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 add ketamine?
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.