Environmental factors, such as chemical exposure, likely contribute to Parkinson’s disease (PD) risk. Golf courses consume large quantities of these chemicals, including herbicides, pesticides and insecticides. A new study from researchers using the Mayo Clinic–driven Rochester Epidemiology Project shows that living near golf courses could increase the risk of Parkinson’s.

Over the last 20 years, evidence has linked certain chemicals used in agriculture to PD. Farm-workers exposed to the weed-killer paraquat or the insecticide rotenone, for instance, develop Parkinson’s at rates two- to three-times higher than people who have never handled those chemicals. In lab settings, research shows that low doses of these compounds can damage dopamine-producing neurons in the brain — the same cells that are impacted in Parkinson’s.

While golf courses are known to be heavily treated with similar chemicals, no research has directly investigated the potential relationship between PD risk and proximity to golf courses.

This new study on golf courses and chemicals covers 25 years of medical data, from 1991 to 2015, and examines residents of several counties in southeastern Minnesota — a region where there are detailed municipal records, well‐depth charts and groundwater maps. Investigators used this information to study whether people who live close to golf courses face higher Parkinson’s risk. Additionally, they explored whether nearby public water systems explain any extra risk.

Study Results

The research team identified 419 men and women whose Parkinson’s diagnosis occurred during the study window (from 1991 to 2015) and matched them with more than 5,000 people of the same age, sex, race and neighborhood who did not have Parkinson’s.

Researchers then calculated the straight-line distance from each participant’s home to the nearest golf course on the date of PD diagnosis. Those addresses were added on maps of municipal water-service areas, the locations and depths of public wells, and geological charts highlighting regions where groundwater is considered “vulnerable,” meaning the soil or bedrock allows surface chemicals to migrate quickly downward.

Overall, the analysis revealed that people who lived within one mile of a golf course were 126% (or 2.26 times) more likely to receive a Parkinson’s diagnosis than those whose homes were six or more miles away. Being farther from the fairway seemed to help; risk steadily tapered off beyond one mile, with the odds of PD diagnoses decreasing by 9% for each mile of distance from a golf course.

Distance is only part of the story. When researchers looked at households served by a public water system that contained at least one golf course, Parkinson’s risk was 96% higher compared to households whose water systems did not have a golf course within their boundaries, and about 50% higher than people who use private wells. Additionally, when a golf course was in an area with groundwater vulnerable to contamination, the risk of Parkinson’s was 82% higher than in less vulnerable areas with a golf course.

Taken together, the findings suggest that the pesticides and herbicides used to keep putting greens immaculate may be leaching into drinking water, increasing Parkinson’s risk for the surrounding area.

Highlights

• Using medical records from 1991 to 2015, researchers pinpointed 419 Minnesotans with a Parkinson’s diagnosis and compared them to a group of more than 5,000 neighbors who were alike in age, sex, race, and residential area with no history of PD.

• For every person in the study, researchers measured how close they lived to the nearest golf course, then overlaid addresses onto maps showing city water-service districts, well water depths and locations, and areas where groundwater is more easily polluted.

• Those living within one mile from a golf course were 2.26 times more likely to be diagnosed with PD compared to those living 6 or more miles from a course. The odds of PD diagnosis decreased by 9% for each mile of distance from a golf course.

• People living in a public-water district with one or more golf courses had almost double the odds of developing Parkinson’s compared to those without a course, and about 50% higher odds than those using private wells.

• When a course was on land more vulnerable to pesticide contamination into the community water source, the risk of Parkinson’s was 82% higher compared to regions with a golf course located on more protective geology.

What does this mean?

This study suggests a strong association between living within close proximity to a golf course with an increased risk of developing PD. Additionally, it highlights water sources surrounding golf courses as a primary means of exposure to the chemicals routinely used on golf courses.

However, this study does not prove cause and effect, and the investigators emphasize that more work is needed before drawing firm conclusions. The research lacks direct measurements of pesticide levels in the water over time, and it cannot rule out the impact of other environmental factors related to golf courses, such as higher-income neighborhoods or traffic patterns.

Still, the clear patterns drawn from this study — highest PD risk closest to golf courses, next-highest in the water systems that share ground with a course, and more risk in areas where contaminants travel easily — gives researchers more compelling evidence about how environmental risks play a role in Parkinson’s. 

What do these findings mean to the people with PD right now?

The connection between golf courses and increased PD risk may help some people living with Parkinson’s better understand one cause — exposure to environmental contaminants, potentially through drinking water. However, the environmental risk factors for PD that golf courses present are potentially preventable, by individuals and regulators. People can choose not to live near golf courses, knowing that it may put them at an increased risk for developing PD. On the other hand, regulators can also acknowledge the potential risks and improve safety measures surrounding golf courses and water sources.

The prevalence of Parkinson’s is on the rise. These findings — and new, similar studies that will most likely result from this one — highlights the need to push for mitigating risk factors for PD. Studies like this one that tie environmental factors to increased risk are shaping the future of PD research by helping people trace a contributor to their diagnosis — and help identify ways to reduce risk for future generations.

Learn More

The Parkinson’s Foundation believes in empowering the Parkinson’s community through education. Learn more about PD and the topics in this article through our below resources, or by calling our free Helpline at 1-800-4PD-INFO (1-800-473-4636) for answers to your Parkinson’s questions.

• Environmental factors

• Episode 122: Environmental Factors and Parkinson’s

• Plastic Waste Contaminants Could Promote Parkinson’s

In a landmark investment to accelerate the path to a Parkinson’s disease (PD) cure, in 2019, the Parkinson’s Foundation awarded $8 million to establish four elite Parkinson’s Foundation Research Centers. Each one received $2 million over four years.

In this series of articles, we will share the story of each center — their goals, successes, surprises and the future of their PD research. In this article, we check in with the Parkinson’s Foundation Research Center at the Yale School of Medicine.

Research Centers

The Parkinson’s Foundation selected four centers for their groundbreaking potential to transform PD research. Together, they launched a series of innovative, interlinked studies aimed at deepening our understanding of PD and translating discoveries into real-world impact for people living with the disease.

Studies ranged from basic science (understanding the disease or how PD affects the brain) to applied science (solving real-life problems associated with PD) to clinical research in humans or a combination of these.

Before The Award

At first, despite housing many scientists and clinicians with interests in PD, Yale School of Medicine did not have a hub specifically focused on the molecular mechanisms causing the disease.

To fill this gap, in 2005 Yale established the Interdepartmental Program in Cellular Neuroscience, Neurodegeneration and Repair (CNNR), and began recruiting top researchers with diverse expertise and the shared goal of advancing the understanding of neurodegenerative diseases like Parkinson’s. The first recruited was Sreeganga Chandra, PhD, who had prior postdoctoral experience in PD research.

“Dr. Chandra played an important role in seeding and promoting interest in the cell biology of PD at Yale” said Pietro De Camilli, MD, a cellular neurobiologist and one of the two founding directors of the CNNR program.

At the time, Dr. De Camilli had no prior track record in PD research, but he soon discovered that two major proteins he was studying were products of two genes implicated in familial early-onset PD, leading him to realign his work around PD disease mechanisms.

Another investigator associated with the CNNR, Shawn Ferguson, PhD, also had never worked on PD, but was “an expert in the cell biology of lysosomes, a cell compartment whose importance in PD pathogenesis, and more generally in neurodegenerative diseases, was being increasingly recognized,” said Dr. De Camilli.

When the Parkinson’s Foundation announced its call for Research Center proposals, Dr. De Camilli invited colleagues Dr. Chandra and Dr. Ferguson to apply together. The idea of the team was to focus on a theme that had emerged in PD genetics and was relevant to each of their labs’ research: endolysosomal dysfunction.

Toward this aim, the team proposed original and high-impact projects. The Parkinson’s Foundation recognized their potential, awarding them Research Center funding to launch three major studies:

1. Understanding how the defect of a protein called auxilin may cause PD (Dr. Chandra)

2. Investigating the link between PD and lysosomes, the recycling stations of the cell (Dr. Ferguson)

3. Uncovering how dysfunction of lipids (fats)-building blocks of the walls of endolysosomal compartments may cause PD (Dr. De Camilli)

Cellular Processes Underlying PD

At a cellular level, there are two key problems that occur in PD. One is a drop in dopamine.  This is the chemical signal that is used for communication between brain cells called neurons and, in turn, helps the body process movement and moods. The other problem is a buildup of a sticky protein called alpha-synuclein inside neurons.

Both issues are linked to defects in how cells manage their internal transport system.  This is the complex movement of materials and nutrients through the cell’s “endolysosomal system.” The endolysomal system uses an intricate array of small containers called vesicles moving inside a cell to handle export, import, sorting, recycling and disposal functions.

To picture this, imagine each neuron as a small city that is in constant communication with other neurons. Each neuronal city depends on the export and import of shipments of supplies through communication centers with other neuronal cities called “synapses.” Cargo is sorted and loaded into the “vesicles,” shipping containers that carry materials where they are needed.  There are major centers inside cells, called “endosomes,” where all the material is sorted. Some special cargo is imported into cells via locked containers called “clathrin-coated vesicles.” Once inside the city, these containers are “unlocked” by shedding their clathrin coat so their content can be delivered to endosomes.

After deliveries are made, the vesicles are reused to take any waste to the cell’s recycling center, called a “lysosome.” These lysosome recycling centers break down waste with enzymes and acid in compartments safely tucked away from the rest of the cell. In so doing, lysosomes liberate nutrients that can be used to build new cellular components. These processes collectively support the ability of neurons to communicate with each other while also preventing the accumulation of cellular trash (including alpha-synuclein buildup) and ensuring a supply of building materials to maintain neuronal health.

The three main research projects supported by the Research Center Award focus on understanding and fixing problems in these cellular transport and recycling systems — processes that are disrupted in Parkinson’s.

Unlocking the Connections Between Auxilin & PD: Dr. Chandra

Following the release of dopamine from one neuron to another, the vesicle containers used to deliver dopamine to the synapse need to be rebuilt. Neurons rebuild them using clathrin-coated vesicles, the cell's locked shipping containers. To unlock these containers, neurons use a special "key" protein called auxilin, which was the focus of Dr. Chandra’s research.

Mutations that cause auxilin defects are linked to early-onset PD, but how auxilin dysfunction contributes to the disease was poorly understood. Dr. Chandra and her team first characterized mice that lack auxilin to see if they were a good model for PD research.

Dr. Chandra said, "the mice lacking auxilin develop cardinal features of Parkinson’s disease: age-dependent motor deficits that are responsive to L-DOPA, the death of dopaminergic neurons in the substantia nigra, and alpha-synuclein pathology.”

Next, Dr. Chandra discovered that being unable to unlock the clathrin containers also impacted the neuron’s ability to rebuild packages containing dopamine. Imagine this as a cellular traffic jam, where the locked containers get stuck in transit.  This prevents them from bringing in other materials, being unlocked and reused for a new shipment.

The shipment of dopamine, the key signal that declines in PD, was also impacted in this neuronal traffic jam. At the synapses, there were fewer containers for it to be loaded into and released for communication with other neurons. Finding a way to unlock containers and prevent traffic jams would be key to making dopamine more available and improving PD symptoms.

With that in mind, Dr. Chandra collaborated with Dalibor Sames, PhD, at Columbia University to test the effects of a repurposed drug called Ariadne on the auxilin-lacking mice.

They found that this drug had a remarkable impact on restoring balance and mobility in the mice, similar to levodopa. While there is still much more to learn about these drug effects, this collaborative research has brought to light Ariadne as a potential future treatment for people with PD, particularly those with auxilin mutations.

Understanding Links Between Disrupted Disposal of Cellular Waste & PD: Dr. Ferguson

Dr. Ferguson was new to PD research before his Research Center involvement. “This provided an opportunity for me to bring my research focused on the intersection between lysosomes and neurodegenerative diseases into the Parkinson’s field,” said Dr. Ferguson.

Lysosomes, the cell’s recycling centers, are managed by different genes and proteins. Dr. Ferguson hypothesized that the protein LRP10, which has documented mutations linked to familial PD, was a recycling facilitator. After investigating how cells behave when LRP10 is turned off, he and his research team found that LRP10 indeed plays a significant role in facilitating lysosome function.

Following the city metaphor, LRP10 helps navigate delivery containers to lysosomes, bringing in proteins that support lysosomal function. Without LRP10’s help, the cells’ ability to build working recycling centers is disrupted. In PD, when lysosomes don’t break down and recycle waste properly, proteins like alpha-synuclein build up. Alpha-synuclein forms toxic clumps that damage brain cells, leading to tremors, stiffness, and other movement and non-movement symptoms.

Dr. Ferguson and his team also developed mice with genetic mutations of LRP10 and looked at how their brains were affected. They found that the loss of LRP10 impacts a specific type of cell in the brain, called microglia, which protect neurons. Dr. Ferguson also uncovered links between microglia and one of the most well-known PD genes LRRK2, revealing new roles for LRRK2 in regulating lysosomes in microglia that were never known before.

The success and breakthroughs from this project have shifted the focus of Dr. Ferguson’s career to PD.

“This Research Center Award was the gateway for my entry into the Parkinson’s disease field and was thus a catalyst that fueled a much broader Parkinson’s program. I am also committed to recruiting additional colleagues with complementary skills into the PD field to increase our collective chances to make the discoveries necessary to end this disease.” - Dr. Ferguson

Connecting lipid dynamics in the endolysosomal system & PD: Dr. De Camilli

“My interest in PD was sparked by the finding that two proteins studied in our lab were identified by human genetic studies as PD proteins,” said Dr. De Camilli, referring to synaptojanin 1 (Synj1, also known by the name PARK20) and VPS13C (also known as PARK23). Both proteins regulate lipids (fats) - building blocks of the walls of different compartments of the endolysosomal system.

These two proteins function at different steps in the cell’s endolysosomal transport system and link Dr. De Camilli’s research directly to his colleagues: Synj1 is a functional partner with Dr. Chandra’s auxilin at the earliest step (clathrin-coated vesicles), and VPS13C is involved with Dr. Ferguson’s lysosomes (the latest step).

Dr. De Camilli and his team discovered that Synj1 is required to begin the unlocking process of clathrin containers after they are imported by modifying the lipids they are made of. In mice with Synj1 mutations, they observed PD-like symptoms.

Working with Dr. Chandra’s lab, they also found that mice with both auxilin and Synj1 mutations have significantly more issues, highlighting that the two proteins have important, cooperative roles in cells. Ongoing work from both researchers is investigating this overlap further.

Dr. De Camilli’s lab also learned that the protein VPS13C, a lipid transport protein, has an important role in repairing damaged lysosomes. As a lysosome is used heavily in recycling, its walls can begin to break down, threatening to leak toxic enzymes and acids into the cell, VPS13C helps bring the lipids needed to rebuild the walls. Most interestingly, in collaboration with Dr. Ferguson, they found that the PD protein LRRK2 works in tandem with VPS13C in lysosome repair, a new discovery.

Understanding how PD mutations affect neuronal function is crucial in designing new PD treatments.

Dr. De Camilli is now highly committed to continue his studies of PD. “In my own lab, I will continue to expand my research on how mutations in Synj1 and VPS13C result in PD. We are very excited for being part of this new era of PD research.”

Building Collaborations as a Parkinson’s Foundation Research Center

Being a Parkinson’s Foundation Research Center not only supported these three main projects but also inspired the growth of PD research across Yale.

The groundbreaking research of the Yale Research Center team motivated other Yale researchers to explore how their own work could contribute to the understanding of PD. This award's dedicated funding for additional pilot projects allowed those researchers to join the PD field for the first time.  

“We have awarded pilot projects to four principal investigators who had never worked on PD, and three of them have continued to work on this disease and are now involved in long-term collaborations with our groups,” said Dr. De Camilli.

“The momentum and enthusiasm for PD research at Yale led to support from numerous other funders devoted to PD scientific breakthroughs, such as Aligning Science Across Parkinson’s (ASAP), the Michael J. Fox Foundation, the Chan Zuckerberg Initiative, the Bumpus Foundation and the McKnight Foundation,” said Dr. Chandra.

This support led to new academic collaborations and joint publications as well, “connecting us to the PD community at large across different institutions in the US and abroad,” said Dr. De Camilli.

What began as three PD experimental proposals being accepted as a Parkinson’s Foundation Research Center has evolved into Yale becoming a nationally recognized hub for PD research.

“Beyond our individual projects, the Parkinson’s disease research community at Yale has grown dramatically over the past five years,” said Dr. Ferguson.

While the Research Center designation has concluded, its impact on the Yale School of Medicine and the scientists investigating PD remains, moving the institution and the greater PD research world toward future new treatments and, someday, a cure.

Learn More

The Parkinson’s Foundation works to improve care for people with PD and advance research toward a cure. Learn more with these resources:

• Discover how we are working to close gaps in knowledge about PD: Advancing Research

• Learn about and enroll in PD GENEration — a global genetics study that provides genetic testing and counseling at no cost for people with Parkinson’s.

• Explore ways to get involved in the Parkinson’s Foundation — from becoming a research advocate to joining a research study.

Every three years, the World Parkinson Coalition welcomes the international Parkinson’s community to gather in person to amplify the voices of the more than 10 million people living with Parkinson’s disease (PD) around the world. This event brings together people living with PD, their loved ones and the community of professionals committed to helping them.

For the first time in 10 years, the 2026 World Parkinson Congress (WPC) will be held in North America, from May 24 - 27 in Phoenix, AZ. The Parkinson’s Foundation is proud to be a WPC Champion Double Platinum event partner at next year’s WPC. We’re already looking forward to connecting with the global community and sharing our latest resources and research.

Here’s what we’re excited about for WPC 2026:

1.  Exploring the latest breakthroughs in PD care and research, including sharing the evolution of PD GENEration: Powered by the Parkinson’s Foundation.

The international research study, which continues to advance, has empowered more than 20,000 people with Parkinson’s with information on genetic risk factors than can influence the course of their disease. The Parkinson’s Foundation will present this and other scientific findings alongside the work of fellow researchers during the WPC poster tours.

See how the Foundation is working to identify the fastest lanes to new therapies for people with PD on our Advancing Research page.

2.  Discovering proven strategies to living well with Parkinson’s.

WPC offers a rare opportunity for people with PD, care partners, doctors, scientists and other wide-ranging healthcare professionals to unite as a community and share strategies to actively engage in wellness, including the May 26 “Living Positively with Parkinson’s” panel discussion.

Read Living Your Best Life: A Guide to Parkinson’s Disease to learn practical tips to live well with Parkinson’s.

3.  Celebrating the ties that unite us.

Leading up to the Congress the Red Thread Project, one of the many WPC art, film, music and writing creativity programs, invites members of the Parkinson’s community to take and submit a photograph of themselves holding a red thread for an onsite art installation that will honor the strength of our connections.

Listen to The Link Between Art and Parkinson’s Disease podcast to learn how practicing art can help manage symptoms of PD.

4.  Learning through pre-Congress courses.

We’re looking forward to taking advantage of WPC’s pre-congress educational opportunities. These includes an Advances in Science, Research & Treatment course, as well as a daylong opportunity to dig into the Fundamentals of Parkinson’s — from exploring the basics of PD to understanding early-onset Parkinson’s. 

Visit the Parkinson’s Foundation Learning Lab if you’re looking for online courses to complete right now, at your own pace.

5.  Diving deep into important topics.

WPC small-group roundtable sessions will give attendees the opportunity for sit-down discussions with different experts in various aspects of Parkinson’s.

Join an online Wellness Wednesday Expert Briefing interview to learn PD management symptoms and more.

6.  Connecting with others in the PD community.

Living with Parkinson’s can increase feelings of loneliness and isolation. Opportunities to connect, especially among people who may share common ground, can make us feel understood and supported.

Along with various networking opportunities for healthcare professionals, the WPC offers a Buddies Program which matches interested participants from across the globe, including many first-time attendees, with one another.

Check out the online PD Conversations community to find year-round shared connection and understanding.

7.  Practicing renewal.

Making wellness part of the daily routine is essential to living your best with Parkinson’s. WPC offers many opportunities to practice well-being — whether learning about the benefits mindfulness, addressing your needs as a care partner or taking a moment to exercise your body and voice in the Renewal Room.

Access PD Health @ Home Mindfulness Mondays and Fitness Fridays for in-home activities designed to boost your health and wellness.

8.  Meeting you!

Stop by the Parkinson’s Foundation booth at WPC to meet staff, explore takeaway items and learn how the Parkinson’s Foundation is here to support you with tools, resources and information to help you build a better life with Parkinson’s.

Contact our Helpline specialists at 1-800-4PD-INFO (1-800-473-4636) to find expert care and support in your area.

Join us! Learn more and register for the 2026 World Parkinson Congress at wpc2026.org.

Dormir bien no sólo es importante para la función cerebral; es esencial para el bienestar de todo el cuerpo. El sueño favorece la salud cardiaca e intestinal, la función inmunitaria y más. Los trastornos del sueño pueden ser frecuentes en la enfermedad de Parkinson (EP), pero dormir bien es posible. Descubra cómo identificar y controlar los síntomas del insomnio, el síndrome de las piernas inquietas (SPI) y el trastorno de la conducta del sueño REM (RBD, por sus siglas en inglés).

El siguiente artículo se basa en una Charla con expertos de la Parkinson's Foundation acerca del manejo de los trastornos del sueño, presentada por el Dr. Roneil G. Malkani, profesor asociado de la Feinberg School of Medicine de Northwestern University y neurólogo del Northwestern Memorial Hospital, un Centro de Excelencia de la Parkinson’s Foundation.

Aunque se supone que las personas pasan alrededor de un tercio del día durmiendo, los cambios cerebrales relacionados con el Parkinson y los síntomas de la enfermedad pueden alterar el reloj interno del cuerpo.

Estos desafíos, junto con un exceso de somnolencia diurna, pueden crear un círculo vicioso. Dormir demasiado durante el día e interrupciones del sueño por la noche pueden causar fatiga e impactar en el movimiento, las funciones, el estado de ánimo y el bienestar.

Afrontar el insomnio

Al igual que la buena salud, el sueño reparador implica esfuerzo, a menudo requiriendo ejercicio diario y tiempo al aire libre con luz natural. Limitar las siestas, relajarse antes de acostarse, reducir al mínimo el tiempo frente a las pantallas, respetar un horario para acostarse y mantener el dormitorio oscuro y fresco también son esenciales para un sueño profundo. A veces, el simple hecho de salir de la cama cuando se siente inquieto para realizar una actividad tranquila hasta que se sienta cansado puede marcar la diferencia.

Sin embargo, incluso cuando se siguen las mejores prácticas para dormir, el insomnio puede persistir en el Parkinson:

• A medida que se desgasta la levodopa, pueden aumentar el temblor u otros síntomas motores, dificultando el darse la vuelta en la cama.

• Los dolores relacionados con la edad o la artritis también pueden agudizarse por la noche.

• La nicturia (la necesidad de orinar con frecuencia durante la noche) puede afectar hasta a un 60% de las personas con la EP. El agrandamiento de la próstata también puede aumentar la urgencia urinaria en los hombres.

• La depresión y la ansiedad, frecuentes y a menudo subtratadas en las personas con la EP, pueden exacerbar el insomnio. También el estrés. Por el contrario, el insomnio puede provocar cambios de humor y estrés.

• La apnea del sueño (la interrupción de la respiración al dormir) puede afectar a casi la mitad de las personas con la EP.

Si sigue dando vueltas en la cama a pesar de dormir en un entorno saludable, hable con su médico, quien puede revisar y ajustar la dosis y el horario de los medicamentos actuales y llegar a la raíz de los problemas de sueño. Las herramientas utilizadas para diagnosticar los trastornos del sueño suelen incluir su historial médico, un diario del sueño o un estudio del sueño.

El tratamiento del insomnio debe personalizarse en función de sus necesidades y síntomas individuales y puede incluir:

• Terapia cognitivo-conductual (TCC): estrategias aprendidas en persona o en línea diseñadas para abordar los comportamientos y pensamientos que impiden dormir bien.

• Técnicas de relajación aprendidas, como la relajación muscular progresiva, la repetición silenciosa de ciertas palabras o frases tranquilizadoras (entrenamiento autógeno) o el uso de la visualización mental positiva (imaginería guiada).

• Restricción del sueño, que inicialmente limita el tiempo en la cama con el objetivo de promover un sueño más largo y profundo.

• Terapia de luz brillante para disminuir la somnolencia diurna.

Su médico puede combinar la terapia del sueño con medicación. Entre los medicamentos habituales para el insomnio están:

• Melatonina

• Hipnóticos z (zolpidem, eszopiclona y zaleplon) y benzodiacepinas (clonazepam y temazepam), que favorecen el sueño.

• Terapias inhibidoras de la vigilia como trazadona, antidepresivos tricíclicos (amitriptilina y doxepina), mirtazapina, antagonistas de la orexina (suvorexant, lemborexant y daridorexant), melatonérgicos (melatonina y ramelteon) y quetiapina

Otras terapias para el insomnio relacionado con la EP pueden ser la safinamida, la doxepina y la eszopiclona.

Síndrome de las piernas inquietas (SPI)

Las personas con la enfermedad de Willis-Ekbom, comúnmente conocida como síndrome de las piernas inquietas, pueden sentir una incómoda necesidad de moverse, así como hormigueo, ardor, dolor o sensación de que algo le camina por las piernas. Aunque no siempre hay una causa conocida, el SPI puede estar relacionado con alteraciones neurológicas, medicamentos, incluidos algunos antidepresivos o carencia de hierro. Cuando se sospecha el SPI con base en los síntomas de una persona, es necesario evaluar los niveles de hierro.

Los tratamientos para la deficiencia de hierro incluyen el hierro oral o intravenoso. Si los niveles de hierro son suficientes y los síntomas persisten, existen otras opciones de tratamiento:

• Ligandos alfa-2-delta: gabapentina, pregabalina y gabapentina enacarbil.

• Benzodiacepinas, incluido el clonazepam.

• Medicamentos como el dipiridamol o la amantadina o, en casos graves, opiáceos.

La activación motora tónica (TOMAC) es un nuevo tratamiento de estimulación nerviosa por debajo de la rodilla, aprobado por la Food and Drug Administration de los EE.UU. para el SPI moderado a severo, que puede utilizarse periódicamente a lo largo del día.

Aunque existe una fuerte relación entre el Parkinson y el SPI, los investigadores están descubriendo que las causas subyacentes de cada enfermedad pueden ser muy diferentes. El Parkinson está relacionado con la pérdida de dopamina en el mesencéfalo, mientras que el SPI parece estar ligado a cambios de señalización en otras zonas del cerebro.

Los fármacos dopaminérgicos utilizados habitualmente para la EP también fueron en su momento uno de los pilares del tratamiento del SPI. Ahora se ha demostrado que el uso prolongado de medicamentos dopaminérgicos en personas con SPI a veces puede empeorar la señalización cerebral y los síntomas del SPI. En alguien con Parkinson, una cuidadosa adaptación de los medicamentos dopaminérgicos utilizados para controlar los síntomas motores también puede ser eficaz para controlar los síntomas del SPI.

Trastorno conductual del sueño REM (RBD)

Durante la fase de movimientos oculares rápidos (REM, por sus siglas en inglés) del sueño, cuando se sueña, normalmente sólo se mueven los ojos. El cerebro bloquea los movimientos grandes del cuerpo como medida de protección. Las enfermedades neurodegenerativas, incluido el Parkinson, están relacionadas con el trastorno conductual del sueño REM (RBD, por sus siglas en inglés), un fallo de este interruptor de encendido y apagado. La apnea del sueño y el consumo de antidepresivos también pueden estar relacionados con el RBD.

El RBD puede hacer que una persona actúe físicamente sus sueños. La persona puede hablar en sueños, utilizar un lenguaje agresivo o gritar, caerse o saltar de la cama. Estos sueños vívidos pueden ser leve o increíblemente perturbadores y pueden causar lesiones al soñador o a su compañero de cama.

Casi un 50% de las personas con Parkinson presentan síntomas de trastorno conductual del sueño REM, que pueden aparecer varios años antes del diagnóstico de Parkinson.

Crear un entorno seguro para dormir es esencial para quien experimenta síntomas de RBD:

• Retire cualquier objeto que suponga un riesgo de lesión.

• Si es posible, baje el colchón para reducir el riesgo de caídas.

• Coloque cojines protectores en las esquinas de los muebles cerca de la cama.

• Añade acolchado a la cabecera, una barandilla a la cama para evitar caídas y una alfombra o tapete junto a la cama para amortiguar las caídas accidentales.

Los compañeros de cama pueden conseguir un sueño más profundo utilizando una barrera de almohadas o durmiendo en otra cama.

Un estudio del sueño puede diagnosticar o descartar el RBD y a menudo se utilizan medicamentos para controlar los síntomas. Los tratamientos pueden incluir:

• Melatonina (de 3 a 12 miligramos)

• Clonazepam (de 0.25 a 2 miligramos antes de acostarse) o pramipexol

• Rivastigmina transdérmica

Aprenda más

Explore nuestros recursos acerca del sueño en el Parkinson: 

• Descargue nuestro libro Preguntas frecuentes

• Hoja informativa Problemas del sueño en el Parkinson

• Lea el artículo Consejos de expertos para dormir bien con Parkinson