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Electrodiagnostic Criteria: A Case Study

Ken Gorson, MD, Neurology, presents a case study and reviews the electrodiagnostic criteria findings that led to a diagnosis.

Transcript

Electrodiagnostic Criteria: A Case Study

Ken Gorson, MD, Neurology, presents a case study and reviews the electrodiagnostic criteria findings that led to a diagnosis.

Hello, my name is Ken Gorson, and I'm professor of neurology at Tufts University School of Medicine, and I'd like to talk about Electrodiagnostic Criteria for CIDP.

First, I'd like to start with a case presentation. This was a 37-year-old woman who came in with symptoms of trouble walking that she's had for about 4 months. She noted that her balance was poor, she was tripping frequently, and had an unsteady gait, and she complained of painless symmetric leg weakness, noting that her hands and arms were unaffected. She was also aware of some subtle tingling and numbness in the feet.

Her medical history is relevant for schizoaffective disease, and she had multiple prior psychiatric evaluations for delusional thinking. She had been stable recently, treated with Tegretol and regular therapy with electroconvulsive treatments. She's had no recent psychotic episodes. Unfortunately, because of years of lithium treatment, she developed secondary endstage renal disease for the last 3 years, and recently started hemodialysis.

On examination, she had reduced grip strength, weakness in the hands and distal muscles of the legs, with normal proximal strength, normal reflexes in the arms, but absent leg reflexes, and loss of touch and vibration in the feet, extending up to the mid-leg, with a Romberg's sign.

Here are her electrodiagnostic findings. What one sees is a generalized reduction in all of the distal motor amplitudes of the nerves in the arms and the legs, with relatively normal conduction velocities, or just slight slowing, commensurate with a degree of axon loss, and relatively normal distal latencies, and no conduction block.

Similarly, her F responses were just slightly prolonged in the legs, and normal or near normal in the arms. Her sensory nerve action potential studies demonstrated absent potentials in the legs, and reduced median and sensory potentials in the upper limbs.

So there are several types of acquired demyelination that are important to recognize. On the first panel off to the left, one sees what looks to be a prolonged distal motor latency, implying distal nerve demyelination. If we look at the panel below, on the left, you see a very classical pattern of what's termed temporal dispersion, where, due to conduction block, conduction failure, or varying degrees of slowness of individual axons in their conduction velocities, the wave forms become prolonged and reduced in amplitude.

On the panel in the lower right, you see a classical pattern of conduction block with proximal nerve stimulation. So the distal waveform in image A looks quite normal, but, following proximal nerve stimulation, not all of the fibers are conducting properly through a presumed demyelinating segment, producing the pattern of conduction block.

If you look at the upper panel, off to the right, you see another example of conduction block, and it's also a form of acquired demyelination, but it, in fact, reflects entrapment neuropathy. So the 2 upper images show the normal median potentials, proximally and distally, and then the third image down shows normal distal conduction of the ulnar nerve at the wrist, normal amplitude at the below groove segment, but marked amplitude reduction with more proximal stimulation at the above groove area, Erb's point and axilla, suggesting entrapment neuropathy ulnar nerve localized to the elbow.

So there are a number of diagnostic criteria for CIDP. They exist but, sadly, they are underutilized. It's very important to recognize these criteria because they guide therapy and prognosis. We have clinical criteria, based on history and examination by a qualified neurologist, and electrophysiologic criteria by a qualified electromyographer. We encounter problems when these criteria are not used because they lead to diagnostic and treatment misadventures.

So the first electrodiagnostic criteria were Albers and Kelly in 1989, where they recognized the parameters of acquired demyelination, showing that conduction velocities below 75% of the lower limit of normal are simply too slow for healthy axons. And it implies there has to be an element of demyelination. Likewise, if there are prolonged distal motor latencies above 125% of the upper limit of normal, this suggests distal demyelination, aside from any associated axonal component. And the same is true with proximal nerve function, looking at prolonged F responses. And they define temporal dispersion, or conduction block, as an amplitude decrement of 30% following proximal nerve stimulation.

They require to see each of these abnormalities in at least 2 nerves to try and demonstrate that this is a widespread demyelinating neuropathy. We now recognize that these parameters are very important in terms of the cutoffs that we use. So there are 4 basic parameters to try and assess nerve demyelination: prolonged or absent F-responses; prolonged distal motor latencies; slowed conduction velocities; and conduction block, or temporal dispersion.

So this was the AAN electrodiagnostic criteria, developed by consensus committee in 1991. And they modulated the cutoff slightly from the Albers and Kelly criteria, noting that they reduced the cutoff to 120% for F-responses in 2 or more nerves. They reduced the degree of prolongation of distal latencies to 120%. Slowed conduction velocities were changed to less than 80% of the lower limit of normal, and they changed conduction block to 20%.

However, they made the criteria stringent in order to diagnose CIDP using these criteria. Three of these 4 abnormalities must be seen in at least 2 nerves. And thus, this was more developed for research criteria with very high specificity at the sacrifice of low sensitivity.

I'd like to move on to the Koski criteria. There weren't many other criteria developed before this, and I'll review them briefly in terms of some difficulties with those self-referential criteria. The Koski criteria are the only validated criteria using stringent scientific methods, and I want to spend a little bit of time on this. This was a committee that was formed from the GBS CIDP Foundation of 13 CIDP experts. And all of these experts submitted clinical cases and data, actual case records and EMG, and all pertinent laboratory data, spinal fluid information, nerve biopsies, and so forth. Each of the members of the committee voted on whether these cases represented CIDP, other acquired forms of demyelinating neuropathy, or other neuropathy, such as toxic neuropathies, diabetic neuropathy, and so forth. There were 267 cases submitted, and 106 cases were defined as CIDP, because 11 or more of the 13 members agreed that they represented CIDP. Then what was done was to use statistical analysis, classification, and regression tree analysis specifically to determine which variables were relevant in making a clinical diagnosis and electrodiagnostic diagnosis.

So all this information was inputted into a computer, and there was a derivation sample. So, from the 267 cases, about half of that sample was used to devise so-called diagnostic rules. And so, the diagnostic rules are presented on the slide. If a patient has a chronic polyneuropathy for at least 8 weeks, they could be classified as having CIDP if there was no evidence of a serum paraprotein, and no documented genetic abnormality.

In that situation, there were clinical rules. Namely, the patient had to have a symmetric onset of symmetrical weakness on examination and involve all 4 limbs, and have to have weakness proximally in at least one limb. There are also electrodiagnostic criteria. And, in this situation, it is very important to study large numbers of nerves and recognize that often we have no responses. So if you don't have a response, you can't classify the nerve, you cannot determine whether the initial inciting nerve injury was axonal or demyelinating.

What that said, if 75% of the motor nerves had a recruitable response, then any of the following conditions would qualify. If more than half of the nerves studied had prolonged distal latency, slowed conduction velocity, or prolonged F-response using the cutoffs for the AAN criteria, they would qualify for electrodiagnostic criteria of CIDP.

So, for example, if 7 nerves were studied, 2 nerves were unresponsive, but 5 nerves were available to assess, if 3 of those 5 nerves showed any of those abnormalities, you can make the electrodiagnosis of CIDP. So, with the derivation sample, as one might anticipate if you applied the rules to the derivation sample, you're going to have very high sensitivity and specificity, as shown in this table. But the key was to apply the rules to the validation sample, the second half of the cohort. And when this was done, you can see excellent sensitivity, at around 83%, and very high specificity for the diagnosis at 97%.

Furthermore, when other criteria were applied to our cohort, for example, AAN criteria, or INCAT criteria, or EFNS criteria, you see that the sensitivity, at least for our 106 patients who had CIDP by classification, had very low sensitivity and limited specificity.

I'd like to move on and talk about the EFNS/PNS electrodiagnostic criteria for CIDP. So this is more for clinical use. Again, this is from a consensus committee of neuromuscular experts. And what you can see is that the number of nerves defined as demyelinating was loosened, such that only 2 nerves need to have the abnormalities, but the cutoffs for defining demyelination were much stricter. So instead of a 20% cutoff for distal latency, of F-response, that's now increased to 50%. Motor conduction velocity was increased, again, slowing had to be at least 30% or more. And partial conduction block was now defined as 50% or more, primarily because subsequent studies were able to demonstrate that one could find partial conduction block due to phase cancellation in normal nerves or in patients with axonopathies.

More frequently, now, the EFNS or Koski criteria are used to establish the electrodiagnosis of CIDP. There are shortcomings in electrodiagnostics and studies in CIDP. As many people see these patients, they recognize that there is often associated axon loss. And if there is substantial axon loss, the amplitudes can be reduced, and make it very difficult to see demyelinating abnormalities. There are rare variants of CIDP that are pure sensory, in which case the motor potentials are unaffected, and the sensory nerve action potentials may be greatly reduced or absent, but no demyelinating criteria are fulfilled.

There are occasional patients who have prominent proximal nerve demyelination, and if one cannot stimulate proximal to the site of conduction block or conduction slowing, we will not be able to determine the demyelinating abnormality to fulfill criteria. So this happens occasionally, where distal nerve segments are relatively spared. And then, of course, in clinical practice, with a combination of all of these issues, we recognize that patients may fulfill clinical criteria but not always fulfill all electrodiagnostic criteria, and yet they still have the disease.

So this is an excellent review paper by my colleague, Mark Bromberg. In 2011, he reviewed, at that time, what were the 16 published electrodiagnostic criteria for CIDP, and he discussed all of the pros and cons of each of the criteria. However, one of the major deficiencies of all of these criteria wasn't recognized, and that's the nature of the self-referential aspects when you establish new diagnostic criteria. So, for example, there are many well-intentioned investigators who feel that published criteria are not sufficient, and they move on to develop their own electrodiagnostic criteria, and then they apply them to their own cases.

Well, this is a problem because the cases that they've culled from their own databases had to get into the database by using some electrodiagnostic criteria, and frequently it may have been that the investigators used their new criteria to identify those CIDP cases. And if that's the situation, one can anticipate that those criteria would have very high sensitivity and specificity. And so, that's not the most ideal scientific method.

So, in summary, there are too many electrodiagnostic criteria for CIDP. So they clearly have design issues. Many are designed strictly for research purposes, others for clinical use. The major take-home message is that many criteria are not applied rigorously and consistently. And, more often than not, most investigators now have settled on either the EFNS or Koski criteria because both seem to have very high sensitivity and specificity. I think, most importantly, we need to educate our colleagues about routinely applying rigorous clinical and electrodiagnostic criteria to establish the diagnosis of CIDP.

Thank you for your attention, and I hope this information is helpful to manage your patients.

Transcript

Electrodiagnostic Criteria: A Case Study

Ken Gorson, MD, Neurology, presents a case study and reviews the electrodiagnostic criteria findings that led to a diagnosis.

Hello, my name is Ken Gorson, and I'm professor of neurology at Tufts University School of Medicine, and I'd like to talk about Electrodiagnostic Criteria for CIDP.

First, I'd like to start with a case presentation. This was a 37-year-old woman who came in with symptoms of trouble walking that she's had for about 4 months. She noted that her balance was poor, she was tripping frequently, and had an unsteady gait, and she complained of painless symmetric leg weakness, noting that her hands and arms were unaffected. She was also aware of some subtle tingling and numbness in the feet.

Her medical history is relevant for schizoaffective disease, and she had multiple prior psychiatric evaluations for delusional thinking. She had been stable recently, treated with Tegretol and regular therapy with electroconvulsive treatments. She's had no recent psychotic episodes. Unfortunately, because of years of lithium treatment, she developed secondary endstage renal disease for the last 3 years, and recently started hemodialysis.

On examination, she had reduced grip strength, weakness in the hands and distal muscles of the legs, with normal proximal strength, normal reflexes in the arms, but absent leg reflexes, and loss of touch and vibration in the feet, extending up to the mid-leg, with a Romberg's sign.

Here are her electrodiagnostic findings. What one sees is a generalized reduction in all of the distal motor amplitudes of the nerves in the arms and the legs, with relatively normal conduction velocities, or just slight slowing, commensurate with a degree of axon loss, and relatively normal distal latencies, and no conduction block.

Similarly, her F responses were just slightly prolonged in the legs, and normal or near normal in the arms. Her sensory nerve action potential studies demonstrated absent potentials in the legs, and reduced median and sensory potentials in the upper limbs.

So there are several types of acquired demyelination that are important to recognize. On the first panel off to the left, one sees what looks to be a prolonged distal motor latency, implying distal nerve demyelination. If we look at the panel below, on the left, you see a very classical pattern of what's termed temporal dispersion, where, due to conduction block, conduction failure, or varying degrees of slowness of individual axons in their conduction velocities, the wave forms become prolonged and reduced in amplitude.

On the panel in the lower right, you see a classical pattern of conduction block with proximal nerve stimulation. So the distal waveform in image A looks quite normal, but, following proximal nerve stimulation, not all of the fibers are conducting properly through a presumed demyelinating segment, producing the pattern of conduction block.

If you look at the upper panel, off to the right, you see another example of conduction block, and it's also a form of acquired demyelination, but it, in fact, reflects entrapment neuropathy. So the 2 upper images show the normal median potentials, proximally and distally, and then the third image down shows normal distal conduction of the ulnar nerve at the wrist, normal amplitude at the below groove segment, but marked amplitude reduction with more proximal stimulation at the above groove area, Erb's point and axilla, suggesting entrapment neuropathy ulnar nerve localized to the elbow.

So there are a number of diagnostic criteria for CIDP. They exist but, sadly, they are underutilized. It's very important to recognize these criteria because they guide therapy and prognosis. We have clinical criteria, based on history and examination by a qualified neurologist, and electrophysiologic criteria by a qualified electromyographer. We encounter problems when these criteria are not used because they lead to diagnostic and treatment misadventures.

So the first electrodiagnostic criteria were Albers and Kelly in 1989, where they recognized the parameters of acquired demyelination, showing that conduction velocities below 75% of the lower limit of normal are simply too slow for healthy axons. And it implies there has to be an element of demyelination. Likewise, if there are prolonged distal motor latencies above 125% of the upper limit of normal, this suggests distal demyelination, aside from any associated axonal component. And the same is true with proximal nerve function, looking at prolonged F responses. And they define temporal dispersion, or conduction block, as an amplitude decrement of 30% following proximal nerve stimulation.

They require to see each of these abnormalities in at least 2 nerves to try and demonstrate that this is a widespread demyelinating neuropathy. We now recognize that these parameters are very important in terms of the cutoffs that we use. So there are 4 basic parameters to try and assess nerve demyelination: prolonged or absent F-responses; prolonged distal motor latencies; slowed conduction velocities; and conduction block, or temporal dispersion.

So this was the AAN electrodiagnostic criteria, developed by consensus committee in 1991. And they modulated the cutoff slightly from the Albers and Kelly criteria, noting that they reduced the cutoff to 120% for F-responses in 2 or more nerves. They reduced the degree of prolongation of distal latencies to 120%. Slowed conduction velocities were changed to less than 80% of the lower limit of normal, and they changed conduction block to 20%.

However, they made the criteria stringent in order to diagnose CIDP using these criteria. Three of these 4 abnormalities must be seen in at least 2 nerves. And thus, this was more developed for research criteria with very high specificity at the sacrifice of low sensitivity.

I'd like to move on to the Koski criteria. There weren't many other criteria developed before this, and I'll review them briefly in terms of some difficulties with those self-referential criteria. The Koski criteria are the only validated criteria using stringent scientific methods, and I want to spend a little bit of time on this. This was a committee that was formed from the GBS CIDP Foundation of 13 CIDP experts. And all of these experts submitted clinical cases and data, actual case records and EMG, and all pertinent laboratory data, spinal fluid information, nerve biopsies, and so forth. Each of the members of the committee voted on whether these cases represented CIDP, other acquired forms of demyelinating neuropathy, or other neuropathy, such as toxic neuropathies, diabetic neuropathy, and so forth. There were 267 cases submitted, and 106 cases were defined as CIDP, because 11 or more of the 13 members agreed that they represented CIDP. Then what was done was to use statistical analysis, classification, and regression tree analysis specifically to determine which variables were relevant in making a clinical diagnosis and electrodiagnostic diagnosis.

So all this information was inputted into a computer, and there was a derivation sample. So, from the 267 cases, about half of that sample was used to devise so-called diagnostic rules. And so, the diagnostic rules are presented on the slide. If a patient has a chronic polyneuropathy for at least 8 weeks, they could be classified as having CIDP if there was no evidence of a serum paraprotein, and no documented genetic abnormality.

In that situation, there were clinical rules. Namely, the patient had to have a symmetric onset of symmetrical weakness on examination and involve all 4 limbs, and have to have weakness proximally in at least one limb. There are also electrodiagnostic criteria. And, in this situation, it is very important to study large numbers of nerves and recognize that often we have no responses. So if you don't have a response, you can't classify the nerve, you cannot determine whether the initial inciting nerve injury was axonal or demyelinating.

What that said, if 75% of the motor nerves had a recruitable response, then any of the following conditions would qualify. If more than half of the nerves studied had prolonged distal latency, slowed conduction velocity, or prolonged F-response using the cutoffs for the AAN criteria, they would qualify for electrodiagnostic criteria of CIDP.

So, for example, if 7 nerves were studied, 2 nerves were unresponsive, but 5 nerves were available to assess, if 3 of those 5 nerves showed any of those abnormalities, you can make the electrodiagnosis of CIDP. So, with the derivation sample, as one might anticipate if you applied the rules to the derivation sample, you're going to have very high sensitivity and specificity, as shown in this table. But the key was to apply the rules to the validation sample, the second half of the cohort. And when this was done, you can see excellent sensitivity, at around 83%, and very high specificity for the diagnosis at 97%.

Furthermore, when other criteria were applied to our cohort, for example, AAN criteria, or INCAT criteria, or EFNS criteria, you see that the sensitivity, at least for our 106 patients who had CIDP by classification, had very low sensitivity and limited specificity.

I'd like to move on and talk about the EFNS/PNS electrodiagnostic criteria for CIDP. So this is more for clinical use. Again, this is from a consensus committee of neuromuscular experts. And what you can see is that the number of nerves defined as demyelinating was loosened, such that only 2 nerves need to have the abnormalities, but the cutoffs for defining demyelination were much stricter. So instead of a 20% cutoff for distal latency, of F-response, that's now increased to 50%. Motor conduction velocity was increased, again, slowing had to be at least 30% or more. And partial conduction block was now defined as 50% or more, primarily because subsequent studies were able to demonstrate that one could find partial conduction block due to phase cancellation in normal nerves or in patients with axonopathies.

More frequently, now, the EFNS or Koski criteria are used to establish the electrodiagnosis of CIDP. There are shortcomings in electrodiagnostics and studies in CIDP. As many people see these patients, they recognize that there is often associated axon loss. And if there is substantial axon loss, the amplitudes can be reduced, and make it very difficult to see demyelinating abnormalities. There are rare variants of CIDP that are pure sensory, in which case the motor potentials are unaffected, and the sensory nerve action potentials may be greatly reduced or absent, but no demyelinating criteria are fulfilled.

There are occasional patients who have prominent proximal nerve demyelination, and if one cannot stimulate proximal to the site of conduction block or conduction slowing, we will not be able to determine the demyelinating abnormality to fulfill criteria. So this happens occasionally, where distal nerve segments are relatively spared. And then, of course, in clinical practice, with a combination of all of these issues, we recognize that patients may fulfill clinical criteria but not always fulfill all electrodiagnostic criteria, and yet they still have the disease.

So this is an excellent review paper by my colleague, Mark Bromberg. In 2011, he reviewed, at that time, what were the 16 published electrodiagnostic criteria for CIDP, and he discussed all of the pros and cons of each of the criteria. However, one of the major deficiencies of all of these criteria wasn't recognized, and that's the nature of the self-referential aspects when you establish new diagnostic criteria. So, for example, there are many well-intentioned investigators who feel that published criteria are not sufficient, and they move on to develop their own electrodiagnostic criteria, and then they apply them to their own cases.

Well, this is a problem because the cases that they've culled from their own databases had to get into the database by using some electrodiagnostic criteria, and frequently it may have been that the investigators used their new criteria to identify those CIDP cases. And if that's the situation, one can anticipate that those criteria would have very high sensitivity and specificity. And so, that's not the most ideal scientific method.

So, in summary, there are too many electrodiagnostic criteria for CIDP. So they clearly have design issues. Many are designed strictly for research purposes, others for clinical use. The major take-home message is that many criteria are not applied rigorously and consistently. And, more often than not, most investigators now have settled on either the EFNS or Koski criteria because both seem to have very high sensitivity and specificity. I think, most importantly, we need to educate our colleagues about routinely applying rigorous clinical and electrodiagnostic criteria to establish the diagnosis of CIDP.

Thank you for your attention, and I hope this information is helpful to manage your patients.


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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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