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EMG and NCS
41 Plays2 months ago
In this bonus episode, Dr. Michael Powers peels back the curtain on electrodiagnostic testing. If you've ever wondered what electromyography (EMG) and nerve conduction studies (NCS) are and how they can help guide clinical decision-making and prognosis, then this episode is for you! After this episode, you will understand how an intentional and well-guided clinical exam can approximate much of the information obtained during EMG and NCS.
All music courtesy of Free Music Archive and used via attribution 4.0 international license.
- Intro and Outro: Stylin' by JMHBM
- Transitional: Our Reality by Ketsa
Contact: neuropowerhour@drmichaelpowers.com
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Transcript
Introduction to Electrodiagnostic Testing
00:00:10
Speaker
Welcome to the NeuroPowerHour. I'm your host and neurological navigator, Dr. Michael Powers, physical therapist, board certified in neurologic physical therapy and clinical electrophysiology.
00:00:22
Speaker
Let's get started. Bonus episode today on EMGs and NCS. Bonus episode as I'm going to be doing a presentation around this content. For our purposes, going be doing EMG and NCS, we can combine those terms into what's also known as electrodiagnostic testing, but in clinical practice, you'll you'll commonly hear people just say EMG.
00:00:43
Speaker
But I do want to be clear that when we say EMG, we're referring to both EMG and NCS.
Understanding EMGs: What, How, and Why
00:00:50
Speaker
What are EMGs and NCS? EMG is electromyography.
00:00:56
Speaker
NCS is nerve conduction studies. These complementary tests performed together give us tremendous insight into the function, generally speaking, of the peripheral nervous system. So when I'm using the term EMG, and again, I'm using that catch-all term to include both EMG and NCS,
00:01:16
Speaker
We're referring to a diagnostic test primarily aimed at looking at the integrity of the peripheral nervous system. In today's discussion, the three content areas we're going to cover are the what, how, and why of EMGs.
00:01:32
Speaker
Then we need to talk about peripheral nerve physiology So peripheral nerve injury and repair. And the reason for that is a lot of what we'll see on our EMGs is going to be somewhat predictable based on our understanding of peripheral nerve injury and repair. There's only a few ways that peripheral nerves can respond to injury and how they can repair themselves.
00:01:53
Speaker
And these will show up on the EMG. So we need to review and make sure we have a good understanding
Clinical Utility of EMG Results
00:01:58
Speaker
that content. And then finally, we'll conclude by talking about the clinical application of EMG. So for many people, you'll never be performing an EMG. You may feel unsure even how to interpret or read an EMG if your patient was sent out for one.
00:02:14
Speaker
So because that's probably a relatively small subset of future clinical practice, I'd rather instead focus on, well, how would you know if maybe your patient would benefit from an EMG And how can you use the information about peripheral nerve injury and repair, considering what's assessed on the EMG, to actually improve your clinical exam? Because I would argue that a well-directed clinical exam can reasonably approximate the information you get from an EMG.
00:02:46
Speaker
I reflect back on my own skill set and knowledge before i became board certified in clinical electrophysiology. And anytime a patient would show up with some numbness tingling, i would feel a little bit unsure. And sometimes just because of where i was located, would little unsure.
00:03:03
Speaker
I would think, well, maybe I should send this person to EMG because it was actually an accessible service. And I didn't fully appreciate that if I took a breath, calmed down, and did a well-guided exam, I could really develop a much stronger hypothesis.
00:03:18
Speaker
I could really help out the person performing the EMG, and I would have a pretty good differential approach. based on the premises or kind of the thought process that goes into even performing an EMG exam. So at the end of today's discussion, I want to leave you with some considerations that you can put into practice right away to improve your clinical exam and improve your decision making on when to refer for EMGs.
00:03:42
Speaker
Let's start then with talking about the kind of what, how, and why of EMGs.
The EMG Examination Process
00:03:49
Speaker
EMG is a two-part test, electromyography, and nerve conduction study.
00:03:55
Speaker
Electromyography involves the insertion of a needle directly into muscle to record electrical activity within the muscle. That needle that's inserted has a small area that it can essentially listen into. We'll we'll see as we insert the needle, we see some waveforms on the screen.
00:04:16
Speaker
But for the EMG practitioner, the sounds we hear is probably even more useful than looking at the waveforms. So that recording area of the EMG needle is relatively small. With each muscle that's being assessed, the EMG examiner will sample or look at different areas within the muscle. So let's say I'm assessing someone's bicep. I insert a needle into the bicep. I'm listening and observing at one area. Then I change the direction of the needle. So I'm looking at different muscle fibers, different motor units within that muscle.
00:04:52
Speaker
During an EMG examination, during the electromyography, the examiner is listening and looking to see what's happening at rest. They're looking to see what happens with some minimal muscle recruitment and then some maximal muscle recruitment.
00:05:08
Speaker
And all that information can be combined to determine whether there appears to be any difficulties or abnormalities within the motor units.
Dynamic Nature of EMGs
00:05:20
Speaker
Biggest thing that I would argue you can find during the needle EMG examination is whether there is some form of what's called axon loss and or denervation. Has the peripheral nerves or the axon's ability to communicate to the muscle been impaired?
00:05:40
Speaker
And if that's happened, you'll get stereotypical resting sounds that you shouldn't normally get, and you may notice abnormalities in recruitment. So that's the EMG electromyography inserting the needle into muscles.
00:05:54
Speaker
looking to see what the activity is, what activity is happening at rest with minimal contraction and with maximal contraction. What happens here is during the needle examination, the EMG examination, the examiner is looking for patterns. Let's make a hypothetical argument that someone has a nerve root injury, cervical radiculopathy. It's severe enough that it's caused some axon damage.
00:06:22
Speaker
And again, we'll talk more about the different types of nerve injury and repair in the second part coming up after the break. But let's say there's some axon damage in at the area of C7. So someone's got a C7 radiculopathy on the right.
00:06:36
Speaker
The needle EMG examination would be expected to find abnormalities throughout C7 innervated muscles. So the examiner may be examining or looking at multiple muscles throughout the right upper extremity, and what would cause the examiner to begin to think that this could be a C7 problem from the EMG itself would be finding abnormalities isolated from to C7 muscles. The EMG examination, therefore, is a dynamic process. There's no necessarily prescriptive here. You need to test these muscles.
00:07:14
Speaker
The examiner is looking at what's the initial hypothesis? What's the referring diagnosis? What did my clinical exam reveal? What am I trying to rule in and rule out?
00:07:26
Speaker
And typically in the upper extremity, you're considering, is this a cervical radiculopathy? Is this possibly a plexus injury? Is this a focal entrapment neuropathy? Could this be something systemic? Could this be a diabetic polyneuropathy? Could this be something acute like Guillain-Barre syndrome? These are all differentials that the examiner is considering.
00:07:47
Speaker
And so during the EMG examination, finding patterns that match up that makes sense with the clinical history, the clinical exam, and are confirmed on the needle EMG really help guide towards ruling in a condition.
00:08:04
Speaker
That's the EMG, the electromyography, 30,000 foot view.
Nerve Conduction Studies Explained
00:08:08
Speaker
Let's talk about the nerve conduction study. The nerve conduction study, when I was in clinical practice, I would perform this part of the examination first, usually a little more well-tolerated, And it gave me information that helped me reconsider what I might want to do during the needle EMG later.
00:08:26
Speaker
Nerve conduction study is the use of current to stimulate peripheral nerves and then record the resulting signals. During the nerve conduction study, some key parameters we're looking at will be latency,
00:08:42
Speaker
And here we can maybe imagine a track and field example. Someone's a runners maybe at the starting block. Latency will be how long from the person hearing the the starting gun till they start running. Then we look at velocity.
00:08:55
Speaker
OK, what's the speed? So if someone's running 100 meter dash, what's the speed? That would be the velocity. We can get that during a nerve conduction study. And then we can also get the amplitude. And maybe the best way I can consider amplitude would be maybe the force that the person is running at at the end. Maybe they go across a ticker line or something. That's the amplitude. What's the summation, the total number of axons that are responding to our stimulation?
00:09:23
Speaker
couple key considerations with nerve conduction studies. Nerve conduction studies are really looking at large diameter myelinated fibers.
00:09:34
Speaker
It's the nature of both the stimulation that's applied and the recording setup. And I don't want to get too far into the and recording setup details here. One thing I will mention, though, is during performance of the nerve conduction studies, there's a lot of computer work that's being done. There's also a lot of blocking of other signals.
00:09:55
Speaker
The purpose or what we're trying to accomplish when we're recording nerve conduction studies is to get biological signals and block everything else out. And based upon the intensity of the current we're applying and the recording montages,
00:10:11
Speaker
The nerve conduction studies really can only see waveforms and results from large diameter myelinated fibers. This is key to consider if you've got a patient maybe that has a painful neuropathy, but it's a small fiber neuropathy, an unmyelinated neuropathy. where unmyelinated fibers are involved. An EMG in NCS test is not going to be able to determine that there's any pathology. So I bring this up to say, you can have situations where someone does have peripheral nerve problems, but it'll be essentially invisible to the nerve conduction study.
00:10:51
Speaker
Let's talk then about the considering the nerve conduction study. So let's say we've got our hypothetical patient. I said we think they've got a cervical radiculopathy on the right.
Setting Up Nerve Conduction Studies
00:11:03
Speaker
I may start out and maybe they say they've got some numbness tingling in the right upper extremis. And maybe I'm just thinking, well, just to make sure i i want to rule out or I want to assess for, you know, could this be carpal tunnel syndrome, cubital tunnel syndrome?
00:11:19
Speaker
So I'll do some nerve conduction studies to assess the integrity nerve. of the median nerve and the ulnar nerve and make sure as those nerves are crossing common compression sites like the wrist for the median nerve, cubital tunnel for the ulnar nerve, that we're getting normal latencies, normal velocities, and normal amplitudes.
00:11:39
Speaker
Now, when we're doing the nerve conduction studies, if you're ever reading a report or looking at an exam, the nerve conduction studies can assess motor and sensory nerve function. If you think about it, so if I'm stimulating the median nerve at the wrist, I put the nerve stimulator over the median nerve and I apply current that's needed,
00:12:02
Speaker
I'm stimulating both motor and sensory fibers. I've had that question. Students commonly ask that question. why aren't you stimulating the entire median nerve? Yes, 100% correct. What determines whether this is a median or I'm sorry, whether this is a motor or a sensory study is the setup of the recording electrodes. If I set up my recording recording electrodes over the abductor pollicis brevis, which is the median motor innervated muscle, and then I put my reference electrode on an area that's electrically silent, so distally on the bone, I get a motor study.
00:12:39
Speaker
If instead I put some ah ring electrodes over the index finger, I decrease the amount of stimulation, my recording setup is set up for sensory, then I'm recording a sensory nerve conduction study.
00:12:52
Speaker
Hopefully that makes sense and that's a little bit helpful in considering how that may look as you're setting up the nerve conduction study. Combining these then, the EMG, the electromyography, and the nerve conduction study, I want to make a couple key points from the vantage point of referring someone for these tests, or when is when is an EMG most appropriate.
Limitations and Specificity of EMG and NCS
00:13:15
Speaker
Big picture view, the electrodiagnostic testing is highly specific. Think back to your evidence-based practice. Specific tests help to rule conditions in. This is not a screening test, and there's a couple reasons for this.
00:13:32
Speaker
One is the resources used in the test, and there is a certain amount of discomfort. Most people tolerate both tests, the yeah EMG and the NCS, very well, but it does involve needle insertion, and it does involve stimulation with current. So It's not the most comfortable exam.
00:13:51
Speaker
Again, the 99% of patients I've worked with tolerate it very well, but there is some discomfort. There's some resources needed, obviously, to set this up. So this is not a test that you're sending every single patient for.
00:14:04
Speaker
The other consideration is that, especially for the nerve conduction studies, most of the normative values are based upon normative studies and then considering abnormal two standard deviations away from those normative values. Because of this, there's a wide range of what would be considered normal.
00:14:25
Speaker
Definitely possible to have someone with symptoms that may be having some mild issues going on, but they don't classically fall into the abnormal range. The abnormal range is set up so far beyond because we're going two standard deviations away from normative values.
00:14:41
Speaker
This is not a test. to rule out. This is a test to rule in. As previously mentioned, nerve conduction studies test large diameter myelinated fibers. So if someone has a small fiber neuropathy, not going to be very helpful.
00:14:57
Speaker
There's a timing consideration to these tests. This will make more sense when we talk about nerve injury and repair. Tests that are performed too early may give false negative results. Because of the timing of nerve injury and what's called Valerian degeneration, the dying back of axons, a test that's performed earlier than maybe one or two weeks, there's some debate about that in the literature, may erroneously indicate a lower severity of injury.
EMGs vs Central Nervous System Assessments
00:15:27
Speaker
That's something key to keep in mind in terms of timing of the exam. Couple other considerations, normative values are not well defined for both the pediatric population and for adults over 65 years old. Doesn't mean you can't still get tests in these populations. your EMG examiner will have to be a little bit more attuned to using that individual patient as their own control. So side-to-side comparisons may be more important.
00:15:56
Speaker
The absence or presence of certain findings on the needle EMG exam. But just keeping in mind that there's not great data on normative values in younger and or older populations. Finally, the point I want to make is, and we mentioned this at the beginning,
00:16:11
Speaker
EMGs are going to be most useful primarily in the peripheral nervous system. Not great at central looking at central problems, so not great at assessing the spinal cord, not great at assessing the brain, obviously. Now, there are some instances where EMGs can be used for intraoperative monitoring. I'm not going to be covering that in this presentation because my goal is for the typical clinician that's considering, well, would I want to refer a patient for an EMG? We're going to keep this towards the peripheral nervous system.
00:16:43
Speaker
So let's say you're working with someone who's had a stroke and they're weak. The EMG is not going to give you much beneficial information. What the EMG is really looking for is whether there's a problem with nerve conduction and connection at the neuromuscular junction out in the periphery.
00:17:03
Speaker
The weakness and difficulties with movement we see with someone who's had a stroke, that's a central problem. And the EMG is unlikely to be of any benefit. It's not going to change your management. It's not going to tell you anything new. And maybe that's what I want to hone in on here before we transition to peripheral nerve injury and repair. If you're thinking about, well, should I refer someone for an EMG? I strongly advise the same consideration that I've advised people on when you think about any additional diagnostic tests like an x-ray, an MRI, EMG. Is it going to change your clinical management?
00:17:39
Speaker
You should have a solid understanding that, yes, this would change my clinical management before thinking that, okay, i want to get this test. If you're at a point where you say, well, I don't know what's going on, so let me get an EMG, in my opinion, that's not appropriate utilization of this test. You need to go back and improve your clinical exam, get a better differential, and then consider, based on the results of the EMG, how might you change your clinical management.
00:18:12
Speaker
Let's shift gears now and talk about peripheral nerve injury and repair. This will be tremendously helpful in recognizing what information the EMG may provide.
00:18:25
Speaker
It'll also give you some information on what to tell patients as they're coming back from various nerve injuries in terms of what to expect from a repair or recovery perspective.
Physiology of Nerve Injury and Repair
00:18:37
Speaker
Let's take one individual neuron, so one nerve cell, for this discussion, keeping in mind, however, that when we talk about a peripheral nerve, a peripheral nerve consists of multiple, multiple neurons bundled together, organized.
00:18:55
Speaker
The initial organization is via fascicles, and then you've got various layers of fascicles combining together into the peripheral nerve. But to better understand nerve injury and repair, let's take one nerve cell. Let's take one neuron.
00:19:11
Speaker
the The main areas that we're focusing on are going to be the myelin sheath. So if you remember, it's kind of that fatty layer of insulation wrapped around the axon, and there's gaps in the myelin sheath. The big purpose here is to speed up, i'm gonna use the term speed again, speed up the speed of the action potential propagation. So the action potential is what leads to depolarization. If we are not myelinated, that action potential has to travel to each individual voltage gate to depolarize, and it slows transmission down substantially by having myelin There's what's called saltatory conduction, so that action potential can jump between those gaps in the myelin because the myelin acts as an insulator, which tremendously increases the speed of our transmission. I use kind of the analogy where I think about track and field a lot, I guess, as I'm thinking about nerve conduction.
00:20:13
Speaker
I think about the triple jump, which I think is just a cool thing to watch when you see the person jumping three times. That's your saltatory conduction. And then I combine that with, embarrassingly enough, the Super Mario Brothers sound of someone jumping because that makes it stick out my head a little bit more. so you got boing, boing, boing. And that action potential is hopping quickly down that myelinated nerve. In cases where we have now demyelination, where because of either compression, any number of cases, and it really does not matter what the offending action item was to the nerve, the responses to injury are going to be the same. So we're going to ignore what the cause is. If we've got demyelination, Starting out, what we're going to get is slower nerve conduction velocity because now instead of having that saltatory conduction, instead of our triple jumper, jump, jump, jump, imagine the triple jumper jumps once, pulled a muscle or something, and now has to slowly walk across the rest of the sandpit. Going to get to the end a lot slower. Still gets there.
00:21:17
Speaker
We have the connection at the end at that neuromuscular junction, if this is a motor neuron, just going to be a lot slower. So on your nerve conduction study, if someone has demyelination, the biggest thing we're going to see is slowness.
00:21:33
Speaker
So when I talked previously about latency, that time from stimulation to response, I talked about velocity, overall speed, these are going to show up as slow. But because our triple jumper still gets to the end point, we're not going to have any difficulty at this level with the amplitude of our response.
00:21:53
Speaker
And because we get to the end point on our EMG, on our needle exam, we're not going to see big abnormalities because ultimately we still get to the end point. The neuromuscular junction is intact. So the big findings we get with demyelination is slowness. That's the take-home easy thing to remember. Demyelination in terms of nerve injury is considered, i don't want to say lowest level, but it's considered the less severe aspect of nerve injury because given the correct environment, removing the offending stimulus, our bodies can actually remyelinate and this can improve. I want to talk to about one additional consideration with focal demyelination, and that's what's called a conduction block.
00:22:40
Speaker
If we have an area of demyelination that's severe enough, we may actually lose the action potential as it's trying to make its way. Let's use a a motor neuron as an example. Maybe we have an area of focal demyelination, so instead of saltatory conduction, that action potential is now having to go up and down through all these voltage-gated channels. And it may get to a point where the action potential gets lost or that signal now gets blocked. How that will look clinically is this is going to show up now as some weakness because our triple jumper jumps once, tries to wander off to get to the end, and then falls over because just can't make it to the end.
00:23:23
Speaker
So our endpoint is never reached. And if this is coming from a motor neuron, we don't get a signal to the muscle to actually contract. What's key here, though, is at the neuromuscular junction,
00:23:38
Speaker
Think about your neuromuscular junction. You've got a lot of acetylcholine that has to go across the junction to get to the muscle. That'll give you your contraction. That transmission of acetylcholine across the neuromuscular junction keeps the muscle healthy. Here I use the analogy of a fish tank.
00:23:55
Speaker
Think about the acetylcholine as you're dropping fish food into the tank. The fish come up and eat it. That is a good, healthy neuromuscular junction. With a conduction block, even though our triple jumper is not getting to the neuromuscular junction, the neuromuscular junction remains intact.
00:24:13
Speaker
Acetylcholine is going across the junction. The muscle stays viable. Clinically, you will not see any atrophy. So I'm jumping ahead a little bit into clinical considerations, but I think this is a good point to do this. If you have someone with a peripheral nerve problem who expresses weakness or talks about weakness and you either visualize the weakness or on your muscle testing, you denote some weakness, but there's no atrophy, you may be thinking this is either early, very early in the process, or this is a conduction block. And the good news about conduction blocks They are extremely reversible.
00:24:51
Speaker
Very common condition would be a radial nerve palsy. It used to be called a Saturday night palsy, sometimes a honeymoon palsy, because these would be common injuries. The Saturday night palsy, maybe not the most politically correct term, someone who went out and partied too much, drank a lot,
00:25:08
Speaker
and passed out or fell asleep with their arm in a weird position. Honeymoon palsy because you're sleeping with your partner in bed and maybe their head's resting on your arm. And essentially from either either cause, you're getting compression on the radial nerve and the person wakes up in the morning and has a wrist drop. The radial nerve is not working. Most of these cases are what's known as a transient conduction block and get better either the next day within days or weeks. The neuromuscular junction was intact. The damage was to myelin. This heals because it was a one-time um ischemic or compression event. And so the prognosis is very good. And I bring this up because it can be very scary when a patient presents with weakness. I've had cases clinically where I've had to educate referring providers that something they thought was tremendously catastrophic was actually likely to get better very quickly.
00:26:07
Speaker
in terms of it being a conduction block. Let's review here then the myelins. The first thing we're looking at, damages to myelin on nerve conduction studies will give you prolonged latencies, slower velocities. Now, if this is a sensory demyelinating condition, the patient will interpret this potentially as tingling because the signals are getting slow. Some of the signals may be dropping out a little bit, so you can absolutely get tingling even if it's a myelin problem.
00:26:35
Speaker
the patient may feel weak, and this is very common in carpal tunnel syndrome. Because of that impaired sensation, they interpret this as weakness because they can't feel the coffee cup and they have to hold on with the other hand.
00:26:48
Speaker
But when you actually look at their median innervated muscles, there's no atrophy. And when you strength test them, they have full strength. So I did want to bring that point up because that's clinically important. Myelin damage, therefore, is the least severe of what you will see has a good prognosis to improve really without either too much intervention or with um removal of the offending whatever is causing that typically compression or ischemia.
00:27:18
Speaker
Let's talk about then, let's move on to the axon.
Detecting Axon Damage with EMG
00:27:21
Speaker
That's more of the structural portion of the neuron. And once we get into axon damage, our categorization changes. Once we have actual damage to the axon, If this is a motor neuron, now we're talking about losing connection from that neuron to the muscle. So we're going to get disruption of the neuromuscular junction. Here is where the needle EMG becomes most beneficial because a muscle that is becoming denervated that has axon loss that has lost its connection from neuron to muscle has distinct...
00:28:01
Speaker
sounds and waveforms when the needle's in the muscle. I previously used the example of feeding a fish as the acetylcholine going across the neuromuscular junction.
00:28:12
Speaker
Now imagine because of axon loss, I can't feed the fish. The neuromuscular junction is not intact. The fish now come up to the surface of the fish tank and they're crying out for help.
00:28:24
Speaker
Maybe this is an extreme example, but it's a good visual. And now they're making certain sounds saying, feed me, feed me. This is what you will get on your needle EMG at rest when you stick the needle in a denervated muscle. This is what makes an EMG outstanding for cases of muscle weakness and or atrophy.
00:28:45
Speaker
You can observe these signals and listen to these signals without any cooperation from the patient. I don't mean to throw that term around lightly. I mean, if the patient is maybe unconscious in the ICU, you can do the needle EMG and see if there's denervation. If you have a patient case where you're worried about is there secondary gain and or malingering, you can do the needle EMG. And if you see and hear these, what are called fibrillations of positive sharp waves, you know there's been axon loss. This is not something that relies on any active input from the patient. I should take a step back and say same thing with nerve conduction studies. As long as the patient is allowing the testing to proceed, the patient is not actively engaging in these test and these tests. So these tests do provide a nice objective way of getting information.
00:29:32
Speaker
Let's say then... We've got some compression. Let's use the carpal tunnel as an example. One of the, I think the most common upper extremity entrapment neuropathy starts out. Maybe there's some compression there and it starts out as a demyelinating condition over time. It starts to get more severe.
00:29:49
Speaker
and now there is actual axon loss. You then get this dying away of the terminal part of the axon. This is what is known as Valerian degeneration. This takes usually one to three weeks. It can vary, but what's happening here is that distal part of the axon is dying away. The body is coming in and cleaning up the area. trying to get things ready, hopefully for a repair. This is why i previously mentioned the timing of when to get a test is important. If someone presents with a one to two day history of numbness, tingling and weakness, and there's no known external injury like a gunshot, a knife wound, a car accident, if you get an EMG, you can get an EMG right away, but you haven't allowed enough time for Wellerian degeneration. So you can't 100%
00:30:43
Speaker
rule in or out axon loss. So you may not have the appropriate severity documented. Now for axon loss, prognosis is good to poor depending upon the injury severity. And the time frame for recovery is typically months. So I mentioned demyelination is is really good prognosis.
00:31:03
Speaker
Days, weeks, maybe months. Axon loss, we're moving into now a little bit worse or quite a bit worse category. The prognosis for recovery here is depending upon the preservation of other axons within the nerve. Let's use our carpal tunnel example again. We know that the median nerve is not one neuron. It's going to be many, many, many, many neurons packed together. So maybe it's possible that some axons have dropped out.
00:31:31
Speaker
but some axons are intact. So we don't have a complete loss of function, but maybe we say half of the axons have dropped out. So we're going to have significant weakness, significant numbness, but our prognosis is a little bit better because of all the other supporting structures are intact. intact, keeping in mind your epineurium, perineurium, endoneurium. I don't want to go into too much detail there, but if the supporting structures around the entire nerve are good, if some of the more internal supporting structures are intact, the nerve doesn't have, the neuron doesn't have to figure out where to go, or as the axon tries to regrow, it's going to know where to go. So a little bit better prognosis there. These cases where you have axon loss is where that common, commonly cited rule of thumb
00:32:18
Speaker
does apply. So you may have heard people say, well, nerves regrow at one to three millimeters per day or one inch a month. That is correct if there's axon loss. If I've lost that terminal connection, or let's even say I've got a laceration somewhere and I see, well, I've got four inches of the nerve left to grow, that would typically take then four months if all things go well. That one inch a month does not apply to demyelinating conditions. And probably because I'm an EMG or that really irks me when I hear therapists or other healthcare providers say your nerve gets better an inch a month. That's only in cases of axon loss. if If it's a demyelinating condition, much quicker than that. And it's not guaranteed that it's an inch a month. All the other conditions have to be correct for that to happen. Let's talk real quickly about axon damage and the two ways that your body can come back.
00:33:14
Speaker
One would be axonal regeneration, where the nerve grows back or that neuron grows back. So we've had willerian degeneration. Distal part of that axon is gone. Neuromuscular junction is not intact for that neuron.
00:33:28
Speaker
And over time, that axon says, I think I can, I think I can, starts pushing out. starts regrowing. So there's a lot of processes involved with that, i'm not going to go into detail there. But that would be one way of returning function and returning neurologic function, essentially axonal regeneration. The other option would be that if there are other intact axons and they see that one has dropped out, this would be you've got a strong team. One of your team members is sick. The team pulls together and says, you know what, I'm going to pick up the we're going to pick up the slack. So the intact axon sends a little offshoot to make up at that neuromuscular junction for the axon that dropped off. This is, you may hear the term giant motor units. This is when other axons have taken over.
00:34:17
Speaker
Their motor units are much, much bigger. And this is what we see in conditions like ALS where axons are dropping out. Others are trying to take over. And this is a viable strategy for a while until the motor units become so big that bigger than one axon can handle and then they start dropping
Recovery Strategies for Nerve Injuries
00:34:36
Speaker
off again. Two ways of axonal recovery after axon injury would be axonal regeneration. That's probably preferred. That's the initial axon actually regrowing, getting back to where it needs to go. The other one is collateral sprouting, which is other axons taking over. And it's a good short-term strategy. And it works, especially if there's not continuing injury to the axon. But over time, those giant motor units via collateral sprouting may fail. Interventions then, if someone's got axon loss, this treatment of precipitating factors, you may be looking now at surgical intervention. So possibly decompression. These would be your carpal tunnel surgeries, cubital tunnel releases, your surgeries for radiculopathy.
00:35:22
Speaker
Depending on maybe if there was a penetrating injury or a laceration, there may also be primary nerve repair. You may talk about grafting. Final category I want to talk about. So we talked about demyelination. We talked about axon loss in cases where you've got a severed nerve in some of the classification schemes. You may hear this called neuromiesis. This is when the axons and connective tissue are completely interrupted. If this were to happen, there's an immediate loss of sensation and muscle paralysis in the area supplied. So this is, let's say there's a full laceration of a nerve. That person is going to be immediately numb in that nerve territory and immediately not going to be able to move the muscles. Well, therein degeneration will still take place.
00:36:06
Speaker
And here in this case, if you have a known mechanism of injury, you could get an EMG. But at this point, if there's been a laceration or something traumatic, most likely the patient is heading to surgery anyway. During surgery, the nerve and the surrounding tissues will be visualized. So you may be looking at primary nerve repair, Down the road, possible nerve grafts, nerve transfers, tendon transfer. So neuromiesis, the nerve is damaged, so axon damage, surrounding structures damage, much worse prognosis.
00:36:39
Speaker
Let's recap then. There's a lot of content about nerve injury and repair.
Differentiating Nerve Injuries
00:36:45
Speaker
Key take-home messages are, I want you to think about, is this problem primarily myelin problem?
00:36:52
Speaker
Is it primarily an axon problem? Or is it the axon and supporting structures? That's really going to guide your prognosis. If you were wondering between severity of nerve injury, because that would guide what treatments might be appropriate for the patient, that would be very a very appropriate distinction or a very appropriate consideration for sending for an EMG exam. If someone's got a demyelinating problem,
00:37:18
Speaker
more conservative measures, maybe some positioning, activity modification, nerve glide slide. Those may be all very appropriate measures. If it's axon damage, probably looking at a little more involved treatment, maybe surgical decompression. This is essentially the the neuron is saying, hey, I've lost connection. If it's a motor neuron, I've lost connection with the neuromuscular junction. This is more severe, and you're probably looking at a more involved intervention. And if you've got axon damage with damage of the surrounding structures, neuromiesis, This is emergent surgical repair.
00:37:55
Speaker
This area needs to get cleaned out. If there's a nerve repair that's possible, that needs to happen there. You'll see in various textbooks, in various descriptions, there's a lot of classification categories.
00:38:07
Speaker
There was Seddon back in, I believe, nineteen forty s that came up with the terms neuropraxia, axonotmesis, neuromiesis. Sunderland had categories one through five. There's some Lundberg categories.
00:38:20
Speaker
I would advise you you, can look at all those different terms. What you're really keeping front and center in your mind is, was myelin damaged? If it was myelin damaged, I'm going to see slow velocities, but my needle EMG should be normal. Myelin damage, good prognosis. If it's axon damage,
00:38:40
Speaker
Usually my nerve conduction velocities will be relatively normal if there's still a connection through, but I'm going to see the needle EMG problems. This is a little more severe. I've lost neuromuscular junction integrity for the affected axons. And then if it's neuromiesis, if it's axon damage and connective tissue damage, more severe, very guarded prognosis.
00:39:10
Speaker
Let's finish up then with talking about how to clinically apply the information we covered, how this information might improve your clinical exam and your decision making on when to refer for
Diagnosing Neuropathies with EMG
00:39:23
Speaker
EMG.
00:39:23
Speaker
I previously discussed that during an EMG examination, the person performing the exam is really using a dynamic process to look for patterns and to see, well, where is the abnormality? And the term that was drilled into my head early on was surround abnormality with normality.
00:39:46
Speaker
What's meant here is for the EMG or going through an exam, if I can localize all my abnormal findings to the median nerve at the wrist, everything else I've assessed is normal. I feel pretty comfortable calling this a compressive problem of the median nerve at the wrist. And I can quantify is there myelin damage and or axon damage. Pretty straightforward. But what if at the right wrist or at the right hand, I'm finding median and ulnar findings?
00:40:19
Speaker
Does the person have carpal tunnel syndrome and cubital tunnel? Do they have a peripheral neuropathy? Do they have a diabetic polyneuropathy? Because I haven't put a boundary around what's happening, I have to keep going. I would then look at the other upper extremity, and i would start I would also by default assess a lower extremity to open up the possibility of this being a polyneuropathy. The reason I bring this up is if you can get in your head that a lot of your clinical exam can approximate
00:40:52
Speaker
an EMG by looking for patterns, you can actually get much closer to a definitive, and I put definitive in air quotes, to a definitive diagnosis or at least a differential diagnosis with your clinical exam.
00:41:06
Speaker
Let's take your muscle testing, for example. Assuming that the patient is relatively cognitive and cognitively intact, is cooperating, if you start going through and assessing various, let's say, upper extremity muscles, and you're finding weakness, and as you follow this back up, let's say, oh, I've got weakness in radially innervated muscles, and and axillary muscles, the common pathway there is the posterior cord of the plexus. Could this be a plexus injury?
00:41:37
Speaker
You're putting then, instead of just saying, well, deltoids at four out of five, wrist extensions, four out of five, everything else is five out of five. Huh, okay. No, you're starting to look at patterns based on peripheral nerve, based on plexus, based on cervical nerve root patterns. That's really, when I do an EMG test,
00:41:58
Speaker
I'm following the nerve from the muscle back up through the brachial plexus, up through cervical nerve roots and in. And I'm seeing, okay, which of those, and I'll use the term roads, seems to be blocked. And that provides the information to determine, okay, where's the problem coming from?
00:42:16
Speaker
Now, if we've got more of a demyelinating problem, your muscle testing should be normal. Your reflexes should be normal. And I should have mentioned your muscle tests and you combine your reflexes as well, obviously, to get that muscle picture.
00:42:30
Speaker
But if it's a demyelinating problem, your strength testing should be normal. Reflexes should be normal. And you're probably going to rely a little bit more on your sensory exam. And really, you may be considering going as deep as Okay, I'll use two-point discrimination in the hand. Maybe I'll use the monofilament and I'll start getting a really good sensory map.
00:42:50
Speaker
Keep in mind, there's also CPGs in terms of some clinical prediction guidelines in terms of what increases and decreases your pre and post test likelihood. And it's not always the clinical exam you may think. So I believe there's a test cluster at the neck for ruling in cervical radiculopathy. There's a test item cluster for carpal tunnel syndrome as well that combines multiple factors. So you can use evidence-based practice to also help you rule in and rule out conditions.
00:43:23
Speaker
One big take home I would advocate for or mention is anytime you see significant muscle atrophy, that's a call to action. That is something that is telling you that there is an interruption of that neuromuscular junction. That muscle is to some extent denervated. It's lost axonal connection. That is something that The patient cannot actively change. That's a call-out sign. That's those fish in the aquarium jumping up saying, hey, someone feed me, feed me. So that is a higher level of severity.
00:43:59
Speaker
And almost by default, by seeing profound atrophy, you can infer that there's going to be some amount of
Clinical Exams vs EMG Findings
00:44:06
Speaker
axon damage. So when you've got if you've got a patient that comes in and you're seeing significant atrophy, you'll obviously take your clinical history, do your exam. But that may be someone that could benefit from an EMG, especially if they've not been worked up to that point before, because they may benefit from a more intense intervention to try and improve nerve function.
00:44:31
Speaker
Anytime I see atrophy, whether it was when I was doing EMGs or even now clinically, I sit up and take notice. It's not that I ignore tingling or sensory disturbances disturbances. Those are a little more challenging, in my opinion, to determine where overall physiologic severity versus the atrophy is something that warrants immediate consideration. Big picture, if we think about we've got a muscle that has some amount of atrophy and we're trying to think about, well, let's refer for an EMG and what is their potential for improvement from a physiologic perspective? Muscle remains viable for re-innervation for about one and a half to two years. Obviously, sooner is better than later. But what will happen over time if the neuromuscular junction is disrupted and those fish in that fish tank aren't fed for a year and a half to two years, the muscle loses its ability to contract. It loses its ability to respond to electrical signals. It becomes non-contractile.
00:45:38
Speaker
I've actually performed needle EMGs on patients who have had atrophy for years. And when you insert the needle into healthy muscle, there's a kinesthetic sense. You can feel the resistance. You feel kind of the give.
00:45:52
Speaker
When you insert a needle into muscle that's been atrophied and is no longer able to contract, it feels gritty. It feels like putting a needle into sand. I say this then to think about from a prognosis perspective, if you've got someone with peripheral nerve damage, they've got axon loss, they've got atrophy, the clock is ticking, you need to get them progressed into some kind of intervention. within a year and a half to two years. And really, I would argue that's the upper, upper, or upper limit. That's the theoretical limit. We want them in much, much sooner than that.
00:46:28
Speaker
To recap here then, what I would like to see for those of you in what I would consider standard practice, maybe you're in an outpatient setting, it doesn't really matter what setting, maybe your patient has some ill-defined neurologic symptoms that you think are peripheral, and you're wondering, should I refer for an EMG? I'd like you to consider what information would the EMG give you that would change the management? Can you refine your clinical exam such that you've now created a pretty good differential diagnosis? So instead of throwing your hands up and saying, I don't know, their their hand is kind of numb and tingly,
00:47:06
Speaker
Okay, let's apply some pre-test likelihoods. Let's see, okay, in this age range, the most likely would be carpal tunnel syndrome. They don't have a history of diabetes, so I put diabetic neuropathy down lower. I need to rule out cervical radiculopathy, so I'm going to do some testing there. I'm going to do some guided muscle tests that combine muscles within groups of peripheral nerves, which within distributions within the plexus and distributions at the cervical nerve root level. I'm going to test reflexes and I'm going to do a good sensory exam. And you can get, believe it or not, very close to what you would get on a well-guided EMG.
Conclusion and Recap
00:47:45
Speaker
Today, then we've covered a lot. We've talked about the what, how, why, of EMG and NCS. Hopefully got a little bit of background there on what the test entails.
00:47:58
Speaker
Talked about peripheral nerve injury and repair. key take homes there being, is this a demyelinating problem or a problem with the myelin? Is this an axon problem or is this a problem with the axon and the supporting structures? And you learned about the relative prognosis for each bucket.
00:48:16
Speaker
And then finally, concluding with really taking a thorough look at your clinical exam, the extensive amount of information you can get from a well-guided clinical exam, getting a good differential diagnosis before you potentially recommend or refer out for an EMG. and thinking about how an EMG may change your clinical decision-making and may change the outcomes for the patient.
00:48:41
Speaker
Thank you for listening to the NeuroPowerHour. I'm your host, Dr. Michael Powers, and I hope to catch you next episode to continue learning.