Diabetic Neuropathies With Dr. Vera Fridman

Diabetic neuropathy is more than a disorder of numbness and pain in the feet. In this episode, Dr. Vera Fridman discusses diabetic neuropathy as a complex, multisystem condition, highlighting the importance of recognizing autonomic involvement, identifying high-risk patients early, and addressing factors that influence progression. Learn practical strategies for screening, prevention, symptom management, and recognizing when symptoms may suggest an alternative diagnosis.

In this episode, Kait Nevel, MD, speaks with Vera Fridman, MD, author of the article “Diabetic Neuropathies” in the Continuum® October 2026 Peripheral Nerve and Motor Neuron Disorders issue.

Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana.

Dr. Fridman is an Associate Professor of Neurology and Neuromuscular Medicine Fellowship Director at the University of Colorado in Aurora, Colorado.

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Read the article: Diabetic Neuropathies

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Full episode transcript available here

Dr. Nevel: Diabetic neuropathy affects millions of people, but in our neurology clinics, are we thinking about it too narrowly? In this clinic, Dr. Vera Fridman emphasizes that diabetic neuropathy is not simply a disease of the feet, revealing it instead as a complex neurologic syndrome with consequences that reach far beyond numbness and pain.

 

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 earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.

 

Dr. Nevel: Hello, this is Dr. Kate Nevel. Today, I'm interviewing Dr. Vera Fridman about her article on diabetic neuropathies. This article appears in the October 2026 Continuum issue on peripheral nerve and motor neuron disorders. Vera, welcome to the podcast, and please introduce yourself to the audience.

 

Dr. Fridman: Hello, it's great to be here. I'm Vera Fridman, and I'm located at the University of Colorado Medical Center. I'm a neuromuscular neurologist with focus on neuropathy clinically and in my research, and it's great to join you.

 

Dr. Nevel: Wonderful. Looking forward to talking to you about your article and learning more. So, I always like to start these interviews with the question, what is the most important takeaway from your article for the practicing neurologist?

 

Dr. Fridman: I think to me, in thinking about this article and writing it, the most important message and take-home is that we need to start thinking about diabetes-associated nerve injury as a complex disorder that's multisystemic. So rather than sort of just focusing on the peripheral nerve involvement we're used to seeing at the bedside, to really start taking that early clinical presentation of numbness or tingling as a warning sign, as a heralding sign of something that is widespread, complex, systemic, the way we might think about other multi-organ systemic disorders.

 

Dr. Nevel: Great. And that leads me into my next question, because you really do emphasize that throughout your article, all the different ways that this kind of more systemic diabetic nerve injury can impact a person and affect their morbidity and even their mortality. So, can you tell us a little bit more about this more widespread diabetic nerve injury beyond the kind of classic diabetic peripheral neuropathy that maybe we think of as neurologists?

 

Dr. Fridman: Yeah, I think the idea here is that we have nerves innervating a lot of different organs, and they are also not siloed. They're interfacing with other parts of our biology, vasculature, you know, the impact of inflammation. All of these things are converging, and they are complicated. And so clinically, when I think about diabetic neuropathy associated with systemic injury, I think about cardiac autonomic neuropathy, about gastrointestinal and urogenital neuropathies, and that these symptoms can be really diverse, and they can be nebulous. And so, in seeing someone who just says, "I have a little bit of numbness and tingling in my toes," I think the clinician has to sort of force themselves to imagine that there's all this asymptomatic disruption in the person's presentation that they have to dig for to understand better.

 

Dr. Nevel: What else should we be asking to kind of delve deeper to investigate or identify a more widespread diabetic nerve injury?

 

Dr. Fridman: When I think about what sort of trainees and early clinicians miss, like when I see histories come from people who haven't been thinking about diabetic neuropathy for a long time, it's usually the autonomic that's missing. Do you have lightheadedness? Have you noticed decreased or increased sweating? Do you get full easily with meals, what we call early satiety? Patients don't know that word. Do you have sexual dysfunction? That's an enormously important question because it can actually herald that there's more widespread neuropathy, more severe neuropathy, and that there's autonomic involvement or potentially vascular involvement. So those are the ones that I see missed. And then the others would be related to the risk of ulceration. What is your foot care approach? Have you had ulcers in the past? I think a lot of people don't realize that having had an ulcer, even if it happened some time ago and healed, is a major risk factor for recurrent ulceration. You're going to pay attention differently to that patient. And then the other question that doesn't necessarily relate to symptoms, but I think is hugely important to ask is, what are your barriers to caring for your diabetes and for yourself? What is getting in the way of those preventative measures, which are really the only really reliable preventative things we can do, right? Like, we don't have good treatments for this disease. So why can't you exercise? What are some of the reasons why you can't? Really in a non-judgmental, guilt-free way, because we know diabetes increases the barrier to these things substantially, and that patients are struggling just to get through their day. So, I think understanding those obstacles early in the therapeutic relationship is where you can make the most impact.

 

Dr. Nevel: Thanks for sharing that. Can you tell us a little bit more about cardiac autonomic neuropathy and why that's so important?

 

Dr. Fridman: Yeah, well, it's important because basically the largest driver of mortality and cardiac death in this population. And I think sometimes even with well-managed diabetes, we are sort of heartbroken to see patients who have gone on to have really terrible outcomes from cardiac autonomic involvement that we didn't necessarily know was there. The other reason it's so important is because it stays asymptomatic for a very long time. So, it's one of these sort of elephant in the room entities that if you don't ask about, you don't look for intentionally, you're just not gonna know, and the patient's not gonna know. They're gonna think they're lightheaded from their medication, which is a very reasonable postulation when someone's taking neuropathic pain medications and blood sugar is going up and down. But it may just be that there's autonomic disease underlying. The other reason it's important is because it's difficult to test for. So even if you have the awareness that you have to think about it and ask about it, it's not always clear to clinicians what they're supposed to do next if those symptoms are there or how to evaluate them. And so, I think for all those reasons, it's probably the most undetected complication, and it's hugely common, and in some cases preventable through aggressive management of disease. So, I think for all those reasons, it comes out as the one that we need to remind ourselves about.

 

Dr. Nevel: How do you evaluate for cardiac autonomic neuropathy in your clinic?

 

Dr. Fridman: That's a great question. I think I start really with the questions that will be included in this article of kind of these detailed questions about symptoms that they may not know come together as indicating autonomic disease. Then at the bedside, I do a

quick heart rate screen to see if they have resting tachycardia. Unfortunately, resting tachycardia is a late manifestation of cardiac autonomic neuropathy, so once you see it, it's probably too late. The next thing is to just perform orthostatic vital signs in the clinic and trying to get in the habit of having the patient lying and sitting and standing and taking the time. And in a busy clinic, that's actually quite a big ask. But if you can get a medical assistant trained and ready to do it on most patients, that I think is really important. If I'm concerned about it, then an EKG, which obviously wouldn't necessarily happen in the same visit, can help look for heart rate variability. And then the next layer is really talking to their primary care about a cardiology referral, because at that point, I think neurologists need help. And that's the other, I think, salient message from my thinking about this field is that this is not something that one practitioner can take on alone, and there has to be a really strong multidisciplinary network, just like we would do for our other complex disorders.

 

Dr. Nevel: Yeah. Do you see in the future there being more multidisciplinary engagement between neurology and cardiology for these patients if this is such a difficult to diagnose problem, but big cause of mortality in these patients?

 

Dr. Fridman: I think that's already happening, but maybe not enough and not in a more algorithmic way. It's happening also through our other diseases that we treat, right? So, we have the emergence of sort of modifying therapies for amyloid, and so that has led to these really close collaborations. I think most neuromuscular clinics now have cardiology that they can contact. And so really broadening that to diabetic neuropathy and creating those pathways for patients early. You have to be a little sensitive that these patients see a lot of doctors, and so, make it as easy as possible. I think that's the key, and getting everyone in one clinic is, of course, financially and sort of logistically very difficult. But having a close relationship to say, "Hey, I saw this patient and noticed this or that on, you know, at the bedside. What would you do next?" I think those relationships are really critical.

 

Dr. Nevel: Yeah. So, kind of moving on into your article, this is kind of a hypothetical situation, but if you could evaluate or only perform one part of your physical exam in a patient with diabetes, what would it be and why?

 

Dr. Fridman: Yeah, I mean, I think looking at their feet and then looking at the sensation at the distal toe, probably with pinprick and light touch, if you had to do one thing. If you have bandwidth to also check vibratory perception, that would be helpful. But I think early on, we know that those small fiber involving neuropathies are more common. And what that tells you in a patient who maybe doesn't even have diabetes, I mean, I think that's another important thing to stress. They may be glucose intolerant and just have a slightly elevated hemoglobin A1c, but we all know that if you look carefully at those patients, a lot of them will have some subtle sensory loss at the toe already. And that's really the patient you want to treat. I mean, that's when you want to intervene. And so, the guidelines currently say to screen at time of diabetes diagnosis, but that's actually probably late. And this isn't discussed in the article because we're sticking to the current day guidelines, but I'm imagining those will be revised as we understand more and more that it's the preempting of the neuropathy that we want to focus on. So, the exam findings of ankle reflexes, for example, that I think a lot of people do sort of semi-automatically in a patient looking for neuropathy, you can have preserved ankle reflexes for quite some time and have important diabetic neuropathy manifestations and cardiac autonomic neuropathy already. And then the foot exam, I think we somehow have to

convince ourselves that really small foot deformities like a hammer toe or a bunion or something that maybe in a non-diabetic patient would never be a big deal is a huge deal because that could be a lost limb. And again, it takes that extra intentionality to think about that, right? But that's when you say, "I really want you to get attention from a podiatrist." And, you know, thinking about things where we can have impact, that sensory loss or loss of protective sensation, those subtle foot deformities, that's the beginning.

 

Dr. Nevel: Yeah. And on that note, you know, early recognition, you emphasize is important so that we can take these preventative measures. What things can our patients do to reduce their risk of progression of their diabetic nerve injury?

 

Dr. Fridman: That's a really complex question, actually. So, what we say kind of formally and based on current knowledge is that they can control their diabetes, and they can control their metabolic risk factors. So, we understand more and more about the contribution of obesity, truncal obesity, metabolic syndrome, hypertriglyceridemia, right? These things that maybe weren't as much emphasized in the past because we were very glycemia-focused. So that's changing, and I think most internal medicine doctors understand that better, and as do neurologists. So, we tell them these things, right? But what we maybe forget to tell them is that in type 2 diabetes, that doesn't necessarily ensure the lack of progression of neuropathy, that they may be doing a wonderful job with their diabetic control and working really hard and still be stuck with a lot of neuropathic pain and progression in the sensory loss. And that's just, that's just a fact, right? And I think it actually is important to communicate that upfront to patients so that they don't blame themselves when things are not going well. The other study-proven research-based intervention is exercise. This is, I think, essential to discuss with every patient with diabetes at every appointment. So, as I'm asking questions, one of my questions will always be, "What do you do for exercise? How often do you exercise? What are the barriers to exercise?" We know that exercise can, in smaller studies, show reinnervation of nerve fiber density. We know that there's reductions in neuropathic pain, that people feel better. Energy is a huge problem in diabetes in general. And so, the hurdle to exercising in type 2 diabetes and type one diabetes is high. And so, our job is to facilitate that they do the minimal amount that will be helpful to them that they can tolerate and then slowly build that up. And there's a recent publication looking at physical activity in patients with diabetes that shows that it's actually just under 10 minutes a day of intense exercise that can make an impact. So, if you think about that, even for people who are having a lot of difficulty starting exercise, five to seven minutes a day is a pretty low bar, and then you work from there. So, I think that's important for us to know, right, that that actually can impact in small amounts.

 

Dr. Nevel: Yeah, that's really helpful, and I imagine as a patient would feel a lot more achievable for somebody maybe who hasn't been engaging in physical exercise to hear from their doctor, "I'm just asking you to try five minutes a day or something like that." 30 minutes or 20 minutes each time that has been kind of previously, I think, the metric.

 

Dr. Fridman: Yeah. Agreed.

 

Dr. Nevel: What are some red flags that should alert the clinician that diabetic peripheral neuropathy may not be the culprit of the patient's symptoms?

 

Dr. Fridman: Always with neuropathies, we think about are they sensory, are they motor, are they symmetric, asymmetric? The classic teaching is that it's gonna be a sensory predominant length-dependent neuropathy that you see with diabetes or other idiopathic sort of slowly progressive nerve disorders. When that is not the case, so when there is initial symptom presentation in the hands, when there is marked asymmetry, and when there's early weakness or early substantial autonomic symptoms like presyncope that comes early in disease, those are all sort of red flags for other etiologies. And because we're in an era where there are some treatable conditions that can mimic slowly progressive sensory loss, such as TTR amyloid, right, I think you have to cast a broader net with patients. Comorbidities, I mean, in patients who have other medical issues, you have to be a little bit careful. I also think there's a tendency to say, "Oh, they have diabetes, and therefore they have a diabetic neuropathy." We see this all the time. But really, if their progression has been subacute and more aggressive than we'd expect in, like, 3 months of sudden onset symptoms, that's not diabetic neuropathy. So just being careful to really ask those questions about timing, progression, symmetry, length dependency, and autonomic symptoms.

 

Dr. Nevel: Yeah. Well, pain is not necessarily universal for patients with diabetic peripheral neuropathy. Obviously, as your article points out, many do experience pain. What do we know? You mentioned spontaneous remission of pain among some patients with diabetic peripheral neuropathy, and how should this knowledge inform our medication management? How do you approach this in your clinic in patients who are on neuropathic medicine who have good control? At what point might you consider tapering them off their medications, or how do you go about that?

 

Dr. Fridman: Yeah, no, that's very important. I'm glad you're highlighting that. There's a few scenarios, and like everything with diabetes and diabetic neuropathy, it's like heterogeneous and it's different for different people. So, some people progress, their neuropathy gets worse, but their pain gets better. I think patients have this kind of perception of, their nerves are dead, like they don't feel anything, and that actually may not be inaccurate, but there's at some point that nociceptive response changes in conjunction with the progression of sensory nerve loss. The other possibility is their neuropathy improves, right? So, they exercise, they get really vigilant with their diabetes, they're really on top of it, and then they're in that lucky category of people for whom there's actual reversal. And there's a paper, a natural history five year study of diabetic neuropathy showing that a small percentage of patients legitimately improve on nerve fiber density testing and electrophysiology. So that's another possibility. How does it guide my treatment? So I hate medications. I find them onerous. I find the side effects really difficult for my patients. And they hate medications. A lot of my patients don't wanna be on these medications. So, I make it a rule to ask at every visit what they're on, what they think it's helping with, what the side effects are. I really work through each drug. Like, is it doing anything? What do you think it's doing? And you'll be surprised when you ask that question. People think they're taking medicines for completely arbitrary indications. They say, "It really helps my back pain." You had no idea you were prescribing their Neurontin, you know, for their back pain. And I'm not arguing it's a bad thing necessarily, but you wanna know. Or they'll say, "I think my numbness got a little better." Or other patients will say, "This medicine doesn't work. It's not helping my numbness." Right? And this is where there's this huge education component of, like, I'm prescribing this medicine for these specific symptoms. I want you to keep track of whether they improve, not these other symptoms, right? Because you wanna know if you're targeting the right symptomatology. If you're not, then I take them off. If they're

feeling better at every visit, if we're achieving control that is adequate for the patient, they're happy where they are, I start a discussion about reducing. And reducing slowly and then bumping back up. As much as I hate medications, I also think it's, on balance, much more important to control pain than to have people living with it because it disrupts sleep, quality of life, it causes mood disorders. And, you know, I think on balance, it's worse for their health to not treat them. So, I tell them that. But if we have room to reduce carefully with monitoring, I think every patient, every visit.

 

Dr. Nevel: Thank you. You mentioned research earlier, and I know that's a big part of your career. What's going on in research in this area that you think is most exciting right now?

 

Dr. Fridman: Yeah, I think I could break it down to a few themes that I think are most exciting. So, one really exciting theme was shifting away from only hyperglycemia as the main area of research, focus of research. I think that that really broadened our understanding of the complexity of this problem in a way that allows for intervention. And there's great animal work looking at dyslipidemia, looking at obesity, looking at the interaction with exercise, all the things that go beyond. Another big theme is thinking about the interactions between axons and Schwann cells, and then also axons and Schwann cells and other cell types in the environment, right? So not thinking about the neuron as like a siloed organ that has this hyperglycemia that it has to manage, but how does, what is the cross-talk with the Schwann cell? What is the role of the Schwann cell in instigating and propelling the diabetic neuropathy biology? Then skin cells, immune cells, all of this sort of micro-environment, right, that we have to really take into account because it appears that these cells that are non-neuronal cells are playing a really important role. And again, I think that lends itself to different and exciting interventions that, that wouldn't have been thought of before. I also think about the study of pathways. So, thinking about pathways that lead to nerve degeneration in this disease and the variable pathways, right? There's, like, many that have been investigated. Some of them interact with each other. And thinking about pathways across different neuropathy types. What are the pathways that diabetic neuropathy might share with genetic neuropathies or chemotherapy-induced neuropathies? We have a good example of that with the SARM1 neurodegeneration pathways and how those might allow for cross-talk across different areas of neuropathy research. So, I think that's all really important. And then the last piece is we're starting in every disease that's common, and though thus far not fully resolved, we're starting to understand the contribution of genetics. If you have a disease where half of the people develop a complication, neuropathy in this case, right, and half don't, it definitely invites the possibility that there may be a genetic contribution. And if we can resolve that, that also gets into more personalized approaches for patients and their risk.

 

Dr. Nevel: Thank you so much for talking with me today. I really enjoyed learning from you, and I really enjoyed your article. So again, I'm gonna encourage all of the listeners, as always, to please read Dr. Fridman's excellent article on diabetic neuropathies in the latest issue of Continuum.

 

Dr. Fridman: Thank you for having me, and I will leave off by telling all the younger clinicians and trainees to please not just read the article, but come join.

 

Dr. Nevel: Absolutely. Wonderful. So again, today I've been interviewing Dr. Vera Fridman about her article on diabetic neuropathies. This article appears in the October

2026 Continuum issue on peripheral nerve and motor neuron disorders. As always, please be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining us 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. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audiocme. Thank you for listening to Continuum Audio.