
Understanding Parkinson Disease Through a Personalized Lens: Perspectives From Kelsey Jensen, MD
Kelsey Jensen, MD, a movement disorders neurologist at Allina Health, discussed Parkinson disease diagnosis, deep brain stimulation candidacy, treatment personalization, and ongoing unmet needs in PD care and research.
Although Parkinson Disease Awareness Month concluded earlier this spring, conversations surrounding diagnosis, access to care, and individualized management strategies continue to remain central across the movement disorders community. Parkinson disease (PD), a clinically heterogeneous neurodegenerative disorder characterized by both motor and nonmotor symptoms, still lacks a definitive disease-modifying therapy despite continued advances in symptomatic management and device-based treatment approaches.
Over the past several years, the treatment landscape for PD has continued to evolve with newer infusion therapies, expanded deep brain stimulation (DBS) technologies, and emerging biomarker-based diagnostic tools. At the same time, clinicians continue to face persistent challenges surrounding early diagnosis, care access in rural communities, and tailoring treatment approaches to highly variable patient presentations and disease trajectories.
In a recent conversation with NeurologyLive®, Kelsey Jensen, MD, board-certified neurologist and movement disorders specialist with Allina Health Brain and Spine Institute, discussed her approach to diagnosing PD, selecting patients for DBS, and personalizing treatment plans across the disease continuum. Throughout the Q&A, Jensen reflects on telemedicine, underserved care regions, and research areas she believes warrant greater attention moving forward.
How do you approach differentiating Parkinson disease from other movement disorders or mimics during the diagnostic process?
Kelsey Jensen, MD: I think the biggest thing when I'm thinking about PD patients is context, right? Everything is interpreted within context. The basic feature is they have to have parkinsonism on exam. Parkinsonism consisting of the 4 core motor features: tremor, which is typically going to be a rest tremor, bradykinesia, rigidity, postural instability. They must have at least 2 of those, and 1 of them has to be bradykinesia to say that somebody has parkinsonism. So, without that on exam, I'm never going to diagnose PD. I may say there's some features, but we'll keep an eye out.
History is critical. This is still a clinical diagnosis, so one, just keeping an eye out for any Parkinson disease mimics. Are they on neuroleptic agents? Are they on other dopamine blockade? Things that I think people think of less frequently than antipsychotics would be anti-nausea medications with dopamine blocking activity. So, Compazine, Reglan, Phenergan, and then also the VMAT2 inhibitors are something that I've definitely seen cause parkinsonism.
Nonmotor features are really important to ask about and look for. So orthostatic symptoms, constipation, loss of sense of smell, dream enactment behavior. It's important to interpret those within context. If they're on diabetes medications that impact bowel movements, maybe their constipation is from metformin. A lot of people get constipated without having PD. In terms of loss of sense of smell, we've been through the COVID pandemic. If it happened when they had COVID, it's hard to know how much weight to put on that.
Oftentimes I have a fairly good sense of where the conversation is going to go within a couple minutes of chatting with somebody and casually observing. Looking at facial expression, is it blunted? Are they blinking as much as I expect? How much are they gesturing? Looking at that global bradykinesia. What's their voice like? I’ve had people come in with soft voices who are just always soft spoken. So really asking about whether this is a change.
I think it's also important when discussing these diagnoses to just be open to uncertainty. I will tell people, this is what I'm seeing on your exam. This is what I'm hearing from your history. This looks like Parkinson disease. That being said, there are atypical syndromes that can look a lot like it early on. You don't have eye movement abnormalities or the kind of falls characteristic of PSP, or cognitive symptoms concerning for Lewy body disease, or prominent orthostatic and autonomic symptoms for MSA, or cortical sensory findings and profound asymmetry concerning for CBD. But that doesn't mean things don't change over time. The way to be certain about the diagnosis is with an autopsy, and for most folks we're just not there yet.
How do you view the current role of biomarkers and diagnostic testing in Parkinson disease?
Yeah, I will also mention, we do have DAT scans looking at dopamine uptake. We have alpha-synuclein skin biopsies available for testing and CSF, kind of depending on where you're practicing. So, there is more biomarker testing available. You can look for certain features on MRI. But I tell folks no test is perfect.
I will use those in cases where I'm debating essential tremor versus PD, or drug-induced versus Parkinson disease. I am generally a lot less aggressive about getting that extra testing because for most people it's just not going to change management.
What factors influence whether a patient may be a candidate for deep brain stimulation?
Yeah, I think the key to doing DBS well is to have a really good team. A neurosurgeon that you like and trust, which I am very fortunate to have, neuropsychology, physical therapy, occupational therapy, speech therapy resources, good support staff. I have a phenomenal clinical coordinator and nurse in my practice, which makes it a lot easier.
In terms of when to consider deep brain stimulation surgery, it's going to be different for everybody because everybody's course with PD is so different. Typically, I'm not going to start thinking about it until we're at least 4 to 5 years into the disease course. That's usually after we've tried a lot of medications and we have more history to say this really looks like Parkinson's as opposed to one of the atypical syndromes. But there are people where it wouldn't be a consideration for 10 or 15 years.
It's really for folks where the medications aren't doing a good enough job controlling symptoms. The 4 indications for DBS in PD are motor fluctuations that are not adequately controlled with medication adjustments, dyskinesias, and what I emphasize there is bothersome dyskinesias, dystonia, and medication refractory tremor. Tremor is notoriously one of the more difficult cardinal features of Parkinson's to treat with medications.
Our process starts with myself or my colleague working with the patient and trying different medications and different ways to address symptoms. If we get to the point where we're thinking DBS should be considered, the first workup step is neuropsychological testing. Dementia is a contraindication to deep brain stimulation. If somebody has diagnosable dementia, or if they're bordering on dementia, we're probably not going to offer DBS.
We also have patients do on/off testing with physical therapy. They come in off medications, complete a UPDRS motor scale, then take their medications and repeat the exam once the medications kick in. With the exception of tremor, the symptoms we expect to improve with DBS are the symptoms that improve with medication. If we're targeting bradykinesia and rigidity, I want to see that they respond to levodopa.
Once we have all of that data, we meet as a team with neuropsychology, physical therapy, and neurosurgery and discuss the patient together before moving forward.
How do you navigate care for patients with Parkinson disease who live in rural or underserved communities?
Yeah, that's a huge challenge. I have folks who drive 1 hour, 5 hours, longer to come see me. Minneapolis itself has a really vibrant movement disorders community. There's a lot of us here. But when you get to other major centers, there are phenomenal neurologists, but not necessarily movement disorder trained neurologists.
The dream answer is just making the medical system better and recruiting more neurologists. This is my call to anybody training or interacting with medical students. Neurology is fun. Make neurology seem fun. I think second-year medical school can turn people off from neurology because the basic science feels complicated and scary, but exposure to clinical neurology is really important because a lot of people are surprised by how much they like it.
From a practical standpoint, telemedicine has been huge. That's probably the one good thing that came out of the pandemic as far as I'm concerned. For initial assessments I really want to see people in person, but after that I can be flexible with follow-up. Particularly during Minnesota winters, I do not want my patients with Parkinson driving through a blizzard.
Sometimes getting people telemedicine access means involving kids, grandkids, friends, or neighbors because there are varying levels of tech savviness. Sometimes it means giving up and doing a phone call instead of a video visit. But we'll make it work.
The other thing that's important is partnering with local physicians. If somebody has a neurologist that's only an hour away and I'm 6 hours away, then maybe they see the local neurologist more regularly and me more on a consulting basis yearly. Primary care often ends up doing a lot of the heavy lifting with coordinating care, and I always make it very clear that I'm here to collaborate.
How do you approach treatment personalization in Parkinson disease?
The first time I'm having the Parkinson diagnosis conversation with somebody, whether I'm diagnosing them or taking over care, I make sure to emphasize that Parkinson disease is incredibly varied. What I tell folks is, if you know 1 person with Parkinson disease, you know their Parkinson's disease.
I'm a huge fan of support groups and PD exercise classes, but what you are absolutely not allowed to do is look around the room and say, “that's going to be me in 10 years,” or “that's going to be me in 5 years,” because we just don't know. PD is incredibly individual, and people's responses to medications are incredibly individual.
The first jumping off point is that if symptoms don't bother you, they don't bother me. If somebody has a little bit of rest tremor and it's not affecting quality of life, we don't necessarily need to treat it. This is still symptomatic management. It's not changing where your disease is going to be in 5 or 10 years.
My preferred agent to start with is always carbidopa-levodopa. It's the best efficacy, usually the best tolerated, an oldie but a goodie. Then we see how they do and make adjustments based on wearing off or symptom control. There's so much flexibility with medication timing and dosing.
The other thing I emphasize is therapy services. Physical therapy, occupational therapy, speech therapy. I'm a huge advocate for doing them proactively. Exercise should be a part of every Parkinson's treatment plan. That's the only thing that's consistently been shown to slow progression in studies. I encourage people to find something safe and fun, whether that's boxing classes, seated exercises, or walking.
I tell my patients they are the captain of the ship. Any change we make is something they're living with. It's their brain and their body. I'm never going to offer anything dangerous, but I'm also not here to bully anybody into doing something they're uncomfortable with. We're making decisions together based on what they're telling me.
What aspects of Parkinson disease research need greater attention moving forward?
Kind of everything. Obviously, the big thing everybody wants and is excited for is disease-modifying therapies. Whether that's something that reliably slows progression or eventually curative treatments.
We've had a lot of advancement in treatments even during the course of my fellowship. Vyalev and Crexont both came out in 2024. Adaptive DBS came out from Medtronic in 2025. Image-guided programming from Boston Scientific came out in 2024. So there have been a lot of treatment advancements, but we still need more and better treatments.
An area of research I'm really excited about is genetics and understanding the pathogenesis of Parkinson disease. There have been more than 100 genes associated with Parkinson risk. Environmental factors are another really important area. There was a study in 2025 showing significantly increased risk of developing Parkinson disease if you live within 1 mile of a golf course. When that study came out, I actually happened to be renting a house 3 doors down from a golf course, so it factored into my recent house hunting decisions.
Understanding environmental contributors can help shape policy and help us think about how we make PD less likely as a society. There are also interesting developments with genetic treatments and stem cell research, although nothing commercially available right now.
Across the spectrum of disease, there's still so much to learn and understand. But it's also encouraging how many people are actively working to solve these questions.
Transcript edited for clarity.


















