Parkinson's Insights

Stop being a passenger, drive your own care with a holistic approach to Parkinson's.

Prof Michael Okun: My Take

Could carbon monoxide hold a clue to why smoking has been linked to a lower risk of Parkinson’s? Carbon monoxide (CO) is a gas best known for its toxicity, however our bodies also produce tiny amounts of CO where it functions as a signaling molecule. Bueno Lopez and colleagues describe in a new paper in JAMA Neurology how higher exhaled CO levels were associated w/ a lower future risk of Parkinson’s disease, including among folks who never smoked. The accompanying editorial by Darweesh, Remz and Goldman asks the provocative question of whether CO could be one piece of the long-standing smoking-Parkinson’s puzzle. Key points: - More than 512,000 adults in China were followed for approximately 12 years, and 1,131 developed Parkinson’s disease. - Among folks who never smoked, higher exhaled CO was associated w/ progressively lower Parkinson’s risk, and the highest CO group had about a 35% lower risk compared w/ the lowest group. - The editorial appropriately pumps the brakes: this is an association, not proof that CO prevents Parkinson’s, and confounding, regional differences and variability in measuring exhaled CO remain important concerns. My take: This is one of those fascinating Parkinson’s observations that should make us curious, but not careless. Smoking is harmful and nobody should smoke or expose themselves to carbon monoxide in an attempt to prevent Parkinson’s. The exciting question is whether we can identify the biological mechanism hiding inside this epidemiologic paradox and someday separate a potentially protective pathway from the enormous harms of smoking and toxic CO exposure. The nicotine story taught us humility: epidemiology suggested a protective association, yet nicotine itself has not translated into benefit in human trials.

Could carbon monoxide hold a clue to why smoking has been linked to a lower risk of Parkinson’s? Carbon monoxide (CO) is a gas best known for its toxicity, however our bodies also produce tiny amounts of CO where it functions as a signaling molecule. Bueno Lopez and colleagues describe in a new paper in JAMA Neurology how higher exhaled CO levels were associated w/ a lower future risk of Parkinson’s disease, including among folks who never smoked. The accompanying editorial by Darweesh, Remz and Goldman asks the provocative question of whether CO could be one piece of the long-standing smoking-Parkinson’s puzzle. Key points: - More than 512,000 adults in China were followed for approximately 12 years, and 1,131 developed Parkinson’s disease. - Among folks who never smoked, higher exhaled CO was associated w/ progressively lower Parkinson’s risk, and the highest CO group had about a 35% lower risk compared w/ the lowest group. - The editorial appropriately pumps the brakes: this is an association, not proof that CO prevents Parkinson’s, and confounding, regional differences and variability in measuring exhaled CO remain important concerns. My take: This is one of those fascinating Parkinson’s observations that should make us curious, but not careless. Smoking is harmful and nobody should smoke or expose themselves to carbon monoxide in an attempt to prevent Parkinson’s. The exciting question is whether we can identify the biological mechanism hiding inside this epidemiologic paradox and someday separate a potentially protective pathway from the enormous harms of smoking and toxic CO exposure. The nicotine story taught us humility: epidemiology suggested a protective association, yet nicotine itself has not translated into benefit in human trials.

PostOpen details
Germany has taken the bold step of recognizing Parkinson’s as an occupational disease when associated with long-term, frequent occupational pesticide exposure, an important acknowledgment that Parkinson’s may sometimes be linked to preventable environmental exposures. At this morning’s Parkinson Stiftung press conference in Berlin, Prof. Jens Volkmann emphasized the growing burden of Parkinson’s and the need to move environmental risk and prevention into the center of research and public policy; Dr. Johannes Wagner stressed that occupational recognition should be a beginning, not an endpoint, calling for safer approaches to pesticides while protecting the livelihoods of farmers and agricultural workers; and I emphasized that pesticides are only part of the story, with evidence also implicating exposures such as industrial solvents and air pollution, and that neurology needs to begin thinking more like cardiology by identifying and reducing modifiable risks before disease appears. The voices of farmers and people living with Parkinson’s brought home why this matters: these are not simply epidemiologic statistics, but lives potentially affected by exposures accumulated over decades. We should be careful not to suggest that every case of Parkinson’s is environmentally caused, but we also should not wait for perfect certainty before acting on avoidable risks. We need a Parkinson’s Plan that brings scientists, clinicians, patients, farmers, industry and governments together around a new goal: not only treating Parkinson’s better, but preventing it whenever we can. Prevention may ultimately prove to be our most powerful treatment. https://www.parkinsonstiftung.de/umwelt-und-parkinson/?utm_source=chatgpt.com https://pdplan.org/

Germany has taken the bold step of recognizing Parkinson’s as an occupational disease when associated with long-term, frequent occupational pesticide exposure, an important acknowledgment that Parkinson’s may sometimes be linked to preventable environmental exposures. At this morning’s Parkinson Stiftung press conference in Berlin, Prof. Jens Volkmann emphasized the growing burden of Parkinson’s and the need to move environmental risk and prevention into the center of research and public policy; Dr. Johannes Wagner stressed that occupational recognition should be a beginning, not an endpoint, calling for safer approaches to pesticides while protecting the livelihoods of farmers and agricultural workers; and I emphasized that pesticides are only part of the story, with evidence also implicating exposures such as industrial solvents and air pollution, and that neurology needs to begin thinking more like cardiology by identifying and reducing modifiable risks before disease appears. The voices of farmers and people living with Parkinson’s brought home why this matters: these are not simply epidemiologic statistics, but lives potentially affected by exposures accumulated over decades. We should be careful not to suggest that every case of Parkinson’s is environmentally caused, but we also should not wait for perfect certainty before acting on avoidable risks. We need a Parkinson’s Plan that brings scientists, clinicians, patients, farmers, industry and governments together around a new goal: not only treating Parkinson’s better, but preventing it whenever we can. Prevention may ultimately prove to be our most powerful treatment. https://www.parkinsonstiftung.de/umwelt-und-parkinson/?utm_source=chatgpt.com https://pdplan.org/

PostOpen details
I had the opportunity to write this piece for The Conversation about something we often underestimate in Tourette syndrome: the extraordinary amount of effort many people expend trying to suppress their tics. People may appear relatively tic-free in a classroom, workplace, clinic or on a stage, but that outward appearance can hide an exhausting internal struggle. Suppression is not simply “stopping” a tic; it can require sustained attention, awareness of premonitory urges and enormous mental energy, and the tics may rebound later. The encouraging part is that this same ability to recognize urges and modify responses is also central to behavioral treatments such as CBIT. I have spent much of my career learning from people living with Tourette syndrome, and I continue to be reminded that what we see from the outside rarely tells the whole story. The lesson for all of us is simple: look beyond the tic, listen to the person, and recognize the effort we may not be able to see. https://theconversation.com/people-with-tourette-syndrome-like-billie-eilish-use-everything-in-their-power-to-suppress-tics-this-exhausting-process-is-key-to-treatment-287277

I had the opportunity to write this piece for The Conversation about something we often underestimate in Tourette syndrome: the extraordinary amount of effort many people expend trying to suppress their tics. People may appear relatively tic-free in a classroom, workplace, clinic or on a stage, but that outward appearance can hide an exhausting internal struggle. Suppression is not simply “stopping” a tic; it can require sustained attention, awareness of premonitory urges and enormous mental energy, and the tics may rebound later. The encouraging part is that this same ability to recognize urges and modify responses is also central to behavioral treatments such as CBIT. I have spent much of my career learning from people living with Tourette syndrome, and I continue to be reminded that what we see from the outside rarely tells the whole story. The lesson for all of us is simple: look beyond the tic, listen to the person, and recognize the effort we may not be able to see. https://theconversation.com/people-with-tourette-syndrome-like-billie-eilish-use-everything-in-their-power-to-suppress-tics-this-exhausting-process-is-key-to-treatment-287277

PostOpen details
Could lumbar belts deserve a second look for low back pain? A lumbar belt is a soft support worn around the lower back that may improve postural control, proprioceptive feedback and reduce mechanical load. Laurent Grange and colleagues describe in a new randomized clinical trial in JAMA Network Open whether adding a nonrigid lumbar belt to usual care can improve nonspecific low back pain. The study included 168 adults whose back pain had lasted 1 to 6 months, so this is really a study of subacute, recently chronic and recurrent pain rather than longstanding chronic back pain. Key points: - After 12 weeks, disability improved more in the lumbar belt group, and pain at rest and during activity also improved more than w/ usual care alone. - 60.5% of folks using the belt achieved at least a 30% improvement in disability compared w/ 40.5% receiving usual care alone. - Folks using the belt were less likely to use pain medications, particularly NSAIDs, and there were no serious device-related adverse events. My take: For years many health care providers, including many of us in neurology, have discouraged lumbar belts because of concerns about dependence, deconditioning and weakening muscles. Interestingly, those concerns have not been consistently supported, and this randomized trial should make us more open-minded. I would be more enthusiastic about time-limited use during an acute-to-subacute flare than indefinite use for chronic low back pain, and importantly this study did not actually test very acute pain lasting only days or weeks. In Parkinson’s disease and other chronic neurological diseases, however, pain can shut down walking, exercise and independence. Could a belt used strategically during painful activities help some folks keep moving rather than retreating to the chair? That is a question worth asking. Here are 3 points that resonated w/ me: 1- Lumbar belts should perhaps not be dismissed simply because we were historically taught to avoid them. 2- The goal should be supporting movement, not replacing muscles or exercise. 3- Short-term targeted use may make more sense than wearing a belt indefinitely for chronic pain.

Could lumbar belts deserve a second look for low back pain? A lumbar belt is a soft support worn around the lower back that may improve postural control, proprioceptive feedback and reduce mechanical load. Laurent Grange and colleagues describe in a new randomized clinical trial in JAMA Network Open whether adding a nonrigid lumbar belt to usual care can improve nonspecific low back pain. The study included 168 adults whose back pain had lasted 1 to 6 months, so this is really a study of subacute, recently chronic and recurrent pain rather than longstanding chronic back pain. Key points: - After 12 weeks, disability improved more in the lumbar belt group, and pain at rest and during activity also improved more than w/ usual care alone. - 60.5% of folks using the belt achieved at least a 30% improvement in disability compared w/ 40.5% receiving usual care alone. - Folks using the belt were less likely to use pain medications, particularly NSAIDs, and there were no serious device-related adverse events. My take: For years many health care providers, including many of us in neurology, have discouraged lumbar belts because of concerns about dependence, deconditioning and weakening muscles. Interestingly, those concerns have not been consistently supported, and this randomized trial should make us more open-minded. I would be more enthusiastic about time-limited use during an acute-to-subacute flare than indefinite use for chronic low back pain, and importantly this study did not actually test very acute pain lasting only days or weeks. In Parkinson’s disease and other chronic neurological diseases, however, pain can shut down walking, exercise and independence. Could a belt used strategically during painful activities help some folks keep moving rather than retreating to the chair? That is a question worth asking. Here are 3 points that resonated w/ me: 1- Lumbar belts should perhaps not be dismissed simply because we were historically taught to avoid them. 2- The goal should be supporting movement, not replacing muscles or exercise. 3- Short-term targeted use may make more sense than wearing a belt indefinitely for chronic pain.

PostOpen details
What resonates with me about this excellent review of gastroparesis is how relevant it is to Parkinson’s disease and parkinsonism, where impaired gastric motility can become much more than a gastrointestinal symptom: delayed emptying can contribute to nausea, bloating and early satiety, but it can also make absorption of critical Parkinson’s medications, particularly levodopa, delayed and unpredictable. The review specifically recognizes Parkinson’s as a neurological risk factor for gastroparesis and reminds us how remarkably limited our therapeutic toolbox remains. Metoclopramide is the only FDA-approved drug for gastroparesis, yet because it blocks dopamine D2 receptors and carries a risk of parkinsonian symptoms and tardive dyskinesia, it is generally a particularly poor choice for people with Parkinson’s and other parkinsonian disorders. This is where I think we should all be making more noise: domperidone (Motilium), a peripheral dopamine antagonist commonly used in many countries, does not readily cross the blood-brain barrier and can be useful in Parkinson’s, yet it remains unavailable as a routinely FDA-approved prescription in the United States because of cardiac safety concerns. We need safer treatments, better trials and a workable regulatory pathway because for people with Parkinson’s, the stomach can determine whether the medication that works beautifully on paper actually reaches the brain when it is needed. You will find domperidone sold all over the world, and here are some of the names it goes by in different countries: Motilium, Motilium Rapid, Peridon, Peridys, Cilroton, Cinet, Costi, Domstal, Domperitop, Nauzelin, Neoperidys, Oroperidys, Permotil, Remotil, Riges, Tametil, Touristil, and Zilium. https://jamanetwork.com/journals/jama/fullarticle/2852115

What resonates with me about this excellent review of gastroparesis is how relevant it is to Parkinson’s disease and parkinsonism, where impaired gastric motility can become much more than a gastrointestinal symptom: delayed emptying can contribute to nausea, bloating and early satiety, but it can also make absorption of critical Parkinson’s medications, particularly levodopa, delayed and unpredictable. The review specifically recognizes Parkinson’s as a neurological risk factor for gastroparesis and reminds us how remarkably limited our therapeutic toolbox remains. Metoclopramide is the only FDA-approved drug for gastroparesis, yet because it blocks dopamine D2 receptors and carries a risk of parkinsonian symptoms and tardive dyskinesia, it is generally a particularly poor choice for people with Parkinson’s and other parkinsonian disorders. This is where I think we should all be making more noise: domperidone (Motilium), a peripheral dopamine antagonist commonly used in many countries, does not readily cross the blood-brain barrier and can be useful in Parkinson’s, yet it remains unavailable as a routinely FDA-approved prescription in the United States because of cardiac safety concerns. We need safer treatments, better trials and a workable regulatory pathway because for people with Parkinson’s, the stomach can determine whether the medication that works beautifully on paper actually reaches the brain when it is needed. You will find domperidone sold all over the world, and here are some of the names it goes by in different countries: Motilium, Motilium Rapid, Peridon, Peridys, Cilroton, Cinet, Costi, Domstal, Domperitop, Nauzelin, Neoperidys, Oroperidys, Permotil, Remotil, Riges, Tametil, Touristil, and Zilium. https://jamanetwork.com/journals/jama/fullarticle/2852115

PostOpen details
What resonates with me about the recent FDA clearances of blood tests for Alzheimer’s disease is that we are crossing an important threshold: biomarkers that largely lived in research studies and specialty centers are rapidly moving into everyday clinical practice. Four FDA-cleared blood-based assays are now available, including two cleared in August 2026, with p-tau217 emerging near the center of this new diagnostic pathway. But clinicians need to understand that ordering the test may be the easy part; managing what comes next will be harder. These are tests for the likelihood of amyloid pathology, not stand-alone tests that diagnose Alzheimer’s disease, and results must be interpreted in the context of the person’s symptoms, age, cognitive testing, comorbidities and pretest probability. A negative result may help some patients avoid more invasive or expensive testing, while intermediate or positive results may lead to amyloid PET or CSF confirmation and potentially consideration of disease-modifying therapy. We also need to think carefully about false positives, particularly when testing people in lower-prevalence populations, and about the counseling required before and after testing. The blood test should therefore never replace the clinician or the clinical history. It should make us better clinicians by helping us put the right patient on the right diagnostic pathway at the right time.

What resonates with me about the recent FDA clearances of blood tests for Alzheimer’s disease is that we are crossing an important threshold: biomarkers that largely lived in research studies and specialty centers are rapidly moving into everyday clinical practice. Four FDA-cleared blood-based assays are now available, including two cleared in August 2026, with p-tau217 emerging near the center of this new diagnostic pathway. But clinicians need to understand that ordering the test may be the easy part; managing what comes next will be harder. These are tests for the likelihood of amyloid pathology, not stand-alone tests that diagnose Alzheimer’s disease, and results must be interpreted in the context of the person’s symptoms, age, cognitive testing, comorbidities and pretest probability. A negative result may help some patients avoid more invasive or expensive testing, while intermediate or positive results may lead to amyloid PET or CSF confirmation and potentially consideration of disease-modifying therapy. We also need to think carefully about false positives, particularly when testing people in lower-prevalence populations, and about the counseling required before and after testing. The blood test should therefore never replace the clinician or the clinical history. It should make us better clinicians by helping us put the right patient on the right diagnostic pathway at the right time.

PostOpen details
What resonates with me about this study is that it moves the CTE conversation from symptoms recalled after death toward something far more rigorous: detailed neuropsychological testing performed during life lined up with what was actually found in the brain at autopsy. In 33 former NFL players with autopsy-confirmed CTE, the clearest pattern was impairment in learning and memory (63%), followed by executive function (52%) and language (41%), while visuospatial function was relatively preserved; importantly, greater p-tau burden tracked with worse learning and memory. What I find particularly compelling is that this pattern largely persisted even after removing cases with Alzheimer’s and other tauopathies, strengthening the possibility that we are beginning to see a recognizable cognitive fingerprint of CTE itself. We are not yet at a point where a neuropsychological profile can diagnose CTE in a living person, and this was a small, selected autopsy cohort, but connecting objective symptoms during life to verified pathology after death is exactly the kind of bridge we need if we hope to eventually diagnose CTE accurately before death. https://cutt.ly/LykT2EWg

What resonates with me about this study is that it moves the CTE conversation from symptoms recalled after death toward something far more rigorous: detailed neuropsychological testing performed during life lined up with what was actually found in the brain at autopsy. In 33 former NFL players with autopsy-confirmed CTE, the clearest pattern was impairment in learning and memory (63%), followed by executive function (52%) and language (41%), while visuospatial function was relatively preserved; importantly, greater p-tau burden tracked with worse learning and memory. What I find particularly compelling is that this pattern largely persisted even after removing cases with Alzheimer’s and other tauopathies, strengthening the possibility that we are beginning to see a recognizable cognitive fingerprint of CTE itself. We are not yet at a point where a neuropsychological profile can diagnose CTE in a living person, and this was a small, selected autopsy cohort, but connecting objective symptoms during life to verified pathology after death is exactly the kind of bridge we need if we hope to eventually diagnose CTE accurately before death. https://cutt.ly/LykT2EWg

PostOpen details
Parkinson’s disease is not only costing lives and independence; it is costing Europe billions. Economic burden means the total financial impact of a disease, including medical care, lost productivity and unpaid caregiving. Welter and colleagues describe in a new paper in Movement Disorders the enormous and growing societal cost of Parkinson’s disease across Europe. Key points: - Parkinson’s disease was estimated to cost Europe €22.8 billion in 2019, equivalent to approximately €28.8 billion in 2025 after adjustment for inflation. - Direct costs accounted for 76% of the economic burden, while informal caregiving accounted for another 19%. - The prevalence rate of Parkinson’s increased 18% in the WHO European region between 2010 and 2019, suggesting the economic challenge may continue to grow. My take: Parkinson’s is not simply a tremor disease and these numbers remind us that its impact extends far beyond the clinic. Families, care partners and health systems are absorbing an enormous burden. We need better treatments, however we should also be thinking upstream about prevention and modifiable risk factors, including environmental exposures. The price of Parkinson’s should be measured not only in euros, but also in independence, caregiver time and lives disrupted. Here are 5 points that resonated w/ me: 1- More Parkinson’s means more disability, more caregiving and more pressure on health systems. 2- Informal caregiving is a major part of the Parkinson’s economy and we should never underestimate what families contribute. 3- Advanced Parkinson’s can be particularly expensive, strengthening the argument for earlier and more effective interventions. 4- Investment in disease modifying therapies could potentially yield returns both for folks living w/ Parkinson’s and for society. 5- Perhaps most importantly, we need to invest not only in treating Parkinson’s, but also in understanding why Parkinson’s is increasing and how we might prevent it. https://movementdisorders.onlinelibrary.wiley.com/doi/10.1002/mds.70491

Parkinson’s disease is not only costing lives and independence; it is costing Europe billions. Economic burden means the total financial impact of a disease, including medical care, lost productivity and unpaid caregiving. Welter and colleagues describe in a new paper in Movement Disorders the enormous and growing societal cost of Parkinson’s disease across Europe. Key points: - Parkinson’s disease was estimated to cost Europe €22.8 billion in 2019, equivalent to approximately €28.8 billion in 2025 after adjustment for inflation. - Direct costs accounted for 76% of the economic burden, while informal caregiving accounted for another 19%. - The prevalence rate of Parkinson’s increased 18% in the WHO European region between 2010 and 2019, suggesting the economic challenge may continue to grow. My take: Parkinson’s is not simply a tremor disease and these numbers remind us that its impact extends far beyond the clinic. Families, care partners and health systems are absorbing an enormous burden. We need better treatments, however we should also be thinking upstream about prevention and modifiable risk factors, including environmental exposures. The price of Parkinson’s should be measured not only in euros, but also in independence, caregiver time and lives disrupted. Here are 5 points that resonated w/ me: 1- More Parkinson’s means more disability, more caregiving and more pressure on health systems. 2- Informal caregiving is a major part of the Parkinson’s economy and we should never underestimate what families contribute. 3- Advanced Parkinson’s can be particularly expensive, strengthening the argument for earlier and more effective interventions. 4- Investment in disease modifying therapies could potentially yield returns both for folks living w/ Parkinson’s and for society. 5- Perhaps most importantly, we need to invest not only in treating Parkinson’s, but also in understanding why Parkinson’s is increasing and how we might prevent it. https://movementdisorders.onlinelibrary.wiley.com/doi/10.1002/mds.70491

PostOpen details
What resonates with me about Abraham Myerson’s original 1944 description of the glabellar “tap reaction” is how remarkably modern some of his observations feel. He described repeated eye closure “against the will of the patient,” contrasted this with the normal habituation that occurs after several taps to the forehead, and, importantly, recognized that the finding was not confined to Parkinson’s disease. Most strikingly, Myerson reported that the response could occur frequently in what was then called “catatonic dementia precox,” could vary with the severity of the catatonic state, and could even disappear during the same examination as the patient’s clinical state changed. Eight decades later, this observation is an important reminder that neurological signs do not exist in diagnostic silos. In the modern era of Parkinson’s disease, catatonia, functional neurological disorders, and other neuropsychiatric syndromes, we should resist assigning a diagnosis based on a single examination sign. The neurological examination is most powerful when we interpret what we see in the context of the history, associated signs and symptoms, medications, longitudinal course, and the patient’s overall clinical picture. https://jamanetwork.com/journals/archneurpsyc/fullarticle/649901

What resonates with me about Abraham Myerson’s original 1944 description of the glabellar “tap reaction” is how remarkably modern some of his observations feel. He described repeated eye closure “against the will of the patient,” contrasted this with the normal habituation that occurs after several taps to the forehead, and, importantly, recognized that the finding was not confined to Parkinson’s disease. Most strikingly, Myerson reported that the response could occur frequently in what was then called “catatonic dementia precox,” could vary with the severity of the catatonic state, and could even disappear during the same examination as the patient’s clinical state changed. Eight decades later, this observation is an important reminder that neurological signs do not exist in diagnostic silos. In the modern era of Parkinson’s disease, catatonia, functional neurological disorders, and other neuropsychiatric syndromes, we should resist assigning a diagnosis based on a single examination sign. The neurological examination is most powerful when we interpret what we see in the context of the history, associated signs and symptoms, medications, longitudinal course, and the patient’s overall clinical picture. https://jamanetwork.com/journals/archneurpsyc/fullarticle/649901

PostOpen details
What resonates with me about this study is how dramatically we may be undercounting the true burden of neurodegenerative disease. Among 202 former NFL players with clinician-adjudicated dementia, only 30.7% had a neurodegenerative disease listed as the underlying cause of death, and the disease was more likely to make it onto the death certificate when cognitive, executive and functional impairment, or the underlying neuropathology, was more severe. This matters well beyond football. We often build our estimates of Alzheimer’s, Parkinson’s and other neurodegenerative diseases from administrative datasets and death certificates, yet this paper reminds us that what gets counted can depend on how advanced and recognizable the disease becomes. The authors make an especially important point: mortality studies may sometimes be identifying factors associated with disease severity or progression rather than the true incidence of disease. If we underestimate neurodegenerative disease, we risk underestimating the people and families affected, the resources they need, and ultimately the urgency of prevention. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2853502?widget=personalizedcontent&previousarticle=0

What resonates with me about this study is how dramatically we may be undercounting the true burden of neurodegenerative disease. Among 202 former NFL players with clinician-adjudicated dementia, only 30.7% had a neurodegenerative disease listed as the underlying cause of death, and the disease was more likely to make it onto the death certificate when cognitive, executive and functional impairment, or the underlying neuropathology, was more severe. This matters well beyond football. We often build our estimates of Alzheimer’s, Parkinson’s and other neurodegenerative diseases from administrative datasets and death certificates, yet this paper reminds us that what gets counted can depend on how advanced and recognizable the disease becomes. The authors make an especially important point: mortality studies may sometimes be identifying factors associated with disease severity or progression rather than the true incidence of disease. If we underestimate neurodegenerative disease, we risk underestimating the people and families affected, the resources they need, and ultimately the urgency of prevention. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2853502?widget=personalizedcontent&previousarticle=0

PostOpen details
The future of DBS is here, and the Rising Stars are ready! One of the things I am most excited about at this year’s DBS Think Tank is our 2026 Rising Stars Junior Investigator Challenge. On Friday, Sept. 4, from 1–3:30 p.m. Eastern Time, six exceptional early-career investigators from across the country will present bold and innovative ideas aimed at advancing deep brain stimulation and neuromodulation. The finalists are Wonkyung Choi, PhD, University of Pennsylvania; Nandini PS, University of California, Berkeley; Garance Meyer, PhD, Harvard; Matthew Baker, PhD, Mayo Clinic; Alexandra Steina, PhD, University of California, San Francisco; and Prerana Acharyya, University of Southern California. Each will present to a panel of DBS experts, followed by discussion and questions. The winner receives a $1,000 prize, and the top three will receive travel, accommodations and attendance for the 2027 DBS Think Tank. What excites me most is not the competition itself. It is getting a glimpse of where the next generation will take our field. And we are opening the doors virtually to everyone. The public is welcome to join us live and free on Zoom. Come hear the ideas, meet the Rising Stars and see what may be coming next in DBS. Register free to watch the Rising Stars Challenge live on Zoom; open to scientists, practitioners, engineers, persons w/ disease, families, industry, stakeholders... https://ufl.zoom.us/webinar/register/WN_ZMtLKhoHQrGzxuHTlaQgCg

The future of DBS is here, and the Rising Stars are ready! One of the things I am most excited about at this year’s DBS Think Tank is our 2026 Rising Stars Junior Investigator Challenge. On Friday, Sept. 4, from 1–3:30 p.m. Eastern Time, six exceptional early-career investigators from across the country will present bold and innovative ideas aimed at advancing deep brain stimulation and neuromodulation. The finalists are Wonkyung Choi, PhD, University of Pennsylvania; Nandini PS, University of California, Berkeley; Garance Meyer, PhD, Harvard; Matthew Baker, PhD, Mayo Clinic; Alexandra Steina, PhD, University of California, San Francisco; and Prerana Acharyya, University of Southern California. Each will present to a panel of DBS experts, followed by discussion and questions. The winner receives a $1,000 prize, and the top three will receive travel, accommodations and attendance for the 2027 DBS Think Tank. What excites me most is not the competition itself. It is getting a glimpse of where the next generation will take our field. And we are opening the doors virtually to everyone. The public is welcome to join us live and free on Zoom. Come hear the ideas, meet the Rising Stars and see what may be coming next in DBS. Register free to watch the Rising Stars Challenge live on Zoom; open to scientists, practitioners, engineers, persons w/ disease, families, industry, stakeholders... https://ufl.zoom.us/webinar/register/WN_ZMtLKhoHQrGzxuHTlaQgCg

PostOpen details
POTS is real but over-diagnosed in clinical practice. It can however be disabling and missed. Postural orthostatic tachycardia syndrome or POTS is a chronic disorder of the autonomic nervous system, the system that automatically regulates functions such as heart rate, blood pressure, sweating and digestion. Tae Hwan Chung and Satish Raj describe in a new review in JAMA what we currently know about POTS, how to recognize it and importantly, how we can treat it. POTS may affect as many as 1% of the US population and can profoundly disrupt school, work and daily life. Key points: - POTS is diagnosed when chronic symptoms of orthostatic intolerance occur w/ a sustained heart rate increase of at least 30 beats/min in adults or 40 beats/min in adolescents within 10 minutes of standing or tilt, w/o orthostatic hypotension. - POTS is much more than a fast heart rate. Folks can experience lightheadedness, palpitations, fatigue, exercise intolerance, sleep disturbance, gastrointestinal symptoms and brain fog, and approximately 70% in one large survey reported substantial functional impairment. - Treatment begins w/ practical strategies including fluids and salt when appropriate, compression garments and carefully structured exercise. - Medications can be individualized to the predominant physiology and symptoms, although the evidence base remains limited. My take: What resonated w/ me is how POTS challenges us to think beyond a single organ. The heart may race, however the problem involves autonomic regulation and can manifest across the brain, cardiovascular system, gastrointestinal system and more. We should also resist dismissing symptoms simply because conventional structural testing is normal. The median diagnostic delay reported in this review was 24 months. That is a long time for someone struggling to stand, think, exercise, attend school or work to wait for an explanation. Be careful as many clinicians call folks POTS that don't have POTS and this can be problematic.

POTS is real but over-diagnosed in clinical practice. It can however be disabling and missed. Postural orthostatic tachycardia syndrome or POTS is a chronic disorder of the autonomic nervous system, the system that automatically regulates functions such as heart rate, blood pressure, sweating and digestion. Tae Hwan Chung and Satish Raj describe in a new review in JAMA what we currently know about POTS, how to recognize it and importantly, how we can treat it. POTS may affect as many as 1% of the US population and can profoundly disrupt school, work and daily life. Key points: - POTS is diagnosed when chronic symptoms of orthostatic intolerance occur w/ a sustained heart rate increase of at least 30 beats/min in adults or 40 beats/min in adolescents within 10 minutes of standing or tilt, w/o orthostatic hypotension. - POTS is much more than a fast heart rate. Folks can experience lightheadedness, palpitations, fatigue, exercise intolerance, sleep disturbance, gastrointestinal symptoms and brain fog, and approximately 70% in one large survey reported substantial functional impairment. - Treatment begins w/ practical strategies including fluids and salt when appropriate, compression garments and carefully structured exercise. - Medications can be individualized to the predominant physiology and symptoms, although the evidence base remains limited. My take: What resonated w/ me is how POTS challenges us to think beyond a single organ. The heart may race, however the problem involves autonomic regulation and can manifest across the brain, cardiovascular system, gastrointestinal system and more. We should also resist dismissing symptoms simply because conventional structural testing is normal. The median diagnostic delay reported in this review was 24 months. That is a long time for someone struggling to stand, think, exercise, attend school or work to wait for an explanation. Be careful as many clinicians call folks POTS that don't have POTS and this can be problematic.

PostOpen details