetic technique is not important, and effects on cortically recorded responses may be ignored

The volatile anesthetics isoflurane, sevoflurane, desflurane, enflurane, and halothane have similar effects in differing degrees on all types of SERs. VEPs are the most sensitive to the effects of volatile anesthetics, and BAEPs are the most resistant to anesthetic-induced changes. Spinal and subcortical SSEP responses are significantly less affected than cortical potentials. [223] [224] [225] SSEPs, because they are the most widely used intraoperative SER technique, are the most completely studied with respect to the effects of anesthetic drugs. The effects of the currently used volatile agents on cortical SSEPs are dose-dependent increases in latency and conduction times and a decrease in amplitude of cortically, but not subcortically recorded signals. [223] [224] [225] [226] [227] When comparing the different volatile agents, studies have reported conflicting results. [223] [225] One study suggests that halothane has a greater impact on cortical SSEPs than either isoflurane or enflurane, [225] whereas another published report supports a greater effect produced by enflurane and isoflurane than halothane. [223] None of these


differences are clinically important and may be ignored by the practicing clinician. With respect to the newer agents, desflurane and sevoflurane seem to have qualitatively and quantitatively similar effects on SERs as isoflurane. [228] [229] [230] [231] [232] In neurologically normal patients, 0.5 to 1 MAC of any of the potent inhaled agents in the presence of nitrous oxide is compatible with monitoring of cortical SSEPs (Figs. 46-18, 46-19, and 46-20 [0180] [0190] [0200]). [223] [227] Neurologically impaired patients may show a significantly greater sensitivity to inhaled agents, even to the point of not tolerating any recordable level of inhaled agent. Generally, better monitoring conditions are obtained, however, with narcotic-based anesthetics with less than 1 MAC total (nitrous oxide plus potent agent) end-tidal inhaled anesthetic concentration.

Figure 46-18 Representative somatosensory evoked potential cortical responses (C-3, C-4-FPz) at various minimum alveolar concentration (MAC) levels of isoflurane. (From Peterson DO, Drummond JC, Todd MM: Effects of halothane, enflurane, isoflurane, and nitrous oxide on somatosensory evoked potentials in humans. Anesthesiology 65:35, 1986.)

Figure 46-19 Representative somatosensory evoked potential cortical responses (C-3, or C-4-FPz) at various minimum alveolar concentration (MAC) levels of enflurane. (From Peterson DO, Drummond JC, Todd MM: Effects of halothane, enflurane, isoflurane, and nitrous oxide on somatosensory evoked potentials in humans. Anesthesiology 65:35, 1986.)

Figure 46-20 Representative somatosensory evoked potential cortical responses (C-3, C-4-FPz) at various minimum alveolar concentration (MAC) levels of halothane. (From Peterson DO, Drummond JC, Todd MM: Effects of halothane, enflurane, isoflurane, and nitrous oxide on somatosensory evoked potentials in humans. Anesthesiology 65:35, 1986.)

The volatile anesthetics result in increases in latency of BAEPs without significantly affecting the amplitude. [227] [233] [234] [235] Volatile anesthetics cause increases in latency and decreases in amplitude in the early (middle latency) cortical responses after auditory stimulation, [234] however, and these middle latency responses are now being used to monitor the hypnotic component of general anesthetics. [32] Adequate monitoring of BAEPs is possible with any clinically useful concentrations of inhaled agents (with or without nitrous oxide) (Figs. 46-21 and 46-22 [0210] [0220]). [227] [233] [234] [235] [236]

Figure 46-21 Influence of isoflurane alone on brainstem auditory evoked potential in a typical subject. Latency of peaks III and IV to V increased at 1.0%, but stabilized with increasing anesthetic depth. (From Manninen PH, Lam AM, Nicholas JF: The effects of isofluraneâ&#x20AC;&#x201C;nitrous oxide anesthesia on brainstem auditory evoked potentials in humans. Anesth Analg 64:43, 1985.)

Figure 46-22 Brainstem auditory evoked potential recording obtained in one patient at different enflurane (Ethrane)-inspired concentrations. (From Dubois MY, Sato S, Chassy J, et al: Effects of enflurane on brainstem auditory evoked responses in humans. Anesth Analg 61:898, 1982.)


Use of the volatile agents during monitoring of VEPs results in dose-dependent increases in latency with or without changes in amplitude. [227] [237] [238] [239] [240] Isoflurane results in dose-dependent increases in latency and decreases in amplitude up to 1.8% in 100% oxygen, at which time the waveform is lost. [227] [237] Enflurane in the absence of hypocarbia also leads to decrease in amplitude. [237] Halothane causes increases in latency without changes in amplitude. [238] [239] Although the data from these studies seem valid, the results are not clinically relevant because the variability of VEPs in anesthetized patients is so great that satisfactory monitoring, in the opinion of many experts, is impossible using any anesthetic technique. Although volatile anesthetics cause significant changes in the SER waveforms, it is possible to provide adequate monitoring intraoperatively in the presence of anesthetic doses of volatile anesthetics. Doses of agents causing significant depression of the response to be monitored must be prevented. In the authorsâ&#x20AC;&#x2122; experience, end-tidal concentrations of inhaled agents totaling greater than 1.3 MAC have a dose-related, increasing probability of obliterating cortical SSEPs even in neurologically normal patients. Equally important, anesthetic concentration should not be changed during the critical periods of intraoperative monitoring. Critical periods are defined as periods in which surgical interventions are most likely to result in damage to neurologic tissue and changes in the SERs. Because the volatile anesthetic-induced changes in SERs are dose-dependent, increasing anesthetic dosage at a crucial point in the operative procedure can result in confusing changes in the SERs that potentially may be caused by the anesthetic, the surgical procedure, or both. The appropriate intervention is difficult to determine. As with the volatile anesthetics, nitrous oxide causes differing effects on the SERs depending on the sensory system monitored. It causes decreases in amplitude without significant changes in latency in SSEPs when used alone or when added to a narcotic-based or volatile anesthetic. [223] [224] [241] The addition of nitrous oxide to a maintenance volatile anesthetic during the monitoring of BAEPs causes no further change. [233] Likewise, use of nitrous oxide alone causes no change in BAEPs, unless gas accumulates in the middle ear. [241] Use of nitrous oxide alone results in an increase in latency and a decrease in amplitude in VEPs, but when it is added to a volatile anesthetic technique, it causes no further changes in VEPs. [237] [241] Intravenous Agents

The effects of barbiturates on SERs have been studied in animal models and in humans. Increasing doses of thiopental in patients result in progressive dose-dependent increases in latency, decreases in amplitude of SSEPs, and progressive increases in latency of wave V in BAEPs. The changes in SSEPs are more pronounced than the changes in BAEPs, and waveforms beyond the initial primary cortical response are quickly obliterated. This finding is consistent with the theories that barbiturates affect synaptic transmission more than axonal conduction. Early waveforms in SERs result primarily from axonal transmission, and later waves depend on multisynaptic pathways in addition to axonal transmission. At doses of thiopental far greater than doses producing an isoelectric EEG, adequate monitoring of early cortical and subcortical SSEPs and BAEPs was preserved. [242] Other barbiturate compounds show similar effects. Somatosensory and auditory SERs were never obliterated even at doses greater than those causing complete suppression of spontaneous EEG activity. [243] This observation is important, especially when attempting to monitor the adequacy of CBF during cerebrovascular surgery when the patient has been given large, â&#x20AC;&#x153;protectiveâ&#x20AC;? doses of barbiturates. The EEG is isoelectric and not helpful for monitoring. The early cortical SSEP waveforms are still preserved, however, and may be very helpful in determining adequacy of CBF. Preserved ability to monitor SSEPs in head-injured patients receiving therapeutic thiopental infusions has been shown. [244] VEPs are much more sensitive to barbiturates. Low barbiturate doses obliterate all except the earliest waveforms. The early potentials persisted with increases in latency even to very high pentobarbital doses. [245] Except for VEPs, adequate perioperative monitoring of SERs is possible even in the presence of high-dose barbiturate therapy as long as the effects of the drug (increased latency with moderately decreased amplitude) are considered.


After bolus administration and intravenous infusions, etomidate causes increases in latency of all waves and prolongation of central conduction time in SSEPs. In contrast to virtually all other commonly used anesthetics, etomidate causes increases in amplitude of the cortical SSEP. [246] [247] This effect may be due to an alteration in the balance of inhibitory and excitatory influences or an increase in the irritability of the CNS. This effect seems to be present in the cortex, but not in the spinal cord. [247] Etomidate infusions have been used to enhance SSEP recording in patients when it was impossible to obtain reproducible responses at the beginning of intraoperative monitoring because of the patients’ pathology ( Fig. 46-23 ). Following baseline responses that could not be monitored, the etomidate augmentation of the SSEP allowed adequate monitoring and detection of intraoperative events leading to compromise of the spinal cord. [247] The effects of etomidate on BAEPs are dose-dependent increases in latency and decreases in amplitude that are not clinically significant. [248]

Figure 46-23 Effects of etomidate on somatosensory evoked potential. A, The top tracings were obtained from a mildly mentally impaired patient with severe kyphoscoliosis during the early maintenance phase of anesthesia using isoflurane and fentanyl. B, The bottom tracings were obtained after discontinuing isoflurane and instituting an etomidate infusion at 20 µg/kg/min. Note dramatically increased amplitude and clarity of the signal in the cortical channels (marked by arrows), which both are recorded with the same amplification scale.

Droperidol in premedicant doses has been shown to have varying effects on SSEPs. In most patients, decreases in amplitude and loss of late waves were noted. In a few patients, increases in amplitude were noted. In all patients, conduction time was prolonged. [249] Effects were not clinically significant. Benzodiazepines also can cause changes in SERs. [250] [251] Diazepam causes increases in latency and decreases in amplitude of SSEPs, increases in latency in the cortical response after auditory stimulation, and no change in BAEPs. [250] [251] Midazolam causes decreases in amplitude without changes in latency of SSEPs. [246] Generally, opioids cause small dose-dependent increases in latency and decreases in amplitude of SSEPs. These changes are not clinically significant. Effects on amplitude are more variable than the latency increases. [252] [253] Even at large doses of fentanyl (60 µg/kg), reproducible SSEPs can be recorded. [253] Other opiates cause similar dose-dependent changes in SSEPs. [252] [254] Opioids can be used even in high doses in patients requiring intraoperative SSEP monitoring without impairment of ability to monitor neurologic function adequately. Opioid-induced changes must be taken into account, however, when evaluating the recordings. Large intravenous bolus administration of opioids should be avoided at times of potential surgical compromise to neurologic function to prevent confusing the interpretation of SEP changes if they develop. BAEPs were resistant to doses of fentanyl of 50 µg/kg with no changes observed in absolute latency, interpeak latency, or amplitude. [255] Based on several case reports and small series, dexmedetomidine seems to be compatible with all types of evoked potential monitoring (including MEPs), and does not produce changes that would be mistaken for a surgically induced change. Data are limited, and large studies are lacking entirely. As the use of this drug increases, more data should become available, but at this time, use of dexmedetomidine does not seem to be problematic. Anesthesia and Motor Evoked Potentials

Except in the case of neurogenic MEPs, effects of anesthetics are surprisingly profound, particularly on MEP recordings from muscle produced by either single pulse transcranial electric or especially magnetic stimulation (see Table 46-3 ). [256] [257] [258] [259] [260] [261] Anesthetic techniques typically used by most anesthesiologists for spine surgery would produce prohibitive depression of the MEP. [262] [263] Investigators showed in several studies that intravenous agents produce significantly less depression, and


techniques using any of a combination of ketamine, opiates, etomidate, and propofol have been described. [264] [265] [266] [267] [268] [269] [270] The authors have had excellent experience with a combination of propofol and remifentanil, which also is supported in the literature. Anesthetic effects on MEP responses recorded at spinal levels seem to be less serious. When responses are recorded from muscle, neuromuscular blocking agents should be monitored quantitatively, maintaining T1 twitch height at around 30% of control values to prevent excessive movement during the operation. [136] [257] When responses are not recorded from muscle, profound relaxation is desirable because gross muscle movement produced by MEP stimulation is eliminated, facilitating the surgical procedure. More recent studies using rapid trains of stimuli with transcranial electric and magnetic stimulus techniques have produced responses that are more resistant to the effects of anesthetic agents, and more “traditional” techniques using inhaled agents and narcotics may be used. [271] [272] [273] Most studies support the use of total intravenous anesthesia as preferable to techniques using nitrous oxide or potent inhaled agents, however. Precise control of the anesthetic and avoidance of boluses during critical monitoring periods seem to be even more important than for SSEPs, and active cooperation of the anesthesia care team is essential for good, reproducible results. Figure 46-24 shows the dramatic effect of introduction of 0.3 MAC isoflurane to a total intravenous technique using propofol and remifentanil.

Figure 46-24 A, Transcranial electrical motor evoked potential recording showing surgically induced change during spine surgery (scoliosis repair). B, Motor evoked potential with an anesthetic-induced change. Note similarity of the change pattern except that in the anesthetic-induced change, the responses in the upper extremity also changed. Left-sided and right-sided responses are shown on the corresponding panel. A single upper extremity response is shown ( top tracing ) in each panel. Responses from four muscle groups in each lower extremity are shown directly below.

Pathophysiologic Effects on the Electroencephalogram Hypoxia

Hypoxia may produce inadequate delivery of oxygen to the cerebral cortex generating EEG, and changes similar to those occurring with ischemia result. Initially, hypoxemia may not result in any EEG changes because the brain can increase blood flow to compensate. When the hypoxemia becomes severe enough, further increases in flow are impossible, and EEG changes occur. “Slowing” of the EEG during hypoxia is a nonspecific global effect. Fast frequencies are lost, and low frequencies dominate. Eventually, the EEG is abolished as the brain shuts down electric activity and diverts all oxygen delivered to maintenance of cellular integrity. Hypotension

In a normal, awake patient, significant levels of hypotension seem to be needed to cause the earliest of CNS signs, as measured by discrimination tests such as the flicker-fusion test. This test examines the flicker rate at which the observer perceives the light to be continuous. In the early days of deliberate hypotension, this test was part of the preoperative evaluation to judge how far the pressure could be reduced during the operation. Clear signs of confusion and inability to concentrate or respond properly to simple commands generally represent very low levels of cerebral perfusion when caused by hypotension because the normal cerebral circulation has a large capacity to vasodilate and maintain normal flow in the face of significant hypotension. The EEG changes associated with even this level of hypotension are not dramatic, although they are clear by comparison with a previously active recording. Herein lies the problem with using intraoperative EEG to determine whether a given level of hypotension has resulted in brain ischemia. EEG changes are not very pronounced and are bilateral. These changes also are nearly identical to the changes caused by increasing


doses of many anesthetic drugs. EEG changes associated with hypotension can be detected, but when the hypotension is induced slowly and associated with changes in anesthetic drugs (e.g., use of isoflurane to reduce blood pressure), the changes are very difficult to interpret. EEG changes associated with acute, severe hypotension such as may be caused by sudden arrhythmias are easier to read. Many patients undergoing surgery do not have a normal cerebral circulation, however. In these individuals, even mild hypotension may result in significant cerebral ischemia. In these individuals, monitoring the EEG during planned hypotension may be helpful, provided that other causes of similar EEG changes may be carefully controlled. There remains little literature to support the use of EEG monitoring during hypotension, but in our opinion, when the EEG is being monitored (e.g., during carotid surgery), EEG changes secondary to hypotension really do represent cerebral ischemia of a significant degree and should be considered an important finding. Hypothermia

During cooling on CPB, the total power and peak power frequency of the high-frequency band were highly correlated with temperature using Fourier analysis and spectral edge data; however, there was significant variability between subjects, especially during cooling. [274] Complete EEG suppression usually develops at 15°C to 18°C. Levy and colleagues [162] showed an improved ability to quantify the effects of hypothermia on the EEG using an EEG processing technique known as “approximate entropy.” Hypercarbia and Hypocarbia

Hypocapnia is known to activate excitable seizure foci, and in rare cases may produce EEG evidence of cerebral ischemia even in awake subjects. [275] Hypercapnia, unless severe and associated with hypoxemia, has only indirect effects secondary to increased CBF. In an anesthetized patient, hypercarbia-associated increases in CBF may have similar effects to the effects seen with increasing end-tidal tension of volatile anesthetics. [276] Untoward Events

One of the suggested reasons for monitoring the brain of an anesthetized patient is to enable detection of injuries to the nervous system that would not be otherwise apparent. Although there are hundreds of such case reports in the literature and many in the authors’ experience, cost-effectiveness of such monitoring is unclear. In a more recent case at the authors’ institution, severe EEG changes occurred at the beginning of a carotid endarterectomy, before surgical incision, and were unassociated with any other vital sign changes or hypotension. Immediate angiography revealed acute carotid occlusion and completely changed the operation performed with this patient, and the patient recovered completely. There are intraoperative events that could lead to CNS insult, which, if detected early, could be rapidly reversed or treated to prevent permanent injury. Given the rarity of such events, however, it is extremely unlikely that such monitoring would be shown to be beneficial in any foreseeable randomized trial. If the “at-risk” patient could be identified preoperatively, perhaps the EEG or other types of neuromonitoring could be useful in detecting untoward CNS events during anesthesia, such as a new stroke after elective general surgery. Physiologic Factors Influencing Sensory Evoked Responses

Numerous physiologic variables, including systemic blood pressure, temperature (local and systemic), and blood gas tensions, can influence SEP recordings. With decreases in mean arterial blood pressure to below levels of cerebral autoregulation owing to either blood loss or vasoactive agents, progressive changes in SERs have been noted. SSEP changes observed are progressive decreases in amplitude until loss of the waveform with no changes in latency. [277] [278] BAEPs are resistant to even profound levels of hypotension (mean arterial pressure of 20 mm Hg in dogs). [277] Cortical (synaptic) function necessary to produce cortical SERs seems to be more sensitive to hypoperfusion than spinal cord or brainstem, nonsynaptic transmission. [278] Rapid decreases in blood pressure to levels above the lower limit of autoregulation also have been associated with transient SSEP changes of decreased amplitude that resolve after several


minutes of continued hypotension at the same level. [279] Reversible SSEP changes at systemic pressures within the normal range have been observed in patients undergoing spinal distraction during scoliosis surgery. These changes resolved with increases of systemic blood pressure to slightly above the patient's normal pressure, suggesting that the combination of surgical manipulation with levels of hypotension generally considered â&#x20AC;&#x153;safeâ&#x20AC;? could result in spinal cord ischemia. [280] Changes in temperature also affect SERs. Hypothermia causes increases in latency and decreases in amplitude of cortical and subcortical SERs after all types of stimulation. [281] [282] [283] Hyperthermia also alters SERs, with increases in temperature leading to decreases in amplitude in SSEPs and loss of SSEPs at 42°C during induced hyperthermia. [284] Changes in arterial blood gas tensions have been reported to alter SERs, probably in relation to changes in blood flow or oxygen delivery to neural structures. [285] [286] Hypoxia produces SSEP changes (decreased amplitude) similar to the changes seen with ischemia. [286] Decreased oxygen delivery associated with anemia during isovolemic hemodilution results in progressive increases in latency of SSEPs and VEPs that become significant at hematocrits less than 15%. Changes in amplitude were variable until very low hematocrits (approximately 7%) were reached, at which point the amplitude of all waveforms decreased. [287] Summary

Regardless of the type of intraoperative neurologic monitor, several principles must be observed for neurologic monitoring to provide potential benefit to the patient. First, the pathway at risk during the surgical procedure must be amenable to monitoring. Second, if evidence of injury to the pathway is detected, there must be some intervention possible. If changes in the neurologic monitor are detected, and no intervention is possible, although the monitor may be of prognostic value, it does not have the potential to provide direct benefit to the patient from early detection of impending neurologic injury. Third, the monitor must provide reliable and reproducible data. If the data have a high degree of variability in the absence of clinical interventions, their utility for detecting clinically significant events is limited. This chapter has reviewed the most common clinically used intraoperative neurologic monitors. Ideally, clinical studies would provide outcome data on the efficacy of a neurologic monitor in a given procedure to improve neurologic outcome. Although there is a wealth of clinical experience with many of these monitoring modalities, there is little in the way of randomized prospective studies evaluating the efficacy of neurologic monitoring. Based on clinical experience with neurologic monitoring and nonrandomized clinical studies in which neurologic monitoring is used and generally compared with historical controls, practice patterns for use of neurologic monitoring have developed. In certain procedures, neurologic monitoring is recommended and used by most centers; in other procedures, monitoring is used almost routinely in some centers, but not in others; and in some procedures, there is no clear clinical experience or evidence that would indicate that monitoring is useful at all (experimental use). Finally, there are procedures in which monitoring is used selectively for patients believed to be at higher-than-usual risk for intraoperative neurologic injury. Table 46-5 provides a summary of current clinical practice. Table 46-5 -- Current Practices in Neurologic Monitoring Procedure Monitors Current Practice Awake patient neurologic NIH recommends use of one of these four available monitors. examination, EEG, Carotid endarterectomy SSEP, TCD CO

Threshold value not determined, inadequate normative population data Monitoring recommended, and may substitute for wake-up


SSEP Scoliosis surgery Wake-up test

testing Largely abandoned in centers using electrophysiologic monitoring. Monitoring is not continuous and false-negative monitoring patterns have been reported.

MEP

Increased clinical use now that transcranial electrical stimulation is FDA approved. Useful in combination with SSEP

Facial nerve monitor

Facial nerve monitoring recommended

BAEP

BAEP shows some clinical evidence of improved outcome in some procedures.

Intracranial aneurysm clipping

SSEP, EEG

Used routinely in some centers; limited clinical data on outcome, but appears clinically useful during anterior circulation procedures

Cranial nerve V decompression

BAEP

Used in some centers, reduces hearing loss

Cranial nerve VII decompression

BAEP

Data from small series show improved hearing preservation

Supratentorial mass lesions

SSEP

Used in some centers in selected high-risk procedures

Infratentorial mass lesions

BAEP/SSEP

BAEP to detect retractor-related cranial nerve VIII injury; SSEP in rare, high-risk lesions adjacent to ascending sensory pathways

Decompression of spinal stenosis

SSEP

Used in some centers in high-risk procedures (more often cervical)

Spinal cord trauma

SSEP/MEP

Used in some centers in high-risk procedures

Acoustic neuroma

Cardiopulmonary EEG, TCD, Sj VO , CO 2 bypass

Used routinely in some centers, actively studied, but no outcome data as of yet

Aortic coarctation

SSEP

Used routinely in a few centers, no widespread acceptance

Aortic aneurysm SSEP repair

Used routinely in a few centers, no widespread acceptance

MEP

Used routinely in a few centers, no widespread acceptance

BAEP, brainstem auditory evoked potential; CO, cerebral oximetry; EEG, electroencephalogram; FDA, U.S. Food and Drug Administration; MEP, motor evoked potential; NIH, National Institutes of Health; Sj VO 2 , jugular bulb venous oxygen saturation; TCD, transcranial Doppler.

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Millers 46th Chapter  

46 – Neurologic Monitoring

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