While being stuck for ideas for a topic to write about from this blog, I sought some inspiration from the theatre team I was about to assist, to which the anaesthetist replied, “I’d love to know some real stats on anaesthetics and electrical potentials”, so here we go.

There is a long-standing love-hate relationship between anaesthetics and neurophysiology. This is because to obtain reliable neurophysiological responses, anaesthesia is often required to be accommodative. Without this adaptive collaboration, neurophysiological data may not be obtained.

Generally speaking- as the neurophysiologist we are looking at the function of the motor and sensory pathways of the brain, spinal cord and/or peripheral nerves. There are many tests that we can perform, but keeping things simple, we monitor the motor pathways through Transcranial Motor Evoked Potentials (TcMEP) where an electrical stimulation is delivered to the motor cortex, the signal is sent down the spinal cord (Corticospinal tract/ Ventral column/ efferently), and out the peripheral nervous system which causes the muscles to contract. This muscle contraction is measured at the beginning, throughout and at the end of the procedure. A baseline trace is obtained at the start of the surgery, which all other stimulations are compared to throughout the procedure. Any variation >50% in amplitude of these muscle contractions may correlate to clinically significant changes and post operative deficit. Similarly, the Sensory pathways are monitored through Somatosensory Evoked Potentials (SSEP), where an averaged response is obtained from a peripheral nerve, where the stimulation travels from the periphery, up the spinal cord and then the response is recorded at the Primary Somatosensory Cortex (Spinothalamic tract/ Dorsal column/ afferently). These baselines are also obtained at the start of the surgery for all other responses to be compared to, with the clinical significance criteria outlining a >50% amplitude reduction or a >10% latency shift. With both motor and sensory responses, the goal is to predict and prevent post operative deficits by providing early feedback to the surgeon, so they can avoid or rectify anything that shows the early signs of neurological damage.

Without going into too much detail into anaesthetics, it is important to understand the main goal in the procedure. Traditionally, optimal anaesthesia has had three main objectives: Analgesia (pain management), Amnesia (memory) and Sedation (depth of consciousness), and although this isn’t the most up to date explanation of objectives according to one anaesthetist I spoke to, it does give a little insight into what’s required for a successful anaesthetic. In addition to this, for the sake of this blog and from feedback I received from the anaesthetist I was speaking to, I’m going to add another category: Paralysis (limiting patient movement during the operation).

So, the anaesthetist is aiming to achieve I. Analgesia, II. Amnesia, III. Sedation and IV. Paralysis, all while considering the medical history and risks of each patient. This in addition to managing the patient’s overall health and wellbeing. This includes and is not limited to the patients cardiac, pulmonary, hepatic, renal and pregnancy related concerns and the medications that interact with each of these conditions. With all these considerations, it is understandable that the anaesthetist is often less than overjoyed when approached by the neurophysiologist to do a sometimes unexpected, last-minute change of anaesthetic plan. This provides the additional challenge of not being able to use Volatiles or Neuromuscular blockades (NMB) for patient paralysis, and therefore having to apply a different approach to what they would usually do to keep the patient still enough for the surgeon to perform the operation. On the other hand, the neurophysiologist is invited into theatre to do an important job too. For procedures where the neural elements are at risk (brain, spinal cord, peripheral nerves), the surgeon may require some feedback on the function of these elements, to identify, to protect and to potentially rectify any harm done.

A common anaesthetic set up may include Volatile agents such as Sevoflurane, or less commonly due to environmental effects, Desflurane. These gasses alone can provide the anaesthetist with an anaesthetic depth they can control easily, suitable amnesia, and reduces patient movement due to the action at the glycine receptor as well as some muscle relaxation at the neuromuscular junction. So, with easy administration and monitoring of these gasses which targets some of the main goals of anaesthesia, these anaesthetic options often become the favoured anaesthetic type when intraoperative neuro-monitoring is not in the equation.

If neuromonitoring is in the equation, what does the anaesthetist do? TIVA. Total Intra-Venous Anaesthetic. A common combination of TIVA medications may include Propofol, Remifentanil and Ketamine infusions, with or without a short acting/small dose of NMB at induction. In fact, this is the anaesthetic that is recommended for procedures in which neurophysiological monitoring is required- assuming it is safe to do so. There are many variations of the medications listed above that can achieve -what I as a neurophysiologist would call “optimal anaesthesia for monitoring”- but as I said earlier, I’d like to keep things as simple as possible for this blog. The three areas I would like to focus on however are: I. TIVA II. NMB and III. Volatile agents.

TIVA is considered the gold standard for anaesthetics when IONM is required. It is a combination of medications delivered intravenously to target the goals of amnesia, analgesia, sedation and paralysis. It’s common to walk into a theatre, greet the anaesthetist who smiles at you, agrees to run TIVA and be filled with joy, because honestly, what more could you want. That in itself is an indication that you’re likely to have a good day. Unfortunately, it’s not as simple as that. Once you’ve crossed that first bridge of getting that TIVA anaesthetic, there are other things to consider. Anaesthetic depth, patient temperature, Mean Arterial Pressure (MAP), and whether there is NMB or Volatiles in the mix (I know, we already ruled this out in our preoperative discussion, but that doesn’t mean a little sneaky volatile can’t be added in). All of these are factors to consider when IONM traces aren’t adding up to expectation. Anaesthetic depth is often measured through a BIS monitor attached to the anaesthetic machine - this is a numeric display of how asleep the patient is with 0 being practically comatose and 100 being fully awake and chatting, with a range of 30-60 being the range of suitable depth of anaesthesia. Another way of identifying if the depth is appropriate for monitoring is an analysis through an intraoperative EEG set up by the neurophysiologist. Again, if the EEG displays complete burst suppression and isoelectric activity, it renders IONM useless. Similarly, a low patient temperature and/or low MAP can supress IONM responses, so it is important to check that these figures are in the normal range when troubleshooting traces.

NMB is a drug given intravenously often during induction/ intubation, to allow for the Endotracheal tube to be inserted into the patient’s airway without significant muscle contraction or coughing to make the process more difficult. As we all know, getting that tube in the right position is a very important part of a procedure, as without oxygenation it can lead to disaster. When TIVA is the anaesthetic of choice, NMB is often extended throughout the procedure to minimise patient movement while the surgeon is operating. When IONM is required, NMB should not be continued during the procedure as the blockage of responses at the neuromuscular junction means that no myogenic responses will be obtained, and no neural feedback can be given. In these cases, other medications may be required to keep the patient movement at a minimum without obstructing neurophysiological data. If NMB is required for intubation, that’s completely fine. A small dose will likely be metabolised before baseline traces are obtained; or for a larger dose, NMB reversal can be given. No worries, happy days... Volatiles on the other hand, not so happy days.

Volatiles. Almost a dirty word in the world of intraoperative neuro monitoring (IONM). This type of anaesthetic has the potential to absolutely ruin your day. Not only does this type of anaesthetic inhibit the ability to obtain most responses in IONM, it also can take much much longer to fully wear off out of the patient’s system than (a) what’s expected and (b) What the anaesthetist says. This in itself can cause some tension between operators. What’s more, this type of anaesthetic isn’t always performed in an all-or-nothing manner, some anaesthetists also like to include Volatile agents into the mix, yet still calling it TIVA. A classic sneaky manoeuvre I like to call PIVA (partial intravenous anaesthetic), which at the same time totally peeves us off.

I often hear the argument from anaesthetists that, “the volatiles are all worn off, it shouldn’t still be affecting your traces”, or “we will just use Volatiles for induction and then we will switch to TIVA” or “it’s fine I’ll only run 0.7MAC of Sevoflurane and you’ll still be able to get responses”, or “I’ll just run a small concentration of gas and you won’t even be able to tell”. In reality, and full disclosure, sometimes we can’t tell. BUT, this is absolutely a case by case situation, as the effect if 1 MAC of volatiles has a bell curve distribution of effects across the population. Some patients will still produce great responses with a high concentration of volatile on board, but this is a minority of cases. More often than not, even a small concentration of volatile can have detrimental effects on the ability to obtain good responses for the entirety of the procedure. And, what’s the point of having neuromonitoring if the traces are unreliable for the entire procedure? That’s just great, a whopper tumour located in the intramedullary space, and we can’t give any functional feedback on the spinal cord function, yep perfect. Surgeon is unhappy with the incredibly high risk of paralysing the patient, the anaesthetist is unhappy because they are being blamed for not being able to get these responses and the neurophysiologist is unhappy because their anaesthetic requests have been dismissed and there are no traces to report. And let’s not even mention how unhappy the patient is going to be when they wake up with no movement or feeling when they’ve been told that these pathways are going to be monitored.

Now, just to be clear, the use of volatile agents and NMB are not always the end of the world in regard to monitoring! There are procedures which warrant the responsible use of volatiles or NMB. By this I mean the primary modality of IONM can still be achieved with these anaesthetics in use, and everybody can be happy. For example, in peripheral nervous system procedures where Triggered EMG (tEMG) is the primary modality the use of volatile agents is acceptable due to the stimulation site being on the peripheral nerve, which is distal to the post synaptic nerve- where the volatile agents take effect. Or similarly, when analysing Compound Nerve Action Potentials (CNAP/NAP), active NMB and volatiles can be utilised due to the location of the stimulating and recording sites both being on the peripheral nerve itself, which occurs more proximal to the neuromuscular junction - where the NMB takes effect; and more distal to the post synaptic nerves- for volatile effect. It is still nice however to have TIVA for secondary modalities, but as was mentioned earlier IONM can cover a broad range of tests and the goal of this blog was to keep things as simple as possible. Therefore, this blog is targeting the more commonly utilised type of monitoring- multimodality, which involves TcMEP and SSEP, among others.

So, with all that said, lets dive into a real-life example.

(14:37) Sevoflurane 0.8MAC

(14:42) TcMEP baseline traces attempted but not able to be obtained. TcMEP attempt pictured below.

(14:46) Surgery start.

(15:00) 0.0 MAC

(15:01) TcMEP baselines obtained. Pictured below.

(15:45) ~45 minutes following anaesthetics announcing, “no volatiles on board”. TcMEP performed with global amplitude increase observed due to volatiles wearing off. TcMEP pictured below.

(16:56) TcMEP amplitude reductions beginning to be observed (baselines had been reset to reflect patients true form following global increase). Anaesthetist announces 0.2 MAC sevoflurane has been running for last 30 mins. Spinal cord perfusion also in question. Reliability of responses unable to be determined due to volatile agents.

Remainder of procedure, amplitude fluctuations were observed. Final traces indicated significant changes; however, these changes were not able to clearly be identified as either surgical manipulation, or anaesthetic involvement, which undermines the relevance of having neuromonitoring in the first place.

I could provide hundreds of examples, but you get the point. In the above examples, where our baselines are only a fraction of the size of the patient’s true motor function, how on earth are we supposed to give reliable feedback to the surgeon when it takes 45 mins-1 hour for the evoked potentials to return to their true form following the MAC concentration returning to 0.0? What if the damage had already been done to the spinal cord and we couldn’t see it because it was hidden among the effect of the sevoflurane? In example 2, that was a real concern. The perfusion of the spinal cord was in question by the surgeon, and unfortunately that question could not be answered confidently due to volatiles being re-added to the mix around the same time the damage had potentially been done. This example is particularly valid and useful, as it outlines the effects of the Sevoflurane at the beginning of the procedure (very much affecting amplitude of traces, even after “volatiles being worn off”), while providing insight in how a late addition can impact the validity of the responses being obtained.

To conclude this blog, I would like to make it known that all anaesthetic agents influence IONM responses to some degree, with even the “good anaesthetics” having depth dependant results. As a final sign off, I would like to present this table from the textbook “Neurophysiology in Neurosurgery - A Modern Approach” (Deletis et al., 2020; page 570), which outlines the effects of some of the common anaesthetic agents on TcMEP and SSEP responses. Just remember, as illustrated in the above examples, the effects of volatiles on TcMEP and SSEP responses can take some time, even when the volatile agents have been switched off.

Table pictured below.

A Volatile Relationship?