Intro

Parkinson disease is a neurodegenerative movement disorder that is increasing in prevalence as the population ages. The symptoms and rate of progression are clinically heterogenous, and medical management is focused on the individual needs of the patient.

In this episode, Kait Nevel MD, speaks with Ashley Rawls, MD, MS, author of the article “Parkinson Disease” in the Continuum® August 2025 Movement 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. Rawls is an assistant professor at the University of Florida Health, Department of Neurology at the Norman Fixel Institute for Neurological Diseases in Gainesville, Florida

Additional Resources

Read the article:  Parkinson Disease

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Host: @IUneurodocmom

Guest: @DrRawlsMoveMD

Full episode transcript available here

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 Kait Nevel. Today I'm interviewing Dr Ashley Rawls about her article on Parkinson disease, which appears in the August 2025 Continuum issue on movement disorders. Ashley, welcome to the podcast, and please introduce yourself to the audience.

Dr Rawls: Thank you, Kait. Hello everyone, my name is Dr Ashley Rawls. I am a movement disorder specialist at the University of Florida Fixel Institute for Neurologic Diseases in Gainesville, Florida. It's a pleasure to be here.

Dr Nevel: Awesome. To start us off talking about your article, can you share what you think is the most important takeaway for the practicing neurologist?

Dr Rawls: Yes. I would say that my most important takeaway for this article is that Parkinson disease remains a clinical diagnosis. I think the field has really been advancing and trying to find a biomarker to help with diagnosis through ancillary testing. For example, with the dopamine transporter, the DAT scan, an alpha-synuclein skin biopsy, an alpha-synuclein amplification assay that can happen in blood and CSF. However, I think it's so critical to make sure that you have a very strong history and a very thorough physical exam and use those biomarkers or other testing to help with, kind of, bolstering your thoughts on what's going on with the patient.

Dr Nevel: Great. And I can't wait to talk a little bit more about the ancillary testing and how you use that. Before we get to that, can you review with us some of the components of the clinical diagnosis of Parkinson disease?

Dr Rawls: Yes. So, when I think about a person that comes in that might have a neurodegenerative disease, I think about two different features, mainly: both motor and Manon motor. So, for my motor features, I'm thinking about resting tremor, bradykinesia---which is fullness of movement with decrement over time---rigidity, and then a specific gait disturbance, a Parkinsonian gait, involving stooped posture, decreased arm swing. They can also have reemergent tremor while walking if they do have tremor as part of their disease process, and also in-block turning as they are walking down the hallway. So, those are my motor features that I look for. So now, when we're talking about a specific diagnosis of Parkinson disease, the one motor feature that you need to have is bradykinesia. The reason why I make sure to speak about bradykinesia, which is slowness of movement with decrement over time, is because people can still have Parkinson disease without having tremor, a resting tremor. So even though that's one of the core cardinal features that most of us will be able to notice very readily, you don't have to necessarily have a resting tremor to be diagnosed with Parkinson' disease. When I talk about nonmotor features, those are going to be the three, particularly the prodromal features that can occur even ten years before people have motor features, can be very prominent early on in the disease process. For example, hyposmia or anosmia for decrease or lack of sense of smell. Another one that we really look for is going to be RBD, or rapid eye movement behavior disorder; or REM behavior disorder, the person acting out their dreams, calling out, flailing their limbs, hitting their bed partner. And then the other one is going to be severe constipation. So those three prodromal nonmotor symptoms of hyposmia/anosmia, RBD or REM behavior disorder, and severe constipation can also make me concerned as a red flag that there is a sort of neurodegenerative issue like a Parkinson disease that may be going on with the patient.

Dr Nevel: Great, thank you so much for that overview. While we're talking about the diagnosis, do you mind kind of going back to what you mentioned in the beginning and talking about the ancillary tests that sometimes are used to kind of help, again, bolster that diagnosis of Parkinson disease? You know, like the DAT or the alpha-synuclein skin biopsy. When should we be using those? Should we be getting these on everyone? And what scenarios should we really consider doing one of those tests?

Dr Rawls: The scenario in which I would order one of the ancillary testing, particularly like a DAT scan or a skin biopsy, looking for alpha-synuclein is going to be when there are potential red flags or a little bit of confusion in regard to the history and physical that I need to have a little bit more clarification on. For example, if I have a patient that has a history of using dopamine blocking agents, for example, for severe depression; or they have a history of cancer diagnosis and they've been on a dopamine agent like metoclopramide; those I want to be mindful because if they're coming in to see me and they're having the symptoms of Parkinsonism---which is going to be resting tremor, bradykinesia rigidity, or gait disturbance---I need to try to figure out is it potentially due to a medication effect, particularly if they're still on the dopamine blockade medication, or is it something where they're actually having a neurodegenerative illness underneath it, like a Parkinson disease?

The other situation that would make me order a DAT skin or a skin biopsy is going to be someone who is coming in that maybe has elements of essential tremor, they have more of a postural or an intention tremor that's very flapping and larger amplitude, and maybe have some mild symptoms and Parkinsonism that might be difficult to distinguish between other musculoskeletal things like arthritis, other imbalance issues from, you know, hip problems or knee problems and what have you. Then I might say, okay, let's see if there is some sort of neurodegeneration underneath this; that may be- that there could be, you know, potentially two elements like a central tremor and Parkinson disease going on. Or is this someone who actually really has Parkinson disease, but there's other factors that are kind of playing into that.

Dr Nevel: Great, thank you for that. Gosh, things have really changed over the past fifteen years or so where we have this ancillary testing that we're able to use more, because what you read in the textbook isn't always what you see in clinic. And as you described, there are patients who… it's not as clear cut, and these tests can be helpful. Could you tell us more about the levodopa challenge test? How is this useful in clinical practice? And what are some key points that we should know about when utilizing this strategy for patients who we think have Parkinson disease?

Dr Rawls: So, before we had all this ancillary testing with the DAT scan, the skin biopsy, the alpha-synuclein amplification assay, many times if you had a suspicion that a person that had Parkinson disease, but you weren't entirely sure, you would say, hey, listen, let us give you back the dopamine that your body may be missing and see if you have an improvement, in particular in your motor symptom. So, when I talk with my patients, I say, listen, I might have a strong suspicion that you have Parkinson disease. Doing a levodopa trial can not only be diagnostic, but also can be therapeutic as well. So, with this levodopa trial, what I end up doing is saying, okay, we're going to start the medication at a low dose because we are looking to see if you have improvement in three of the main cardinal motor symptoms. Obviously, tremor is much easier for us to see if it gets better. It's very obvious on exam, and the patients are more readily able to see it. Whereas stiffness and slowness is much harder to quantify and try to figure out. Am I stiff and slow because of potential muscle tightness from Parkinson disease, or is it something that's more of a musculoskeletal issue? So, I will tell persons, okay, we're looking for improvement in these three cardinal motor symptoms, and things that we're looking for is getting into and out of a car, into and out of a chair, turning over in bed, seeing how do we navigate ourselves in our daily lives? I give people the example of going through the grocery store, going through a busy airport. Are we able to move better and respond better to different changes in our environment which can give us a better clue of if our stiffness and slowness in particular are being improved with the medication?

The other part of this is talking about potential side effects of the carbidopa- of the levodopa in particular. One big thing that I think limits people initially is going to be the nausea, vomiting, potential GI upset when starting this medication initially. So, oftentimes I will find people coming in, oh, you know, my outside doctor started me immediately on one tab of carbidopa/levodopa three times per day. I got nauseous, I threw up, and I never took the medication again. So often times I will start low and go slow because once someone throws up my medication, they are not going to want to take it again---with good reason. So, often times I will ask the patient, hey listen, are you very sensitive to medications? If you are very sensitive, we might start one tablet per day for a week, one tablet twice a day, and then go up until we get to two tablets three times a day if we're talking about carbidopa/levodopa. If someone is not as sensitive then I might go up a little bit quicker. What do we mean when we talk about 600 milligrams per day? So usually, the amount that I use is carbidopa/levodopa, 25/100; so, 100 milligrams being the levodopa portion. Many people just start off at 1 tab 3 times a day, which gives you 300 milligrams of levodopa, and they say, oh, it didn't work, I must not have Parkinson or something else. Well, it just may have been that we did not give an adequate trial and adequate dose to the person. Now if they're not able to tolerate the medication because of the side effects, that's something different. But if they don't have side effects and don't notice a difference, there is room to increase the carbidopa/levodopa or the levodopa replacement that you are using so that you can give it, you know, a very good try to see, is it actually improving resting tremor, bradykinesia and rigidity?

Dr Nevel: Yeah, great. Thanks for that. When you diagnose a patient with Parkinson disease, how do you counsel that patient? How do you break that difficult news? And how do you counsel them on what to expect in the future and goals of treatment? I know that's a lot in that question, but it also is a lot that you do in one visit, oftentimes, or at least introduce these kind of concepts to patients in a single visit.

Dr Rawls: One thing that I think is helpful for me is trying to understand where the patients and their families are when they come in. Because some of the patients come in and have no prior inkling that they may have a neurodegenerative illness like Parkinson disease. Some of my patients come in and say, I'm here for a second opinion for Parkinson disease. So, then I have an idea of where we are in regard to potential understanding of how to start the conversation going forward. If it is someone who is coming in and has not heard about Parkinson disease, or their family has not been made aware that that's the one reason why they're coming to see a movement disorder specialist, then I will start at the beginning After we finish our history, do a very thorough physical exam, I will talk about things that I heard in the history and that I see on the physical exam that make me concerned for a disease like Parkinson disease. I make sure to tell them where I'm getting my criteria from and not just start off, I think you have Parkinson, here's your medication. I think that's very jarring when you're talking with patients and their families, particularly if they had no idea that this could be a potential diagnosis on the table. Like I said, I will start off with recounting, this is what I've heard in your history that makes me concerned. This is what I've seen on your physical exam that makes me concerned. And I think you have Parkinson disease and here is why. And I'll tell them about the tenants like we discussed about Parkinson disease, both the motor and nonmotor symptoms that we see. So that's kind of the first part is, I make sure to lay it out and then open the room up for some questions and clarification. The other portion of this is that, when I'm talking about counseling the patient, I say, we do not expect Parkinson disease to decrease your lifespan. However, over time, our persons, because it is a neurodegenerative illnesses will accumulate deficits over time. So, more stiffness, more slowness, more walking problems. They may, if they have tremor, the tremor may become worse. If they don't have tremor, they might develop tremor in the future. If we're talking about the nonmotor symptoms that we talk about, the main ones are going to be issues with urinary problems, issues with bowels, and then the other thing is going to be neuropsychiatric issues like anxiety and depression. And those things become more prominent, usually, the nonmotor symptoms later on in the disease process, and then also cognitive impairment as well. I really want to make sure that they have the information that I'm seeing, and if there's anything that they want to correct on their end, as in they're saying, oh wait, well, actually I noticed something else, then that's usually when that comes out around kind of the wrapping-up portion of the visit.

So, I think that's really important to, one, be very clear in what I am seeing and if there's red flags, and then tell them, okay this is not going to shorten your lifespan. However, over time, we do have other issues and problems that will arise and we can support you as best as we can through that. The one thing I also been very open with people about is- because our patients will say, is there anything I can do? What can be done? Is there any medication to slow down or stop things? And I let people know that unfortunately, right now there's not an intervention that slows down, stops, or reverses disease progression, with the exception of exercise. Consistent exercise has been found to help to slow down disease progression, okay? And also, it can help to release the dopamine already being made innately in the brain. And also, it can help with our cardiovascular health in the big thing: being balanced. Core strength, quadricep strength. So that's also something that people can work on that they should. And I let people know that exercise is as important as the medications themselves.

Dr Nevel: Absolutely. And it's incredible how much they incorporate exercise into their daily lives and get active, people who weren't active before their diagnosis, and how much that can help. One question that I think patients sometimes ask is, when they understand how carbidopa/levodopa works and what the expectations are for that medication, that it's not a disease-modifying medication, but that it can help with their symptoms. And then they kind of hear, well as time goes on, they need higher doses or, you know, it doesn't control their motor symptoms as well. They'll say, okay well, is it better to wait then? Should I wait to start carbidopa/levodopa? Like in my mind, I'm only maybe going to get X amount of time from carbidopa/levodopa. So, I'd rather wait to start it than start it now. What do you say to them and how do you counsel them through that?

Dr Rawls: So that is a common question that I do get with my patients. So, I tell people, I'm here for you. And it really depends on how you feel at this time. Because you have to weigh the risks and benefits of the medication itself. If someone who's very, very mild decides to take the medication, they feel nauseous, they're just going to say, hey, listen, it's not for me right now. I don't feel like I need it, and then stop, which is with definitely within their right. But what I always counsel patients as well is to say, the dopamine-producing neurons in the substantia nigra are starting to die over time. That is why we are getting the signs and symptoms of Parkinson disease. At some point, your brain is not going to produce enough dopamine that is needed for you to move when you want to move and not move when you don't want to move. Okay? Giving you at least the motor symptoms of Parkinson disease. With this, it's not that the medication stops working, it's just that you need more dopamine to help replace the dopamine that's being lost. However, the dopamine that you are taking or levodopa that you're taking orally is not going to be released as consistently as it is in your brain on demand and shut off when you don't need it. Hence the reason we get more motor fluctuations. Also, potential side effects in the medication like orthostatic hypertension, hallucinations, impulse control disorders. Because you're having to take more escalating doses, those side effects can become more prominent and also lead us to have to balance between the side effects and the medication itself. So, it's not that the medication does not work, your body needs more of it.

Some people will say, oh, well, I want to wait, and I say, that's completely fine. However, my cutoff is basically saying, if you are finding that you, as the person who's afflicted is not able to get up in the morning like you want to, you're avoiding going to walk your dog or working in your garden, you know, because you feel stiff and feel slow; you're avoiding, you know, going out to the community, having lunch with your friends or your family because you're embarrassed by your tremor; this is something that is keeping you from living your life. And that's the time that we need to strongly consider starting the medications. So, a person afflicted will accumulate deficits. However, it's how much the deficits are going to affect you. So, if it's really affecting your life, we have tools and ways to help mitigate that.

Dr Nevel: Yeah, absolutely. Are there any aspects of Parkinson disease management that you feel are maybe underrecognized or perhaps underutilized? In other words, you know, are there things that we the listeners should be maybe more aware of or think about offering or recommending to our patients that you think maybe aren't as much as they could be?

Dr Rawls: I will say the nonmotor symptoms---in particular the neuropsychiatric symptoms with the anxiety and depression, usually later on disease process but also can be earlier as well---I think that is going to be something that is recognized but maybe undertreated in a lot of our patient population. I think part of that is also the fluctuations in dopamine that are occurring naturally in the person, but also, our patients, oftentimes with their medication regimen, really have to be on the ball taking the medication. If they're even 15 minutes late, 10 minutes late, 5 minutes late, we're now off, and now we're waiting for it to kick in. And so that can cause a lot of anxiousness even throughout the day. And then knowing that slowly over time that they're going to accumulate these motor and nonmotor deficits can definitely be problematic as well. There is obvious reason for this underlying potential anxiety and depression. And while we do talk about that and bring that up, sometimes patients will say, oh well, I don't think it's a problem right now. I don't have to mess with this. But usually at some point it does become an issue that usually the family members will bring up and saying, hey, you know, my loved one is very anxious. Or I've noticed that they're just really disengaged from what's going on in their lives and they are not talking as much, they're not going out as much. Again, that could be a combination of depression/anxiety, but it also can be a physical- a combination of, I'm not physically able to do these things, or, they're much more difficult for me to initiate doing these activities. I always want to be mindful. If my patients come in and they already have a diagnosis of depression or anxiety and they're already being treated by a mental health counselor, provider, or a psychiatrist, then I will work with providers so that we can try to optimize their medication regimen. The other thing is, well, if this is the first time that they're really being seen by someone and talking about their anxiety and depression, then oftentimes I will have them go back to their primary care and see if maybe an SSRI or SNRI will be helpful to try to help with the neuropsychiatric symptoms they may be experiencing.

So that's one big one. Another one that I think that might be a little bit underappreciated is going to be drooling. Sometimes I'll come in and see my patients and notice some drooling that's happening with the mouth being open, not being able to initiate the swallowing reflex consistently throughout the day. Or they may be patting their face a lot with a napkin or a towel and then bringing that up and bringing it to light. Oh yeah. I have a lot of drooling while I'm awake. It's on my shirt. It's embarrassing. I feel like it's a little bit too much for me or my family. We have to put a bib on because I'm just drooling all throughout the day. That can really be uncomfortable and cause skin breakdown. It can also be socially embarrassing. So, there are some tools that I talk to people about with drooling. One thing I start with is going to be using sugar-free gum or candy while the person is awake to help initiate the swallow reflex, and sometimes that's all that's needed. There are other agents that can be used---like glycopyrrolate, sublingual atropine drops, and scopolamine patches---that can help with decreasing saliva production. But there can be side effects of making the entire body feel dry, and then also potential cardiac arrhythmias. If those are not helpful or they're contraindicated with the patient, another thing is going to be botulinum toxin injections. So those can be done on the parotid and salivary glands to decrease the amount of saliva that's being produced. So oftentimes people will come to me, because I'm also a botulinum toxin injector. I've been sent by some of my colleagues to inject our persons that have significant sialorrhea.

Dr Nevel: Wonderful. Well, thank you so much for chatting with me today about your article. Again, today I've been interviewing Dr Ashley Rawls about her article on Parkinson disease, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes from this and other issues. And thank you to our listeners for joining today. And thank you, Ashley, for sharing all your knowledge with us today.

Dr Rawls: Thank you, Kate, I appreciate your time. And have a great day, everyone.

Dr Monteith: This is Dr Teshmae 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.