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Chris Martin Speaks at TxANA Part VI: Evoked Potentials Carotid Endarterectomy

Posted: Feb 6, 2017 11:00:00 AM


Speaker:
 Chris Martin, Surgical Neurophysiologist (4:48) speaks at TxANA Conference Part VI

In August, 2016, Neuro Alert exhibited at the TxANA Annual Convention & Trade Show. Here, Chris Martin, one of Neuro Alert's Senior Surgical Neurophysiologists, was asked to present "Introduction to Intraoperative Neurophysiology" and "Intraoperative Monitoring Applications and Considerations." In this six-part presentation, Martin walks us through the origins of Intraoperative Monitoring to present-day applications.

Transcripts to follow:

Chris Martin, CNIM, Surgical Neurophysiologist:

Let's go do another carotid. This time, we're  going to add some evoked potentials to it instead of just EEG. Sensory evoked potentials, obviously, are mediated. We don't need neuromuscular junction unblocked for sensory stuff, so again, running them on the Rockville case is perfectly reasonable. Now we're down to half a MAC of Sevo and we've got some Propofol, so this is more of like a Teva plus technique. Really, Teva should be Teva and if you're adding Sevo, it's not Teva, but we'll let you slide on that, call it a Teva plus. Anyways, this is perfectly reasonable when you're having evoked potentials. Again, half a MAC of Sevoflurane is probably  going toallow you to record some decent sensory evoked potentials. Don't let people tell you that you can't run it at all even in the context of the rest of your Teva technique.

On the other hand, if they have a underlying pathology and they don't have very solid baseline sensories, this would be the first thing to think about cutting off. Here are  the baselines from an overkill point of view. They were monitoring both ulnar and median nerves in the wrists and the left and right EEG, so it's kind of displayed a little bit differently than the other case was on the windows, but again, where it says "right," this is the side of stimulation, so this is the right side stimulation of the median nerve and right side stimulation of the ulnar nerve. This response is being recorded from the left brain, so it's a little bit confusing unless you keep that in mind.

Now, we're starting to see some evidence of insufficient perfusion. The EEG on the left side has definitely gotten lower and slower. There's a little bit of a drop-off in these evoked potentials on the left brain from right stimulation than there had been at baseline. You can see that a little bit there, and then there's the EEG. Compared to the right brain, it's looking like there's less fast frequency and lower amplitude. A shunt was placed, as was in the last case, because we had these changes, except this time, the SSEP changes worsened and essentially disappeared. They're gone. The EEG is still asymmetric on the side that's shunted now, still slower and lower amplitude than the right side, so the shunt is not making these signals rebound like it did the last time.

The surgeon took that one out and put a second shunt in, and then the signals came back. The EEG is still asymmetric here, but the sensory evoked potentials are starting to improve. It's improving on the EEG, but there's still a little bit of asymmetry. Sensories are all the way back. Upper extremity sensory evoked potentials are really good for carotids, because it's a specific area of the cortex that's perfused by M1 right off the carotid, so you're getting a very specific part of the brain that's going to be affected by any blood flow changes from the carotid clamping. EEG is very sensitive, so you get specificity and sensitivity if you combine both of these modalities for a carotid.

Here, by the end of the case, the EEG is basically now back all the way to baseline, looks pretty good. One thing that you might have noted when we were looking at the sensory evoked potential changes is that the corticals dropped out but the subcorticals didn't, so these are cervical medullary junction at the top of the spinal cord, and these are in the cortex itself, so you can see that the hypoperfusion was not affecting as you would expect. It wasn't affecting down low, it was really only specific to the brain, which really gives us confidence that that's what was going on there.

The first shunt, then, was evaluated and determined to be faulty, and that's why he removed it and put a second shunt in, which then led to these improvements in the signals back to, essentially, baseline. The patient did wake up with a mild hemiparesis, but this resolved over the next several weeks, so again, this is sort of a mild sequela that could have been much more dense or permanent, and the surgeon had placed the shunt correctly, so by continuing to monitor and not just saying, "Okay, the shunt's in. We're saved," he was able to determine that that wasn't adequately perfusing the brain again and took it out and put a second shunt in, which did work.

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