The neuromonitoring Technician: Friend or Foe?

A couple of days ago I took over a posterior lumbar interbody fusion from L2 to S1.  The case had started at 7:45 am that morning, and I came into the room at 3pm.  The report I received from the CRNA was that the patient had been stable for the entire case until just recently when the blood pressure began to sag.  The CRNA had already checked a Hgb and ordered two units of blood which were on there way.  It was clear from a brief glance at the surgical field that this case had a ways to go and there was continual bleeding from the field.  A cell saver machine was working and the patient had received about 300 mL from the cell saver machine already.  I checked the UO and it was low and appeared to be concentrated.  The patient was being maintained on Desflurane at 4% with a dexmedetomidine infusion at about 0.15 mcg/kg/hr which had been discontinued due to low blood pressure.  The patient had a history of COPD and was 68 years old, but other wise had no significant medical history that would impact his anesthetic.  Neuromonitoring consisted of SSEPS, MEPS and running EMGS.  No paralysis was being used. 

The patient had already received 4.5 L of crystalloid and 1 L of Hespan.  Due to the prolonged case and the prone position, this patient was at some risk for perioperative visual loss (POVL).  An ASA task force on perioperative blindness (consisting of 12 ASA members) recently published guidelines to help clinicians better deal with this potential outcome.  The task force culled the most recent literature to make recommendations.  They identified several preoperative risk factors which include: hypertension, glaucoma, carotid artery disease, smoking, obesity and diabetes.  This patient was mildly obese and had a prolonged smoking history having ceased just 6 weeks prior to surgery.  The task force also identified surgery lasting longer than 6.5 hours, preoperative anemia, large volume blood loss (i.e. 44% of blood volume) and also prolonged procedures combined with large blood loss cases.  The task force also identified several intraoperative events that are linked to POVL.  These included intraoperative hypotension, anemia, hypovolemia, hypoxia, hemodilution, edem of face and use of vasopressors, infusion of large amounts of fluid, pressure on the eyes, prone positioning (or head down), and increased venous pressure. This case included several of the above risk factors including long duration procedure with large volume fluid ressuscitation, intraoperative and preoperative anemia.  There was ongoing blood loss and it wasn't clear the total volume that would ultimately be lost during the procedure.

At this point all clinical indicators were that the patient was hypovolemic due to blood loss.  I focused on giving blood and volume while attempting to avoid phenylephrine as much as possible. During this time the Neuromonitor technician notified the surgeon that MEPs on the left lower leg had decreased significantly.  The blood pressure was low (MAP of 60s) at this time so I continued to work on increasing this with rapid blood transfusion (3 units) and crystalloid. (2L).  After this volume the blood pressure improved slightly but began sagging again.  It was clear that the patient was still hypovolemic.  I drew more labs and started pumping in more fluid.  During this time the neuromonitoring technician told the surgeon that we needed to put the patient on 3% Desflurane and start a propofol infusion.  I immediately told the neuromonitoring tech I would not be starting a propofol infusion under any circumstances at this point.

He disagreed with me and began telling me why I was wrong to believe that we shouldn't do as he suggested.  He indicated that I was derelict in my duties because I was not following the established protocol for neuromonitoring and that if he should decide, he could write me up and bring me before peer review for my refusal to follow the protocol.

A brief discussion of the current recommendations for anesthetic technique during neuromonitoring is warranted.  Also, I would recommend looking over previous posts on this topic. 1) MEPs with dexmedetomidine and 2) MEPS in AIDCF.

In a review article on intraoperative monitoring (IOM), it states, "These findings support the current position of propofol being the standard anesthetic approach for IOM recording of MEPs." [1].  "These findings" in the above quote refers to a study done in 1998 by Pechstein et al.[2].  In fact, this study is the  basis for the recommendations made and thus serves as the basis for propofol being the automatic "go to" anesthetic for IOM with MEPS during spine surgery.  It should be noted that in the study by Pechstein et al. there were two study groups of 17 (group A) and 13 (group B) patients.  Group A received TIVA (total intravenous anesthesia) with propofol and alfentanil.  In Group B, patients received Nitrous oxide (66%), isoflurane and fentanyl.  MEPS could be recorded in 88% vs. 8% of group A patients vs. Group B patients.  Therefore, this small study was able to show that mixing nitrous oxide with isoflurane is likely to make it difficult to record MEPs.  It certainly does not allow us to conclude that propofol is the gold standard anesthetic for IOM.  It has been well demonstrated that nitrous oxide can also suppress completely MEPs when given with propofol as well [4]. Another study found that both 50% nitrous or doubling the propofol dose both could decrease the amplitude of tc MEP [5].  Zentner [6] found that using 66% nitrous oxide reduced the recorded MEPS to 6% of baseline.  Todd Sloan, in a review of motor evoked potential monitoring stated, "when compared at equipotent anesthetic concentrations, nitrous oxide produces more profound changes in myogenic tcMEP than any other inhalational anesthetic agent.
 On the other hand, more recent work, has found that desflurane can be utilized effectively when IOM is required. Lo et al. successfully measured MEPS in 9/10 patients undergoing scoliosis surgery with Desflurane (mean 3.3%) + 60% nitrous oxide [3].   In fact, Desflurane + nitrous oxide was compared to a propofol narcotic technique when measuring MEPS [7].  They compared 20 consecutive patients randomly  assigned to one of the two groups (10 in each group).  The Desflurane group received a mean ET concentration of 3.4% + 66% nitrous oxide.  MEPS were adequate in all 20 cases. In fact, prior to instrumentation, amplitudes were higher in the Desflurane group (85 mV vs. 59.1 mV).    These studies (done with nitrous) combined with the evidence that nitrous oxide is a potent inhibitor of MEPS recording, supports the technique of using Desflurane without nitrous oxide with minor effect on MEPS.
Published results suggest that to accomplish the 1 MAC equivalent with propofol, it is required to achieve plasma levels of 6 mcg/mL.  This requires an infusion of approximately 200 mcg/kg/min.  Other authors have already shown that MEPS are reduced when propofol is given at much lower dosages than this. Therefore, on a dose equivalent basis, propofol's advantage over Desflurane is likely very small.  Additionally, most studies using propofol for MEPS recording used infusion rates of around 100 mcg/kg/min.
       Propofol does indeed provide for easy recording of MEPS, and in particular, with pulti pulse stimulation, seems to allow very good signals.  However, when dealing with a hypovolemic patient with multiple risk factors for POVL, adding propofol to the equation in to improve MEPS is risky.  Furthermore, as propofol will likely worsen MAP, in reality, the signals are likely not to improve or worsen as low MAP is particularly inhibitory to the recording of MEPS.
       In reality, the key is to obtain good baseline readings, and then maintain a steady anesthetic state.  Whether propofol or desflurane is used is less important than keeping the baseline anesthetic stable. If during a procedure, attenuation of the signal occurs in one part of the body, it is important to find the source of this inhibition.  Any changes to the anesthetic would be important to note. However, anesthetics will result in global signal reduction, not focal.  Other causes of global signal reduction include, severe anemia, hypotension, and hypoxia.  Focal reduction of signal is most likely related to focal ischemia or mechanical trauma..  If this can be ruled out, then lead placement or other mechanical issues related to the measuring process such as impedance should be ruled out first.  In the above presented case, the patient had significant ongoing bleeding with decreased blood pressure.  He had significant anemia (nadir of about 7 gm/dL) and his blood pressure was suppressed (MAP of 58 to 62 mmHg).   I was running desflurane at a steady concentration of 4% which had not changed during the case.  Dexmedetomine was being titrated to effect and had been decreased due to the patients decreased blood pressure.  The technician's request to switch to 3% desflurane + a propofol infusion was not logical for a number of reasons.  First, as mentioned, a stable anesthetic level will aid in the intepretation of MEPS.  Decreasing the desflurane and adding propofol (he didn't specify what dose he wanted) would disrupt this.   Propofol also suppresses the MEPS to a degree not much less than desflurane if you consider the dose equivalent amount.  Another important factor is the risk for sudden patient movement.   As referenced in a previous post, patients are far more likely to move suddenly during propofol anesthesia than when receiving volatile anesthetics.  Of all the potent inhaled anesthetics, some evidence suggests Desflurane is the most effective in the prevention of patient movement [8].  Therefore, despite that propofol is the best from a neuromonitoring stand point, it is not that much better than desflurane and has the disadvantages of not effectively inhibiting patient movement, inability to monitor real time plasma concentration levels, and causing profound hypotension in anemic hypovolemic patients.  There is one other major disadvantage of propofol.  In the setting of spinal surgery with instrumentation, the whole goal with neuromonitoring is to avoid causing injury to the spinal cord or roots.  The injury is often ischemic in nature although mechanical trauma is also a possibility.  The potent inhalational agents have the beneficial property of anesthetic preconditioning which protects organs against ischemic reperfusion damage. This would be pertinent not only for spinal cord/nerve root ischemic protection, but also, retinal  ischemic protection.

So, if propofol is a poor choice in this setting, what are some other options.  Todd Sloan reports in his review on MEPS that in addition to use a mulit pulse technique, the interstimulus interval (ISI) made need to be varied until the optimal response is found.  For example, he states that at low concentrations of Isoflurane (i.e. 0.2%) a wide ISI  (i.e. 2-5 ms).  However, at higher concentrations (i.e. 0.4-0.6%), a wider ISI is better (i.e. 4-5 ms). At even higher concentrations (1%), the most effective ISI was 1 ms.  In short, its likely best to optimize the ISI to the concentration early on in the case.  Other considerations when its difficult to record MEPS are other anesthetics.  Ketamine and Etomidate are both ideal in that do not effect MEPS to any appreciable degree and also increase SSEP recordings.  Both of these also have positive hemodynamic profiles. Unfortunately, etomidate as an infusion suppresses adrenal function and, therefore, has fallen out of favor.  Ketamine at appropriate dosages (0.25 mg/kg/hr to 0.5 mg/kg/hr), is less likely to cause the negative psychological side effects (hallucinations). Several studies have found ketamine to have a protective analgesia effect in general surgical cases and one study in particular found that intraoperative ketamine reduces post operative morphine consumption in patients on chronic opioid pain therapy undergoing spinal surgery [9].  Todd Sloan reports in a review of IOM that in patients where MEPS are "very sensitive" to inhalational agents and neuromuscular blockers, he uses propofol and then adds ketamine if this isn't sufficient.  His typical protocol calls for:  Mix ketamine into propofol 50 cc's at 2mg ketamine to 1 cc (10mg/cc) Propofol.  He then titrates down on the ketamine concentration for each subsequent 50 cc syringe infused over the duration of the case; i.e. 1st syringe 2mg Ketamine/cc Propofol, 2nd syrine 1.5 mg Ketamine/cc Propofol, 3rd syringe; 1mg Ketamine/cc Propofol infused. etc.  The lasty syringe contains only Propofol.  Of course, Propofol can be avoided altogether in many cases.

In conclusion; IOM is becoming very prevalent and in particular, Motor Evoked Potentials are ever more common.  The anesthesiologist needs to be aware of those things that will affect the IOM and how to adjust the anesthetic so that IOM can be successful while considering the other important aspects of the anesthetic: Immobility, Anesthesia, and Amnesia.





1. Pajewski TN, Arlet V, Phillips LH.  Current approach on spinal cord monitoring: the point of view of the neurologist, the anesthesiologist and the spine surgeon.  Eur Spine J. 2007:18. 115-129.

2.  Pechstein U et al.  Isoflurane plus nitrous oxide vs. propofol for recording of motor evoked potentials after high frequency repetitive electrical stimulation.  Electroencephalogr Clin Neurophysiol. 1998: 108(2): 175-81.

3. Lo YL, Dan YF et al.  Intraoperative monitoring in scoliosis surgery with multi-pulse cortical stimuli and desflurane anesthesia.  Spinal Cord. 2004;42: 342-5.

4.  Kunisawa T et al.  A comparison of the absolute amplitude of motor evoked potentials among groups of patients with various concentrations of nitrous oxide.  J Anesth. 2004;18:181-4.
5.  van Dongen EP. et al.  The influence of nitrous oxide to supplement fentanyl/low-dose propofol anesthesia on trancranial myogenic motor-evoked potentials during thoracic aortic surgery.  J cardiothorac Vasc Anesth.  1999; 13:30-4.
6.  Zentner J et al. Influence of anesthetics-nitrous oxide in particular-on electromyogrphaic response by tc electrical stimulation of the cortex.  Neurosurgery. 1989; 24:253-6.
7.  Lo YL et al. Intraoperative motor-evoked potential monitoring in scoliosis surgery: comparison of desflurane/nitrous oxide with propofol total intraenous anesthetic regimens.  J Neurosurg Anesthesiol. 2006; 18:211-4.
8.  Wulf H. et al. Neuromuscular blocking effects of rocuronium during desflurane, isoflurane, and sevoflurane anaesthesia.  Can J Anaesth. 1998;45: 526-32.
9. Loftus R et al.  Intraoperative Ketamine reduces Perioperative Opiate Consumption in Opiate-Dependent Patients with Chronic Back Pain Undergoing Back Surgery. Anesthesiology. 2010;113: 639-46.

Neuromonitoring mishap for ACDIF

A female patient with neck pain radiating to her arms comes for a two level anterior decompression and instrumentation for fusion of C5-6 C6-7. She has a history of Asthma for which she has been hospitalized in the recent past. She has no other relevant PMH and has taken several puffs from her inhaler prior to proceeding to the operating room. Induction is smooth and intubation without incident. Neuromonitoring utilizing somatosensory evoked potentials (SSEPs) and motor evoked potentials (MEPs) will be used for the case to ensure that the anterior and posterior tracts of the spinal cord are not compromised. Anesthesia is maintained with desflurane at 5%, fentanyl with intermittent boluses, and an infusion of dexmedotomidine (Precedex) is begun at a rate of 0.4 mcg/kg/hr. No paralysis is used. The patient's vital signs remained stable throughout case.




After the instrumention is placed and the surgeon is ready to close, the technicion notifies the surgeon that while the SSEPs remain at baseline, the MEPs have declined dramatically, although still present and otherwise normal in appearance. Based on this information from the neuromonitoring tech, the surgeon removes the some of the hardware. This action provides no improvement in the MEPs. Within 30 minutes, MEPS improve back toward baseline. At the time MEPs decreased desflurane was decreased to aproximately 3%, and vital signs were carefully monitored.

Currently, motor evoked potentials (MEPs) and somatosensory evoked potentials (SSEPs) have become routine for some types of spinal surgery. When used together, they have been shown to provide more sensitivity in predicting negative post operative neurologic outcomes. The corticospinal tract is located anteriorly in the spinal cord which is served by the anterior spinal artery, while the dorsal columns relay sensory information to the brain and are served by two posterior spinal arteries. Because SSEPs only monitor the posterior half of the spinal cord, they are less sensitive, and as a result, negative neurologic outcomes have occurred despite no changes in SSEPs intraoperatively.

In monitoring MEPs amplitude and latency are both visualized. Ischemia and general anesthetics principally effect the measured amplitude, whereas hypothermia tends to have a greater affect on latency. In addition to anesthetics, hypoxia, severe anemia (Hct around 15%), decreased blood flow (systemic hypotension, distraction from instrumentation, severe hypocarbia, increased ICP etc.) will also dampen the measured voltage (amplitude) of MEPs. Furthermore, in some cases dramatic metabolic conditions like hypoglycemia, and marked hyper/hyponatremia or kalemia can affect the amplitude as well. Thus, changes associated from a hypothermic patient can be easily distinguished in most cases from those occuring from other causes (i.e. inhalational anesthetics, ischemia).

In clinical practice, motor evoked potentials can be evoked by either direct stimulation of the motor cortex via electrodes placed in the scalp (most common) or by magnetic stimulation. Because magnetic stimulation is difficult in the OR and is far more susceptible to general anesthetics, it is rarely used. Furthermore, stimulation of the motor cortex can be done by a single pulse, or can be accomplished by multiple pusles which have been shown to overcome the inhibitory effects of anesthetics at the synaptic clefts by creating a summation of excitatory postsynaptic potentials (EPSPs). Presently, a train of 3 to 6 pulses, with an interstimulus interval of 2 ms (500 hz) is recommended for use for transcranial electrical stimulation under GA. Stimulus intensity is typically between 100 to 800 V. Upon stimulating the motor cortex via the anode (positive) electrode a direct (or D) wave is elicited which is nearly entirely resistant to anesthetics since it has not passed through any synapses. As the cortical neurons stimulate in turn various subcortical internuncial neurons, indirect (or I) waves are generated which then summate at the alpha motor neuron for elicitation of a motor response. It is these 'I' waves that are decreased in amplitude by the general anesthetics. In the surgical setting, myogenic responses are most commonly measured since they capture information about the entire corticospinsal tract and the anterior horn neurons leading to the motor neuron and neuromuscular junction. Furthermore, myogenic responses can be measured on each side giving information about which side of the patient is depressed. Lastly, myogenic responses (in contrast to responses measured in the epidural space) require relatively noninvasive placement of electrodes into the various muscle groups (usually tibialis anterior, abductor hallucis, flexar carpi radialis, abductor pollicus, etc.).


While the gold standard in the measurement of MEPs is considered to be a TIVA technique using propofol (+/-) nitrous oxide + remifentanil; this is certainly not the only method available. While it is true that propofol as a constant infusion causes less inhibition of motor evoked potentials in most studies, it still is inhibitory and boluses can cause severe and lasting reductions of the measured amplitudes as shown by Kalkman et al. Latency does not seem to be affected by the general anesthetics. A common cited study to support the use of propofol was done by Pelosi et al. comparing a regimen using a propofol infusion + nitrous oxide to isoflurane (0.78%) + nitrous oxide. MEPs were obtained in 97% of those in the propofol group vs. only 61% in the isoflurance group. Furthermore, it was found that the isoflurane group had smaller amplitudes and more variability of the baseline. Variability is indeed one of the buggaboos of MEP. This is a result of a myriad of factors affecting the internal milieu in which the many neurons and synapses are operating. This is a critical principal to understand. Pathologic decrements tend to overestimate the degreee of corticospinal system compromise, therefore, only disappearance or marked attenuation amounting to virtual desappearance of a previously consistent muscle MEP is genereally accepted as significant. In the above presented case, the MEP was still measurable, and in fact, did not have low volatages. For this reason, cause for concern should have been lessened and an alternative source should have been the primary consideration.

At present, most centers utilizing motor evoked potentials in addition to SSEPs, utilize a multi pulsed direct electrical stimulation method of the motor cortex. Consequently, an inhalational technique is often successful in allowing MEPs to be measured. Of the inhalational anesthetics, desflurane is best suited because it allows rapid changes in anesthetic depth if MEP amplitude should be attenuated during the case. Using multipulsed transcranial stimulation, Lo et al. showed that desflurane at 3.4% + nitrous 66% was not worse than a TIVA technique using propofol and fentanyl. Given that nitrous reduces MEPs in a dose dependent fashion, as shown by Pechstein U et al. avoiding nitrous would improve the results found above by Lo YL et al. Avoiding nitrous oxide allows one to utilize higher desflurane concentrations. This is beneficial in clinical practice because nitrous oxide has large effects on SSEPs.







There are two intravenous anesthetics that do not cause any decrement (and perhaps a slight increase) in amplitude: Etomidate and Ketamine. Therefore, in patients that have pre existing neurologic deficits where the measurment of MEPs is anticipated to be difficult, utilizing etomidate and ketamine may be useful.







Because most MEPs are measuring the compound action potential at a target muscle, neuromuscular blockade must be done with care. Some surgeons prefer a degree of neuromuscular blockade to avoid patient movement during surgery. The downside to this is a proportionate decrement in the response measured. Studies and experience suggest that if neuromuscular blockade is going to be undertaken, maitaining a constant blockade at T1 at between 5 to 20% of baseline is required. This corresponds to a TOF of two twitches out of four being present. Sloan reports in his review on MEPs that at a T1 of 20% of baseline results in a measured MEP reduction of 50 to 60%.







So how does one proceed when a patient presents who is going to undergo a surgical procedure on the spine where MEPs are going to be measured. First, it should be noted that SSEPs are also going to be measured. This must be considered as well. SSEPs are very sensitive to nitrous oxide and when nitrous oxide is added to halogenated agents, the suppression of SSEPs is additive. Therefore, avoidance of nitrous in order to enhance SSEPs is likely beneficial.






A patient coming to surgery as this patient for a cervical decompression and instrumentation for stabilization who does not have ongoing weakness and is otherwise neurologically intact who will be monitored with MEPs and SSEPs, probably would benefit from an inhalational technique using desflurane and fentanyl + ketamine as small bolus (subanesthetic) doses Q 30 min during surgery with minimal neuromuscular blocking agents as an infusion. Maintenance of at least 2 twitches is necessary if neuromuscular blockade is used and an infusion is recommended.






Why not TIVA?






TIVA is certainly an acceptable option but does have some negative aspects that make it an alternative regimen. First, propofol, the typical maintenance anesthetic for TIVA does reduce MEPs, although slightly less than inhalational agents. Second, for a prolonged case such as this, using a propofol infusion will increases costs in comparison to low flow (closed circuit) desflurane at around 3.5 to 4%. Third, for a two level fusion this surgery lasted between 2 to 3 hours, and consequently, a delayed wake up is a possibility unless BIS monitoring is utilized which increases cost even more. Furthermore, the MACawake for potent inhalational agents is about 0.3 to 0.4 MAC whereas it is 0.2 MAC for propofol. This means that in order for patients to respond after a propofol anesthetic, it must be cleared to a far greater degree from the body before the patient will respond. This, in theory, could delay any neurologic exam attempted immediately after surgery. Fourth, patients are far more likely to move unintentionally during a propofol infusion for anesthesia compared to those receiving a potent inhalational agent (40% movment w/ propofol vs <10%).>

Why fentanyl and not remifentanil?

First, remifentanil is more costly than fentanyl. Secondly, there is added effort and time required for set up of an additional infusion pump and tubing, plus preparation. Thirdly, remifentanil (more than other opioids) has been associated with acute opioid tolerance/hyperalgesia.(2,3, 4,5).

Why not utilize nitrous oxide?

First, Nitrous oxide is associated with PONV in high risk patients. (6,7) In this case, the modified Apfel score is 3 (out of a total of 4 possible), giving her a post operative risk of PONV of 60% according to Apfel, which I would consider to be high risk. Nitrous is best avoided for this reason alone. Second, many investigators have demonstrated that nitrous in addition to attenuating SSEPs significantly attenuates MEPs. Kunisawa used a TCES technique utiziling a train-of-five stimulus to elicit myogenic responses in patients given a propofol infusion alone or with 50% nitrous or 66% nitrous. The patients given either 50% or 66% nitrous had equally attenuated MEP amplitude (from 4 mV down to 1 mV). (8) Thirdly, Nitrous is not known to effectively produce effective preconditioning as has desflurane. In these cases where the spinal cord is at sufficient risk that MEPs have been deemed necessary to prevent a deficit which is ischemic in nature, avoiding nitrous and adding an inhalational agent in its place (MACS are additive), could make sense.
Why add ketamine?

Ketamine is your friend when it comes to both SSEPs and MEPs. In multiple studies ketmaine has been shown to not have an effect on MEPs at all. In fact, Kalkman et al. (9) showed that using magnetic MEPs 1 mg/kg of ketamine did not cause significant alterations in volunteers. This significant in that MEPs are reduced to virtually zero in the presence of inhalational or propofol when using a magnet as the source of stimulation. Ketamine is an NMDA inhibitor. This is important in that the NMDA receptor in the spinal column has been shown to mediate post surgical chronic pain syndromes, wind up, post surgical allondynia, and post surgical hyperalgesia. Furthermore, Mao in a review of the NMDA receptor and opioids notes that opioids can induce tolerance and hyperalgesia by themselves and that this is mediated by the NMDA receptor. Ketamine, however, can result in significant psychological affects (i.e. hallucinations) which is more common in the elderly or in those with organic brain disease. By utiziling doses of less than 0.5 mg/kg every 30 min. these side effects are minimized while preserving ketamines beneficial attributes.

Does dexmedetomidine have a role when monitoring motor evoked potentials?

Dexmedetomidine can be very useful in many patients by inhibiting sympathetic outflow from the CNS which is almost always desirable in healthy patients undergoing routine surgery. Furthermore, it has a limited inhibitory effect on myogenic motor evoked potentials per recent studies. (10) Titrating dexmedetomidine to blood pressure is being utilized more frequently intraoperatively in many types of cases as it is known that alpha one receptors modulate hyperalgesia, and as dexmedetomidine can reduce MAC for inhalational agents. Unfortunately, this is an expensive agent. Nevertheless, in cases where MEP measurements are necessary and a quick wakeup is important, dexmedetomidine is an ideal adjuvant in that it does not affect MEPs at dosages of 0.4mcg/kg/hr as shown in the study cited above, it allows a rapid patient wake up at the end of the case, and provides additional analgesia reducing the dosage of narcotics necessary potentially preventing acute opioid induced hyperalgesia.
In conclusion, the approach to any patient who will require neuromonitoring should be balanced against the patient's medical status and the needs of the neuromonitoring technician. In most patients who have no preoperative neurological deficits, a standard anesthetic (desflurane + short acting narcotic + ketamine) is ideal. However, a back up plan should always be available in case there is difficulty in measuring MEPs. In this case, decreasing the inhalational agent and using a low dose propofol infusion + dexmedotomidine and ketamine will be beneficial.

1. Tang J, white PF, Wender RH et al. Fast-Track office-based anesthesia: A comparison of propofol vs. desflurane with antiemetic prophylaxis in spontaneously breathing patients. Anesth Analg 2001;92:95-9.

2. Guignard B, Bossard AE, Coste C, et al. Acute opioid tolerance: intraoperative remifentanil increases postoperative pain and morphine requirement. Anesthesiology 2000; 93: 409–17.

3. Vinik HR, Kissin I. Rapid development of tolerance to analgesia during remifentanil infusion in humans. Anesth Analg 1998; 86: 1307–11.

4. Luginbuhl M, Gerber A, Schnider T, Petersen S, Arendt-Nielsen, and Curatolo. Modulation of Remifentanil-induced Analgesia, Hyperalgesia, and Tolerance by small-Dose Ketamine in humans. Anesth Analg 2003;96:726-32.

5. Joly V, Richebe P, Guignard B, Fletcher D, et al. Remifentanil-induced postoperative hyperalgesia and its prevention with small-dose ketamine. Anesthesiology 2005 Jul; 103: 147-55.

6. See Enigma trial

7. Apfel CC, Korttila K, Abdalla M, Kerger H, Turan A, Vedder I, Zernak C, Danner K, Jokela R, Pocock SJ, Trenkler S, Kredel M, Biedler A, Sessler DI, Roewer N. A factorial Trial of six interventions for the prevention of postoperative Nauesea and vomiting. NEJM 350:2441.

8. Kunisawa T, Nagata O, et al. A comparison of the absolute amplitude of motor evoked potentials among groups of patients with various concentrations of nitrous oxide. J Anesthesia 2004:18:181-4.

9. Kalkman CJ, Drummond JC, Patel PM, Sano T, Chesnut RM. Effects of dreoperidol, pentobarbital, and ketamine on myogenic trancransial magnetic motor-evoked responses in humans. Neruosurgery 1994;35:1066-71.

10. Motor and Somatosensory Evoked Potentials Are Well Maintained in Patients Given Dexmedetomidine During Spine Surgery. Survey of Anesthesiology: June 2009;53:136-7.

11. Bala E, Sessler D, Nair D, McLain R, Dalton JE, Farag E. Motor and Sensory evoked potentials are well maintained in patients given dexmedetomidine during spine surgery. Anesthesiology 2008; 109:417.