Transcranial Motor Evoked Potentials - Springer

Chapter 2

Transcranial Motor Evoked Potentials Leslie C. Jameson

Keywords Basics • Motor-evoked potential monitoring • Operating room • Somatosenory evoked potential • Intraoperative neurophysiologic monitoring • Central nervous system • Motor pathway blood supply • Technical aspects • Risk

Motor-evoked potentials (MEPs) are the most recent addition to routine intraoperative neurophysiologic monitoring (IOM). Enthusiastic reports of improved outcomes obtained with the use of somatosenory evoked potential (SEP) monitoring, primarily for scoliosis procedures in children and young adults, were quickly followed by case reports of isolated postoperative motor injury without sensory changes [1]. These reports reflected the reality of the anatomy and physiology of motor/sensory pathways. MEP and SEP pathways are located in different topographic and vascular regions of the cerebral cortex, brainstem, and spinal cord. Motor functional pathways are more sensitive to ischemic insults than SEP pathways [2].

L.C. Jameson (*) Department of Anesthesiology, School of Medicine, University of Colorado, University of Colorado Hospital, 12401 E 17th Place 7th Floor Room 737, Aurora, CO 80045, USA e-mail: [email protected] A. Koht et al. (eds.), Monitoring the Nervous System for Anesthesiologists and Other Health Care Professionals, DOI 10.1007/978-1-4614-0308-1_2, © Springer Science+Business Media, LLC 2012

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Rare isolated motor injury without sensory changes after idiopathic scoliosis procedures was not the only driving force behind the wide spread adoption of MEP monitoring. Increasing surgical volume and operative complexity in the central nervous system (CNS) and spine in high risk adults also fueled the demand to separately assess motor function; MEPs facilitated better intraoperative decision making in all patient groups. As surgical techniques (instrumentation, diagnostic imaging, intraoperative imaging) advanced and perioperative anesthetic management improved, the aged or injured population were scheduled for surgeries that would not have been attempted only a few years ago before. Thus MEP monitoring has been embraced by spine and neurological surgeons as a method to help prevent surgical intervention from exceeding safe limits where risk and severity of the potential surgical injury exceeds the functional gain [3]. Since MEP monitoring, particularly in spinal surgery, has a better correlation with good postoperative motor outcome than the use of SEPs, many experts advocate MEP monitoring for all surgeries (1) surgical correction of axial skeletal deformity [4–7], (2) intramedullary spinal cord tumors [8–11], (3) intracranial tumors [12–14], and (4) CNS vascular lesions [15–17]. Uses of MEPs continue to expand. More recently MEPs have been used for preemptive assessment of outcome in stroke [18–20] and spinal cord function during thoracoabdominal aneurysm repair [18].

Motor Pathway Blood Supply To understand why MEPs provide essential information for spine surgery, it is necessary to review the blood supply of the spinal cord and understand the relationship between ischemia, electrophysiology, and infarction. A detailed discussion is found in Chap. 37. The spinal cord is supplied by the anterior spinal artery (ASA) and the posterior spinal artery (PSA). Spinal cord motor tracts are primarily supplied by the ASA, a vascular network that supplies the metabolically anterior two-thirds to four-fifths of the anterior cord including the gray matter and anterior horn cells. The sensory tracts are supplied primarily by the PSA, a vascular network that supplies the dorsal columns and a small part of the posterior funiculi. Both

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arteries arise as branches of the vertebral arteries in the brainstem and then descend along the spinal cord providing perforators into the spinal cord. They receive blood from radicular arteries which originate in the aorta. The PSA also receives a relatively luxuriant blood flow from the intercostal arteries while the ASA receives a much more limited blood flow from the radicular arteries off the aorta [21]. The ASA blood supply by spinal cord region: • Cervical region – arising from the cervical or subclavian arteries there are 3 vessels at C3, 5, 7. • Thoracic region – arising from intercostal arteries, aorta or iliac artery there is 1 vessel arising from T2 or 3 and 1 vessel between T7-L4 (aka Artery of Adamkiewicz). The AA provides the blood supply for about 75% of the spinal cord supplied by the ASA, making it essential to anterior spinal cord blood flow [22]. The reduced number of radicular arteries, the increased distance traversed, and increased metabolic demand makes areas of the spinal cord perfused by the ASA more susceptible to hypoperfusion. While axons are quite resistant to ischemia, the anterior cord contains many more cells and synapses which explains the rapid changes seen in MEPs when inadequate perfusion occurs. Direct injury to the vessels is not necessarily the cause of hypoperfusion during the correction of scoliosis but can result from the elongation and narrowing of the AA. Intracranial blood supply to motor areas is also vulnerable. Perforator arteries and the lenticulostriate arteries supply the motor cortex and internal capsule and arise from the middle cerebral artery. These vessels transverse a significant distance and are vulnerable to hypoperfusion with decrease in cerebral perfusion pressure (CPP) (MAP-ICP or CSFP) or disruption of the source vessels (e.g., aneurysm or AVM). The distance and caliber of these vessels creates a watershed area making motor function more vulnerable to hypoperfusion than the ascending sensory tracts [23, 24]. The normal spinal cord and brain will autoregulate blood flow to maintain normal perfusion. Autoregulation occurs over a CPP approximately between 50 and 150 mmHg [22]. If the perfusion pressure falls below this range autoregulation is lost and spinal cord blood flow is directly dependant on perfusion pressure. Hypoperfusion, as measured by a change in evoked activity, can be caused by reductions in

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CPP and oxygen delivery (e.g., anemia, hypovolemia). MEP monitoring provides unique information about the functional status of the anterior spinal cord and internal capsule.

Technical Aspects of MEP Monitoring MEP monitoring for IOM requires transcranial stimulation of the motor cortex by electrical or magnetic means to produce a descending response that traverses the corticospinal tracts and eventually generates a measurable response in the form of muscle activity (compound muscle action potential, CMAP) or a spinal cord synaptic response in the anterior horn cells (Direct wave, D wave) (Fig. 2.1).

Fig. 2.1 Depiction of the neurologic response pathway with motor-evoked potentials. Stimulation of the motor cortex (arrow) results in a response that is propagated through the brain and spinal cord to cause a muscle contraction. The response typically is recorded near the muscle as a compound muscle action potential (CMAP) or EMG. The response can also be recorded over the spinal column as a D wave followed by a series of I waves (used with permission from Jameson and Sloan [35])

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Standard IOM MEPs use electrical current (measured in volts) to stimulate pyramidal cells of the motor cortex resulting in a wave of depolarization that often only activates 4–5% of the corticospinal tract [25]. The motor pathway descends from the motor cortex, crosses the midline in the brainstem, and descends in the ipsilateral anterior funiculi of the spinal cord. Attempts to monitor the motor tracts of the spinal cord have been made by other means. Stimulation of the spinal cord using stimulating electrodes placed into the epidural space (see Chap. 6) or needle electrodes near the lamina of the appropriate spine segment (neurogenic motor-evoked potentials, NMEP) were primarily used before 1995 to bypass the difficulties presented by anesthetic effects on motor cortex but have now largely been abandoned as a monitoring technique. With a spinal cord stimulation technique, it is not possible to determine laterality of the response. In addition, another and perhaps more important reason is the evidence that has indicated that NMEP are not mediated by motor pathways but instead by antidromic conduction in sensory pathways and therefore are not a motor response at all [6, 26]. Today transcranial electrical stimulation is the standard method used to generate an MEP response. Direct cortical or spinal cord stimulation using a strip electrode placed directly on the spinal cord or cerebral cortex to stimulate motor pathways continues to be used to map or identify neural tissue with motor functionality. A detailed treatment of motor mapping techniques is found in Chaps. 7 and 8. Transcranial electrical stimulation consists of usually 3–7 electrical pulses of 100–400 V (up to 1,000 V is possible) through electrodes most commonly placed a few centimeters anterior to the somatosenory electrodes at C3¢-C4¢ (International 10–20 system). The stimulus is most often 0.2 ms in duration but can be varied up to 0.5 ms and the interstimulus interval (ISI) (period between stimuli) likewise can vary between 2 and 4 ms (Table 2.1) [27]. Cork screw scalp electrodes increase surface area and reduce the risk of burns from the high energy stimulus. Manipulation in the number of stimuli, ISI, pulse duration, and strength allow optimization of the stimulus. These changes overcome some of the impediments to propagation such as anesthetic effect on the anterior horn cell synapse, preexisting neuropathy, distance of the motor cortex from the stimuli, reductions in motor neuron function, and age. The time required to obtain a MEP is less than 10 s [28, 29].

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Table 2.1 Effect of varying the interstimulus interval (ISI) and the stimulus pulse duration on the threshold stimulus necessary to obtain a MEP muscle response ISI (ms) Pulse duration (ms) 0.1 ms 0.2 ms 0.5 ms Mean Motor Threshold (mA) 2 158 ± 67 105 ± 33 76 ± 26 3 140 ± 55 97 ± 33 64 ± 20 4 126 ± 56 91 ± 35 61 ± 19 5 170 ± 74 120 ± 45 83 ± 31 Stimulus was applied at C3/C4. All combinations of ISI and pulse duration are significantly different from each other at the p-value of 50 V, increases in number of stimuli required, or significant decreases in amplitude (usually >80%) from the initial responses (without muscle relaxant) are generally considered significant changes [39]. Other groups raise concerns when the complexity (number of peaks) of the waveform simplifies. This indicates the broad range of views on the topic. The degree that changing response amplitudes or their latencies reflect the degree of postoperative neurologic change has not been determined. Certainly, loss of CMAP responses requires notification of the surgeon and anesthesiologist to correct, when possible, the physiologic issues contributing to the MEP change.

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Fig. 2.2 Standard normal MEP response. The CMAP response, a large polyphasic wave, is obtained from the upper extremity traditionally using the abductor policis brevis (APB) and from the lower extremity using tibialis anterior (TA) and abductor hallicus (AH) brevis. Two lower extremity muscle groups are used due to the increased difficulty obtaining a consistant response particularly in adults. Other upper and lower extremity muscles can be used depending on the needs of the specific patient. Obtained from the author’s archive

Application of MEP Monitoring Monitoring during structural spine surgery and spinal cord surgery is customarily multimodal and includes somatosensory evoked potentials (SSEP), MEPs, and electromyography (EMG, free running and stimulated). MEP monitoring is considered essential whenever spinal cord parenchyma is at risk. Thus, MEP monitoring is usually performed when the surgery includes the spinal cord and may be performed during spine surgery from C1 to sacrum since the location of the spinal cord varies by age and anatomic factors (e.g., tethered cord) [40, 41]. At risk situations include any surgery where compromise of spinal cord perfusion or direct injury to motor tracks or nerve roots could occur. Consensus opinion is that the evidence supports MEP monitoring in the following specific spine procedures • Spinal deformities with scoliosis greater than 45° rotation. • Congenital spine anomalies. • Resections of intramedullary and extramedullary tumors. – Extensive anterior and/or posterior decompressions in spinal stenosis with myelopathy. – Functional disturbance of the cauda equina and/or individual nerve roots.

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However the evidence does not meet the level 1 standard (large randomized, placebo controlled, double blind studies). The evidence is based on large case series and meta analysis (level 2, 3 evidence) where MEP changes predicted immediate postsurgical neurological findings [10, 42–44]. MEP monitoring can be challenging in some patient populations. It often requires an alteration in anesthetic management to obtain “readable” waveforms. This may require negotiations with the anesthesiologist and surgeon. Many of the older prospective series used SSEPs and EMG but only rarely MEPs due to this issue. In one study of 1,055 adult patients undergoing cervical spine surgery between 2000 and 2005, MEP studies were attempted and obtained in only 26 of 1,055 patients. These were the highest risk patients for spinal cord injury. When used, MEP had 100% sensitivity, 96% specificity, and a positive predictive value of 96% [45]. In smaller studies, adults with cervical myelopathy had about a 12% incidence of MEP only alerts (no EMG or SEP changes); these alerts were usually followed by resolution after alterations in anesthetic and surgical management occurred. Nonetheless, the authors believed that the MEP monitoring provided 100% sensitivity and 90% specificity [46, 47]. MEP changes are relatively infrequent. One group reported that in 172 pediatric spinal deformity corrective procedures, there were 15 intraoperative MEP alerts; all of which resolved with changes in management. None of the patients (MEP-alert and MEP-unchanged patients) had new neurological deficits. This group concluded that MEP alone was adequate for spinal deformity surgery with a MEP monitoring sensitivity of 1.0 and a specificity of 0.97 [7]. The largest (1,121 procedures) multimodality IOM study in idiopathic scoliosis patients had 38 alerts with 17 alerts involving only MEP signal changes and the remainder (21) involving both SSEP and MEP changes. Patients with persistent MEP changes all had immediate postoperative motor deficits. SSEP changes when present lagged significantly behind the MEP changes and often did not predict outcome [48, 49]. Consensus opinion supports and new studies strongly suggest that the use of intraoperative spinal cord motor mapping improves longterm motor function in intramedullary spinal cord tumor resection [8–10, 50, 51]. The MEP is the only reliable monitor of motor pathways and is an earlier predictor of impending damage to the cord than the SSEP due to the more precarious nature of the blood supply. In an anterior approach to an intramedullary spinal cord tumor resection,

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focal injury to the anterior spinal vasculature or motor tracts are often not detected or detected many minutes after injury with SSEP monitoring alone [4, 16, 52, 53]. MEP monitoring and spinal cord stimulation has been successfully used to define the “edge” of the intramedullary spinal tumor; this maximizes the resection while minimizing motor impairment. During intramedullary spinal tumor mapping, the D wave as well as the CMAP may allow better correlation with motor outcome [54]. Direct MEP cortical stimulation is used to map motor function during intracranial procedures and to delineate the demarcation between tumor and functional tissue. This technique may replace or augment awake craniotomy procedures in the supratentorial area when eloquent areas (e.g., speech, vision) or motor only pathways (e.g., internal capsule, motor cortex, premotor cortex) are at risk. The technique involves placing a stimulator on various portions of the cortex or placing a strip electrodes under the dura. These techniques use the same pattern of stimulation but much lower stimulus strength (maximum 2–10 mA vs. 100–400 V) [53]. Vascular injury is possible with the placement of the strip electrodes. Recent large case reports have documented that MEP monitoring assists in delineating the edge between tumor cells and functioning neural tissue. A recent report on 404 patients with low grade glioma lesions that involved motor areas illustrates the point. The group reported that MEP mapping substantially reduced number and severity of permanent motor deficits while increasing the number of total resections. While there were 100 motor deficits at wakeup, they proved to be temporary since only 4 (1%) remained at 3 months after surgery. Total or subtotal tumor resection was done in only 11% of patients prior to motor mapping but 69.8% after motor mapping was initiated [55]. A number of other groups have published similar reports and noted that the long-term outcome is significantly improved by more extensive tumor resection in both children and adults for all supratentorial tumors [56, 57]. Neurologic injury to the posterior fossa can have devastating consequences. Motor mapping is an effective way to identify both tumor margins and safe entry zones into the floor of the fourth ventricle. Stimulation can be either transcranial or more frequently direct brainstem stimulation [58]. Intracranial aneurysms and arteriovenous malformations can result in areas of hypoperfusion during the endovascular embolization, resection, or temporary and permanent clipping. Since MEPs

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rapidly change in response to alterations in perfusion to motor areas, MEPs will identify hypoperfusion in motor areas and adjacent perfused areas. Fortunately, identification of change followed by therapeutic intervention appears to substantially reduce permanent injury. Two large studies with 108 and 129 supratentorial aneurysm clippings found that in cases where no MEP changes occurred, none of the patients had deficits. One of these studies confirmed adequate flow with microvascular Doppler ultrasonography. Both studies found between 13 and 33% of patients had reversible MEP changes; these patients had no neurologic changes immediately after the procedure or had only transient neurologic changes from which they fully recovered. Patients with permanent MEP change (about 20%), all had permanent neurologic deficits, some quite severe [15, 16, 59–61]. Similar findings are published in other small case series reports. The neurosurgical community has reported improved outcome during aneurysm occlusion on basilar, vertebral, and middle cerebral artery aneurysms. All reports have found MEP changes occur more rapidly than SSEP changes and better reflect ultimate outcome when the involved vessels provide perfusion to motor pathways. SSEP usage is addressed in Chap. 1.

Contribution of Anesthesiology to Effective MEP Monitoring Without the cooperation and support of the anesthesia care provider, the detection of MEP response changes and effective treatment is not possible. In addition to the surgical events, physiological management and anesthetic drug choices will impact neural function and MEP responses (see Chap. 15). All are managed by the anesthesiologist and stress the importance of the team effort in the operating room (i.e., surgeon, anesthesiologist, and IOM team). Hypotension is of particular interest since deliberate hypotension to reduce blood loss was once considered a management technique; particularly in the idiopathic scoliosis procedures and during aneurysm clipping. There is a growing appreciation that the presumed lower limit of autoregulation is not always adequate for tissues undergoing surgical stress [62]. Mean BP that is adequate for a young adult patient may not be adequate for an older adult with many coexisting diseases. Hence, increasing perfusion pressure

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Fig. 2.3 Recovery of MEP response after intraoperative loss. During a posterior cervical fusion of C5 to T4 the patient abruptly lost MEP responses in both lower extremities (14:13:15). After BP elevation and steroid administration, MEP response returned only on the left (18:35:53). Patient had weakness on the left, which resolved over 2 weeks. On the right, patient had a dense hemiparesis that had not changed 3 months after surgery (source author’s archive)

effectively treats many impending hypoperfusion injuries. The acceptable lower limit for hemoglobin has also come under question. Anemia can be compensated for only within the limits of the patient’s physiologic ability to increase cardiac output and local tissue perfusion. The acceptable lower limit of blood pressure and hemoglobin is unlikely to be the same for all situations and is poorly predictable. Hence, MEP monitoring allows a functional assessment of adequate blood pressure and oxygen carrying capacity. When neurological monitoring signals deteriorate, increasing the systemic blood pressure to the patient’s preoperative value is the most common and most effective response the anesthesia care team can provide (Fig. 2.3).

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Transfusion is also an effective therapeutic intervention when appropriate [63]. Maintenance of “normal” physiologic conditions within the brain and spinal cord can be difficult but results in the ideal monitoring conditions and the best neurologic outcomes. A recent anesthetic development deserves special comment, which is the impact of dexmedetomidine on MEP monitoring; particularly during pediatric spine procedures. Propofol syndrome [64] is diagnosed primarily pediatric patients. Thus, reductions in the use of propofol for monitoring is especially desirable. Literature reports regarding the use of dexmedetomidine range from no negative effect to loss of effective MEP monitoring [65–71]. Two recent carefully performed studies found a clinically and statistically significant attenuation in the amplitudes of transcranial electric MEPs when the targeted plasma concentrations exceeded 0.6–0.8 ng/mL [66, 70]. Dexmedetomidine in low plasma concentrations appears to reduce the need for other anesthetic agents but must be used with some caution due to its long context sensitive half life.

Risk of MEP Monitoring MEP monitoring is not without risk. The Federal Drug Administration has specified relative MEP contraindications. The most common concern was direct cortical thermal injury (kindling) but over the last 15 years only two cases of cortical thermal injury have been reported [53]. In a 2002 survey of the literature, published complications include: tongue laceration (n = 29), cardiac arrhythmia (n = 5), scalp burn at the site of stimulating electrodes (n = 2), jaw fracture (n = 1) and awareness (n = 1) [72]. Tongue laceration can be ameliorated by placing a bite block between both molars. Notably no new-onset seizures, epidural hematomas or infections from epidural electrodes or movement injuries (e.g., surgical, joint dislocation), neuropsychiatric disease, headaches, and endocrine abnormalities have been reported. Common relative MEP contraindications include epilepsy, cortex lesion, skull defects, high intracranial pressure, intracranial apparatus (electrodes, vascular clips, and shunts), cardiac pacemakers, or other implanted pumps. A well recognized and relatively more common side effect is sore muscles [53]. Needle placement will lead to bleeding and bruising at the insertion site. Infection is always possible. The prevalence of even minor problems is astonishingly low [73].

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The movement that can occur with MEP utilization requires close coordination with the surgeon prior to eliciting a MEP. The current multipulse stimulation has reduced movement and has made testing possible without disrupting surgical activity.

Conclusion Clearly the goal of intraoperative monitoring is to provide the greatest degree of assistance to the operative team for optimal intraoperative decision making. The current literature suggests MEP monitoring provides excellent specificity and sensitivity whenever motor tracts are involved. As such the real question for consideration is not whether MEP monitoring makes the other techniques unnecessary but rather which of the techniques available should be used to complement MEP monitoring in individual patients.

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