October 2026 Peripheral Nerve and Motor Neuron Disorders Issue With Dr. Noah Kolb

In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Noah A. Kolb, MD, who served as the guest editor of the October 2026 Peripheral Nerve and Motor Neuron Disorders issue. They provide a preview of the issue, which publishes on October 2, 2026.

Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota.

Dr. Kolb is a professor of neurological sciences at the Robert Larner College of Medicine at the University of Vermont in Burlington, Vermont.

Additional Resources

Read the issue: continuum.aan.com

Subscribe to Continuum®: shop.lww.com/Continuum

Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud

More about the American Academy of Neurology: aan.com

Social Media

facebook.com/continuumcme

@ContinuumAAN

Host: @LyellJ

Full episode transcript available here

Dr. Jones: The human brain is incredibly complex. That's one of the reasons we like to study it and care for patients with neurologic problems. But to translate cognition into action, we need a functioning sensorimotor and autonomic peripheral nervous system. What do we do when those peripheral systems aren't working? Today, we're speaking with Dr. Noah Kolb, guest editor of our latest issue of Continuum on peripheral nerve and motor neuron disorders.

Dr. Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about subscribing to the journal, listening to verbatim recordings of the articles, and exclusive access to interviews not featured on the podcast.

Dr. Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today, I'm interviewing Dr. Noah Kolb, who is Continuum's guest editor for our latest issue on peripheral nerve and motor neuron disorders. Dr. Kolb is a professor of neurology at the University of Vermont Larner College of Medicine in Burlington, Vermont, where he specializes in the care of patients with neuromuscular disorders, including patients with peripheral neuropathy and other immune-mediated neuromuscular diseases. Dr. Kolb, welcome. Thank you for joining us today. Why don't you introduce yourself to our listeners?

Dr. Kolb: Well, thank you very much for having me. Please call me Noah. I've been a longtime listener of Continuum, dating all the way back to when they came on CDs, so it's really a pleasure to be here. Like you said, I'm a neuromuscular doctor up in Vermont. I take care of the whole scope of neuromuscular disease, but kind of wear 3 different hats. I focus my research primarily in chemotherapy-induced neuropathy, but also do other diseases as well. Obviously, see patients clinically, and then I'm an educator as well, so I run the neurology clerkship and the acting AIs for the medical school. So, it's a fun job.

Dr. Jones: Well, thanks for sharing that little bit of history on Continuum Audio, Noah. I got to be honest with you, I don't know if I've ever seen a Continuum Audio CD. If anybody out there in the audience has a Continuum Audio CD, post a picture online and we'll like and share it. I wonder how many of those are still out there. I really appreciate you not just joining us today, Noah, but also putting together this really stellar issue, a very timely update and overview of peripheral nerve and motor neuron disorders. A lot of good topics for us to dig into today. What I'm going to do before we get into questions is ask our audience Continuum Audio's trivia question. Dr. Kolb and I were talking about this before we started recording here. So, the trivia question, just to frame it up a little bit, the transthyretin or TTR protein receives a lot of attention in neuromuscular medicine as the protein behind the most common causes of acquired and familial amyloidosis. But transthyretin is known in clinical settings by a different name and checked for an entirely different reason. So, the trivia question is, what is the other common name for transthyretin? Stick around, and we'll share the answer at the end of our interview. So, let's get right to it. Our listeners know that peripheral neuropathy is common, right? It affects 2 to 3 percent of the general population and 6 to 7 percent of patients who are older than 60. In your mind, Noah, what's the main thing you would like clinicians to know or do differently in the care of these patients?

Dr. Kolb: Yeah, that's a great question. I think it's something that we spend a lot of time teaching our residents and working with our fellows about is understanding the right workup for people presenting with neuropathy because it's very easy to overdo it with more labs and a broader workup than you need. So, when somebody presents with sort of a garden variety neuropathy that doesn't have red flags, the important things to order in terms of a workup are hemoglobin A1C, B12, and SPEP with IFE, potentially serum light chains, and some thyroid studies as well. Because those are really the most common reasons, and then to make sure that they ask the most important historical questions, like about alcohol use, et cetera. If you're going to find a cause for neuropathy, particularly if it's slowly progressive and sensory predominant, oftentimes the answer is found right in that basic workup.

Dr. Jones: Got it. And I think that's very well taken. And I think one of the questions that commonly comes up in the neuromuscular, but also in the broader neurology setting is, when you're evaluating a patient, especially an older patient who has a new onset length-dependent sensorimotor peripheral neuropathy, you've identified the neuropathy, and you're starting to consider what are those potential underlying disorders or risk factors that that neuropathy could be a warning sign of, right? So, you look for metabolic disease, B12 deficiency, paraproteinemia, et cetera. Where do you stop? In what settings do you do more expanded evaluations, genetic testing, et cetera?

Dr. Kolb: Yeah, and I think this kind of goes back a little bit to the last question where the primary focus of the workup that we do is driven by the most common causes. That's why hemoglobin A1C is so important. And so, thinking through what is likely to be the cause in the specific patient setting is kind of really critical. And again, if you don't have red flags, then the labs that we mentioned previously are probably sufficient in terms of a workup. But if there are any of the other red flags, it's really important specifically because there may be treatable causes of neuropathy or things that would affect the prognosis that'd be important to understand earlier so we can make sure we either engage the right therapies or do a broader diagnostic workup. An important part of that is understanding when to use EMG nerve conduction studies and when not to. So obviously, as a neuromuscular doc who does EMGs, I'm very fond of them. But we regularly see patients in our lab who perhaps don't need one. If somebody has a sensory predominant, slowly progressive neuropathy, particularly if you have an etiology, those patients usually don't need an EMG nerve conduction study. When it's asymmetric, when there's prominent weakness, when there's a lot of autonomic symptoms, those are the times when it can be a lot more informative and helpful to try to get an EMG nerve conduction study to see if we can get at what the underlying etiology is.

Dr. Jones: That's very helpful, Noah. Thank you. And so, let's think about a scenario that I think many of our listeners may have encountered in their practice. You're seeing a patient who has a somewhat rapidly progressive, painful neuropathy, which has some small fiber characteristics. They've got a little bit of autonomic dysfunction, and you worry about the possibility of amyloidosis. How do you approach that evaluation and treatment, and why is it important to think about that diagnosis?

Dr. Kolb: Yeah, that's great. It's important to think about that diagnosis because we now have good treatments for AL amyloid and for ATTR-based amyloid. So, because these are treatable disorders, it's really critical that you identify them. And the reality is it's not always straightforward making a diagnosis of amyloid. As you would with any other type of neuropathy, the workup is gonna begin with serum free light chains, SPEP, trying to see if there are any monoclonal gammopathies or elevation in light chains. But importantly, you need to think about what the next diagnostic steps are and understanding how likely those tests are to be abnormal in the setting of amyloid is important as well, because the easier to obtain tests don't have perfect sensitivity. So, once you've moved on kind of from the basic labs, we think about a fat aspirate or a skin biopsy to look and see if there's any evidence of amyloid. But if your clinical suspicion is high enough, it's important to move to a sural nerve biopsy and genetic testing. That's really the best way to confirm this diagnosis.

Dr. Jones: Very helpful. And obviously, that's not just academic, as it might have been at one point. This is something that we now have good disease-modifying therapies for, which leads to another question that I think our listeners may encounter in their practice. When you think about all the available gene tests in panels and other genomic tools that we have to investigate patients, when do you do a broad genetic evaluation for patients with neuropathy?

Dr. Kolb: Yeah, it's a good question. It depends partly on specifically what we're looking for. I think that as with many things in neurology, one of the reasons I got interested in it, and many people did, is we like doing detective work, and the history often lies in the examination and in our clinical history at the bedside. And for that reason, often just in getting the initial history with a patient, you start to get clues that there may be a hereditary component. Sometimes it's in the history where you're able to elicit a family history of disorder, and they may or may not know that the patient had neuropathy, but it may be that somebody walked funny later in life or somebody always complained of foot pain. Or it may simply be when a patient takes their shoes off, or in Vermont, they're wearing sandals, and you see that they have characteristic changes of a neuropathy that is much more longstanding than the patient even recognizes. That's often the case with some of these forms of hereditary neuropathy because sometimes they don't have a lot of pain. And so, you see those characteristic changes in the foot, and it cues you to the need for genetic testing. In my world where I see a lot of patients with chemotherapy-induced neuropathy, I also think about it in patients who seem to be specifically sensitive to neurotoxic agents, where they get a much worse neuropathy than you would expect with exposure to drug, and it's important to consider it in those times as well.

Dr. Jones: That's a great framing. I appreciate the way you put that. One of the great points in the issue is that patients who have sensory findings out of proportion to their sensory complaints, a lot of times it's worth thinking about a familial or genetic mechanism and then digging a little more into that family history, right?

Dr. Kolb: I agree.

Dr. Jones: Yeah. So, let's think of a different scenario. I know you do a lot of work with immune-mediated acquired neuropathies, and we're fortunate now, obviously, we have a

lot of immunotherapy tools for the treatment of patients with neuropathies like chronic inflammatory demyelinating polyradiculoneuropathy. When it comes to CIDP, Noah, what's your initial approach to immunotherapy? That's one question. And another is, how do you incorporate some of the newer agents like efgartigimod? What's the role of that drug, or when do you go to rituximab or rozanolixizumab? Walk us through your approach to that.

Dr. Kolb: Yeah, so I think it depends a lot on what the clinical presentation looks like and kind of what the patient's preference is. In taking care of neuropathy patients for what's been quite a while now, you find that some patients have a differing comfort level with sort of the newer drugs like efgartigimod versus some of the therapies that have been around for years and years and are tried and true. So, we know, for instance, that plasmapheresis and IVIG work well. In certain cases, we use steroids because they can work well as well, but also have long-term toxicities that you want to be aware of. It's been really exciting to see that efgartigimod is a new therapy that's on the market, and it's been a really interesting space to be involved in, in neuromuscular medicine as some of these new disease-modifying therapies have come out. The trials for efgartigimod are really exciting, and it was very important to our field when efgartigimod became available. But there have been other trials that showed similar drugs weren't that effective, and there are many studies happening right now for complement inhibition with varying results. So, it's been sort of one of these hot topics in neuromuscular medicine, trying to see what these new therapies are and figuring out how to integrate them. I find that oftentimes with patients, we'll start with the tried and true therapies like IVIG or plasmapheresis, but don't hesitate to reach to efgartigimod, particularly if it's more convenient for the patient. I think the other important point to make, and this is addressed nicely throughout some of the manuscripts, is that there are specific instances where certain drugs are preferred. So, for instance, if you're seeing somebody with CIDP that has hard-to-treat symptoms, is not responding to the normal therapies that we use, it's important to think about whether they may have a paranodal form of CIDP, in which case we often reach for things like rituximab instead because it works better.

Dr. Jones: Outstanding. And so, I think that speaks to the importance of phenotyping, right? As we learn more about these acquired immune-mediated neuropathies, we're splitting, right? We're finding that the mechanisms are different in the tools that we have, the treatments are going to be more tailored, and more personalized to the patient. I think that's a great takeaway from the issue. So, Noah, you're in a unique position here, right? You're a world-renowned neuromuscular expert, and you have just edited a bunch of articles on neuromuscular medicine, peripheral nerve, motor neuron disorders written by experts in their respective fields. So, you have this bird's eye view of the specialty up to the minute, what's the latest. When you think about the entire issue, what would you say is the one topic that our readers or listeners could go to, to close the most important education gap in neuromuscular medicine?

Dr. Kolb: It's a great question. It's akin to asking who my favorite child is, of which is all of them, but I would say that when Amro Estino and Ben Becker submitted their manuscript on paraproteinemic neuropathies, after I read it, I wrote an email back to them just telling them how well I thought it was organized and that it really addressed an issue that constantly plagues trainees and practitioners, is how to deal with monoclonal

gammopathies and paraproteinemic neuropathies. It's a nice example of what happens when you give smart people the creative space to organize something in a way that they think makes sense. I certainly learned about the topic reading that, and I think it'd be very high yield for people reading Continuum.

Dr. Jones: Totally agree. It's a wonderful article among many great articles, and that is a persistent education gap. So, I would direct our listeners to that article as well. You know, one of the things that I think about, you're an educator, I'm a clinician educator myself, thinking about the really interesting world of neuromuscular medicine, right? I have a significant part of my practice is in neuromuscular medicine and EMG, and I enjoy that very much. What do you think about trainees who might be interested in neuromuscular medicine, and they want to focus in it or pursue it as a career? How should they approach it? What does the training landscape look like from your perspective?

Dr. Kolb: Yeah, that's a great question and an important one. So, I think that the case to be made for neuromuscular medicine is strong. I talk with the residents and my medical students about this regularly, but I think it's hard to find a place in medicine where the field is evolving more rapidly than it is in neuromuscular medicine, which makes it sometimes hard to stay up to date with everything that's happening, but it also makes it really interesting. To have new medicines coming online for us to change the paradigm for the way we've been treating patients for years and years is very exciting, and I think that those changes are only going to grow. Part of the future of neuromuscular medicine really is going to be in better genetic testing and broader genetic therapies. When you think about hereditary neuropathy as an example, there are tons of emerging therapies that are in pre-clinical trials and some starting in clinical trials. And so, the future of neuromuscular medicine is going to be constantly evolving where we can now treat disorders that we couldn't treat before. I mean, the easiest example is SMA, where previously that was a universally fatal disease for infants, right? And now we have treatments that are very effective. And there are multiple diseases where we're starting to develop therapies like this, so it's really exciting. From a training perspective, there are lots of opportunities for residents as they approach fellowship. There are tons of great neuromuscular fellowships around the program. I would include UVM in there as well, where there's really a wide variety of neuromuscular things that you can learn. And it's a wide and varied field, so people are learning ultrasound, which has been an emerging part of neuromuscular medicine, EMG, electrodiagnostics, Botox, but then also treating autoimmune disorders, hereditary disorders. So, it's really quite a broad field, and you can really sort of super sub-specialize into different areas, which allows you to really focus if that's what you want to do.

Dr. Jones: So now it's time for the answer to our Continuum Audio Trivia question. Just to remind our listeners, what is the other common name for transthyretin? We think about transthyretin a lot, as Noah mentioned, in terms of acquired and familial amyloidosis, but what is the other name for it? Dr. Kolb, do you want to give the answer to our audience?

Dr. Kolb: That would be prealbumin.

Dr. Jones: Prealbumin. Again, we talk about transthyretin all the time because of the neurologic and cardiac presentations of ATTR wild type and variant transthyretin

amyloidosis. But the protein itself, in the non-pathologic setting, in the non-amyloid setting, is a stable tetramer. Its normal function is to transport thyroxine and vitamin A throughout the body, but it also has a relatively short half-life. And on electrophoretic gels, it segregates near the albumin band, and therefore, for a long time was just called prealbumin because it was near the albumin band. And because of that short half-life, it's used as a rough or loose marker of nutritional status. So, all those times when I was a medical student and a resident ordering prealbumin to assess nutritional status, I was really checking transthyretin, and I had no idea.

Dr. Jones: All right. So, Dr. Kolb, I really want to thank you for joining us. Thank you for such an outstanding conversation about peripheral nerve and motor neuron disease in the latest issue of Continuum. I learned a lot reading this issue. I learned a lot in our conversation today. I hope our listeners did too. I'm really grateful for your hard work taking on this issue, which I think will come in handy not only to our more junior listeners and subscribers, but also, our more experienced listeners as well.

Dr. Kolb: Thanks for the opportunity to chat with you. I'm excited for the public to see the Continuum manuscripts. I think there's a lot to learn, and it's an exciting issue.

Dr. Jones: I agree. Again, today we've been speaking with Dr. Noah Kolb, guest editor of Continuum's most recent issue on peripheral nerve and motor neuron disorders. Please check it out, and thank you to our listeners for joining today.

Dr. Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. Thank you for listening to Continuum Audio.