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Diagnosing CIDP with Nerve Conduction Studies

Mark B. Bromberg, MD, PhD, Neurology, talks about the use of nerve conduction studies to help diagnose CIDP and differentiate it from other neuropathies.

Transcript

Diagnosing CIDP with Nerve Conduction Studies

Mark B. Bromberg, MD, PhD, Neurology, talks about the use of nerve conduction studies to help diagnose CIDP and differentiate it from other neuropathies.

My name is Mark Bromberg. I'm a professor of neurology at the University of Utah. I began my career with a doctoral degree in neurophysiology. When I decided to go into clinical medicine, I chose neurology with the subspecialization in nerve and muscle disorders and clinical neurophysiology. Today I would like to talk about diagnosing inflammatory neuropathies using nerve conduction studies, and the inflammatory neuropathy we're going to be focusing on is chronic inflammatory demyelinating polyradiculoneuropathy, or CIDP.

There are other forms to consider. One is a variant of CIDP called multifocal acquired demyelinating sensory and motor neuropathy with conduction block, also abbreviated MADSAM or called Lewis-Sumner syndrome. And then there are others that are rare, multifocal motor neuropathy with conduction block, or MMN. But the key for this with respect to the demyelination is that there's greater slowing than expected for the degree of axonal loss. And there is focal conduction block that is away from common entrapment sites. Please keep in mind that when you start electrodiagnostic study, you will always need to have the historical context of what the patient is describing to you. Second, you need to examine the patient and then you have that information going into the nerve conduction studies.

So first there's a history. And so for inflammatory neuropathies, we're talking about acute neuropathies and chronic neuropathies. For neuromuscular disorders, the time course for acute is really over about 4 weeks. And the time course for chronic is greater than 8 weeks. So we can easily separate for the most part Guillain-Barré syndrome, AIDP, and AMAN from what we're talking about CIDP by the time course. Because CIDP has to have a progression of greater than 8 weeks. On the examination, the more common kind of neuropathy is a primary axonal neuropathy, which has mostly distal involvement, whereas CIDP has both distal symptoms and proximal symptoms. The second is that CIDP has involvement of both motor and sensory fibers, whereas AMAN and MMN has involvement of only motor fibers. And then the reflexes are going to be in CIDP, certainly absent in the legs, and reduced in the arms or globally absent in legs and arms. So going into the neuropathy from the patient's history and examination, we have a reasonable idea that we're looking for evidence of primary demyelination.

Now when we do nerve conductions, we have a choice of stimulating and recording from sensory nerves or motor nerves. Now keep in mind that with sensory nerves, you're stimulating the nerve and you're recording from the nerve. So you're looking in the sensory nerve action potential. You're looking at the summation of nerve fiber action potentials, which are small in amplitude. So overall, the amplitude of sensory nerve action potentials is in microvolts. The problem is, as you begin to lose sensory nerves from secondary axonal loss; when you've lost about two-thirds of them, then the response goes to zero. So if you have zero response, you can't look at timing or conduction velocity.

In contrast, with motor nerve conductions of the compound muscle action potential, you're stimulating the nerve but you're recording from muscle fiber action potentials. And there's an amplification of the number of muscle fiber action potentials. Muscle fibers are larger in diameter, so overall, the compound muscle action potential is measured in millivolts. And that means we have the ability, except in the most severe cases, of being able to record conduction velocity and other measurements. Therefore, most of our information that we use to try to determine primary demyelinating and primary axonal pathology comes from motor nerve conduction studies. I will show a little later on there are some sensory findings, if present, can help you with the diagnosis.

Now when you do your nerve conductions, there are going to be metrics. There are going to be things that you measure. And I try to divide them into 2 categories. One is measures that give you some idea of the number of axons and that would be the amplitude of the compound muscle action potential. Or as I'll show you, probably a little more robust measure is the area. And then the other ones are going to be timing that is the integrity of the myelin.

Now back to the amplitude. There is a caveat and that is that as you begin to lose motor fibers, you're going to have collateral sprouting. And that's going to raise the amplitude or reduce the drop in the amplitude of the compound muscle action potential, so that's why it's only roughly proportional. And the second is that with the slowing of conduction, you're going to have a spread out of the rival times of the individual potentials that contribute to the compound muscle action potential, and that's abnormal temporal dispersion. And this is an important concept that we'll spend more time on in a moment. For the timing, which is the integrity of the myelin, we have 3 major measures that we look at. We look at the distal latency, the F-wave latency, the conduction velocity. And then in there, there's another one, which is the duration of the compound potential. Again, we'll talk about that.

One major issue is how much slowing would you expect if you just lost axons. So here we have a diagram showing 4 different axons…the compound potential that goes into making the compound potential. And you can see that there's one at the top that arrives soonest and then the others come a little bit later and they summarize. And so when you do your timing measurements, you're really recording from the single fastest fiber, which is the top left-hand one. And so we have there a conduction velocity of 55 meters per second and that little horizontal arrows are the latency.

In the middle one, we have lost the fastest fiber, so the pathology arbitrarily involved the fastest fiber. So now, the first one that gets there is not the fastest one, and you can see the conduction velocity is now only 51 meters per second and that distal latency is a little bit longer. In the right side, we lose 2 fibers. Conduction velocity is now even lower and the distal latency is longer. So you have to appreciate that as the amplitude of the compound potential decreases, the distal latency and the conduction velocity will increase to a marginal degree.

Now another way to look at the arrival time of these individual potentials that go to make up the compound potential is to envision a field of runners. We have the fastest runners that consistently run at 6-minute miles and we have the slowest runner who consistently runs at 7-minute miles. So if the race is over 1 mile, then the distribution of the runners crossing the finish line will be 1 minute. On the other hand, if the race is 10 miles and everybody is consistent with the running rate, you can see that the distribution will be 10 minutes. So this is the normal temporal distribution of the action potentials that go to make up the compound muscle action potential over longer distances. And the measure of this is that dispersion, and you can see that with the dark arrow.

Now I want to show you some models of how abnormal temporal dispersion affects the amplitude of the compound potential. I'm going to take you back to your medical school physiology. And you can see in 1939 or so when they were first beginning to show that the compound potential was due to the sum of the underlying elements, they used triangles there. The other component we have to keep in mind is that the phases of the potentials are biphasic. We've got a negative and a positive and there's a phase to it. And there's going to be phase cancellation. And so here you see on the upper right is a real single motor unit wave form. And below that is the triangular representation. And by convention, negative is up and positive is down. And you can see that the negative component is about 4 milliseconds in duration. The positive component is about 2 milliseconds in duration. So the whole element is about 6 to 8 milliseconds in duration. The other important thing is to keep in mind that of the spectrum of different diameters of motor fibers, the fastest conduct at about 55 meters per second and the slowest conduct at about 40 meters per second.

So let's put this together to show you how there is phase cancellation to get the compound potential. So you can see that we have 4 motor units shown here. One arrived sooner than the other, so they're dispersed in time. And you can see it's not the simple summation of the amplitude of the negative and positive peaks, but it's the algebraic summation. You can see the summary sign below there. That's the consequence that gives you the compound muscle potential amplitude.

Now let's put this together in a real context. So as you can see here, these are the wave forms stimulating at the wrist for the first one, stimulating below the elbow for the second one, above the elbow for the third one, in the axilla for the fourth one, and at Erb's point for the fifth one. And you can see that the amplitude drops to a small degree, 21%. But as I mentioned earlier, the area may be a more robust measure because it drops only 19%. And the duration of this gets spread out of it. The same way the runners running over 1 mile versus 10 miles, it spreads out about 11%. So that's the negative peak duration.

Now that you've seen in this slide the change that you'd expect in a normal compound potential, let us look in pathologic situations, factoring in how much axonal loss there is. In particular, how much change in distal latency, F-wave latency, and conduction velocity would be expected with axonal loss? One way to put this into general terms is to use or express it as the laboratory's upper and lower limits of normal. The pathologic condition that we can take, which is pure axonal loss, is amyotrophic lateral sclerosis, or ALS. So there, there is death of axons and no change in the myelin. So when you look at the data from a large number of patients with ALS, you can look at the limits of slowing based on axonal loss. So for conduction velocity, there is slowing that is less than 25% so their values will be greater than 75% of the lower limit of normal. For distal latency and F-wave latency, there'll be prolongation that's less than 25%. So those values will be less than 125% of the upper limit of normal.

Now let's look at the effects, not of axonal loss, but abnormal temporal dispersion. So we're now looking at the change when we go back to the analogy of runners where we're looking at the spread out of the arrival times of the runners over a longer distance. So here we have our diagram where we have 3 motor units illustrated by the biphasic triangles in the upper left when you stimulate distally. And then when you stimulate more proximally, so there's travel over this longer distance, there will be a normal degree of temporal dispersion. And you can see that the amplitude of the compound potential is slightly lower in amplitude.

Now let's contrast that with abnormal temporal dispersion in the lower set. On the left, we have it at distal stimulation and the right, we have it at proximal stimulation where they've had greater spread out of the arrival times of those 3 potentials. And with phase cancellation, the amplitude has dropped quite a bit, but also there's increase in duration of the negative potential. So that drop in amplitude can be monitored or marked by also looking at the degree of abnormal temporal dispersion as measured by the negative peak duration. So that's another number to keep in mind when you're analyzing your nerve conduction studies.

So there are some corollaries that we can use to our advantage. In other words, if we want to estimate how much abnormal temporal dispersion there is, we want to record over a longer distance. And the ulnar nerve is a good example for that, because we can stimulate as I showed you in the several slides earlier, not only at the wrist, below, and above the elbow, but also in the axilla and sometimes at Erb's point. So we can get a much longer segment of nerve to look at. I would caution not doing the same with the median nerve, because the median and ulnar nerve are relatively close together in the axilla at Erb's point, and you may be overstimulating the median nerve and bringing in ulnar nerve responses, which would confuse the compound muscle action potential that you're recording from.

As I mentioned before, CIDP is characterized by focal demyelination, which can cause focal conduction block. That means different foci along the nerve. So here's a cartoon showing 9 nerve fibers. The top one is the smallest diameter fiber. The bottom one is the largest diameter fiber. And you can see there that some of the nerve segments are missing and hence that represents focal demyelination. In the top cartoon, we're stimulating distally and the bottom cartoon, we're stimulating proximally. When we stimulate distally, there can be slowing of some of the nerve fibers getting to the electrode, so the distal latency may be a little bit longer. When we stimulate proximally, you can see that some of those fibers are blocked. So the amplitude of the response is going to be a good bit lower because those fibers are not contributing to the compound potential. So you can appreciate that if we stimulate even more proximally with a longer distance of nerves to accumulate the multifocal demyelination, we might find even greater loss of amplitude.

And so here's an example. On the left, we have normal nerve conduction stimulating at the wrist, below and above, the elbow, and the right we have a patient who's got clear multifocal demyelination. And you can see that the amplitude drops markedly in part because of conduction block. And the negative peak duration spreads out, which would be due to abnormal temporal dispersion, and that also will contribute to the reduction in the amplitude. So on the right-hand side, we have a very nice example of multifocal demyelination as would be seen in CIDP.

Thank you. And I hope that my talk with you today has helped you understand how to use nerve conduction studies to confirm the diagnosis of CIDP.

Transcript

Diagnosing CIDP with Nerve Conduction Studies

Mark B. Bromberg, MD, PhD, Neurology, talks about the use of nerve conduction studies to help diagnose CIDP and differentiate it from other neuropathies.

My name is Mark Bromberg. I'm a professor of neurology at the University of Utah. I began my career with a doctoral degree in neurophysiology. When I decided to go into clinical medicine, I chose neurology with the subspecialization in nerve and muscle disorders and clinical neurophysiology. Today I would like to talk about diagnosing inflammatory neuropathies using nerve conduction studies, and the inflammatory neuropathy we're going to be focusing on is chronic inflammatory demyelinating polyradiculoneuropathy, or CIDP.

There are other forms to consider. One is a variant of CIDP called multifocal acquired demyelinating sensory and motor neuropathy with conduction block, also abbreviated MADSAM or called Lewis-Sumner syndrome. And then there are others that are rare, multifocal motor neuropathy with conduction block, or MMN. But the key for this with respect to the demyelination is that there's greater slowing than expected for the degree of axonal loss. And there is focal conduction block that is away from common entrapment sites. Please keep in mind that when you start electrodiagnostic study, you will always need to have the historical context of what the patient is describing to you. Second, you need to examine the patient and then you have that information going into the nerve conduction studies.

So first there's a history. And so for inflammatory neuropathies, we're talking about acute neuropathies and chronic neuropathies. For neuromuscular disorders, the time course for acute is really over about 4 weeks. And the time course for chronic is greater than 8 weeks. So we can easily separate for the most part Guillain-Barré syndrome, AIDP, and AMAN from what we're talking about CIDP by the time course. Because CIDP has to have a progression of greater than 8 weeks. On the examination, the more common kind of neuropathy is a primary axonal neuropathy, which has mostly distal involvement, whereas CIDP has both distal symptoms and proximal symptoms. The second is that CIDP has involvement of both motor and sensory fibers, whereas AMAN and MMN has involvement of only motor fibers. And then the reflexes are going to be in CIDP, certainly absent in the legs, and reduced in the arms or globally absent in legs and arms. So going into the neuropathy from the patient's history and examination, we have a reasonable idea that we're looking for evidence of primary demyelination.

Now when we do nerve conductions, we have a choice of stimulating and recording from sensory nerves or motor nerves. Now keep in mind that with sensory nerves, you're stimulating the nerve and you're recording from the nerve. So you're looking in the sensory nerve action potential. You're looking at the summation of nerve fiber action potentials, which are small in amplitude. So overall, the amplitude of sensory nerve action potentials is in microvolts. The problem is, as you begin to lose sensory nerves from secondary axonal loss; when you've lost about two-thirds of them, then the response goes to zero. So if you have zero response, you can't look at timing or conduction velocity.

In contrast, with motor nerve conductions of the compound muscle action potential, you're stimulating the nerve but you're recording from muscle fiber action potentials. And there's an amplification of the number of muscle fiber action potentials. Muscle fibers are larger in diameter, so overall, the compound muscle action potential is measured in millivolts. And that means we have the ability, except in the most severe cases, of being able to record conduction velocity and other measurements. Therefore, most of our information that we use to try to determine primary demyelinating and primary axonal pathology comes from motor nerve conduction studies. I will show a little later on there are some sensory findings, if present, can help you with the diagnosis.

Now when you do your nerve conductions, there are going to be metrics. There are going to be things that you measure. And I try to divide them into 2 categories. One is measures that give you some idea of the number of axons and that would be the amplitude of the compound muscle action potential. Or as I'll show you, probably a little more robust measure is the area. And then the other ones are going to be timing that is the integrity of the myelin.

Now back to the amplitude. There is a caveat and that is that as you begin to lose motor fibers, you're going to have collateral sprouting. And that's going to raise the amplitude or reduce the drop in the amplitude of the compound muscle action potential, so that's why it's only roughly proportional. And the second is that with the slowing of conduction, you're going to have a spread out of the rival times of the individual potentials that contribute to the compound muscle action potential, and that's abnormal temporal dispersion. And this is an important concept that we'll spend more time on in a moment. For the timing, which is the integrity of the myelin, we have 3 major measures that we look at. We look at the distal latency, the F-wave latency, the conduction velocity. And then in there, there's another one, which is the duration of the compound potential. Again, we'll talk about that.

One major issue is how much slowing would you expect if you just lost axons. So here we have a diagram showing 4 different axons…the compound potential that goes into making the compound potential. And you can see that there's one at the top that arrives soonest and then the others come a little bit later and they summarize. And so when you do your timing measurements, you're really recording from the single fastest fiber, which is the top left-hand one. And so we have there a conduction velocity of 55 meters per second and that little horizontal arrows are the latency.

In the middle one, we have lost the fastest fiber, so the pathology arbitrarily involved the fastest fiber. So now, the first one that gets there is not the fastest one, and you can see the conduction velocity is now only 51 meters per second and that distal latency is a little bit longer. In the right side, we lose 2 fibers. Conduction velocity is now even lower and the distal latency is longer. So you have to appreciate that as the amplitude of the compound potential decreases, the distal latency and the conduction velocity will increase to a marginal degree.

Now another way to look at the arrival time of these individual potentials that go to make up the compound potential is to envision a field of runners. We have the fastest runners that consistently run at 6-minute miles and we have the slowest runner who consistently runs at 7-minute miles. So if the race is over 1 mile, then the distribution of the runners crossing the finish line will be 1 minute. On the other hand, if the race is 10 miles and everybody is consistent with the running rate, you can see that the distribution will be 10 minutes. So this is the normal temporal distribution of the action potentials that go to make up the compound muscle action potential over longer distances. And the measure of this is that dispersion, and you can see that with the dark arrow.

Now I want to show you some models of how abnormal temporal dispersion affects the amplitude of the compound potential. I'm going to take you back to your medical school physiology. And you can see in 1939 or so when they were first beginning to show that the compound potential was due to the sum of the underlying elements, they used triangles there. The other component we have to keep in mind is that the phases of the potentials are biphasic. We've got a negative and a positive and there's a phase to it. And there's going to be phase cancellation. And so here you see on the upper right is a real single motor unit wave form. And below that is the triangular representation. And by convention, negative is up and positive is down. And you can see that the negative component is about 4 milliseconds in duration. The positive component is about 2 milliseconds in duration. So the whole element is about 6 to 8 milliseconds in duration. The other important thing is to keep in mind that of the spectrum of different diameters of motor fibers, the fastest conduct at about 55 meters per second and the slowest conduct at about 40 meters per second.

So let's put this together to show you how there is phase cancellation to get the compound potential. So you can see that we have 4 motor units shown here. One arrived sooner than the other, so they're dispersed in time. And you can see it's not the simple summation of the amplitude of the negative and positive peaks, but it's the algebraic summation. You can see the summary sign below there. That's the consequence that gives you the compound muscle potential amplitude.

Now let's put this together in a real context. So as you can see here, these are the wave forms stimulating at the wrist for the first one, stimulating below the elbow for the second one, above the elbow for the third one, in the axilla for the fourth one, and at Erb's point for the fifth one. And you can see that the amplitude drops to a small degree, 21%. But as I mentioned earlier, the area may be a more robust measure because it drops only 19%. And the duration of this gets spread out of it. The same way the runners running over 1 mile versus 10 miles, it spreads out about 11%. So that's the negative peak duration.

Now that you've seen in this slide the change that you'd expect in a normal compound potential, let us look in pathologic situations, factoring in how much axonal loss there is. In particular, how much change in distal latency, F-wave latency, and conduction velocity would be expected with axonal loss? One way to put this into general terms is to use or express it as the laboratory's upper and lower limits of normal. The pathologic condition that we can take, which is pure axonal loss, is amyotrophic lateral sclerosis, or ALS. So there, there is death of axons and no change in the myelin. So when you look at the data from a large number of patients with ALS, you can look at the limits of slowing based on axonal loss. So for conduction velocity, there is slowing that is less than 25% so their values will be greater than 75% of the lower limit of normal. For distal latency and F-wave latency, there'll be prolongation that's less than 25%. So those values will be less than 125% of the upper limit of normal.

Now let's look at the effects, not of axonal loss, but abnormal temporal dispersion. So we're now looking at the change when we go back to the analogy of runners where we're looking at the spread out of the arrival times of the runners over a longer distance. So here we have our diagram where we have 3 motor units illustrated by the biphasic triangles in the upper left when you stimulate distally. And then when you stimulate more proximally, so there's travel over this longer distance, there will be a normal degree of temporal dispersion. And you can see that the amplitude of the compound potential is slightly lower in amplitude.

Now let's contrast that with abnormal temporal dispersion in the lower set. On the left, we have it at distal stimulation and the right, we have it at proximal stimulation where they've had greater spread out of the arrival times of those 3 potentials. And with phase cancellation, the amplitude has dropped quite a bit, but also there's increase in duration of the negative potential. So that drop in amplitude can be monitored or marked by also looking at the degree of abnormal temporal dispersion as measured by the negative peak duration. So that's another number to keep in mind when you're analyzing your nerve conduction studies.

So there are some corollaries that we can use to our advantage. In other words, if we want to estimate how much abnormal temporal dispersion there is, we want to record over a longer distance. And the ulnar nerve is a good example for that, because we can stimulate as I showed you in the several slides earlier, not only at the wrist, below, and above the elbow, but also in the axilla and sometimes at Erb's point. So we can get a much longer segment of nerve to look at. I would caution not doing the same with the median nerve, because the median and ulnar nerve are relatively close together in the axilla at Erb's point, and you may be overstimulating the median nerve and bringing in ulnar nerve responses, which would confuse the compound muscle action potential that you're recording from.

As I mentioned before, CIDP is characterized by focal demyelination, which can cause focal conduction block. That means different foci along the nerve. So here's a cartoon showing 9 nerve fibers. The top one is the smallest diameter fiber. The bottom one is the largest diameter fiber. And you can see there that some of the nerve segments are missing and hence that represents focal demyelination. In the top cartoon, we're stimulating distally and the bottom cartoon, we're stimulating proximally. When we stimulate distally, there can be slowing of some of the nerve fibers getting to the electrode, so the distal latency may be a little bit longer. When we stimulate proximally, you can see that some of those fibers are blocked. So the amplitude of the response is going to be a good bit lower because those fibers are not contributing to the compound potential. So you can appreciate that if we stimulate even more proximally with a longer distance of nerves to accumulate the multifocal demyelination, we might find even greater loss of amplitude.

And so here's an example. On the left, we have normal nerve conduction stimulating at the wrist, below and above, the elbow, and the right we have a patient who's got clear multifocal demyelination. And you can see that the amplitude drops markedly in part because of conduction block. And the negative peak duration spreads out, which would be due to abnormal temporal dispersion, and that also will contribute to the reduction in the amplitude. So on the right-hand side, we have a very nice example of multifocal demyelination as would be seen in CIDP.

Thank you. And I hope that my talk with you today has helped you understand how to use nerve conduction studies to confirm the diagnosis of CIDP.


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Terms to know

IG=immune globulin, CIDP=chronic inflammatory demyelinating polyneuropathy, PIDD=primary immunodeficiency disease, ITP=idiopathic thrombocytopenic purpura, Sub Q=subcutaneous, IV=intravenous, ICE=10% caprylate-chromatography purified immune globulin intravenous (IGIV-C) CIDP efficacy.

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