Movement Disorders

Weeks after Jeannie Volpe caught COVID-19 in November 2020, she could no longer do her job running sexual assault support groups in Anniston, Ala., because she kept forgetting the details that survivors had shared with her. “People were telling me they were having to revisit their traumatic memories, which isn’t fair to anybody,” the 47-year-old says.

Ms. Volpe has been diagnosed with long-COVID autonomic dysfunction, which includes severe muscle pain, depression, anxiety, and a loss of thinking skills. Some of her symptoms are more commonly known as brain fog, and they’re among the most frequent problems reported by people who have long-term issues after a bout of COVID-19.

Many experts and medical professionals say they haven’t even begun to scratch the surface of what impact this will have in years to come. 

“I’m very worried that we have an epidemic of neurologic dysfunction coming down the pike,” says Pamela Davis, MD, PhD, a research professor at Case Western Reserve University, Cleveland.

In the 2 years Ms. Volpe has been living with long COVID, her executive function – the mental processes that enable people to focus attention, retain information, and multitask – has been so diminished that she had to relearn to drive. One of the various doctors assessing her has suggested speech therapy to help Ms. Volpe relearn how to form words. “I can see the words I want to say in my mind, but I can’t make them come out of my mouth,” she says in a sluggish voice that gives away her condition. 

All of those symptoms make it difficult for her to care for herself. Without a job and health insurance, Ms. Volpe says she’s researched assisted suicide in the states that allow it but has ultimately decided she wants to live. 

“People tell you things like you should be grateful you survived it, and you should; but you shouldn’t expect somebody to not grieve after losing their autonomy, their career, their finances.”

The findings of researchers studying the brain effects of COVID-19 reinforce what people with long COVID have been dealing with from the start. Their experiences aren’t imaginary; they’re consistent with neurological disorders – including myalgic encephalomyelitis, also known as chronic fatigue syndrome, or ME/CFS – which carry much more weight in the public imagination than the term brain fog, which can often be used dismissively.

Studies have found that COVID-19 is linked to conditions such as strokes; seizures; and mood, memory, and movement disorders. 

While there are still a lot of unanswered questions about exactly how COVID-19 affects the brain and what the long-term effects are, there’s enough reason to suggest people should be trying to avoid both infection and reinfection until researchers get more answers.

Worldwide, it’s estimated that COVID-19 has contributed to more than 40 million new cases of neurological disorders, says Ziyad Al-Aly, MD, a clinical epidemiologist and long COVID researcher at Washington University in St. Louis. In his latest study of 14 million medical records of the U.S. Department of Veterans Affairs, the country’s largest integrated health care system, researchers found that regardless of age, gender, race, and lifestyle, people who have had COVID-19 are at a higher risk of getting a wide array of 44 neurological conditions after the first year of infection.

He noted that some of the conditions, such as headaches and mild decline in memory and sharpness, may improve and go away over time. But others that showed up, such as stroke, encephalitis (inflammation of the brain), and Guillain-Barré syndrome (a rare disorder in which the body’s immune system attacks the nerves), often lead to lasting damage. Dr. Al-Aly’s team found that neurological conditions were 7% more likely in those who had COVID-19 than in those who had never been infected. 

What’s more, researchers noticed that compared with control groups, the risk of post-COVID thinking problems was more pronounced in people in their 30s, 40s, and 50s – a group that usually would be very unlikely to have these problems. For those over the age of 60, the risks stood out less because at that stage of life, such thinking problems aren’t as rare.

Another study of the veterans system last year showed that COVID-19 survivors were at a 46% higher risk of considering suicide after 1 year.

“We need to be paying attention to this,” says Dr. Al-Aly.  “What we’ve seen is really the tip of the iceberg.” He worries that millions of people, including youths, will lose out on employment and education while dealing with long-term disabilities – and the economic and societal implications of such a fallout. “What we will all be left with is the aftermath of sheer devastation in some people’s lives,” he says.

Igor Koralnik, MD, chief of neuro-infectious disease and global neurology at Northwestern University, Chicago, has been running a specialized long COVID clinic. His team published a paper in March 2021 detailing what they saw in their first 100 patients. “About half the population in the study missed at least 10 days of work. This is going to have persistent impact on the workforce,” Dr. Koralnik said in a podcast posted on the Northwestern website. “We have seen that not only [do] patients have symptoms, but they have decreased quality of life.”

For older people and their caregivers, the risk of potential neurodegenerative diseases that the virus has shown to accelerate, such as dementia, is also a big concern. Alzheimer’s is already the fifth leading cause of death for people 65 and older. 

In a recent study of more than 6 million people over the age of 65, Dr. Davis and her team at Case Western found the risk of Alzheimer’s in the year after COVID-19 increased by 50%-80%. The chances were especially high for women older than 85.

To date, there are no good treatments for Alzheimer’s, yet total health care costs for long-term care and hospice services for people with dementia topped $300 billion in 2020. That doesn’t even include the related costs to families.

“The downstream effect of having someone with Alzheimer’s being taken care of by a family member can be devastating on everyone,” she says. “Sometimes the caregivers don’t weather that very well.” 

When Dr. Davis’s own father got Alzheimer’s at age 86, her mother took care of him until she had a stroke one morning while making breakfast. Dr. Davis attributes the stroke to the stress of caregiving. That left Dr. Davis no choice but to seek housing where both her parents could get care. 

Looking at the broader picture, Dr. Davis believes widespread isolation, loneliness, and grief during the pandemic, and the disease of COVID-19 itself, will continue to have a profound impact on psychiatric diagnoses. This in turn could trigger a wave of new substance abuse as a result of unchecked mental health problems.

Still, not all brain experts are jumping to worst-case scenarios, with a lot yet to be understood before sounding the alarm. Joanna Hellmuth, MD, a neurologist and researcher at the University of California, San Francisco, cautions against reading too much into early data, including any assumptions that COVID-19 causes neurodegeneration or irreversible damage in the brain. 

Even with before-and-after brain scans by University of Oxford, England, researchers that show structural changes to the brain after infection, she points out that they didn’t actually study the clinical symptoms of the people in the study, so it’s too soon to reach conclusions about associated cognitive problems.

“It’s an important piece of the puzzle, but we don’t know how that fits together with everything else,” says Dr. Hellmuth. “Some of my patients get better. … I haven’t seen a single person get worse since the pandemic started, and so I’m hopeful.”

A version of this article first appeared on WebMD.com.

Weeks after Jeannie Volpe caught COVID-19 in November 2020, she could no longer do her job running sexual assault support groups in Anniston, Ala., because she kept forgetting the details that survivors had shared with her. “People were telling me they were having to revisit their traumatic memories, which isn’t fair to anybody,” the 47-year-old says.

Ms. Volpe has been diagnosed with long-COVID autonomic dysfunction, which includes severe muscle pain, depression, anxiety, and a loss of thinking skills. Some of her symptoms are more commonly known as brain fog, and they’re among the most frequent problems reported by people who have long-term issues after a bout of COVID-19.

Many experts and medical professionals say they haven’t even begun to scratch the surface of what impact this will have in years to come. 

“I’m very worried that we have an epidemic of neurologic dysfunction coming down the pike,” says Pamela Davis, MD, PhD, a research professor at Case Western Reserve University, Cleveland.

In the 2 years Ms. Volpe has been living with long COVID, her executive function – the mental processes that enable people to focus attention, retain information, and multitask – has been so diminished that she had to relearn to drive. One of the various doctors assessing her has suggested speech therapy to help Ms. Volpe relearn how to form words. “I can see the words I want to say in my mind, but I can’t make them come out of my mouth,” she says in a sluggish voice that gives away her condition. 

All of those symptoms make it difficult for her to care for herself. Without a job and health insurance, Ms. Volpe says she’s researched assisted suicide in the states that allow it but has ultimately decided she wants to live. 

“People tell you things like you should be grateful you survived it, and you should; but you shouldn’t expect somebody to not grieve after losing their autonomy, their career, their finances.”

The findings of researchers studying the brain effects of COVID-19 reinforce what people with long COVID have been dealing with from the start. Their experiences aren’t imaginary; they’re consistent with neurological disorders – including myalgic encephalomyelitis, also known as chronic fatigue syndrome, or ME/CFS – which carry much more weight in the public imagination than the term brain fog, which can often be used dismissively.

Studies have found that COVID-19 is linked to conditions such as strokes; seizures; and mood, memory, and movement disorders. 

While there are still a lot of unanswered questions about exactly how COVID-19 affects the brain and what the long-term effects are, there’s enough reason to suggest people should be trying to avoid both infection and reinfection until researchers get more answers.

Worldwide, it’s estimated that COVID-19 has contributed to more than 40 million new cases of neurological disorders, says Ziyad Al-Aly, MD, a clinical epidemiologist and long COVID researcher at Washington University in St. Louis. In his latest study of 14 million medical records of the U.S. Department of Veterans Affairs, the country’s largest integrated health care system, researchers found that regardless of age, gender, race, and lifestyle, people who have had COVID-19 are at a higher risk of getting a wide array of 44 neurological conditions after the first year of infection.

He noted that some of the conditions, such as headaches and mild decline in memory and sharpness, may improve and go away over time. But others that showed up, such as stroke, encephalitis (inflammation of the brain), and Guillain-Barré syndrome (a rare disorder in which the body’s immune system attacks the nerves), often lead to lasting damage. Dr. Al-Aly’s team found that neurological conditions were 7% more likely in those who had COVID-19 than in those who had never been infected. 

What’s more, researchers noticed that compared with control groups, the risk of post-COVID thinking problems was more pronounced in people in their 30s, 40s, and 50s – a group that usually would be very unlikely to have these problems. For those over the age of 60, the risks stood out less because at that stage of life, such thinking problems aren’t as rare.

Another study of the veterans system last year showed that COVID-19 survivors were at a 46% higher risk of considering suicide after 1 year.

“We need to be paying attention to this,” says Dr. Al-Aly.  “What we’ve seen is really the tip of the iceberg.” He worries that millions of people, including youths, will lose out on employment and education while dealing with long-term disabilities – and the economic and societal implications of such a fallout. “What we will all be left with is the aftermath of sheer devastation in some people’s lives,” he says.

Igor Koralnik, MD, chief of neuro-infectious disease and global neurology at Northwestern University, Chicago, has been running a specialized long COVID clinic. His team published a paper in March 2021 detailing what they saw in their first 100 patients. “About half the population in the study missed at least 10 days of work. This is going to have persistent impact on the workforce,” Dr. Koralnik said in a podcast posted on the Northwestern website. “We have seen that not only [do] patients have symptoms, but they have decreased quality of life.”

For older people and their caregivers, the risk of potential neurodegenerative diseases that the virus has shown to accelerate, such as dementia, is also a big concern. Alzheimer’s is already the fifth leading cause of death for people 65 and older. 

In a recent study of more than 6 million people over the age of 65, Dr. Davis and her team at Case Western found the risk of Alzheimer’s in the year after COVID-19 increased by 50%-80%. The chances were especially high for women older than 85.

To date, there are no good treatments for Alzheimer’s, yet total health care costs for long-term care and hospice services for people with dementia topped $300 billion in 2020. That doesn’t even include the related costs to families.

“The downstream effect of having someone with Alzheimer’s being taken care of by a family member can be devastating on everyone,” she says. “Sometimes the caregivers don’t weather that very well.” 

When Dr. Davis’s own father got Alzheimer’s at age 86, her mother took care of him until she had a stroke one morning while making breakfast. Dr. Davis attributes the stroke to the stress of caregiving. That left Dr. Davis no choice but to seek housing where both her parents could get care. 

Looking at the broader picture, Dr. Davis believes widespread isolation, loneliness, and grief during the pandemic, and the disease of COVID-19 itself, will continue to have a profound impact on psychiatric diagnoses. This in turn could trigger a wave of new substance abuse as a result of unchecked mental health problems.

Still, not all brain experts are jumping to worst-case scenarios, with a lot yet to be understood before sounding the alarm. Joanna Hellmuth, MD, a neurologist and researcher at the University of California, San Francisco, cautions against reading too much into early data, including any assumptions that COVID-19 causes neurodegeneration or irreversible damage in the brain. 

Even with before-and-after brain scans by University of Oxford, England, researchers that show structural changes to the brain after infection, she points out that they didn’t actually study the clinical symptoms of the people in the study, so it’s too soon to reach conclusions about associated cognitive problems.

“It’s an important piece of the puzzle, but we don’t know how that fits together with everything else,” says Dr. Hellmuth. “Some of my patients get better. … I haven’t seen a single person get worse since the pandemic started, and so I’m hopeful.”

A version of this article first appeared on WebMD.com.

Weeks after Jeannie Volpe caught COVID-19 in November 2020, she could no longer do her job running sexual assault support groups in Anniston, Ala., because she kept forgetting the details that survivors had shared with her. “People were telling me they were having to revisit their traumatic memories, which isn’t fair to anybody,” the 47-year-old says.

Ms. Volpe has been diagnosed with long-COVID autonomic dysfunction, which includes severe muscle pain, depression, anxiety, and a loss of thinking skills. Some of her symptoms are more commonly known as brain fog, and they’re among the most frequent problems reported by people who have long-term issues after a bout of COVID-19.

Many experts and medical professionals say they haven’t even begun to scratch the surface of what impact this will have in years to come. 

“I’m very worried that we have an epidemic of neurologic dysfunction coming down the pike,” says Pamela Davis, MD, PhD, a research professor at Case Western Reserve University, Cleveland.

In the 2 years Ms. Volpe has been living with long COVID, her executive function – the mental processes that enable people to focus attention, retain information, and multitask – has been so diminished that she had to relearn to drive. One of the various doctors assessing her has suggested speech therapy to help Ms. Volpe relearn how to form words. “I can see the words I want to say in my mind, but I can’t make them come out of my mouth,” she says in a sluggish voice that gives away her condition. 

All of those symptoms make it difficult for her to care for herself. Without a job and health insurance, Ms. Volpe says she’s researched assisted suicide in the states that allow it but has ultimately decided she wants to live. 

“People tell you things like you should be grateful you survived it, and you should; but you shouldn’t expect somebody to not grieve after losing their autonomy, their career, their finances.”

The findings of researchers studying the brain effects of COVID-19 reinforce what people with long COVID have been dealing with from the start. Their experiences aren’t imaginary; they’re consistent with neurological disorders – including myalgic encephalomyelitis, also known as chronic fatigue syndrome, or ME/CFS – which carry much more weight in the public imagination than the term brain fog, which can often be used dismissively.

Studies have found that COVID-19 is linked to conditions such as strokes; seizures; and mood, memory, and movement disorders. 

While there are still a lot of unanswered questions about exactly how COVID-19 affects the brain and what the long-term effects are, there’s enough reason to suggest people should be trying to avoid both infection and reinfection until researchers get more answers.

Worldwide, it’s estimated that COVID-19 has contributed to more than 40 million new cases of neurological disorders, says Ziyad Al-Aly, MD, a clinical epidemiologist and long COVID researcher at Washington University in St. Louis. In his latest study of 14 million medical records of the U.S. Department of Veterans Affairs, the country’s largest integrated health care system, researchers found that regardless of age, gender, race, and lifestyle, people who have had COVID-19 are at a higher risk of getting a wide array of 44 neurological conditions after the first year of infection.

He noted that some of the conditions, such as headaches and mild decline in memory and sharpness, may improve and go away over time. But others that showed up, such as stroke, encephalitis (inflammation of the brain), and Guillain-Barré syndrome (a rare disorder in which the body’s immune system attacks the nerves), often lead to lasting damage. Dr. Al-Aly’s team found that neurological conditions were 7% more likely in those who had COVID-19 than in those who had never been infected. 

What’s more, researchers noticed that compared with control groups, the risk of post-COVID thinking problems was more pronounced in people in their 30s, 40s, and 50s – a group that usually would be very unlikely to have these problems. For those over the age of 60, the risks stood out less because at that stage of life, such thinking problems aren’t as rare.

Another study of the veterans system last year showed that COVID-19 survivors were at a 46% higher risk of considering suicide after 1 year.

“We need to be paying attention to this,” says Dr. Al-Aly.  “What we’ve seen is really the tip of the iceberg.” He worries that millions of people, including youths, will lose out on employment and education while dealing with long-term disabilities – and the economic and societal implications of such a fallout. “What we will all be left with is the aftermath of sheer devastation in some people’s lives,” he says.

Igor Koralnik, MD, chief of neuro-infectious disease and global neurology at Northwestern University, Chicago, has been running a specialized long COVID clinic. His team published a paper in March 2021 detailing what they saw in their first 100 patients. “About half the population in the study missed at least 10 days of work. This is going to have persistent impact on the workforce,” Dr. Koralnik said in a podcast posted on the Northwestern website. “We have seen that not only [do] patients have symptoms, but they have decreased quality of life.”

For older people and their caregivers, the risk of potential neurodegenerative diseases that the virus has shown to accelerate, such as dementia, is also a big concern. Alzheimer’s is already the fifth leading cause of death for people 65 and older. 

In a recent study of more than 6 million people over the age of 65, Dr. Davis and her team at Case Western found the risk of Alzheimer’s in the year after COVID-19 increased by 50%-80%. The chances were especially high for women older than 85.

To date, there are no good treatments for Alzheimer’s, yet total health care costs for long-term care and hospice services for people with dementia topped $300 billion in 2020. That doesn’t even include the related costs to families.

“The downstream effect of having someone with Alzheimer’s being taken care of by a family member can be devastating on everyone,” she says. “Sometimes the caregivers don’t weather that very well.” 

When Dr. Davis’s own father got Alzheimer’s at age 86, her mother took care of him until she had a stroke one morning while making breakfast. Dr. Davis attributes the stroke to the stress of caregiving. That left Dr. Davis no choice but to seek housing where both her parents could get care. 

Looking at the broader picture, Dr. Davis believes widespread isolation, loneliness, and grief during the pandemic, and the disease of COVID-19 itself, will continue to have a profound impact on psychiatric diagnoses. This in turn could trigger a wave of new substance abuse as a result of unchecked mental health problems.

Still, not all brain experts are jumping to worst-case scenarios, with a lot yet to be understood before sounding the alarm. Joanna Hellmuth, MD, a neurologist and researcher at the University of California, San Francisco, cautions against reading too much into early data, including any assumptions that COVID-19 causes neurodegeneration or irreversible damage in the brain. 

Even with before-and-after brain scans by University of Oxford, England, researchers that show structural changes to the brain after infection, she points out that they didn’t actually study the clinical symptoms of the people in the study, so it’s too soon to reach conclusions about associated cognitive problems.

“It’s an important piece of the puzzle, but we don’t know how that fits together with everything else,” says Dr. Hellmuth. “Some of my patients get better. … I haven’t seen a single person get worse since the pandemic started, and so I’m hopeful.”

A version of this article first appeared on WebMD.com.

Google the word “dopamine” and you will learn that its nicknames are the “happy hormone” and the “pleasure molecule” and that it is among the most important chemicals in our brains. With The Guardian branding it “the Kim Kardashian of neurotransmitters,” dopamine has become a true pop-science darling – people across the globe have attempted to boost their mood with dopamine fasts and dopamine dressing.

A century ago, however, newly discovered dopamine was seen as an uninspiring chemical, nothing more than a precursor of noradrenaline. It took several stubborn and hardworking scientists to change that view.
 

Levodopa: An indifferent precursor

When Casimir Funk, PhD, a Polish biochemist and the discoverer of vitamins, first synthesized the dopamine precursor levodopa in 1911, he had no idea how important the molecule would prove to be in pharmacology and neurobiology. Nor did Markus Guggenheim, PhD, a Swiss biochemist, who isolated levodopa in 1913 from the seeds of a broad bean, Vicia faba. Dr. Guggenheim administered 1 g of levodopa to a rabbit, with no apparent negative consequences. He then prepared a larger dose (2.5 g) and tested it on himself. “Ten minutes after taking it, I felt very nauseous, I had to vomit twice,” he wrote in his paper. In the body, levodopa is converted into dopamine, which may act as an emetic – an effect Dr. Guggenheim didn’t understand. He simply abandoned his human study, erroneously concluding, on the basis of his animal research, that levodopa is “pharmacologically fairly indifferent.”

Around the same time, several scientists across Europe successfully synthesized dopamine, but those discoveries were shelved without much fanfare. For the next 3 decades, dopamine and levodopa were pushed into academic obscurity. Just before World War II, a group of German scientists showed that levodopa is metabolized to dopamine in the body, while another German researcher, Hermann Blaschko, MD, discovered that dopamine is an intermediary in the synthesis of noradrenaline. Even these findings, however, were not immediately accepted.

The dopamine story picked up pace in the post-war years with the observation that the hormone was present in various tissues and body fluids, although nowhere as abundantly as in the central nervous system. Intrigued, Dr. Blaschko, who (after escaping Nazi Germany, changing his name to Hugh, and starting work at Oxford [England] University) hypothesized that dopamine couldn’t be an unremarkable precursor of noradrenaline – it had to have some physiologic functions of its own. He asked his postdoctoral fellow, Oheh Hornykiewicz, MD, to test a few ideas. Dr. Hornykiewicz soon confirmed that dopamine lowered blood pressure in guinea pigs, proving that dopamine indeed had physiologic activity that was independent of other catecholamines.
 

Reserpine and rabbit ears

While Dr. Blaschko and Dr. Hornykiewicz were puzzling over dopamine’s physiologic role in the body, across the ocean at the National Heart Institute in Maryland, pharmacologist Bernard Brodie, PhD and colleagues were laying the groundwork for the discovery of dopamine’s starring role in the brain.

Spoiler alert: Dr. Brodie’s work showed that a new psychiatric drug known as reserpine was capable of fully depleting the brain’s stores of serotonin and – of greatest significance, as it turned out – mimicking the neuromuscular symptoms typical of Parkinson’s disease. The connection to dopamine would be made by new lab colleague Arvid Carlsson, MD, PhD, who would go on to win a Nobel Prize.

Derived from Rauwolfia serpentina (a plant that for centuries has been used in India for the treatment of mental illness, insomnia, and snake bites), reserpine was introduced in the West as a treatment for schizophrenia.

It worked marvels. In 1954, the press lauded the “dramatic” and seemingly “incredible”: results in treating “hopelessly insane patients.” Reserpine had a downside, however. Reports soon changed in tone regarding the drug’s severe side effects, including headaches, dizziness, vomiting, and, far more disturbingly, symptoms mimicking Parkinson’s disease, from muscular rigidity to tremors.

Dr. Brodie observed that, when reserpine was injected, animals became completely immobile. Serotonin nearly vanished from their brains, but bizarrely, drugs that spur serotonin production did not reverse the rabbits’ immobility.

Dr. Carlsson realized that other catecholamines must be involved in reserpine’s side effects, and he began to search for the culprits. He moved back to his native Sweden and ordered a spectrophotofluorimeter. In one of his experiments, Carlsson injected a pair of rabbits with reserpine, which caused the animals to become catatonic with flattened ears. After the researchers injected the animals with levodopa, within 15 minutes, the rabbits were hopping around, ears proudly vertical. “We were just as excited as the rabbits,” Dr. Carlsson later recalled in a 2016 interview. Dr. Carlsson realized that, because there was no noradrenaline in the rabbits’ brains, dopamine depletion must have been directly responsible for producing reserpine’s motor inhibitory effects.
 

Skeptics are silenced

In 1960, however, the medical community was not yet ready to accept that dopamine was anything but a boring intermediate between levodopa and noradrenaline. At a prestigious London symposium, Dr. Carlsson and his two colleagues presented their hypothesis that dopamine may be a neurotransmitter, thus implicating it in Parkinson’s disease. They were met with harsh criticism. Some of the experts said levodopa was nothing more than a poison. Dr. Carlsson later recalled facing “a profound and nearly unanimous skepticism regarding our points of view.”

That would soon change. Dr. Hornykiewicz, the biochemist who had earlier discovered dopamine’s BP-lowering effects, tested Dr. Carlsson’s ideas using the postmortem brains of Parkinson’s disease patients. It appeared Dr. Carlsson was right: Unlike in healthy brains, the striatum of patients with Parkinson’s disease contained almost no dopamine whatsoever. Beginning in 1961, in collaboration with neurologist Walther Birkmayer, MD, Hornykiewicz injected levodopa into 20 patients with Parkinson’s disease and observed a “miraculous” (albeit temporary) amelioration of rigidity, motionlessness, and speechlessness.

By the late 1960s, levodopa and dopamine were making headlines. A 1969 New York Times article described similar stunning improvements in patients with Parkinson’s disease who were treated with levodopa. A patient who had arrived at a hospital unable to speak, with hands clenched and rigid expression, was suddenly able to stride into his doctor’s office and even jog around. “I might say I’m a human being,” he told reporters. Although the treatment was expensive – equivalent to $210 in 2022 – physicians were deluged with requests for “dopa.” To this day, levodopa remains a gold standard in the treatment of Parkinson’s disease.
 

Still misunderstood

The history of dopamine, however, is not only about Parkinson’s disease but extends to the treatment of schizophrenia and addiction. When in the1940s a French military surgeon started giving a new antihistamine drug, promethazine, to prevent shock in soldiers undergoing surgery, he noticed a bizarre side effect: the soldiers would become euphoric yet oddly calm at the same time.

After the drug was modified by adding a chlorine atom and renamed chlorpromazine, it fast became a go-to treatment for psychosis. At the time, no one made the connection to dopamine. Contemporary doctors believed that it calmed people by lowering body temperature (common treatments for mental illness back in the day included swaddling patients in cold, wet sheets). Yet just like reserpine, chlorpromazine produced range of nasty side effects that closely mimicked Parkinson’s disease. This led a Dutch pharmacologist, Jacques van Rossum, to hypothesize that dopamine receptor blockade could explain chlorpromazine’s antipsychotic effects – an idea that remains widely accepted today.

In the 1970s, dopamine was linked with addiction through research on rodents, and this novel idea caught people’s imagination over the coming decades. A story on dopamine titled, “How We Get Addicted,” made the cover of Time in 1997.

Yet as the dopamine/addiction connection became widespread, it also became oversimplified. According to a 2015 article in Nature Reviews Neuroscience, a wave of low-quality research followed – nonreplicated, insufficient – which led the authors to conclude that we are “addicted to the dopamine theory of addiction.” Just about every pleasure under the sun was being attributed to dopamine, from eating delicious foods and playing computer games to sex, music, and hot showers. As recent science shows, however, dopamine is not simply about pleasure – it’s about reward prediction, response to stress, memory, learning, and even the functioning of the immune system. Since its first synthesis in the early 20th century, dopamine has often been misunderstood and oversimplified – and it seems the story is repeating itself now.

In one of his final interviews, Dr. Carlsson, who passed away in 2018 at the age of 95, warned about playing around with dopamine and, in particular, prescribing drugs that have an inhibitory action on this neurotransmitter. “Dopamine is involved in everything that happens in our brains – all its important functions,” he said.

We should be careful how we handle such a delicate and still little-known system.

A version of this article first appeared on Medscape.com.

Google the word “dopamine” and you will learn that its nicknames are the “happy hormone” and the “pleasure molecule” and that it is among the most important chemicals in our brains. With The Guardian branding it “the Kim Kardashian of neurotransmitters,” dopamine has become a true pop-science darling – people across the globe have attempted to boost their mood with dopamine fasts and dopamine dressing.

A century ago, however, newly discovered dopamine was seen as an uninspiring chemical, nothing more than a precursor of noradrenaline. It took several stubborn and hardworking scientists to change that view.
 

Levodopa: An indifferent precursor

When Casimir Funk, PhD, a Polish biochemist and the discoverer of vitamins, first synthesized the dopamine precursor levodopa in 1911, he had no idea how important the molecule would prove to be in pharmacology and neurobiology. Nor did Markus Guggenheim, PhD, a Swiss biochemist, who isolated levodopa in 1913 from the seeds of a broad bean, Vicia faba. Dr. Guggenheim administered 1 g of levodopa to a rabbit, with no apparent negative consequences. He then prepared a larger dose (2.5 g) and tested it on himself. “Ten minutes after taking it, I felt very nauseous, I had to vomit twice,” he wrote in his paper. In the body, levodopa is converted into dopamine, which may act as an emetic – an effect Dr. Guggenheim didn’t understand. He simply abandoned his human study, erroneously concluding, on the basis of his animal research, that levodopa is “pharmacologically fairly indifferent.”

Around the same time, several scientists across Europe successfully synthesized dopamine, but those discoveries were shelved without much fanfare. For the next 3 decades, dopamine and levodopa were pushed into academic obscurity. Just before World War II, a group of German scientists showed that levodopa is metabolized to dopamine in the body, while another German researcher, Hermann Blaschko, MD, discovered that dopamine is an intermediary in the synthesis of noradrenaline. Even these findings, however, were not immediately accepted.

The dopamine story picked up pace in the post-war years with the observation that the hormone was present in various tissues and body fluids, although nowhere as abundantly as in the central nervous system. Intrigued, Dr. Blaschko, who (after escaping Nazi Germany, changing his name to Hugh, and starting work at Oxford [England] University) hypothesized that dopamine couldn’t be an unremarkable precursor of noradrenaline – it had to have some physiologic functions of its own. He asked his postdoctoral fellow, Oheh Hornykiewicz, MD, to test a few ideas. Dr. Hornykiewicz soon confirmed that dopamine lowered blood pressure in guinea pigs, proving that dopamine indeed had physiologic activity that was independent of other catecholamines.
 

Reserpine and rabbit ears

While Dr. Blaschko and Dr. Hornykiewicz were puzzling over dopamine’s physiologic role in the body, across the ocean at the National Heart Institute in Maryland, pharmacologist Bernard Brodie, PhD and colleagues were laying the groundwork for the discovery of dopamine’s starring role in the brain.

Spoiler alert: Dr. Brodie’s work showed that a new psychiatric drug known as reserpine was capable of fully depleting the brain’s stores of serotonin and – of greatest significance, as it turned out – mimicking the neuromuscular symptoms typical of Parkinson’s disease. The connection to dopamine would be made by new lab colleague Arvid Carlsson, MD, PhD, who would go on to win a Nobel Prize.

Derived from Rauwolfia serpentina (a plant that for centuries has been used in India for the treatment of mental illness, insomnia, and snake bites), reserpine was introduced in the West as a treatment for schizophrenia.

It worked marvels. In 1954, the press lauded the “dramatic” and seemingly “incredible”: results in treating “hopelessly insane patients.” Reserpine had a downside, however. Reports soon changed in tone regarding the drug’s severe side effects, including headaches, dizziness, vomiting, and, far more disturbingly, symptoms mimicking Parkinson’s disease, from muscular rigidity to tremors.

Dr. Brodie observed that, when reserpine was injected, animals became completely immobile. Serotonin nearly vanished from their brains, but bizarrely, drugs that spur serotonin production did not reverse the rabbits’ immobility.

Dr. Carlsson realized that other catecholamines must be involved in reserpine’s side effects, and he began to search for the culprits. He moved back to his native Sweden and ordered a spectrophotofluorimeter. In one of his experiments, Carlsson injected a pair of rabbits with reserpine, which caused the animals to become catatonic with flattened ears. After the researchers injected the animals with levodopa, within 15 minutes, the rabbits were hopping around, ears proudly vertical. “We were just as excited as the rabbits,” Dr. Carlsson later recalled in a 2016 interview. Dr. Carlsson realized that, because there was no noradrenaline in the rabbits’ brains, dopamine depletion must have been directly responsible for producing reserpine’s motor inhibitory effects.
 

Skeptics are silenced

In 1960, however, the medical community was not yet ready to accept that dopamine was anything but a boring intermediate between levodopa and noradrenaline. At a prestigious London symposium, Dr. Carlsson and his two colleagues presented their hypothesis that dopamine may be a neurotransmitter, thus implicating it in Parkinson’s disease. They were met with harsh criticism. Some of the experts said levodopa was nothing more than a poison. Dr. Carlsson later recalled facing “a profound and nearly unanimous skepticism regarding our points of view.”

That would soon change. Dr. Hornykiewicz, the biochemist who had earlier discovered dopamine’s BP-lowering effects, tested Dr. Carlsson’s ideas using the postmortem brains of Parkinson’s disease patients. It appeared Dr. Carlsson was right: Unlike in healthy brains, the striatum of patients with Parkinson’s disease contained almost no dopamine whatsoever. Beginning in 1961, in collaboration with neurologist Walther Birkmayer, MD, Hornykiewicz injected levodopa into 20 patients with Parkinson’s disease and observed a “miraculous” (albeit temporary) amelioration of rigidity, motionlessness, and speechlessness.

By the late 1960s, levodopa and dopamine were making headlines. A 1969 New York Times article described similar stunning improvements in patients with Parkinson’s disease who were treated with levodopa. A patient who had arrived at a hospital unable to speak, with hands clenched and rigid expression, was suddenly able to stride into his doctor’s office and even jog around. “I might say I’m a human being,” he told reporters. Although the treatment was expensive – equivalent to $210 in 2022 – physicians were deluged with requests for “dopa.” To this day, levodopa remains a gold standard in the treatment of Parkinson’s disease.
 

Still misunderstood

The history of dopamine, however, is not only about Parkinson’s disease but extends to the treatment of schizophrenia and addiction. When in the1940s a French military surgeon started giving a new antihistamine drug, promethazine, to prevent shock in soldiers undergoing surgery, he noticed a bizarre side effect: the soldiers would become euphoric yet oddly calm at the same time.

After the drug was modified by adding a chlorine atom and renamed chlorpromazine, it fast became a go-to treatment for psychosis. At the time, no one made the connection to dopamine. Contemporary doctors believed that it calmed people by lowering body temperature (common treatments for mental illness back in the day included swaddling patients in cold, wet sheets). Yet just like reserpine, chlorpromazine produced range of nasty side effects that closely mimicked Parkinson’s disease. This led a Dutch pharmacologist, Jacques van Rossum, to hypothesize that dopamine receptor blockade could explain chlorpromazine’s antipsychotic effects – an idea that remains widely accepted today.

In the 1970s, dopamine was linked with addiction through research on rodents, and this novel idea caught people’s imagination over the coming decades. A story on dopamine titled, “How We Get Addicted,” made the cover of Time in 1997.

Yet as the dopamine/addiction connection became widespread, it also became oversimplified. According to a 2015 article in Nature Reviews Neuroscience, a wave of low-quality research followed – nonreplicated, insufficient – which led the authors to conclude that we are “addicted to the dopamine theory of addiction.” Just about every pleasure under the sun was being attributed to dopamine, from eating delicious foods and playing computer games to sex, music, and hot showers. As recent science shows, however, dopamine is not simply about pleasure – it’s about reward prediction, response to stress, memory, learning, and even the functioning of the immune system. Since its first synthesis in the early 20th century, dopamine has often been misunderstood and oversimplified – and it seems the story is repeating itself now.

In one of his final interviews, Dr. Carlsson, who passed away in 2018 at the age of 95, warned about playing around with dopamine and, in particular, prescribing drugs that have an inhibitory action on this neurotransmitter. “Dopamine is involved in everything that happens in our brains – all its important functions,” he said.

We should be careful how we handle such a delicate and still little-known system.

A version of this article first appeared on Medscape.com.

Google the word “dopamine” and you will learn that its nicknames are the “happy hormone” and the “pleasure molecule” and that it is among the most important chemicals in our brains. With The Guardian branding it “the Kim Kardashian of neurotransmitters,” dopamine has become a true pop-science darling – people across the globe have attempted to boost their mood with dopamine fasts and dopamine dressing.

A century ago, however, newly discovered dopamine was seen as an uninspiring chemical, nothing more than a precursor of noradrenaline. It took several stubborn and hardworking scientists to change that view.
 

Levodopa: An indifferent precursor

When Casimir Funk, PhD, a Polish biochemist and the discoverer of vitamins, first synthesized the dopamine precursor levodopa in 1911, he had no idea how important the molecule would prove to be in pharmacology and neurobiology. Nor did Markus Guggenheim, PhD, a Swiss biochemist, who isolated levodopa in 1913 from the seeds of a broad bean, Vicia faba. Dr. Guggenheim administered 1 g of levodopa to a rabbit, with no apparent negative consequences. He then prepared a larger dose (2.5 g) and tested it on himself. “Ten minutes after taking it, I felt very nauseous, I had to vomit twice,” he wrote in his paper. In the body, levodopa is converted into dopamine, which may act as an emetic – an effect Dr. Guggenheim didn’t understand. He simply abandoned his human study, erroneously concluding, on the basis of his animal research, that levodopa is “pharmacologically fairly indifferent.”

Around the same time, several scientists across Europe successfully synthesized dopamine, but those discoveries were shelved without much fanfare. For the next 3 decades, dopamine and levodopa were pushed into academic obscurity. Just before World War II, a group of German scientists showed that levodopa is metabolized to dopamine in the body, while another German researcher, Hermann Blaschko, MD, discovered that dopamine is an intermediary in the synthesis of noradrenaline. Even these findings, however, were not immediately accepted.

The dopamine story picked up pace in the post-war years with the observation that the hormone was present in various tissues and body fluids, although nowhere as abundantly as in the central nervous system. Intrigued, Dr. Blaschko, who (after escaping Nazi Germany, changing his name to Hugh, and starting work at Oxford [England] University) hypothesized that dopamine couldn’t be an unremarkable precursor of noradrenaline – it had to have some physiologic functions of its own. He asked his postdoctoral fellow, Oheh Hornykiewicz, MD, to test a few ideas. Dr. Hornykiewicz soon confirmed that dopamine lowered blood pressure in guinea pigs, proving that dopamine indeed had physiologic activity that was independent of other catecholamines.
 

Reserpine and rabbit ears

While Dr. Blaschko and Dr. Hornykiewicz were puzzling over dopamine’s physiologic role in the body, across the ocean at the National Heart Institute in Maryland, pharmacologist Bernard Brodie, PhD and colleagues were laying the groundwork for the discovery of dopamine’s starring role in the brain.

Spoiler alert: Dr. Brodie’s work showed that a new psychiatric drug known as reserpine was capable of fully depleting the brain’s stores of serotonin and – of greatest significance, as it turned out – mimicking the neuromuscular symptoms typical of Parkinson’s disease. The connection to dopamine would be made by new lab colleague Arvid Carlsson, MD, PhD, who would go on to win a Nobel Prize.

Derived from Rauwolfia serpentina (a plant that for centuries has been used in India for the treatment of mental illness, insomnia, and snake bites), reserpine was introduced in the West as a treatment for schizophrenia.

It worked marvels. In 1954, the press lauded the “dramatic” and seemingly “incredible”: results in treating “hopelessly insane patients.” Reserpine had a downside, however. Reports soon changed in tone regarding the drug’s severe side effects, including headaches, dizziness, vomiting, and, far more disturbingly, symptoms mimicking Parkinson’s disease, from muscular rigidity to tremors.

Dr. Brodie observed that, when reserpine was injected, animals became completely immobile. Serotonin nearly vanished from their brains, but bizarrely, drugs that spur serotonin production did not reverse the rabbits’ immobility.

Dr. Carlsson realized that other catecholamines must be involved in reserpine’s side effects, and he began to search for the culprits. He moved back to his native Sweden and ordered a spectrophotofluorimeter. In one of his experiments, Carlsson injected a pair of rabbits with reserpine, which caused the animals to become catatonic with flattened ears. After the researchers injected the animals with levodopa, within 15 minutes, the rabbits were hopping around, ears proudly vertical. “We were just as excited as the rabbits,” Dr. Carlsson later recalled in a 2016 interview. Dr. Carlsson realized that, because there was no noradrenaline in the rabbits’ brains, dopamine depletion must have been directly responsible for producing reserpine’s motor inhibitory effects.
 

Skeptics are silenced

In 1960, however, the medical community was not yet ready to accept that dopamine was anything but a boring intermediate between levodopa and noradrenaline. At a prestigious London symposium, Dr. Carlsson and his two colleagues presented their hypothesis that dopamine may be a neurotransmitter, thus implicating it in Parkinson’s disease. They were met with harsh criticism. Some of the experts said levodopa was nothing more than a poison. Dr. Carlsson later recalled facing “a profound and nearly unanimous skepticism regarding our points of view.”

That would soon change. Dr. Hornykiewicz, the biochemist who had earlier discovered dopamine’s BP-lowering effects, tested Dr. Carlsson’s ideas using the postmortem brains of Parkinson’s disease patients. It appeared Dr. Carlsson was right: Unlike in healthy brains, the striatum of patients with Parkinson’s disease contained almost no dopamine whatsoever. Beginning in 1961, in collaboration with neurologist Walther Birkmayer, MD, Hornykiewicz injected levodopa into 20 patients with Parkinson’s disease and observed a “miraculous” (albeit temporary) amelioration of rigidity, motionlessness, and speechlessness.

By the late 1960s, levodopa and dopamine were making headlines. A 1969 New York Times article described similar stunning improvements in patients with Parkinson’s disease who were treated with levodopa. A patient who had arrived at a hospital unable to speak, with hands clenched and rigid expression, was suddenly able to stride into his doctor’s office and even jog around. “I might say I’m a human being,” he told reporters. Although the treatment was expensive – equivalent to $210 in 2022 – physicians were deluged with requests for “dopa.” To this day, levodopa remains a gold standard in the treatment of Parkinson’s disease.
 

Still misunderstood

The history of dopamine, however, is not only about Parkinson’s disease but extends to the treatment of schizophrenia and addiction. When in the1940s a French military surgeon started giving a new antihistamine drug, promethazine, to prevent shock in soldiers undergoing surgery, he noticed a bizarre side effect: the soldiers would become euphoric yet oddly calm at the same time.

After the drug was modified by adding a chlorine atom and renamed chlorpromazine, it fast became a go-to treatment for psychosis. At the time, no one made the connection to dopamine. Contemporary doctors believed that it calmed people by lowering body temperature (common treatments for mental illness back in the day included swaddling patients in cold, wet sheets). Yet just like reserpine, chlorpromazine produced range of nasty side effects that closely mimicked Parkinson’s disease. This led a Dutch pharmacologist, Jacques van Rossum, to hypothesize that dopamine receptor blockade could explain chlorpromazine’s antipsychotic effects – an idea that remains widely accepted today.

In the 1970s, dopamine was linked with addiction through research on rodents, and this novel idea caught people’s imagination over the coming decades. A story on dopamine titled, “How We Get Addicted,” made the cover of Time in 1997.

Yet as the dopamine/addiction connection became widespread, it also became oversimplified. According to a 2015 article in Nature Reviews Neuroscience, a wave of low-quality research followed – nonreplicated, insufficient – which led the authors to conclude that we are “addicted to the dopamine theory of addiction.” Just about every pleasure under the sun was being attributed to dopamine, from eating delicious foods and playing computer games to sex, music, and hot showers. As recent science shows, however, dopamine is not simply about pleasure – it’s about reward prediction, response to stress, memory, learning, and even the functioning of the immune system. Since its first synthesis in the early 20th century, dopamine has often been misunderstood and oversimplified – and it seems the story is repeating itself now.

In one of his final interviews, Dr. Carlsson, who passed away in 2018 at the age of 95, warned about playing around with dopamine and, in particular, prescribing drugs that have an inhibitory action on this neurotransmitter. “Dopamine is involved in everything that happens in our brains – all its important functions,” he said.

We should be careful how we handle such a delicate and still little-known system.

A version of this article first appeared on Medscape.com.

Resistance training can help improve several symptoms of Parkinson’s disease – but is not superior to other physical activities, new research suggests.

A meta-analysis, which included 18 randomized controlled trials and more than 1,000 patients with Parkinson’s disease, showed that those who underwent resistance training had significantly greater improvement in motor impairment, muscle strength, and mobility/balance than their peers who underwent passive or placebo interventions.

However, there was no significant difference between patients who participated in resistance training and those who participated in other active physical interventions, including yoga.

Overall, the results highlight the importance that these patients should participate in some type of physical exercise, said the study’s lead author, Romina Gollan, MSc, an assistant researcher in the division of medical psychology, University of Cologne, Germany. “Patients should definitely be doing exercises, including resistance training, if they want to. But the type of exercise is of secondary interest,” she said.

The findings were presented at the International Congress of Parkinson’s Disease and Movement Disorders.
 

Positive but inconsistent

Previous reviews have suggested resistance training has positive effects on motor function in Parkinson’s disease. However, results from the included studies were inconsistent; and few reviews have examined nonmotor outcomes of resistance training in this population, the investigators noted.

After carrying out a literature search of studies that examined the effects of resistance training in Parkinson’s disease, the researchers included 18 randomized controlled trials in their current review. Among the 1,134 total participants, the mean age was 66 years, the mean Hoehn & Yahr stage was 2.3 (range 0-4), and the mean duration of Parkinson’s disease was 7.5 years.

The investigation was grouped into two meta-analysis groups: one examining resistance training versus a passive or placebo intervention and the other assessing resistance training versus active physical interventions, such as yoga.

During resistance training, participants use their full strength to do a repetition, working muscles to overcome a certain threshold, said Ms. Gollan. In contrast, a placebo intervention is “very low intensity” and involves a much lower threshold, she added.

Passive interventions include such things as stretching where the stimulus “is not high enough for muscles to adapt” and build strength, Ms. Gollan noted.

A passive intervention might also include “treatment as usual” or normal daily routines.
 

Patient preference important

The meta-analysis comparing resistance training groups with passive control groups showed significant large effects on muscle strength (standard mean difference, –0.84; 95% confidence interval, –1.29 to –0.39; P = .0003), motor impairment (SMD, –0.81; 95% CI, –1.34 to –0.27; P = .003), and mobility and balance (SMD, –1.80; 95% CI, –3.13 to –0.49; P  = .007).

The review also showed significant but small effects on quality of life.

However, the meta-analysis that assessed resistance training versus other physical interventions showed no significant between-group differences.

Ms. Gollan noted that although there were some assessments of cognition and depression, the data were too limited to determine the impact of resistance training on these outcomes.

“We need more studies, especially randomized controlled trials, to investigate the effects of resistance training on nonmotor outcomes like depression and cognition,” she said.

Co-investigator Ann-Kristin Folkerts, PhD, who heads the University of Cologne medical psychology working group, noted that although exercise in general is beneficial for patients with Parkinson’s disease, the choice of activity should take patient preferences into consideration.

It is important that patients choose an exercise they enjoy “because otherwise they probably wouldn’t adhere to the treatment,” Dr. Folkerts said. “It’s important to have fun.”

Specific goals or objectives, such as improving quality of life or balance, should also be considered, she added.
 

Oversimplification?

Commenting on the research, Alice Nieuwboer, PhD, professor in the department of rehabilitation sciences and head of the neurorehabilitation research group at the University of Leuven, Belgium, disagreed that exercise type is of secondary importance in Parkinson’s disease.

“In my view, it’s of primary interest, especially at the mid- to later stages,” said Dr. Nieuwboer, who was not involved with the research.

She noted it is difficult to carry out meta-analyses of resistance training versus other interventions because studies comparing different exercise types “are rather scarce.”

“Another issue is that the dose may differ, so you’re comparing apples with pears,” said Dr. Nieuwboer.

She did agree that all patients should exercise, because it is “better than no exercise,” and they should be “free to choose a mode that interests them.”

However, she stressed that exercise requires significant effort on the part of patients with Parkinson’s disease, requires “sustained motivation,” and has to become habit-forming. This makes “exercise targeting” very important, with the target changing over the disease course, Dr. Nieuwboer said.

For example, for a patient at an early stage of the disease who can still move quite well, both resistance training and endurance training can improve fitness and health; but at a mid-stage, it is perhaps better for patients to work on balance and walking quality “to preempt the risk of falls and developing freezing,” she noted.

Later on, as movement becomes very difficult, “the exercise menu is even more restricted,” said Dr. Nieuwboer.

The bottom line is that a message saying “any movement counts” is an oversimplification, she added.

The study was funded by a grant from the German Federal Ministry of Education and Research. The investigators and Dr. Nieuwboer have reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Resistance training can help improve several symptoms of Parkinson’s disease – but is not superior to other physical activities, new research suggests.

A meta-analysis, which included 18 randomized controlled trials and more than 1,000 patients with Parkinson’s disease, showed that those who underwent resistance training had significantly greater improvement in motor impairment, muscle strength, and mobility/balance than their peers who underwent passive or placebo interventions.

However, there was no significant difference between patients who participated in resistance training and those who participated in other active physical interventions, including yoga.

Overall, the results highlight the importance that these patients should participate in some type of physical exercise, said the study’s lead author, Romina Gollan, MSc, an assistant researcher in the division of medical psychology, University of Cologne, Germany. “Patients should definitely be doing exercises, including resistance training, if they want to. But the type of exercise is of secondary interest,” she said.

The findings were presented at the International Congress of Parkinson’s Disease and Movement Disorders.
 

Positive but inconsistent

Previous reviews have suggested resistance training has positive effects on motor function in Parkinson’s disease. However, results from the included studies were inconsistent; and few reviews have examined nonmotor outcomes of resistance training in this population, the investigators noted.

After carrying out a literature search of studies that examined the effects of resistance training in Parkinson’s disease, the researchers included 18 randomized controlled trials in their current review. Among the 1,134 total participants, the mean age was 66 years, the mean Hoehn & Yahr stage was 2.3 (range 0-4), and the mean duration of Parkinson’s disease was 7.5 years.

The investigation was grouped into two meta-analysis groups: one examining resistance training versus a passive or placebo intervention and the other assessing resistance training versus active physical interventions, such as yoga.

During resistance training, participants use their full strength to do a repetition, working muscles to overcome a certain threshold, said Ms. Gollan. In contrast, a placebo intervention is “very low intensity” and involves a much lower threshold, she added.

Passive interventions include such things as stretching where the stimulus “is not high enough for muscles to adapt” and build strength, Ms. Gollan noted.

A passive intervention might also include “treatment as usual” or normal daily routines.
 

Patient preference important

The meta-analysis comparing resistance training groups with passive control groups showed significant large effects on muscle strength (standard mean difference, –0.84; 95% confidence interval, –1.29 to –0.39; P = .0003), motor impairment (SMD, –0.81; 95% CI, –1.34 to –0.27; P = .003), and mobility and balance (SMD, –1.80; 95% CI, –3.13 to –0.49; P  = .007).

The review also showed significant but small effects on quality of life.

However, the meta-analysis that assessed resistance training versus other physical interventions showed no significant between-group differences.

Ms. Gollan noted that although there were some assessments of cognition and depression, the data were too limited to determine the impact of resistance training on these outcomes.

“We need more studies, especially randomized controlled trials, to investigate the effects of resistance training on nonmotor outcomes like depression and cognition,” she said.

Co-investigator Ann-Kristin Folkerts, PhD, who heads the University of Cologne medical psychology working group, noted that although exercise in general is beneficial for patients with Parkinson’s disease, the choice of activity should take patient preferences into consideration.

It is important that patients choose an exercise they enjoy “because otherwise they probably wouldn’t adhere to the treatment,” Dr. Folkerts said. “It’s important to have fun.”

Specific goals or objectives, such as improving quality of life or balance, should also be considered, she added.
 

Oversimplification?

Commenting on the research, Alice Nieuwboer, PhD, professor in the department of rehabilitation sciences and head of the neurorehabilitation research group at the University of Leuven, Belgium, disagreed that exercise type is of secondary importance in Parkinson’s disease.

“In my view, it’s of primary interest, especially at the mid- to later stages,” said Dr. Nieuwboer, who was not involved with the research.

She noted it is difficult to carry out meta-analyses of resistance training versus other interventions because studies comparing different exercise types “are rather scarce.”

“Another issue is that the dose may differ, so you’re comparing apples with pears,” said Dr. Nieuwboer.

She did agree that all patients should exercise, because it is “better than no exercise,” and they should be “free to choose a mode that interests them.”

However, she stressed that exercise requires significant effort on the part of patients with Parkinson’s disease, requires “sustained motivation,” and has to become habit-forming. This makes “exercise targeting” very important, with the target changing over the disease course, Dr. Nieuwboer said.

For example, for a patient at an early stage of the disease who can still move quite well, both resistance training and endurance training can improve fitness and health; but at a mid-stage, it is perhaps better for patients to work on balance and walking quality “to preempt the risk of falls and developing freezing,” she noted.

Later on, as movement becomes very difficult, “the exercise menu is even more restricted,” said Dr. Nieuwboer.

The bottom line is that a message saying “any movement counts” is an oversimplification, she added.

The study was funded by a grant from the German Federal Ministry of Education and Research. The investigators and Dr. Nieuwboer have reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Resistance training can help improve several symptoms of Parkinson’s disease – but is not superior to other physical activities, new research suggests.

A meta-analysis, which included 18 randomized controlled trials and more than 1,000 patients with Parkinson’s disease, showed that those who underwent resistance training had significantly greater improvement in motor impairment, muscle strength, and mobility/balance than their peers who underwent passive or placebo interventions.

However, there was no significant difference between patients who participated in resistance training and those who participated in other active physical interventions, including yoga.

Overall, the results highlight the importance that these patients should participate in some type of physical exercise, said the study’s lead author, Romina Gollan, MSc, an assistant researcher in the division of medical psychology, University of Cologne, Germany. “Patients should definitely be doing exercises, including resistance training, if they want to. But the type of exercise is of secondary interest,” she said.

The findings were presented at the International Congress of Parkinson’s Disease and Movement Disorders.
 

Positive but inconsistent

Previous reviews have suggested resistance training has positive effects on motor function in Parkinson’s disease. However, results from the included studies were inconsistent; and few reviews have examined nonmotor outcomes of resistance training in this population, the investigators noted.

After carrying out a literature search of studies that examined the effects of resistance training in Parkinson’s disease, the researchers included 18 randomized controlled trials in their current review. Among the 1,134 total participants, the mean age was 66 years, the mean Hoehn & Yahr stage was 2.3 (range 0-4), and the mean duration of Parkinson’s disease was 7.5 years.

The investigation was grouped into two meta-analysis groups: one examining resistance training versus a passive or placebo intervention and the other assessing resistance training versus active physical interventions, such as yoga.

During resistance training, participants use their full strength to do a repetition, working muscles to overcome a certain threshold, said Ms. Gollan. In contrast, a placebo intervention is “very low intensity” and involves a much lower threshold, she added.

Passive interventions include such things as stretching where the stimulus “is not high enough for muscles to adapt” and build strength, Ms. Gollan noted.

A passive intervention might also include “treatment as usual” or normal daily routines.
 

Patient preference important

The meta-analysis comparing resistance training groups with passive control groups showed significant large effects on muscle strength (standard mean difference, –0.84; 95% confidence interval, –1.29 to –0.39; P = .0003), motor impairment (SMD, –0.81; 95% CI, –1.34 to –0.27; P = .003), and mobility and balance (SMD, –1.80; 95% CI, –3.13 to –0.49; P  = .007).

The review also showed significant but small effects on quality of life.

However, the meta-analysis that assessed resistance training versus other physical interventions showed no significant between-group differences.

Ms. Gollan noted that although there were some assessments of cognition and depression, the data were too limited to determine the impact of resistance training on these outcomes.

“We need more studies, especially randomized controlled trials, to investigate the effects of resistance training on nonmotor outcomes like depression and cognition,” she said.

Co-investigator Ann-Kristin Folkerts, PhD, who heads the University of Cologne medical psychology working group, noted that although exercise in general is beneficial for patients with Parkinson’s disease, the choice of activity should take patient preferences into consideration.

It is important that patients choose an exercise they enjoy “because otherwise they probably wouldn’t adhere to the treatment,” Dr. Folkerts said. “It’s important to have fun.”

Specific goals or objectives, such as improving quality of life or balance, should also be considered, she added.
 

Oversimplification?

Commenting on the research, Alice Nieuwboer, PhD, professor in the department of rehabilitation sciences and head of the neurorehabilitation research group at the University of Leuven, Belgium, disagreed that exercise type is of secondary importance in Parkinson’s disease.

“In my view, it’s of primary interest, especially at the mid- to later stages,” said Dr. Nieuwboer, who was not involved with the research.

She noted it is difficult to carry out meta-analyses of resistance training versus other interventions because studies comparing different exercise types “are rather scarce.”

“Another issue is that the dose may differ, so you’re comparing apples with pears,” said Dr. Nieuwboer.

She did agree that all patients should exercise, because it is “better than no exercise,” and they should be “free to choose a mode that interests them.”

However, she stressed that exercise requires significant effort on the part of patients with Parkinson’s disease, requires “sustained motivation,” and has to become habit-forming. This makes “exercise targeting” very important, with the target changing over the disease course, Dr. Nieuwboer said.

For example, for a patient at an early stage of the disease who can still move quite well, both resistance training and endurance training can improve fitness and health; but at a mid-stage, it is perhaps better for patients to work on balance and walking quality “to preempt the risk of falls and developing freezing,” she noted.

Later on, as movement becomes very difficult, “the exercise menu is even more restricted,” said Dr. Nieuwboer.

The bottom line is that a message saying “any movement counts” is an oversimplification, she added.

The study was funded by a grant from the German Federal Ministry of Education and Research. The investigators and Dr. Nieuwboer have reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Sport climbing can help improve posture in patients with Parkinson’s disease, including older patients, new research suggests.

In a randomized controlled study, those who participated in scaling a wall using ropes and fixed anchors were less stooped at 12 weeks than was a control group that participated in some form of unsupervised physical activity.

The results underscore that it is never too late to learn a new sport or type of movement – and that this type of intervention may have big health payoffs, said study investigator Heidemarie Zach, MD, associate professor of neurology, Medical University of Vienna, Austria.

“There’s no hurdle too high over which you can’t climb, or burden you can’t conquer,”  said Dr. Zach. “As long as you can walk independently and walk up a stair, you can go climbing.”

The findings were presented at the International Congress of Parkinson’s Disease and Movement Disorders.
 

Common feature of Parkinson’s disease

The analysis is part of a larger project that included a 2021 study showing a reduced Unified Parkinson’s Disease Rating Scale Part III (UPDRS-III) score by almost 13 points in patients who participated in sport climbing. The activity was also significantly associated with improved bradykinesia, rigidity, and tremor.

The current analysis focused on stooped posture, which in addition to motor symptoms is a common feature of Parkinson’s disease. This postural deformity can result in significant discomfort, pain, and decreased quality of life.

Pharmaceutical treatments are mostly ineffective for postural deformities, the researchers noted. Physical therapy may help improve symptoms, but only a few randomized studies have examined improved posture in patients with Parkinson’s disease using physiotherapy in general and alternative sports in particular.

Sport climbing is “really unique” in Parkinson’s disease, said Dr. Zach, who has yet to come across other research on this intervention. A climber herself, she recommended it to one of her patients: A 79-year old man with Parkinson’s disease who was a walker and hiker, and who ended up loving the sport. She called him her “pilot patient.”

The single-center study included 48 adult participants up to age 78 years (mean age, 65) with mild to moderate Parkinson’s disease. Most were at Hoehn & Yahr stage 2, with some at stage 3. All had no previous climbing experience. Exclusion criteria included having a condition other than Parkinson’s disease.

The researchers randomly assigned participants to a sport climbing course or to a control group.

The sport climbing group had a 90-minute climbing session each week for 12 weeks in an indoor gym. Under the supervision of an instructor, they were harnessed and connected to ropes with mats placed on the ground for safety.

The climbing wall was about 15 meters (50 feet) high. Participants typically started at 2 or 3 meters (6.5 to 9.5 feet) and worked their way up, Dr. Zach noted.

Those in the control group were asked to participate for 12 weeks in unsupervised physical activity, as recommended by the World Health Organization and the European Physiotherapy Guidelines for Parkinson’s Disease. This included at least 2.5 hours of moderate-intensity activity or 75 minutes of vigorous activity each week.
 

Whole-body workout

The primary outcome was improvement in posture, measured using a “simple” but highly reliable tool, said Dr. Zach. While the patients stood with their backs straight against a wall, researchers measured the distance in centimeters between the C7 sagittal vertical axis (C7SVA) and the wall.

The mean C7SVA at baseline did not significantly differ between the two groups, at 8.2 cm for the climbing group versus  7.7 cm for the control group. However, results showed only sport climbing was associated with significantly lessened forward flexion of the cervical spine.

The climbing group showed a decrease of the C7SVA by 1.7 cm (95% confidence interval [CI], 0.8-2.6 cm). “So climbers were more erect and less stooped after 12 weeks,” Dr. Zach said.

She noted that the mean difference in the control group was 0.5 cm (95% confidence interval [CI], –0.2 to 1.3 cm), which “is almost nothing.”

There did not seem to be any predictor, such as age, sex, or body mass index, for what patient subgroups benefit the most from the intervention, Dr. Zach noted.

In explaining why climbing helps posture, she said it is akin to “a whole-body workout.” The activity increases upper-body strength by using back and shoulder girdle muscles, as well as joint flexibility, Dr. Zach noted. Movements involved in climbing, such as repeated reaching for a distant hold, stretch the muscles of the hip flexors and hip.

As these movements reduce rigidity, the climbing action may also promote an upright posture. And as wall climbing involves planning and executing movements, it trains spatial body awareness, an important component of maintaining and correcting posture, she said.

Dr. Zach noted a motivational group dynamic likely also contributed to the success of the intervention. “They were cheering each other at the bottom” of the climbing wall, she said.

The results show that posture can be added to the improvements in Parkinson’s disease already documented from climbing, including improved motor symptoms, rigidity, and tremor, she said. The next step on the research agenda is to show whether the intervention has a positive impact on gait, Dr. Zach added.
 

‘Quite adventurous’

Commenting on the research, Rebecca Gilbert, MD, PhD, chief scientific officer at the American Parkinson Disease Association, said she welcomes “any new idea” to help patients with Parkinson’s disease – and that sport climbing sounds “quite adventurous.”

“The general concept that you’re asking the body to move in a novel way is a good thing for everyone and especially for people with Parkinson’s disease,” said Dr. Gilbert, who was not involved with the research.

She noted that in Parkinson’s disease, an ideal exercise intervention includes a combination of four modalities: stretching, balance, aerobics, and strengthening. Rope climbing involves many of these, in addition to a cognitive element, Dr. Gilbert said. It’s also important that patients with Parkinson’s disease participate in an activity they enjoy, she added.

However, she stressed that safety has to be “weighed,” especially for patients with stage 3 Parkinson’s disease, who often have balance problems. “It may be difficult to climb a rope if you have balance problems,” Dr. Gilbert said. “The intervention needs to be tailored to the existing disability, and perhaps this activity is more a reasonable thing for patients at milder stages.”

Dr. Zach and Dr. Gilbert have reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Sport climbing can help improve posture in patients with Parkinson’s disease, including older patients, new research suggests.

In a randomized controlled study, those who participated in scaling a wall using ropes and fixed anchors were less stooped at 12 weeks than was a control group that participated in some form of unsupervised physical activity.

The results underscore that it is never too late to learn a new sport or type of movement – and that this type of intervention may have big health payoffs, said study investigator Heidemarie Zach, MD, associate professor of neurology, Medical University of Vienna, Austria.

“There’s no hurdle too high over which you can’t climb, or burden you can’t conquer,”  said Dr. Zach. “As long as you can walk independently and walk up a stair, you can go climbing.”

The findings were presented at the International Congress of Parkinson’s Disease and Movement Disorders.
 

Common feature of Parkinson’s disease

The analysis is part of a larger project that included a 2021 study showing a reduced Unified Parkinson’s Disease Rating Scale Part III (UPDRS-III) score by almost 13 points in patients who participated in sport climbing. The activity was also significantly associated with improved bradykinesia, rigidity, and tremor.

The current analysis focused on stooped posture, which in addition to motor symptoms is a common feature of Parkinson’s disease. This postural deformity can result in significant discomfort, pain, and decreased quality of life.

Pharmaceutical treatments are mostly ineffective for postural deformities, the researchers noted. Physical therapy may help improve symptoms, but only a few randomized studies have examined improved posture in patients with Parkinson’s disease using physiotherapy in general and alternative sports in particular.

Sport climbing is “really unique” in Parkinson’s disease, said Dr. Zach, who has yet to come across other research on this intervention. A climber herself, she recommended it to one of her patients: A 79-year old man with Parkinson’s disease who was a walker and hiker, and who ended up loving the sport. She called him her “pilot patient.”

The single-center study included 48 adult participants up to age 78 years (mean age, 65) with mild to moderate Parkinson’s disease. Most were at Hoehn & Yahr stage 2, with some at stage 3. All had no previous climbing experience. Exclusion criteria included having a condition other than Parkinson’s disease.

The researchers randomly assigned participants to a sport climbing course or to a control group.

The sport climbing group had a 90-minute climbing session each week for 12 weeks in an indoor gym. Under the supervision of an instructor, they were harnessed and connected to ropes with mats placed on the ground for safety.

The climbing wall was about 15 meters (50 feet) high. Participants typically started at 2 or 3 meters (6.5 to 9.5 feet) and worked their way up, Dr. Zach noted.

Those in the control group were asked to participate for 12 weeks in unsupervised physical activity, as recommended by the World Health Organization and the European Physiotherapy Guidelines for Parkinson’s Disease. This included at least 2.5 hours of moderate-intensity activity or 75 minutes of vigorous activity each week.
 

Whole-body workout

The primary outcome was improvement in posture, measured using a “simple” but highly reliable tool, said Dr. Zach. While the patients stood with their backs straight against a wall, researchers measured the distance in centimeters between the C7 sagittal vertical axis (C7SVA) and the wall.

The mean C7SVA at baseline did not significantly differ between the two groups, at 8.2 cm for the climbing group versus  7.7 cm for the control group. However, results showed only sport climbing was associated with significantly lessened forward flexion of the cervical spine.

The climbing group showed a decrease of the C7SVA by 1.7 cm (95% confidence interval [CI], 0.8-2.6 cm). “So climbers were more erect and less stooped after 12 weeks,” Dr. Zach said.

She noted that the mean difference in the control group was 0.5 cm (95% confidence interval [CI], –0.2 to 1.3 cm), which “is almost nothing.”

There did not seem to be any predictor, such as age, sex, or body mass index, for what patient subgroups benefit the most from the intervention, Dr. Zach noted.

In explaining why climbing helps posture, she said it is akin to “a whole-body workout.” The activity increases upper-body strength by using back and shoulder girdle muscles, as well as joint flexibility, Dr. Zach noted. Movements involved in climbing, such as repeated reaching for a distant hold, stretch the muscles of the hip flexors and hip.

As these movements reduce rigidity, the climbing action may also promote an upright posture. And as wall climbing involves planning and executing movements, it trains spatial body awareness, an important component of maintaining and correcting posture, she said.

Dr. Zach noted a motivational group dynamic likely also contributed to the success of the intervention. “They were cheering each other at the bottom” of the climbing wall, she said.

The results show that posture can be added to the improvements in Parkinson’s disease already documented from climbing, including improved motor symptoms, rigidity, and tremor, she said. The next step on the research agenda is to show whether the intervention has a positive impact on gait, Dr. Zach added.
 

‘Quite adventurous’

Commenting on the research, Rebecca Gilbert, MD, PhD, chief scientific officer at the American Parkinson Disease Association, said she welcomes “any new idea” to help patients with Parkinson’s disease – and that sport climbing sounds “quite adventurous.”

“The general concept that you’re asking the body to move in a novel way is a good thing for everyone and especially for people with Parkinson’s disease,” said Dr. Gilbert, who was not involved with the research.

She noted that in Parkinson’s disease, an ideal exercise intervention includes a combination of four modalities: stretching, balance, aerobics, and strengthening. Rope climbing involves many of these, in addition to a cognitive element, Dr. Gilbert said. It’s also important that patients with Parkinson’s disease participate in an activity they enjoy, she added.

However, she stressed that safety has to be “weighed,” especially for patients with stage 3 Parkinson’s disease, who often have balance problems. “It may be difficult to climb a rope if you have balance problems,” Dr. Gilbert said. “The intervention needs to be tailored to the existing disability, and perhaps this activity is more a reasonable thing for patients at milder stages.”

Dr. Zach and Dr. Gilbert have reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Sport climbing can help improve posture in patients with Parkinson’s disease, including older patients, new research suggests.

In a randomized controlled study, those who participated in scaling a wall using ropes and fixed anchors were less stooped at 12 weeks than was a control group that participated in some form of unsupervised physical activity.

The results underscore that it is never too late to learn a new sport or type of movement – and that this type of intervention may have big health payoffs, said study investigator Heidemarie Zach, MD, associate professor of neurology, Medical University of Vienna, Austria.

“There’s no hurdle too high over which you can’t climb, or burden you can’t conquer,”  said Dr. Zach. “As long as you can walk independently and walk up a stair, you can go climbing.”

The findings were presented at the International Congress of Parkinson’s Disease and Movement Disorders.
 

Common feature of Parkinson’s disease

The analysis is part of a larger project that included a 2021 study showing a reduced Unified Parkinson’s Disease Rating Scale Part III (UPDRS-III) score by almost 13 points in patients who participated in sport climbing. The activity was also significantly associated with improved bradykinesia, rigidity, and tremor.

The current analysis focused on stooped posture, which in addition to motor symptoms is a common feature of Parkinson’s disease. This postural deformity can result in significant discomfort, pain, and decreased quality of life.

Pharmaceutical treatments are mostly ineffective for postural deformities, the researchers noted. Physical therapy may help improve symptoms, but only a few randomized studies have examined improved posture in patients with Parkinson’s disease using physiotherapy in general and alternative sports in particular.

Sport climbing is “really unique” in Parkinson’s disease, said Dr. Zach, who has yet to come across other research on this intervention. A climber herself, she recommended it to one of her patients: A 79-year old man with Parkinson’s disease who was a walker and hiker, and who ended up loving the sport. She called him her “pilot patient.”

The single-center study included 48 adult participants up to age 78 years (mean age, 65) with mild to moderate Parkinson’s disease. Most were at Hoehn & Yahr stage 2, with some at stage 3. All had no previous climbing experience. Exclusion criteria included having a condition other than Parkinson’s disease.

The researchers randomly assigned participants to a sport climbing course or to a control group.

The sport climbing group had a 90-minute climbing session each week for 12 weeks in an indoor gym. Under the supervision of an instructor, they were harnessed and connected to ropes with mats placed on the ground for safety.

The climbing wall was about 15 meters (50 feet) high. Participants typically started at 2 or 3 meters (6.5 to 9.5 feet) and worked their way up, Dr. Zach noted.

Those in the control group were asked to participate for 12 weeks in unsupervised physical activity, as recommended by the World Health Organization and the European Physiotherapy Guidelines for Parkinson’s Disease. This included at least 2.5 hours of moderate-intensity activity or 75 minutes of vigorous activity each week.
 

Whole-body workout

The primary outcome was improvement in posture, measured using a “simple” but highly reliable tool, said Dr. Zach. While the patients stood with their backs straight against a wall, researchers measured the distance in centimeters between the C7 sagittal vertical axis (C7SVA) and the wall.

The mean C7SVA at baseline did not significantly differ between the two groups, at 8.2 cm for the climbing group versus  7.7 cm for the control group. However, results showed only sport climbing was associated with significantly lessened forward flexion of the cervical spine.

The climbing group showed a decrease of the C7SVA by 1.7 cm (95% confidence interval [CI], 0.8-2.6 cm). “So climbers were more erect and less stooped after 12 weeks,” Dr. Zach said.

She noted that the mean difference in the control group was 0.5 cm (95% confidence interval [CI], –0.2 to 1.3 cm), which “is almost nothing.”

There did not seem to be any predictor, such as age, sex, or body mass index, for what patient subgroups benefit the most from the intervention, Dr. Zach noted.

In explaining why climbing helps posture, she said it is akin to “a whole-body workout.” The activity increases upper-body strength by using back and shoulder girdle muscles, as well as joint flexibility, Dr. Zach noted. Movements involved in climbing, such as repeated reaching for a distant hold, stretch the muscles of the hip flexors and hip.

As these movements reduce rigidity, the climbing action may also promote an upright posture. And as wall climbing involves planning and executing movements, it trains spatial body awareness, an important component of maintaining and correcting posture, she said.

Dr. Zach noted a motivational group dynamic likely also contributed to the success of the intervention. “They were cheering each other at the bottom” of the climbing wall, she said.

The results show that posture can be added to the improvements in Parkinson’s disease already documented from climbing, including improved motor symptoms, rigidity, and tremor, she said. The next step on the research agenda is to show whether the intervention has a positive impact on gait, Dr. Zach added.
 

‘Quite adventurous’

Commenting on the research, Rebecca Gilbert, MD, PhD, chief scientific officer at the American Parkinson Disease Association, said she welcomes “any new idea” to help patients with Parkinson’s disease – and that sport climbing sounds “quite adventurous.”

“The general concept that you’re asking the body to move in a novel way is a good thing for everyone and especially for people with Parkinson’s disease,” said Dr. Gilbert, who was not involved with the research.

She noted that in Parkinson’s disease, an ideal exercise intervention includes a combination of four modalities: stretching, balance, aerobics, and strengthening. Rope climbing involves many of these, in addition to a cognitive element, Dr. Gilbert said. It’s also important that patients with Parkinson’s disease participate in an activity they enjoy, she added.

However, she stressed that safety has to be “weighed,” especially for patients with stage 3 Parkinson’s disease, who often have balance problems. “It may be difficult to climb a rope if you have balance problems,” Dr. Gilbert said. “The intervention needs to be tailored to the existing disability, and perhaps this activity is more a reasonable thing for patients at milder stages.”

Dr. Zach and Dr. Gilbert have reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

A high baseline intake of vitamin B₁₂ is linked to lower risk of developing Parkinson’s disease, new research suggests. “The results leave the door open for the possibility that vitamin B₁₂ may have a beneficial effect in protecting against Parkinson’s disease,” said lead author Mario H. Flores, PhD, a research fellow at Harvard T.H. Chan School of Public Health, Boston.

The findings were presented at the International Congress of Parkinson’s Disease and Movement Disorders.
 

B vitamins and Parkinson’s disease

Previous preclinical studies have suggested that B vitamins protect against Parkinson’s disease by decreasing plasma homocysteine levels and through other neuroprotective effects. However, there have been only two epidemiologic studies of B vitamins in Parkinson’s disease – and their results were inconsistent, Dr. Flores noted.

The new study included 80,965 women from the Nurses’ Health Study and 48,837 men from the Health Professionals Follow-up Study. All completed a food frequency questionnaire at baseline and every 4 years.

Researchers collected information on dietary, supplemental, and total intake of folate, vitamin B₆, and vitamin B₁₂ over the course of about 30 years up to 2012. They estimated hazard ratios and 95% confidence intervals for Parkinson’s disease according to quintiles of cumulative average intake.

During follow-up, 495 women and 621 men were diagnosed with Parkinson’s disease.

The investigators adjusted for potential confounders, including age, year, smoking status, physical activity, intake of alcohol or caffeine, hormone use (in women), intake of dairy and flavonoids, and Mediterranean diet score.

Analyses of cumulative average total folate, B₆, and B₁₂ intake were not associated with Parkinson’s disease risk. “The results of the primary analysis of cumulative intake were not significant for any of the vitamins we looked at,” said Dr. Flores.

Researchers also conducted secondary analyses, including assessment of how the most recent intake of B vitamins related to Parkinson’s disease risk. This analysis also did not find a significant association.

However, when examining baseline intake of vitamin B₁₂, “we saw some suggestion for a potential inverse association with Parkinson’s disease,” Dr. Flores said.

Among individuals with higher total intake of vitamin B₁₂, there was a lower risk for Parkinson’s disease (pooled hazard ratio for top vs. bottom quintile, 0.74; 95% confidence interval [CI], 0.60-0.89; P for trend, .001). Intake from both diet and supplements contributed to this inverse association, the investigators noted.

Dietary sources of vitamin B₁₂ include poultry, meat, fish, and dairy products; however, the main sources in this study were multivitamins/supplements and enriched foods such as cereals, said Dr. Flores.
 

Several limitations

In an attempt to overcome risk for reverse causality, the researchers examined B₁₂ intake during four lagged exposure periods: 8-, 12-, 16- and 20-year lags. They found a significant relationship between intake for the 20-year lag time and development of Parkinson’s disease.

Overall, the study results provide support for a possible protective effect of early intake of vitamin B₁₂ on the development of Parkinson’s disease, Dr. Flores noted.

In addition to being involved in the regulation of homocysteine levels, vitamin B₁₂ may help regulate leucine-rich repeat kinase 2 (LRRK2), an enzyme implicated in the pathogenesis of Parkinson’s disease, he said.

However, the study did not examine how B₁₂ deficiency might relate to risk for Parkinson’s disease, which “is something worth looking at in future studies,” said Dr. Flores.

He added that although findings from a single study cannot translate into recommendations on ideal vitamin B₁₂ intake to prevent or delay Parkinson’s disease onset, the median intake in the highest quintile that the study linked to less Parkinson’s disease risk was 18 mcg/d at baseline. The amount in multivitamins can vary from 5 to 25 mcg.

Dr. Flores said a limitation of the study was that it included U.S. health care professionals, “most of whom arguably have very good nutritional status.”

As well, assessment of vitamin B intake was self-reported, so there might have been measurement error – and there may have been an unmeasured confounding factor that could explain the associations.

Dr. Flores also stressed that the effect of B₁₂ on Parkinson’s disease risk “was very modest,” and the results need to be confirmed in other studies “ideally looking at circulating levels of vitamin B₁₂.”
 

Not ready to recommend

Commenting on the research, Michael S. Okun, MD, medical adviser at the Parkinson’s Foundation and professor and director of the Norman Fixel Institute for Neurological Diseases at the University of Florida, Gainesville, noted that other recent studies have suggested high-dose B₁₂ may be preventive and a possible treatment in Parkinson’s disease.

“Although only a secondary aim of the current study, there was a reported potential benefit” in this new study, too, said Dr. Okun, who was not involved with the research.

However, the evidence is still not strong enough to change prescribing habits, he noted. “We do not recommend high-dose B₁₂ either for those at genetic risk of Parkinson’s or those already with the disease,” Dr. Okun said.

He added that because multiple recent studies have questioned the beneficial effects for multivitamin combinations used to prevent neurologic diseases, “it wasn’t surprising to see results showing a lack of protection against later-onset Parkinson’s disease with [cumulative] folate, B₆, and B₁₂ intake” in the current study.

The study was supported by the NIH. Dr. Flores and Dr. Okun have reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

A high baseline intake of vitamin B₁₂ is linked to lower risk of developing Parkinson’s disease, new research suggests. “The results leave the door open for the possibility that vitamin B₁₂ may have a beneficial effect in protecting against Parkinson’s disease,” said lead author Mario H. Flores, PhD, a research fellow at Harvard T.H. Chan School of Public Health, Boston.

The findings were presented at the International Congress of Parkinson’s Disease and Movement Disorders.
 

B vitamins and Parkinson’s disease

Previous preclinical studies have suggested that B vitamins protect against Parkinson’s disease by decreasing plasma homocysteine levels and through other neuroprotective effects. However, there have been only two epidemiologic studies of B vitamins in Parkinson’s disease – and their results were inconsistent, Dr. Flores noted.

The new study included 80,965 women from the Nurses’ Health Study and 48,837 men from the Health Professionals Follow-up Study. All completed a food frequency questionnaire at baseline and every 4 years.

Researchers collected information on dietary, supplemental, and total intake of folate, vitamin B₆, and vitamin B₁₂ over the course of about 30 years up to 2012. They estimated hazard ratios and 95% confidence intervals for Parkinson’s disease according to quintiles of cumulative average intake.

During follow-up, 495 women and 621 men were diagnosed with Parkinson’s disease.

The investigators adjusted for potential confounders, including age, year, smoking status, physical activity, intake of alcohol or caffeine, hormone use (in women), intake of dairy and flavonoids, and Mediterranean diet score.

Analyses of cumulative average total folate, B₆, and B₁₂ intake were not associated with Parkinson’s disease risk. “The results of the primary analysis of cumulative intake were not significant for any of the vitamins we looked at,” said Dr. Flores.

Researchers also conducted secondary analyses, including assessment of how the most recent intake of B vitamins related to Parkinson’s disease risk. This analysis also did not find a significant association.

However, when examining baseline intake of vitamin B₁₂, “we saw some suggestion for a potential inverse association with Parkinson’s disease,” Dr. Flores said.

Among individuals with higher total intake of vitamin B₁₂, there was a lower risk for Parkinson’s disease (pooled hazard ratio for top vs. bottom quintile, 0.74; 95% confidence interval [CI], 0.60-0.89; P for trend, .001). Intake from both diet and supplements contributed to this inverse association, the investigators noted.

Dietary sources of vitamin B₁₂ include poultry, meat, fish, and dairy products; however, the main sources in this study were multivitamins/supplements and enriched foods such as cereals, said Dr. Flores.
 

Several limitations

In an attempt to overcome risk for reverse causality, the researchers examined B₁₂ intake during four lagged exposure periods: 8-, 12-, 16- and 20-year lags. They found a significant relationship between intake for the 20-year lag time and development of Parkinson’s disease.

Overall, the study results provide support for a possible protective effect of early intake of vitamin B₁₂ on the development of Parkinson’s disease, Dr. Flores noted.

In addition to being involved in the regulation of homocysteine levels, vitamin B₁₂ may help regulate leucine-rich repeat kinase 2 (LRRK2), an enzyme implicated in the pathogenesis of Parkinson’s disease, he said.

However, the study did not examine how B₁₂ deficiency might relate to risk for Parkinson’s disease, which “is something worth looking at in future studies,” said Dr. Flores.

He added that although findings from a single study cannot translate into recommendations on ideal vitamin B₁₂ intake to prevent or delay Parkinson’s disease onset, the median intake in the highest quintile that the study linked to less Parkinson’s disease risk was 18 mcg/d at baseline. The amount in multivitamins can vary from 5 to 25 mcg.

Dr. Flores said a limitation of the study was that it included U.S. health care professionals, “most of whom arguably have very good nutritional status.”

As well, assessment of vitamin B intake was self-reported, so there might have been measurement error – and there may have been an unmeasured confounding factor that could explain the associations.

Dr. Flores also stressed that the effect of B₁₂ on Parkinson’s disease risk “was very modest,” and the results need to be confirmed in other studies “ideally looking at circulating levels of vitamin B₁₂.”
 

Not ready to recommend

Commenting on the research, Michael S. Okun, MD, medical adviser at the Parkinson’s Foundation and professor and director of the Norman Fixel Institute for Neurological Diseases at the University of Florida, Gainesville, noted that other recent studies have suggested high-dose B₁₂ may be preventive and a possible treatment in Parkinson’s disease.

“Although only a secondary aim of the current study, there was a reported potential benefit” in this new study, too, said Dr. Okun, who was not involved with the research.

However, the evidence is still not strong enough to change prescribing habits, he noted. “We do not recommend high-dose B₁₂ either for those at genetic risk of Parkinson’s or those already with the disease,” Dr. Okun said.

He added that because multiple recent studies have questioned the beneficial effects for multivitamin combinations used to prevent neurologic diseases, “it wasn’t surprising to see results showing a lack of protection against later-onset Parkinson’s disease with [cumulative] folate, B₆, and B₁₂ intake” in the current study.

The study was supported by the NIH. Dr. Flores and Dr. Okun have reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

A high baseline intake of vitamin B₁₂ is linked to lower risk of developing Parkinson’s disease, new research suggests. “The results leave the door open for the possibility that vitamin B₁₂ may have a beneficial effect in protecting against Parkinson’s disease,” said lead author Mario H. Flores, PhD, a research fellow at Harvard T.H. Chan School of Public Health, Boston.

The findings were presented at the International Congress of Parkinson’s Disease and Movement Disorders.
 

B vitamins and Parkinson’s disease

Previous preclinical studies have suggested that B vitamins protect against Parkinson’s disease by decreasing plasma homocysteine levels and through other neuroprotective effects. However, there have been only two epidemiologic studies of B vitamins in Parkinson’s disease – and their results were inconsistent, Dr. Flores noted.

The new study included 80,965 women from the Nurses’ Health Study and 48,837 men from the Health Professionals Follow-up Study. All completed a food frequency questionnaire at baseline and every 4 years.

Researchers collected information on dietary, supplemental, and total intake of folate, vitamin B₆, and vitamin B₁₂ over the course of about 30 years up to 2012. They estimated hazard ratios and 95% confidence intervals for Parkinson’s disease according to quintiles of cumulative average intake.

During follow-up, 495 women and 621 men were diagnosed with Parkinson’s disease.

The investigators adjusted for potential confounders, including age, year, smoking status, physical activity, intake of alcohol or caffeine, hormone use (in women), intake of dairy and flavonoids, and Mediterranean diet score.

Analyses of cumulative average total folate, B₆, and B₁₂ intake were not associated with Parkinson’s disease risk. “The results of the primary analysis of cumulative intake were not significant for any of the vitamins we looked at,” said Dr. Flores.

Researchers also conducted secondary analyses, including assessment of how the most recent intake of B vitamins related to Parkinson’s disease risk. This analysis also did not find a significant association.

However, when examining baseline intake of vitamin B₁₂, “we saw some suggestion for a potential inverse association with Parkinson’s disease,” Dr. Flores said.

Among individuals with higher total intake of vitamin B₁₂, there was a lower risk for Parkinson’s disease (pooled hazard ratio for top vs. bottom quintile, 0.74; 95% confidence interval [CI], 0.60-0.89; P for trend, .001). Intake from both diet and supplements contributed to this inverse association, the investigators noted.

Dietary sources of vitamin B₁₂ include poultry, meat, fish, and dairy products; however, the main sources in this study were multivitamins/supplements and enriched foods such as cereals, said Dr. Flores.
 

Several limitations

In an attempt to overcome risk for reverse causality, the researchers examined B₁₂ intake during four lagged exposure periods: 8-, 12-, 16- and 20-year lags. They found a significant relationship between intake for the 20-year lag time and development of Parkinson’s disease.

Overall, the study results provide support for a possible protective effect of early intake of vitamin B₁₂ on the development of Parkinson’s disease, Dr. Flores noted.

In addition to being involved in the regulation of homocysteine levels, vitamin B₁₂ may help regulate leucine-rich repeat kinase 2 (LRRK2), an enzyme implicated in the pathogenesis of Parkinson’s disease, he said.

However, the study did not examine how B₁₂ deficiency might relate to risk for Parkinson’s disease, which “is something worth looking at in future studies,” said Dr. Flores.

He added that although findings from a single study cannot translate into recommendations on ideal vitamin B₁₂ intake to prevent or delay Parkinson’s disease onset, the median intake in the highest quintile that the study linked to less Parkinson’s disease risk was 18 mcg/d at baseline. The amount in multivitamins can vary from 5 to 25 mcg.

Dr. Flores said a limitation of the study was that it included U.S. health care professionals, “most of whom arguably have very good nutritional status.”

As well, assessment of vitamin B intake was self-reported, so there might have been measurement error – and there may have been an unmeasured confounding factor that could explain the associations.

Dr. Flores also stressed that the effect of B₁₂ on Parkinson’s disease risk “was very modest,” and the results need to be confirmed in other studies “ideally looking at circulating levels of vitamin B₁₂.”
 

Not ready to recommend

Commenting on the research, Michael S. Okun, MD, medical adviser at the Parkinson’s Foundation and professor and director of the Norman Fixel Institute for Neurological Diseases at the University of Florida, Gainesville, noted that other recent studies have suggested high-dose B₁₂ may be preventive and a possible treatment in Parkinson’s disease.

“Although only a secondary aim of the current study, there was a reported potential benefit” in this new study, too, said Dr. Okun, who was not involved with the research.

However, the evidence is still not strong enough to change prescribing habits, he noted. “We do not recommend high-dose B₁₂ either for those at genetic risk of Parkinson’s or those already with the disease,” Dr. Okun said.

He added that because multiple recent studies have questioned the beneficial effects for multivitamin combinations used to prevent neurologic diseases, “it wasn’t surprising to see results showing a lack of protection against later-onset Parkinson’s disease with [cumulative] folate, B₆, and B₁₂ intake” in the current study.

The study was supported by the NIH. Dr. Flores and Dr. Okun have reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Mexican researchers found no direct association between SARS-CoV-2 vaccination and worsening symptoms among 60 patients with Parkinson’s disease. Nonmotor symptoms seemed to improve after SARS-CoV-2 vaccination, although the investigators could not verify a causal relationship.

Vaccination programs should continue for patients with Parkinson’s disease, they said, reporting their clinical results at the International Congress of Parkinson’s Disease and Movement Disorders.

The International Parkinson and Movement Disorder Society has recommended vaccining patients with Parkinson’s disease. “All approved mRNA-based and viral vector vaccines are not expected to interact with Parkinson’s disease, but patients [still] report concern with regard to the benefits, risks, and safeness in Parkinson’s disease,” Mayela Rodríguez-Violante, MD, MSc, and colleagues wrote in an abstract of their findings.

Social isolation may be contributing to these beliefs and concerns, though this is inconclusive.

Investigators from Mexico City conducted a retrospective study of patients with Parkinson’s disease to see how COVID-19 vaccination affected motor and nonmotor symptoms. They enlisted 60 patients (66.7% were male; aged 65.7 ± 11.35 years) who received either a vector-viral vaccine (Vaxzevria Coronavirus) or an mRNA vaccine (BNT162b2).

A Wilcoxon signed-rank test assessed scale differences before and after vaccination, measuring motor involvement (Unified Parkinson’s Disease Rating Scale), nonmotor involvement (Non-Motor Rating Scale [NMSS]), cognitive impairment (Montreal Cognitive Assessment), and quality of life (8-item Parkinson’s Disease Questionnaire index).

Investigators found no significant difference between scales, although they did notice a marked improvement in non-motor symptoms.

“The main takeaway is that vaccination against COVID-19 does not appear to worsen motor or nonmotor symptoms in persons with Parkinson’s disease. The benefits outweigh the risks,” said Dr. Rodríguez-Violante, the study’s lead author and a movement disorder specialist at the National Institute of Neurology and Neurosurgery, Mexico City.

Next steps are to increase the sample size to see if it’s possible to have a similar number in terms of type of vaccine, said Dr. Rodríguez-Violante. “Also, the data presented refers to primary series doses so booster effects will also be studied.”

Few studies have looked at vaccines and their possible effects on this patient population. However, a 2021 study of 181 patients with Parkinson’s disease reported that 2 (1.1%) had adverse effects after receiving the BNT162b2 mRNA vaccine. One of the patients, a 61-year-old woman with a decade-long history of Parkinson’s disease, developed severe, continuous, generalized dyskinesia 6 hours after a first dose of vaccine. The second patient was 79 years old and had Parkinson’s disease for 5 years. She developed fever, confusion, delusions, and continuous severe dyskinesia for 3 days following her vaccination.

“This highlights that there is a variability in the response triggered by the vaccine that might likely depend on individual immunological profiles … clinicians should be aware of this possibility and monitor their patients after they receive their vaccination,” Roberto Erro, MD, PhD and colleagues wrote in the Movement Disorders journal.

Mexican researchers found no direct association between SARS-CoV-2 vaccination and worsening symptoms among 60 patients with Parkinson’s disease. Nonmotor symptoms seemed to improve after SARS-CoV-2 vaccination, although the investigators could not verify a causal relationship.

Vaccination programs should continue for patients with Parkinson’s disease, they said, reporting their clinical results at the International Congress of Parkinson’s Disease and Movement Disorders.

The International Parkinson and Movement Disorder Society has recommended vaccining patients with Parkinson’s disease. “All approved mRNA-based and viral vector vaccines are not expected to interact with Parkinson’s disease, but patients [still] report concern with regard to the benefits, risks, and safeness in Parkinson’s disease,” Mayela Rodríguez-Violante, MD, MSc, and colleagues wrote in an abstract of their findings.

Social isolation may be contributing to these beliefs and concerns, though this is inconclusive.

Investigators from Mexico City conducted a retrospective study of patients with Parkinson’s disease to see how COVID-19 vaccination affected motor and nonmotor symptoms. They enlisted 60 patients (66.7% were male; aged 65.7 ± 11.35 years) who received either a vector-viral vaccine (Vaxzevria Coronavirus) or an mRNA vaccine (BNT162b2).

A Wilcoxon signed-rank test assessed scale differences before and after vaccination, measuring motor involvement (Unified Parkinson’s Disease Rating Scale), nonmotor involvement (Non-Motor Rating Scale [NMSS]), cognitive impairment (Montreal Cognitive Assessment), and quality of life (8-item Parkinson’s Disease Questionnaire index).

Investigators found no significant difference between scales, although they did notice a marked improvement in non-motor symptoms.

“The main takeaway is that vaccination against COVID-19 does not appear to worsen motor or nonmotor symptoms in persons with Parkinson’s disease. The benefits outweigh the risks,” said Dr. Rodríguez-Violante, the study’s lead author and a movement disorder specialist at the National Institute of Neurology and Neurosurgery, Mexico City.

Next steps are to increase the sample size to see if it’s possible to have a similar number in terms of type of vaccine, said Dr. Rodríguez-Violante. “Also, the data presented refers to primary series doses so booster effects will also be studied.”

Few studies have looked at vaccines and their possible effects on this patient population. However, a 2021 study of 181 patients with Parkinson’s disease reported that 2 (1.1%) had adverse effects after receiving the BNT162b2 mRNA vaccine. One of the patients, a 61-year-old woman with a decade-long history of Parkinson’s disease, developed severe, continuous, generalized dyskinesia 6 hours after a first dose of vaccine. The second patient was 79 years old and had Parkinson’s disease for 5 years. She developed fever, confusion, delusions, and continuous severe dyskinesia for 3 days following her vaccination.

“This highlights that there is a variability in the response triggered by the vaccine that might likely depend on individual immunological profiles … clinicians should be aware of this possibility and monitor their patients after they receive their vaccination,” Roberto Erro, MD, PhD and colleagues wrote in the Movement Disorders journal.

Mexican researchers found no direct association between SARS-CoV-2 vaccination and worsening symptoms among 60 patients with Parkinson’s disease. Nonmotor symptoms seemed to improve after SARS-CoV-2 vaccination, although the investigators could not verify a causal relationship.

Vaccination programs should continue for patients with Parkinson’s disease, they said, reporting their clinical results at the International Congress of Parkinson’s Disease and Movement Disorders.

The International Parkinson and Movement Disorder Society has recommended vaccining patients with Parkinson’s disease. “All approved mRNA-based and viral vector vaccines are not expected to interact with Parkinson’s disease, but patients [still] report concern with regard to the benefits, risks, and safeness in Parkinson’s disease,” Mayela Rodríguez-Violante, MD, MSc, and colleagues wrote in an abstract of their findings.

Social isolation may be contributing to these beliefs and concerns, though this is inconclusive.

Investigators from Mexico City conducted a retrospective study of patients with Parkinson’s disease to see how COVID-19 vaccination affected motor and nonmotor symptoms. They enlisted 60 patients (66.7% were male; aged 65.7 ± 11.35 years) who received either a vector-viral vaccine (Vaxzevria Coronavirus) or an mRNA vaccine (BNT162b2).

A Wilcoxon signed-rank test assessed scale differences before and after vaccination, measuring motor involvement (Unified Parkinson’s Disease Rating Scale), nonmotor involvement (Non-Motor Rating Scale [NMSS]), cognitive impairment (Montreal Cognitive Assessment), and quality of life (8-item Parkinson’s Disease Questionnaire index).

Investigators found no significant difference between scales, although they did notice a marked improvement in non-motor symptoms.

“The main takeaway is that vaccination against COVID-19 does not appear to worsen motor or nonmotor symptoms in persons with Parkinson’s disease. The benefits outweigh the risks,” said Dr. Rodríguez-Violante, the study’s lead author and a movement disorder specialist at the National Institute of Neurology and Neurosurgery, Mexico City.

Next steps are to increase the sample size to see if it’s possible to have a similar number in terms of type of vaccine, said Dr. Rodríguez-Violante. “Also, the data presented refers to primary series doses so booster effects will also be studied.”

Few studies have looked at vaccines and their possible effects on this patient population. However, a 2021 study of 181 patients with Parkinson’s disease reported that 2 (1.1%) had adverse effects after receiving the BNT162b2 mRNA vaccine. One of the patients, a 61-year-old woman with a decade-long history of Parkinson’s disease, developed severe, continuous, generalized dyskinesia 6 hours after a first dose of vaccine. The second patient was 79 years old and had Parkinson’s disease for 5 years. She developed fever, confusion, delusions, and continuous severe dyskinesia for 3 days following her vaccination.

“This highlights that there is a variability in the response triggered by the vaccine that might likely depend on individual immunological profiles … clinicians should be aware of this possibility and monitor their patients after they receive their vaccination,” Roberto Erro, MD, PhD and colleagues wrote in the Movement Disorders journal.

Two studies from different parts of the world demonstrated telehealth’s ability to increase access to care and manage symptoms of Parkinson’s disease and other movement disorders. Researchers presented their findings at the International Congress of Parkinson’s Disease and Movement Disorders.

Serving the underserved

One of the studies – from Kenya, Africa – documented a 2-year experience with telemedicine in a rural patient population.

Kenya suffers from a dearth of neurologists and movement disorder specialists. Most are based in the capital city of Nairobi, “leaving regions with a population of more than 30 million without access to their care,” wrote the study’s investigators. Internists with an interest in neurology usually manage the bulk of these patients.

Telemedicine has helped to bridge gaps between providers in this part of Africa.

Investigators in their study reviewed all cases of movement disorders at Meru Teaching and Referral Hospital and an affiliated clinic, Oregon Health Services, Meru, Kenya, during 2020 and 2021.

They also reviewed WhatsApp messaging, video calls via WhatsApp, patient videos, and phone calls to see how final diagnoses were arrived at using these platforms.

“For instance, a relative would send a video of a patient experiencing a tremor,” explained lead study author Bundi Karau, MD, a consultant physician. “We also shared the diagnostic challenges with experienced neurologists in Kenya and abroad by forwarding WhatsApp and recorded videos of the patients,” he added.

Telemedicine bridged the gap between rural doctors and patients in several ways. It enabled physicians to discuss cases with neurologists in and out of Kenya. “We were able to advise on medical management or further investigations in a more structured pattern and without spending months to make a diagnosis,” said Dr. Karau.

Patients no longer had to travel to Nairobi for care.  “Where a direct link could be expensive or out of reach, we bridged this and consequently brought care closer to the patient,” he added.

More than 100 patients were diagnosed with a movement disorder and enrolled in care and follow-up during this 2-year time. Patients averaged about 62 years of age and more than 60% were male. Parkinson’s disease was the most common diagnosed condition (38.9%) followed by drug-induced movement disorders (30.6%), dystonia (11.1%), and functional movement disorders (11.1%).

Investigators found 3 cases of diabetic striatopathy, 8 cases of myoclonus, and 2 cases of Sydenham’s chorea.

Looking ahead, Dr. Karau and colleagues plan to do a cost benefit analysis vis-a-vis traditional physician visits and a trial model for follow-up visits for other neurological diseases.
 

Wearable devices and apps improve care

Moving from Africa to Greece, investigators in another study assessed the feasibility of using wearable devices to monitor symptoms in patients with Parkinson’s disease.

Such devices may enhance physical exams during virtual visits. Studies have shown that patients can commit to using such devices or mobile apps. What’s lacking is real-world data from everyday device usage, noted lead author George Rigas, PhD, and colleagues.

Fifty-two private physicians instructed a total of 133 patients to wear a device for Parkinson’s disease motor symptom telemonitoring for 1 week per month during waking hours.

Patients used a mobile app to report symptoms, medication, and nutrition adherence and to message their doctor.

The study team noticed that adherence rates stayed above 70% over a 12-month period. Medication and nutrition were among the most popular app features, an encouraging finding given that patients averaged 67 years of age.

“The high adherence percentage is significant, considering the target population and the early stage of telemedicine in Greece,” they concluded. Additional real-world data could help better inform longer-term adherence.

“These studies from all over the world demonstrate that we are only scratching the surface of the telehealth’s potential to improve care and the lives of individuals with Parkinson’s disease,” said Ray Dorsey, MD, a professor of neurology with the Center for Health + Technology at the University of Rochester (N.Y.).

Dr. Dorsey was not involved with the studies but has written and researched extensively on this topic.

Dr. Dorsey is a consultant for and has equity interests in Mediflix and Included Health, two digital health companies.

Two studies from different parts of the world demonstrated telehealth’s ability to increase access to care and manage symptoms of Parkinson’s disease and other movement disorders. Researchers presented their findings at the International Congress of Parkinson’s Disease and Movement Disorders.

Serving the underserved

One of the studies – from Kenya, Africa – documented a 2-year experience with telemedicine in a rural patient population.

Kenya suffers from a dearth of neurologists and movement disorder specialists. Most are based in the capital city of Nairobi, “leaving regions with a population of more than 30 million without access to their care,” wrote the study’s investigators. Internists with an interest in neurology usually manage the bulk of these patients.

Telemedicine has helped to bridge gaps between providers in this part of Africa.

Investigators in their study reviewed all cases of movement disorders at Meru Teaching and Referral Hospital and an affiliated clinic, Oregon Health Services, Meru, Kenya, during 2020 and 2021.

They also reviewed WhatsApp messaging, video calls via WhatsApp, patient videos, and phone calls to see how final diagnoses were arrived at using these platforms.

“For instance, a relative would send a video of a patient experiencing a tremor,” explained lead study author Bundi Karau, MD, a consultant physician. “We also shared the diagnostic challenges with experienced neurologists in Kenya and abroad by forwarding WhatsApp and recorded videos of the patients,” he added.

Telemedicine bridged the gap between rural doctors and patients in several ways. It enabled physicians to discuss cases with neurologists in and out of Kenya. “We were able to advise on medical management or further investigations in a more structured pattern and without spending months to make a diagnosis,” said Dr. Karau.

Patients no longer had to travel to Nairobi for care.  “Where a direct link could be expensive or out of reach, we bridged this and consequently brought care closer to the patient,” he added.

More than 100 patients were diagnosed with a movement disorder and enrolled in care and follow-up during this 2-year time. Patients averaged about 62 years of age and more than 60% were male. Parkinson’s disease was the most common diagnosed condition (38.9%) followed by drug-induced movement disorders (30.6%), dystonia (11.1%), and functional movement disorders (11.1%).

Investigators found 3 cases of diabetic striatopathy, 8 cases of myoclonus, and 2 cases of Sydenham’s chorea.

Looking ahead, Dr. Karau and colleagues plan to do a cost benefit analysis vis-a-vis traditional physician visits and a trial model for follow-up visits for other neurological diseases.
 

Wearable devices and apps improve care

Moving from Africa to Greece, investigators in another study assessed the feasibility of using wearable devices to monitor symptoms in patients with Parkinson’s disease.

Such devices may enhance physical exams during virtual visits. Studies have shown that patients can commit to using such devices or mobile apps. What’s lacking is real-world data from everyday device usage, noted lead author George Rigas, PhD, and colleagues.

Fifty-two private physicians instructed a total of 133 patients to wear a device for Parkinson’s disease motor symptom telemonitoring for 1 week per month during waking hours.

Patients used a mobile app to report symptoms, medication, and nutrition adherence and to message their doctor.

The study team noticed that adherence rates stayed above 70% over a 12-month period. Medication and nutrition were among the most popular app features, an encouraging finding given that patients averaged 67 years of age.

“The high adherence percentage is significant, considering the target population and the early stage of telemedicine in Greece,” they concluded. Additional real-world data could help better inform longer-term adherence.

“These studies from all over the world demonstrate that we are only scratching the surface of the telehealth’s potential to improve care and the lives of individuals with Parkinson’s disease,” said Ray Dorsey, MD, a professor of neurology with the Center for Health + Technology at the University of Rochester (N.Y.).

Dr. Dorsey was not involved with the studies but has written and researched extensively on this topic.

Dr. Dorsey is a consultant for and has equity interests in Mediflix and Included Health, two digital health companies.

Two studies from different parts of the world demonstrated telehealth’s ability to increase access to care and manage symptoms of Parkinson’s disease and other movement disorders. Researchers presented their findings at the International Congress of Parkinson’s Disease and Movement Disorders.

Serving the underserved

One of the studies – from Kenya, Africa – documented a 2-year experience with telemedicine in a rural patient population.

Kenya suffers from a dearth of neurologists and movement disorder specialists. Most are based in the capital city of Nairobi, “leaving regions with a population of more than 30 million without access to their care,” wrote the study’s investigators. Internists with an interest in neurology usually manage the bulk of these patients.

Telemedicine has helped to bridge gaps between providers in this part of Africa.

Investigators in their study reviewed all cases of movement disorders at Meru Teaching and Referral Hospital and an affiliated clinic, Oregon Health Services, Meru, Kenya, during 2020 and 2021.

They also reviewed WhatsApp messaging, video calls via WhatsApp, patient videos, and phone calls to see how final diagnoses were arrived at using these platforms.

“For instance, a relative would send a video of a patient experiencing a tremor,” explained lead study author Bundi Karau, MD, a consultant physician. “We also shared the diagnostic challenges with experienced neurologists in Kenya and abroad by forwarding WhatsApp and recorded videos of the patients,” he added.

Telemedicine bridged the gap between rural doctors and patients in several ways. It enabled physicians to discuss cases with neurologists in and out of Kenya. “We were able to advise on medical management or further investigations in a more structured pattern and without spending months to make a diagnosis,” said Dr. Karau.

Patients no longer had to travel to Nairobi for care.  “Where a direct link could be expensive or out of reach, we bridged this and consequently brought care closer to the patient,” he added.

More than 100 patients were diagnosed with a movement disorder and enrolled in care and follow-up during this 2-year time. Patients averaged about 62 years of age and more than 60% were male. Parkinson’s disease was the most common diagnosed condition (38.9%) followed by drug-induced movement disorders (30.6%), dystonia (11.1%), and functional movement disorders (11.1%).

Investigators found 3 cases of diabetic striatopathy, 8 cases of myoclonus, and 2 cases of Sydenham’s chorea.

Looking ahead, Dr. Karau and colleagues plan to do a cost benefit analysis vis-a-vis traditional physician visits and a trial model for follow-up visits for other neurological diseases.
 

Wearable devices and apps improve care

Moving from Africa to Greece, investigators in another study assessed the feasibility of using wearable devices to monitor symptoms in patients with Parkinson’s disease.

Such devices may enhance physical exams during virtual visits. Studies have shown that patients can commit to using such devices or mobile apps. What’s lacking is real-world data from everyday device usage, noted lead author George Rigas, PhD, and colleagues.

Fifty-two private physicians instructed a total of 133 patients to wear a device for Parkinson’s disease motor symptom telemonitoring for 1 week per month during waking hours.

Patients used a mobile app to report symptoms, medication, and nutrition adherence and to message their doctor.

The study team noticed that adherence rates stayed above 70% over a 12-month period. Medication and nutrition were among the most popular app features, an encouraging finding given that patients averaged 67 years of age.

“The high adherence percentage is significant, considering the target population and the early stage of telemedicine in Greece,” they concluded. Additional real-world data could help better inform longer-term adherence.

“These studies from all over the world demonstrate that we are only scratching the surface of the telehealth’s potential to improve care and the lives of individuals with Parkinson’s disease,” said Ray Dorsey, MD, a professor of neurology with the Center for Health + Technology at the University of Rochester (N.Y.).

Dr. Dorsey was not involved with the studies but has written and researched extensively on this topic.

Dr. Dorsey is a consultant for and has equity interests in Mediflix and Included Health, two digital health companies.

Medical cannabis doesn’t appear to exacerbate disease or neuropsychiatric symptoms in patients with movement disorders, two Israeli research teams reported.

The practice calls for careful monitoring of patients and additional study, said the researchers, who presented their findings at the International Congress of Parkinson’s Disease and Movement Disorders.
 

Cannabis for Parkinson’s disease

One retrospective study focused on Parkinson’s disease, evaluating the safety and effects of long-term treatment with medical cannabis, which has become a widely available treatment for controlling symptoms in Parkinson’s disease and other pain disorders. Studies have demonstrated its efficacy in patients with Parkinson’s disease, but long-term safety has never been examined in Parkinson’s disease compared with untreated patients.

Their study included 152 patients with idiopathic Parkinson’s disease (mean age at diagnosis: 55.6 plus or minus 9.5 years) from the Sheba Medical Center Movement Disorders Institute who had been issued a license for medical cannabis. Seventy-six patients treated with cannabis were compared with 76 patients with similar characteristics who were not treated with cannabis.

Investigators collected data on patients who were followed at the institute between 2008 and 2022. Average follow-up period was 3.6 years.

Specifically, they collected data on levodopa equivalent daily dose (LEDD), Hoehn and Yahr scale progression, and patient-reported outcome measures on cognitive impairment, depressive, and psychotic symptoms, at baseline and at follow-up.

The Hoehn and Yahr scale allows for the quantification of different disease stages and LEDD provides a summary of the total daily medication a patient is receiving, explained Tomer Goldberg, BSc, the study’s lead author. Both are widely accepted motor severity and progression measures for Parkinson’s disease. “We wanted to check whether cannabis treatment influences these two motor parameters,” said Mr. Goldberg, who is affiliated with Tel Aviv University and the Movement Disorders Institute at Sheba Medical Center.

The medical cannabis–treated group and the untreated group had no significant differences in the mean annual change in LEDD or Hoehn and Yahr score. At 1, 2, and 3 years of follow-up, the treated group showed no signs of psychotic, depressive, or cognitive deterioration (P = .10-.68). The groups in Kaplan-Meier analyses also exhibited no differences in these nonmotor symptoms over time (P = .27-.93).

The findings suggest that cannabis treatment appears to be safe and has no negative effect on disease progression, said Mr. Goldberg. “It is important to note that we did not investigate all of the potential side effects of this treatment, and that prescribing medical cannabis for patients with Parkinson’s disease should be done with careful monitoring of each patient’s individual response to the treatment,” he added.
 

Cannabis for Huntington’s disease

Another study, targeting Huntington’s disease, drew similar conclusions. Psychiatric symptoms and cognitive decline are often present in Huntington’s disease patients, who have few treatment options. “An overall improvement in chorea and in neuropsychiatric symptoms was reported following cannabis treatment in several studies both in humans and in murine models,” wrote the study authors.

In this study, a certified Huntington’s disease specialist reviewed the medical records of 150 patients who were being followed in an Huntington’s disease clinic. Study metrics included the Unified Huntington’s Disease Rating Scale and Montreal Cognitive Assessment scores, indications for treatment, and adverse events related to treatment. Among the 150 patients, 19 had received cannabis treatment for indications such as sleep disorders, behavioral anomalies, and chorea. All but one patient reported an improvement in symptoms (94%). No adverse events were recorded, although one patient died from a COVID-19 infection.

Overall, medical cannabis appeared to safely relieve symptoms in patients with Huntington’s disease. A double-blind randomized controlled trial should further examine efficacy of these findings, the study authors recommended.

Mr. Goldberg had no disclosures or conflicts of interest in reporting his research.

Medical cannabis doesn’t appear to exacerbate disease or neuropsychiatric symptoms in patients with movement disorders, two Israeli research teams reported.

The practice calls for careful monitoring of patients and additional study, said the researchers, who presented their findings at the International Congress of Parkinson’s Disease and Movement Disorders.
 

Cannabis for Parkinson’s disease

One retrospective study focused on Parkinson’s disease, evaluating the safety and effects of long-term treatment with medical cannabis, which has become a widely available treatment for controlling symptoms in Parkinson’s disease and other pain disorders. Studies have demonstrated its efficacy in patients with Parkinson’s disease, but long-term safety has never been examined in Parkinson’s disease compared with untreated patients.

Their study included 152 patients with idiopathic Parkinson’s disease (mean age at diagnosis: 55.6 plus or minus 9.5 years) from the Sheba Medical Center Movement Disorders Institute who had been issued a license for medical cannabis. Seventy-six patients treated with cannabis were compared with 76 patients with similar characteristics who were not treated with cannabis.

Investigators collected data on patients who were followed at the institute between 2008 and 2022. Average follow-up period was 3.6 years.

Specifically, they collected data on levodopa equivalent daily dose (LEDD), Hoehn and Yahr scale progression, and patient-reported outcome measures on cognitive impairment, depressive, and psychotic symptoms, at baseline and at follow-up.

The Hoehn and Yahr scale allows for the quantification of different disease stages and LEDD provides a summary of the total daily medication a patient is receiving, explained Tomer Goldberg, BSc, the study’s lead author. Both are widely accepted motor severity and progression measures for Parkinson’s disease. “We wanted to check whether cannabis treatment influences these two motor parameters,” said Mr. Goldberg, who is affiliated with Tel Aviv University and the Movement Disorders Institute at Sheba Medical Center.

The medical cannabis–treated group and the untreated group had no significant differences in the mean annual change in LEDD or Hoehn and Yahr score. At 1, 2, and 3 years of follow-up, the treated group showed no signs of psychotic, depressive, or cognitive deterioration (P = .10-.68). The groups in Kaplan-Meier analyses also exhibited no differences in these nonmotor symptoms over time (P = .27-.93).

The findings suggest that cannabis treatment appears to be safe and has no negative effect on disease progression, said Mr. Goldberg. “It is important to note that we did not investigate all of the potential side effects of this treatment, and that prescribing medical cannabis for patients with Parkinson’s disease should be done with careful monitoring of each patient’s individual response to the treatment,” he added.
 

Cannabis for Huntington’s disease

Another study, targeting Huntington’s disease, drew similar conclusions. Psychiatric symptoms and cognitive decline are often present in Huntington’s disease patients, who have few treatment options. “An overall improvement in chorea and in neuropsychiatric symptoms was reported following cannabis treatment in several studies both in humans and in murine models,” wrote the study authors.

In this study, a certified Huntington’s disease specialist reviewed the medical records of 150 patients who were being followed in an Huntington’s disease clinic. Study metrics included the Unified Huntington’s Disease Rating Scale and Montreal Cognitive Assessment scores, indications for treatment, and adverse events related to treatment. Among the 150 patients, 19 had received cannabis treatment for indications such as sleep disorders, behavioral anomalies, and chorea. All but one patient reported an improvement in symptoms (94%). No adverse events were recorded, although one patient died from a COVID-19 infection.

Overall, medical cannabis appeared to safely relieve symptoms in patients with Huntington’s disease. A double-blind randomized controlled trial should further examine efficacy of these findings, the study authors recommended.

Mr. Goldberg had no disclosures or conflicts of interest in reporting his research.

Medical cannabis doesn’t appear to exacerbate disease or neuropsychiatric symptoms in patients with movement disorders, two Israeli research teams reported.

The practice calls for careful monitoring of patients and additional study, said the researchers, who presented their findings at the International Congress of Parkinson’s Disease and Movement Disorders.
 

Cannabis for Parkinson’s disease

One retrospective study focused on Parkinson’s disease, evaluating the safety and effects of long-term treatment with medical cannabis, which has become a widely available treatment for controlling symptoms in Parkinson’s disease and other pain disorders. Studies have demonstrated its efficacy in patients with Parkinson’s disease, but long-term safety has never been examined in Parkinson’s disease compared with untreated patients.

Their study included 152 patients with idiopathic Parkinson’s disease (mean age at diagnosis: 55.6 plus or minus 9.5 years) from the Sheba Medical Center Movement Disorders Institute who had been issued a license for medical cannabis. Seventy-six patients treated with cannabis were compared with 76 patients with similar characteristics who were not treated with cannabis.

Investigators collected data on patients who were followed at the institute between 2008 and 2022. Average follow-up period was 3.6 years.

Specifically, they collected data on levodopa equivalent daily dose (LEDD), Hoehn and Yahr scale progression, and patient-reported outcome measures on cognitive impairment, depressive, and psychotic symptoms, at baseline and at follow-up.

The Hoehn and Yahr scale allows for the quantification of different disease stages and LEDD provides a summary of the total daily medication a patient is receiving, explained Tomer Goldberg, BSc, the study’s lead author. Both are widely accepted motor severity and progression measures for Parkinson’s disease. “We wanted to check whether cannabis treatment influences these two motor parameters,” said Mr. Goldberg, who is affiliated with Tel Aviv University and the Movement Disorders Institute at Sheba Medical Center.

The medical cannabis–treated group and the untreated group had no significant differences in the mean annual change in LEDD or Hoehn and Yahr score. At 1, 2, and 3 years of follow-up, the treated group showed no signs of psychotic, depressive, or cognitive deterioration (P = .10-.68). The groups in Kaplan-Meier analyses also exhibited no differences in these nonmotor symptoms over time (P = .27-.93).

The findings suggest that cannabis treatment appears to be safe and has no negative effect on disease progression, said Mr. Goldberg. “It is important to note that we did not investigate all of the potential side effects of this treatment, and that prescribing medical cannabis for patients with Parkinson’s disease should be done with careful monitoring of each patient’s individual response to the treatment,” he added.
 

Cannabis for Huntington’s disease

Another study, targeting Huntington’s disease, drew similar conclusions. Psychiatric symptoms and cognitive decline are often present in Huntington’s disease patients, who have few treatment options. “An overall improvement in chorea and in neuropsychiatric symptoms was reported following cannabis treatment in several studies both in humans and in murine models,” wrote the study authors.

In this study, a certified Huntington’s disease specialist reviewed the medical records of 150 patients who were being followed in an Huntington’s disease clinic. Study metrics included the Unified Huntington’s Disease Rating Scale and Montreal Cognitive Assessment scores, indications for treatment, and adverse events related to treatment. Among the 150 patients, 19 had received cannabis treatment for indications such as sleep disorders, behavioral anomalies, and chorea. All but one patient reported an improvement in symptoms (94%). No adverse events were recorded, although one patient died from a COVID-19 infection.

Overall, medical cannabis appeared to safely relieve symptoms in patients with Huntington’s disease. A double-blind randomized controlled trial should further examine efficacy of these findings, the study authors recommended.

Mr. Goldberg had no disclosures or conflicts of interest in reporting his research.

A history of head trauma may predict a more rapid decline in patients with Parkinson’s disease, new research suggests.

In a longitudinal online study, among patients with Parkinson’s disease who had a history of head injury, motor impairment developed 25% faster and cognitive impairment developed 45% faster than among those without such a history.

In addition, severe head injuries were associated with an even more rapid onset of impairment. The results give weight to the idea that “it’s head injuries themselves” prior to the development of Parkinson’s disease that might exacerbate motor and cognitive symptoms, said study investigator Ethan Brown, MD, assistant professor, Weill Institute of Neurosciences, department of neurology, University of California, San Francisco.

The findings emphasize the importance of “doing everything we can” to prevent falls and head injuries for patients with Parkinson’s disease, Dr. Brown said.

The findings were presented at the International Congress of Parkinson’s Disease and Movement Disorders.
 

Reverse causality concerns

Head injury is a risk factor for Parkinson’s disease, but its relationship to Parkinson’s disease progression is not well established. “There has always been this concern in Parkinson’s disease that maybe it’s problems with motor impairment that lead to head injuries, so reverse causality is an issue,” said Dr. Brown. “We wanted to look at whether risk factors we know relate to the development of Parkinson’s disease can also have a bearing on its progression,” he added.

The analysis was part of the online Fox Insight study that is evaluating motor and nonmotor symptoms in individuals with and those without Parkinson’s disease. The study included participants who had completed questionnaires on such things as head trauma.

The study included 1,065 patients (47% women; mean age, 63 years) with Parkinson’s disease who reported having had a head injury at least 5 years prior to their diagnosis. Among the participants, the mean duration of Parkinson’s disease was 7.5 years.

The investigators employed a 5-year lag time in their study to exclude head injuries caused by early motor dysfunction, they noted. “We wanted to look at people who had these head injuries we think might be part of the cause of Parkinson’s disease as opposed to a result of them,” Dr. Brown said.

In this head injury group, 51% had received one head injury, 28% had received two injuries, and 22% had received more than two injuries.

The study also included 1,457 participants (56% women; mean age, 65 years) with Parkinson’s disease who had not had a head injury prior to their diagnosis. Of these patients, the mean time with a Parkinson’s disease diagnosis was 8 years.

Dr. Brown noted that the age and sex distribution of the study group was “probably representative” of the general Parkinson’s disease population. However, because the participants had to be able to go online and complete questionnaires, it is unlikely that, among these patients, Parkinson’s disease was far advanced, he said.

The investigators adjusted for age, sex, years of education, and Parkinson’s disease duration.

Two-hit hypothesis?

The researchers compared time from diagnosis to the development of significant motor impairment, such as the need for assistance with walking, and cognitive impairment, such as having a score of less than 43 on the Penn Daily Activities Questionnaire.

They also examined the role of more severe head injuries. In the head injury group, over half (54%) had had a severe head injury, including 543 who had lost consciousness and others who had suffered a fracture or had had a seizure.

Results showed that the adjusted hazard ratio for developing motor impairment among those with a head injury, compared with those who had not had a head injury was 1.24 (95% confidence interval, 1.01-1.53; P = .037). For severe injuries, the aHR for motor impairment was 1.44 (95% CI, 1.13-1.83; P = .003).

For cognitive impairment, the aHR for those with versus without head injuries was 1.45 (95% CI, 1.14-1.86; P = .003); and for severe injuries, the aHR was 1.49 (95% CI, 1.11-2.0; P = .008).

Aside from severity, the researchers did not examine subgroups. However, Dr. Brown reported that his team would like to stratify results by sex and other variables in the future.

He noted that various mechanisms may explain why Parkinson’s disease progression is faster for patients who have a history of head injury, compared with others. Chronic inflammation due to the injury and “co-pathology” might play some role, he said. He noted that head injuries are associated with cognitive impairment in other conditions, including Alzheimer’s disease.

There is also the “two hit” hypothesis, Dr. Brown said. “A head injury could cause such broad damage that once people develop Parkinson’s disease, it’s harder for them to compensate.”

Dr. Brown also noted there might have been a “higher magnitude” of a difference between groups had the study captured participants with more severe symptoms.
 

‘Provocative’ findings

Michael S. Okun, MD, medical advisor at the Parkinson’s Foundation and professor and director at the Norman Fixel Institute for Neurological Diseases, University of Florida, Gainesville, said the new data are “provocative.”

“The idea that a head injury may be important in predicting how quickly and how severely deficits will manifest could be important to the treating clinician,” said Dr. Okun, who was not involved with the research.

He noted that the results suggest clinicians should elicit more information from patients about head trauma. “They should be seeking more than a binary ‘yes or no’ answer to head injury when questioning patients,” he added.

Dr. Okun reiterated that head injury is a “known and important risk factor” not only for Parkinson’s disease but also for other neurodegenerative diseases. “It’s important to counsel patients about the association,” he said.

The study was supported by the Michael J. Fox Foundation. Dr. Brown reports having received grant support from the Michael J. Fox Foundation. Dr. Okun has reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

A history of head trauma may predict a more rapid decline in patients with Parkinson’s disease, new research suggests.

In a longitudinal online study, among patients with Parkinson’s disease who had a history of head injury, motor impairment developed 25% faster and cognitive impairment developed 45% faster than among those without such a history.

In addition, severe head injuries were associated with an even more rapid onset of impairment. The results give weight to the idea that “it’s head injuries themselves” prior to the development of Parkinson’s disease that might exacerbate motor and cognitive symptoms, said study investigator Ethan Brown, MD, assistant professor, Weill Institute of Neurosciences, department of neurology, University of California, San Francisco.

The findings emphasize the importance of “doing everything we can” to prevent falls and head injuries for patients with Parkinson’s disease, Dr. Brown said.

The findings were presented at the International Congress of Parkinson’s Disease and Movement Disorders.
 

Reverse causality concerns

Head injury is a risk factor for Parkinson’s disease, but its relationship to Parkinson’s disease progression is not well established. “There has always been this concern in Parkinson’s disease that maybe it’s problems with motor impairment that lead to head injuries, so reverse causality is an issue,” said Dr. Brown. “We wanted to look at whether risk factors we know relate to the development of Parkinson’s disease can also have a bearing on its progression,” he added.

The analysis was part of the online Fox Insight study that is evaluating motor and nonmotor symptoms in individuals with and those without Parkinson’s disease. The study included participants who had completed questionnaires on such things as head trauma.

The study included 1,065 patients (47% women; mean age, 63 years) with Parkinson’s disease who reported having had a head injury at least 5 years prior to their diagnosis. Among the participants, the mean duration of Parkinson’s disease was 7.5 years.

The investigators employed a 5-year lag time in their study to exclude head injuries caused by early motor dysfunction, they noted. “We wanted to look at people who had these head injuries we think might be part of the cause of Parkinson’s disease as opposed to a result of them,” Dr. Brown said.

In this head injury group, 51% had received one head injury, 28% had received two injuries, and 22% had received more than two injuries.

The study also included 1,457 participants (56% women; mean age, 65 years) with Parkinson’s disease who had not had a head injury prior to their diagnosis. Of these patients, the mean time with a Parkinson’s disease diagnosis was 8 years.

Dr. Brown noted that the age and sex distribution of the study group was “probably representative” of the general Parkinson’s disease population. However, because the participants had to be able to go online and complete questionnaires, it is unlikely that, among these patients, Parkinson’s disease was far advanced, he said.

The investigators adjusted for age, sex, years of education, and Parkinson’s disease duration.

Two-hit hypothesis?

The researchers compared time from diagnosis to the development of significant motor impairment, such as the need for assistance with walking, and cognitive impairment, such as having a score of less than 43 on the Penn Daily Activities Questionnaire.

They also examined the role of more severe head injuries. In the head injury group, over half (54%) had had a severe head injury, including 543 who had lost consciousness and others who had suffered a fracture or had had a seizure.

Results showed that the adjusted hazard ratio for developing motor impairment among those with a head injury, compared with those who had not had a head injury was 1.24 (95% confidence interval, 1.01-1.53; P = .037). For severe injuries, the aHR for motor impairment was 1.44 (95% CI, 1.13-1.83; P = .003).

For cognitive impairment, the aHR for those with versus without head injuries was 1.45 (95% CI, 1.14-1.86; P = .003); and for severe injuries, the aHR was 1.49 (95% CI, 1.11-2.0; P = .008).

Aside from severity, the researchers did not examine subgroups. However, Dr. Brown reported that his team would like to stratify results by sex and other variables in the future.

He noted that various mechanisms may explain why Parkinson’s disease progression is faster for patients who have a history of head injury, compared with others. Chronic inflammation due to the injury and “co-pathology” might play some role, he said. He noted that head injuries are associated with cognitive impairment in other conditions, including Alzheimer’s disease.

There is also the “two hit” hypothesis, Dr. Brown said. “A head injury could cause such broad damage that once people develop Parkinson’s disease, it’s harder for them to compensate.”

Dr. Brown also noted there might have been a “higher magnitude” of a difference between groups had the study captured participants with more severe symptoms.
 

‘Provocative’ findings

Michael S. Okun, MD, medical advisor at the Parkinson’s Foundation and professor and director at the Norman Fixel Institute for Neurological Diseases, University of Florida, Gainesville, said the new data are “provocative.”

“The idea that a head injury may be important in predicting how quickly and how severely deficits will manifest could be important to the treating clinician,” said Dr. Okun, who was not involved with the research.

He noted that the results suggest clinicians should elicit more information from patients about head trauma. “They should be seeking more than a binary ‘yes or no’ answer to head injury when questioning patients,” he added.

Dr. Okun reiterated that head injury is a “known and important risk factor” not only for Parkinson’s disease but also for other neurodegenerative diseases. “It’s important to counsel patients about the association,” he said.

The study was supported by the Michael J. Fox Foundation. Dr. Brown reports having received grant support from the Michael J. Fox Foundation. Dr. Okun has reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

A history of head trauma may predict a more rapid decline in patients with Parkinson’s disease, new research suggests.

In a longitudinal online study, among patients with Parkinson’s disease who had a history of head injury, motor impairment developed 25% faster and cognitive impairment developed 45% faster than among those without such a history.

In addition, severe head injuries were associated with an even more rapid onset of impairment. The results give weight to the idea that “it’s head injuries themselves” prior to the development of Parkinson’s disease that might exacerbate motor and cognitive symptoms, said study investigator Ethan Brown, MD, assistant professor, Weill Institute of Neurosciences, department of neurology, University of California, San Francisco.

The findings emphasize the importance of “doing everything we can” to prevent falls and head injuries for patients with Parkinson’s disease, Dr. Brown said.

The findings were presented at the International Congress of Parkinson’s Disease and Movement Disorders.
 

Reverse causality concerns

Head injury is a risk factor for Parkinson’s disease, but its relationship to Parkinson’s disease progression is not well established. “There has always been this concern in Parkinson’s disease that maybe it’s problems with motor impairment that lead to head injuries, so reverse causality is an issue,” said Dr. Brown. “We wanted to look at whether risk factors we know relate to the development of Parkinson’s disease can also have a bearing on its progression,” he added.

The analysis was part of the online Fox Insight study that is evaluating motor and nonmotor symptoms in individuals with and those without Parkinson’s disease. The study included participants who had completed questionnaires on such things as head trauma.

The study included 1,065 patients (47% women; mean age, 63 years) with Parkinson’s disease who reported having had a head injury at least 5 years prior to their diagnosis. Among the participants, the mean duration of Parkinson’s disease was 7.5 years.

The investigators employed a 5-year lag time in their study to exclude head injuries caused by early motor dysfunction, they noted. “We wanted to look at people who had these head injuries we think might be part of the cause of Parkinson’s disease as opposed to a result of them,” Dr. Brown said.

In this head injury group, 51% had received one head injury, 28% had received two injuries, and 22% had received more than two injuries.

The study also included 1,457 participants (56% women; mean age, 65 years) with Parkinson’s disease who had not had a head injury prior to their diagnosis. Of these patients, the mean time with a Parkinson’s disease diagnosis was 8 years.

Dr. Brown noted that the age and sex distribution of the study group was “probably representative” of the general Parkinson’s disease population. However, because the participants had to be able to go online and complete questionnaires, it is unlikely that, among these patients, Parkinson’s disease was far advanced, he said.

The investigators adjusted for age, sex, years of education, and Parkinson’s disease duration.

Two-hit hypothesis?

The researchers compared time from diagnosis to the development of significant motor impairment, such as the need for assistance with walking, and cognitive impairment, such as having a score of less than 43 on the Penn Daily Activities Questionnaire.

They also examined the role of more severe head injuries. In the head injury group, over half (54%) had had a severe head injury, including 543 who had lost consciousness and others who had suffered a fracture or had had a seizure.

Results showed that the adjusted hazard ratio for developing motor impairment among those with a head injury, compared with those who had not had a head injury was 1.24 (95% confidence interval, 1.01-1.53; P = .037). For severe injuries, the aHR for motor impairment was 1.44 (95% CI, 1.13-1.83; P = .003).

For cognitive impairment, the aHR for those with versus without head injuries was 1.45 (95% CI, 1.14-1.86; P = .003); and for severe injuries, the aHR was 1.49 (95% CI, 1.11-2.0; P = .008).

Aside from severity, the researchers did not examine subgroups. However, Dr. Brown reported that his team would like to stratify results by sex and other variables in the future.

He noted that various mechanisms may explain why Parkinson’s disease progression is faster for patients who have a history of head injury, compared with others. Chronic inflammation due to the injury and “co-pathology” might play some role, he said. He noted that head injuries are associated with cognitive impairment in other conditions, including Alzheimer’s disease.

There is also the “two hit” hypothesis, Dr. Brown said. “A head injury could cause such broad damage that once people develop Parkinson’s disease, it’s harder for them to compensate.”

Dr. Brown also noted there might have been a “higher magnitude” of a difference between groups had the study captured participants with more severe symptoms.
 

‘Provocative’ findings

Michael S. Okun, MD, medical advisor at the Parkinson’s Foundation and professor and director at the Norman Fixel Institute for Neurological Diseases, University of Florida, Gainesville, said the new data are “provocative.”

“The idea that a head injury may be important in predicting how quickly and how severely deficits will manifest could be important to the treating clinician,” said Dr. Okun, who was not involved with the research.

He noted that the results suggest clinicians should elicit more information from patients about head trauma. “They should be seeking more than a binary ‘yes or no’ answer to head injury when questioning patients,” he added.

Dr. Okun reiterated that head injury is a “known and important risk factor” not only for Parkinson’s disease but also for other neurodegenerative diseases. “It’s important to counsel patients about the association,” he said.

The study was supported by the Michael J. Fox Foundation. Dr. Brown reports having received grant support from the Michael J. Fox Foundation. Dr. Okun has reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

A World Health Organization (WHO) consultation workshop on global disparities in Parkinson’s disease has suggested six avenues for action to address the needs of these patients.

Since 2000, Parkinson’s disease has increased 81% and related deaths have increased 100% globally. In addition, many patients affected by Parkinson’s disease live in low- and middle-income countries and experience large inequalities in access to neurologic care and essential medicines.

To address these issues, the Brain Health Unit at the WHO developed six “action steps” it says are urgently required to combat global disparities in Parkinson’s disease.

The need for action is great, said lead author Nicoline Schiess, MD, MPH, a neurologist and technical officer in the WHO’s Brain Health Unit in Geneva.

“In adults, disorders of the nervous system are the leading cause of disability adjusted life years, or DALYs, and the second leading cause of death globally, accounting for 9 million deaths per year,” Dr. Schiess said.

The WHO’s recommendations were published online recently as a “Special Communication” in JAMA Neurology.
 

Serious public health challenge

Parkinson’s disease is the fastest growing disorder in terms of death and disability, and it is estimated that it caused 329,000 deaths in 2019 – an increase of more than 100% since 2000.

“The rise in cases is thought to be multifactorial and is likely affected by factors such as aging populations and environmental exposures, such as certain pesticides. With these rapidly increasing numbers, compounded by a lack of specialists and medicines in low- and middle-income countries, Parkinson’s disease presents a serious public health challenge,” Dr. Schiess  said.

The publication of the six action steps is targeted toward clinicians and researchers who work in Parkinson’s disease, she added. The steps address the following areas:

• 1. Disease burden
• 2. Advocacy and awareness
• 3. Prevention and risk reduction
• 4. Diagnosis, treatment, and care
• 5. Caregiver support
• 6. Research

Dr. Schiess noted that data on disease burden are lacking in certain areas of the world, such as low- and middle-income countries, and information “based on race and ethnicity are inconsistent. Studies are needed to establish more representative epidemiological data.”

She said that advocacy and awareness are particularly important since young people may not be aware they can also develop Parkinson’s disease, and sex and race differences can factor in to the potential for delays in diagnosis and care. “This is often due to the incorrect perception that Parkinson’s disease only affects older people,” she noted.

In addition, “a substantial need exists to identify risks for Parkinson’s disease – in particular the risks we can mitigate,” said Dr. Schiess, citing pesticide exposure as one example. “The evidence linking pesticide exposure, for example paraquat and chlorpyrifos, with the risk of developing Parkinson’s disease is substantial. And yet in many countries, these products are still being used.”

Under the heading of diagnosis, treatment, and care, Dr. Schiess noted that patients with Parkinson’s disease in “low resource settings” and low- to middle-income countries are unable to obtain “even the most basic medications” to treat Parkinson’s disease.

“Strengthening health and social systems, and building capacity to improve medical care, including rehabilitation and palliative care and medication access, are vital. Also, education and training of primary health care professionals, growing the neurological workforce, and increasing the use of digital technology such as telemedicine, are key mechanisms to improving diagnosis and sustainability of care,” she said.

For caregiver support, Dr. Schiess pointed out that the progressive nature of the disease and timing of onset are contributors to increased caregiver burden. Other contributors, as the disease advances in a patient, include the development of cognitive impairment, psychiatric manifestations, and sleep disruption.

“Solutions that could decrease the burden on caregivers include providing an accurate and timely diagnosis and training and education to caregivers, such as the WHO iSUPPORT program, as well as psychosocial, financial, and community-based support,” said Dr. Schiess.

For research, she noted that the amount of studies in the field of Parkinson’s disease has grown because of increased funding and a greater number of initiatives over the past 2 decades.

“Continuing to build on this momentum is important in order to generate new treatment options, better care, and research capacity, especially in low- and middle-income countries,” she said.

Dr. Schiess emphasized the urgency for adopting these measures as cases of Parkinson’s disease continue to rise.

“The take-away message for clinicians is that Parkinson disease is a growing global public health issue. There is a pressing need for a global public health response to address health and social requirements for people with Parkinson’s disease,” she said.

Dr. Schiess reports having received grants from the Edmond J. Safra Foundation paid to her institution during the conduct of the study.

A version of this article first appeared on Medscape.com.

A World Health Organization (WHO) consultation workshop on global disparities in Parkinson’s disease has suggested six avenues for action to address the needs of these patients.

Since 2000, Parkinson’s disease has increased 81% and related deaths have increased 100% globally. In addition, many patients affected by Parkinson’s disease live in low- and middle-income countries and experience large inequalities in access to neurologic care and essential medicines.

To address these issues, the Brain Health Unit at the WHO developed six “action steps” it says are urgently required to combat global disparities in Parkinson’s disease.

The need for action is great, said lead author Nicoline Schiess, MD, MPH, a neurologist and technical officer in the WHO’s Brain Health Unit in Geneva.

“In adults, disorders of the nervous system are the leading cause of disability adjusted life years, or DALYs, and the second leading cause of death globally, accounting for 9 million deaths per year,” Dr. Schiess said.

The WHO’s recommendations were published online recently as a “Special Communication” in JAMA Neurology.
 

Serious public health challenge

Parkinson’s disease is the fastest growing disorder in terms of death and disability, and it is estimated that it caused 329,000 deaths in 2019 – an increase of more than 100% since 2000.

“The rise in cases is thought to be multifactorial and is likely affected by factors such as aging populations and environmental exposures, such as certain pesticides. With these rapidly increasing numbers, compounded by a lack of specialists and medicines in low- and middle-income countries, Parkinson’s disease presents a serious public health challenge,” Dr. Schiess  said.

The publication of the six action steps is targeted toward clinicians and researchers who work in Parkinson’s disease, she added. The steps address the following areas:

• 1. Disease burden
• 2. Advocacy and awareness
• 3. Prevention and risk reduction
• 4. Diagnosis, treatment, and care
• 5. Caregiver support
• 6. Research

Dr. Schiess noted that data on disease burden are lacking in certain areas of the world, such as low- and middle-income countries, and information “based on race and ethnicity are inconsistent. Studies are needed to establish more representative epidemiological data.”

She said that advocacy and awareness are particularly important since young people may not be aware they can also develop Parkinson’s disease, and sex and race differences can factor in to the potential for delays in diagnosis and care. “This is often due to the incorrect perception that Parkinson’s disease only affects older people,” she noted.

In addition, “a substantial need exists to identify risks for Parkinson’s disease – in particular the risks we can mitigate,” said Dr. Schiess, citing pesticide exposure as one example. “The evidence linking pesticide exposure, for example paraquat and chlorpyrifos, with the risk of developing Parkinson’s disease is substantial. And yet in many countries, these products are still being used.”

Under the heading of diagnosis, treatment, and care, Dr. Schiess noted that patients with Parkinson’s disease in “low resource settings” and low- to middle-income countries are unable to obtain “even the most basic medications” to treat Parkinson’s disease.

“Strengthening health and social systems, and building capacity to improve medical care, including rehabilitation and palliative care and medication access, are vital. Also, education and training of primary health care professionals, growing the neurological workforce, and increasing the use of digital technology such as telemedicine, are key mechanisms to improving diagnosis and sustainability of care,” she said.

For caregiver support, Dr. Schiess pointed out that the progressive nature of the disease and timing of onset are contributors to increased caregiver burden. Other contributors, as the disease advances in a patient, include the development of cognitive impairment, psychiatric manifestations, and sleep disruption.

“Solutions that could decrease the burden on caregivers include providing an accurate and timely diagnosis and training and education to caregivers, such as the WHO iSUPPORT program, as well as psychosocial, financial, and community-based support,” said Dr. Schiess.

For research, she noted that the amount of studies in the field of Parkinson’s disease has grown because of increased funding and a greater number of initiatives over the past 2 decades.

“Continuing to build on this momentum is important in order to generate new treatment options, better care, and research capacity, especially in low- and middle-income countries,” she said.

Dr. Schiess emphasized the urgency for adopting these measures as cases of Parkinson’s disease continue to rise.

“The take-away message for clinicians is that Parkinson disease is a growing global public health issue. There is a pressing need for a global public health response to address health and social requirements for people with Parkinson’s disease,” she said.

Dr. Schiess reports having received grants from the Edmond J. Safra Foundation paid to her institution during the conduct of the study.

A version of this article first appeared on Medscape.com.

A World Health Organization (WHO) consultation workshop on global disparities in Parkinson’s disease has suggested six avenues for action to address the needs of these patients.

Since 2000, Parkinson’s disease has increased 81% and related deaths have increased 100% globally. In addition, many patients affected by Parkinson’s disease live in low- and middle-income countries and experience large inequalities in access to neurologic care and essential medicines.

To address these issues, the Brain Health Unit at the WHO developed six “action steps” it says are urgently required to combat global disparities in Parkinson’s disease.

The need for action is great, said lead author Nicoline Schiess, MD, MPH, a neurologist and technical officer in the WHO’s Brain Health Unit in Geneva.

“In adults, disorders of the nervous system are the leading cause of disability adjusted life years, or DALYs, and the second leading cause of death globally, accounting for 9 million deaths per year,” Dr. Schiess said.

The WHO’s recommendations were published online recently as a “Special Communication” in JAMA Neurology.
 

Serious public health challenge

Parkinson’s disease is the fastest growing disorder in terms of death and disability, and it is estimated that it caused 329,000 deaths in 2019 – an increase of more than 100% since 2000.

“The rise in cases is thought to be multifactorial and is likely affected by factors such as aging populations and environmental exposures, such as certain pesticides. With these rapidly increasing numbers, compounded by a lack of specialists and medicines in low- and middle-income countries, Parkinson’s disease presents a serious public health challenge,” Dr. Schiess  said.

The publication of the six action steps is targeted toward clinicians and researchers who work in Parkinson’s disease, she added. The steps address the following areas:

• 1. Disease burden
• 2. Advocacy and awareness
• 3. Prevention and risk reduction
• 4. Diagnosis, treatment, and care
• 5. Caregiver support
• 6. Research

Dr. Schiess noted that data on disease burden are lacking in certain areas of the world, such as low- and middle-income countries, and information “based on race and ethnicity are inconsistent. Studies are needed to establish more representative epidemiological data.”

She said that advocacy and awareness are particularly important since young people may not be aware they can also develop Parkinson’s disease, and sex and race differences can factor in to the potential for delays in diagnosis and care. “This is often due to the incorrect perception that Parkinson’s disease only affects older people,” she noted.

In addition, “a substantial need exists to identify risks for Parkinson’s disease – in particular the risks we can mitigate,” said Dr. Schiess, citing pesticide exposure as one example. “The evidence linking pesticide exposure, for example paraquat and chlorpyrifos, with the risk of developing Parkinson’s disease is substantial. And yet in many countries, these products are still being used.”

Under the heading of diagnosis, treatment, and care, Dr. Schiess noted that patients with Parkinson’s disease in “low resource settings” and low- to middle-income countries are unable to obtain “even the most basic medications” to treat Parkinson’s disease.

“Strengthening health and social systems, and building capacity to improve medical care, including rehabilitation and palliative care and medication access, are vital. Also, education and training of primary health care professionals, growing the neurological workforce, and increasing the use of digital technology such as telemedicine, are key mechanisms to improving diagnosis and sustainability of care,” she said.

For caregiver support, Dr. Schiess pointed out that the progressive nature of the disease and timing of onset are contributors to increased caregiver burden. Other contributors, as the disease advances in a patient, include the development of cognitive impairment, psychiatric manifestations, and sleep disruption.

“Solutions that could decrease the burden on caregivers include providing an accurate and timely diagnosis and training and education to caregivers, such as the WHO iSUPPORT program, as well as psychosocial, financial, and community-based support,” said Dr. Schiess.

For research, she noted that the amount of studies in the field of Parkinson’s disease has grown because of increased funding and a greater number of initiatives over the past 2 decades.

“Continuing to build on this momentum is important in order to generate new treatment options, better care, and research capacity, especially in low- and middle-income countries,” she said.

Dr. Schiess emphasized the urgency for adopting these measures as cases of Parkinson’s disease continue to rise.

“The take-away message for clinicians is that Parkinson disease is a growing global public health issue. There is a pressing need for a global public health response to address health and social requirements for people with Parkinson’s disease,” she said.

Dr. Schiess reports having received grants from the Edmond J. Safra Foundation paid to her institution during the conduct of the study.

A version of this article first appeared on Medscape.com.