User login
Children with autism show distinct brain features related to motor impairment
Previous research suggests that individuals with ASD overlap in motor impairment with those with DCD. But these two conditions may differ significantly in some areas, as children with ASD tend to show weaker skills in social motor tasks such as imitation, wrote Emil Kilroy, PhD, of the University of Southern California, Los Angeles, and colleagues.
The neurobiological basis of autism remains unknown, despite many research efforts, in part because of the heterogeneity of the disease, said corresponding author Lisa Aziz-Zadeh, PhD, also of the University of Southern California, in an interview.
Comorbidity with other disorders is a strong contributing factor to heterogeneity, and approximately 80% of autistic individuals have motor impairments and meet criteria for a diagnosis of DCD, said Dr. Aziz-Zadeh. “Controlling for other comorbidities, such as developmental coordination disorder, when trying to understand the neural basis of autism is important, so that we can understand which neural circuits are related to [core symptoms of autism] and which ones are related to motor impairments that are comorbid with autism, but not necessarily part of the core symptomology,” she explained. “We focused on white matter pathways here because many researchers now think the underlying basis of autism, besides genetics, is brain connectivity differences.”
In their study published in Scientific Reports, the researchers reviewed data from whole-brain correlational tractography for 22 individuals with autism spectrum disorder, 16 with developmental coordination disorder, and 21 normally developing individuals, who served as the control group. The mean age of the participants was approximately 11 years; the age range was 8-17 years.
Overall, patterns of brain diffusion (movement of fluid, mainly water molecules, in the brain) were significantly different in ASD children, compared with typically developing children.
The ASD group showed significantly reduced diffusivity in the bilateral fronto-parietal cingulum and the left parolfactory cingulum. This finding reflects previous studies suggesting an association between brain patterns in the cingulum area and ASD. But the current study is “the first to identify the fronto-parietal and the parolfactory portions of the cingulum as well as the anterior caudal u-fibers as specific to core ASD symptomatology and not related to motor-related comorbidity,” the researchers wrote.
Differences in brain diffusivity were associated with worse performance on motor skills and behavioral measures for children with ASD and children with DCD, compared with controls.
Motor development was assessed using the Total Movement Assessment Battery for Children-2 (MABC-2) and the Florida Apraxia Battery modified for children (FAB-M). The MABC-2 is among the most common tools for measuring motor skills and identifying clinically relevant motor deficits in children and teens aged 3-16 years. The test includes three subtest scores (manual dexterity, gross-motor aiming and catching, and balance) and a total score. Scores are based on a child’s best performance on each component, and higher scores indicate better functioning. In the new study, The MABC-2 total scores averaged 10.57 for controls, compared with 5.76 in the ASD group, and 4.31 in the DCD group.
Children with ASD differed from the other groups in social measures. Social skills were measured using several tools, including the Social Responsivity Scale (SRS Total), which is a parent-completed survey that includes a total score designed to reflect the severity of social deficits in ASD. It is divided into five subscales for parents to assess a child’s social skill impairment: social awareness, social cognition, social communication, social motivation, and mannerisms. Scores for the SRS are calculated in T-scores, in which a score of 50 represents the mean. T-scores of 59 and below are generally not associated with ASD, and patients with these scores are considered to have low to no symptomatology. Scores on the SRS Total in the new study were 45.95, 77.45, and 55.81 for the controls, ASD group, and DCD group, respectively.
Results should raise awareness
“The results were largely predicted in our hypotheses – that we would find specific white matter pathways in autism that would differ from [what we saw in typically developing patients and those with DCD], and that diffusivity in ASD would be related to socioemotional differences,” Dr. Aziz-Zadeh said, in an interview.
“What was surprising was that some pathways that had previously been thought to be different in autism were also compromised in DCD, indicating that they were common to motor deficits which both groups shared, not to core autism symptomology,” she noted.
A message for clinicians from the study is that a dual diagnosis of DCD is often missing in ASD practice, said Dr. Aziz-Zadeh. “Given that approximately 80% of children with ASD have DCD, testing for DCD and addressing potential motor issues should be more common practice,” she said.
Dr. Aziz-Zadeh and colleagues are now investigating relationships between the brain, behavior, and the gut microbiome. “We think that understanding autism from a full-body perspective, examining interactions between the brain and the body, will be an important step in this field,” she emphasized.
The study was limited by several factors, including the small sample size, the use of only right-handed participants, and the use of self-reports by children and parents, the researchers noted. Additionally, they noted that white matter develops at different rates in different age groups, and future studies might consider age as a factor, as well as further behavioral assessments, they said.
Small sample size limits conclusions
“Understanding the neuroanatomic differences that may contribute to the core symptoms of ASD is a very important goal for the field, particularly how they relate to other comorbid symptoms and neurodevelopmental disorders,” said Michael Gandal, MD, of the department of psychiatry at the University of Pennsylvania, Philadelphia, and a member of the Lifespan Brain Institute at the Children’s Hospital of Philadelphia, in an interview.
“While this study provides some clues into how structural connectivity may relate to motor coordination in ASD, it will be important to replicate these findings in a much larger sample before we can really appreciate how robust these findings are and how well they generalize to the broader ASD population,” Dr. Gandal emphasized.
The study was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development. The researchers had no financial conflicts to disclose. Dr. Gandal had no financial conflicts to disclose.
Previous research suggests that individuals with ASD overlap in motor impairment with those with DCD. But these two conditions may differ significantly in some areas, as children with ASD tend to show weaker skills in social motor tasks such as imitation, wrote Emil Kilroy, PhD, of the University of Southern California, Los Angeles, and colleagues.
The neurobiological basis of autism remains unknown, despite many research efforts, in part because of the heterogeneity of the disease, said corresponding author Lisa Aziz-Zadeh, PhD, also of the University of Southern California, in an interview.
Comorbidity with other disorders is a strong contributing factor to heterogeneity, and approximately 80% of autistic individuals have motor impairments and meet criteria for a diagnosis of DCD, said Dr. Aziz-Zadeh. “Controlling for other comorbidities, such as developmental coordination disorder, when trying to understand the neural basis of autism is important, so that we can understand which neural circuits are related to [core symptoms of autism] and which ones are related to motor impairments that are comorbid with autism, but not necessarily part of the core symptomology,” she explained. “We focused on white matter pathways here because many researchers now think the underlying basis of autism, besides genetics, is brain connectivity differences.”
In their study published in Scientific Reports, the researchers reviewed data from whole-brain correlational tractography for 22 individuals with autism spectrum disorder, 16 with developmental coordination disorder, and 21 normally developing individuals, who served as the control group. The mean age of the participants was approximately 11 years; the age range was 8-17 years.
Overall, patterns of brain diffusion (movement of fluid, mainly water molecules, in the brain) were significantly different in ASD children, compared with typically developing children.
The ASD group showed significantly reduced diffusivity in the bilateral fronto-parietal cingulum and the left parolfactory cingulum. This finding reflects previous studies suggesting an association between brain patterns in the cingulum area and ASD. But the current study is “the first to identify the fronto-parietal and the parolfactory portions of the cingulum as well as the anterior caudal u-fibers as specific to core ASD symptomatology and not related to motor-related comorbidity,” the researchers wrote.
Differences in brain diffusivity were associated with worse performance on motor skills and behavioral measures for children with ASD and children with DCD, compared with controls.
Motor development was assessed using the Total Movement Assessment Battery for Children-2 (MABC-2) and the Florida Apraxia Battery modified for children (FAB-M). The MABC-2 is among the most common tools for measuring motor skills and identifying clinically relevant motor deficits in children and teens aged 3-16 years. The test includes three subtest scores (manual dexterity, gross-motor aiming and catching, and balance) and a total score. Scores are based on a child’s best performance on each component, and higher scores indicate better functioning. In the new study, The MABC-2 total scores averaged 10.57 for controls, compared with 5.76 in the ASD group, and 4.31 in the DCD group.
Children with ASD differed from the other groups in social measures. Social skills were measured using several tools, including the Social Responsivity Scale (SRS Total), which is a parent-completed survey that includes a total score designed to reflect the severity of social deficits in ASD. It is divided into five subscales for parents to assess a child’s social skill impairment: social awareness, social cognition, social communication, social motivation, and mannerisms. Scores for the SRS are calculated in T-scores, in which a score of 50 represents the mean. T-scores of 59 and below are generally not associated with ASD, and patients with these scores are considered to have low to no symptomatology. Scores on the SRS Total in the new study were 45.95, 77.45, and 55.81 for the controls, ASD group, and DCD group, respectively.
Results should raise awareness
“The results were largely predicted in our hypotheses – that we would find specific white matter pathways in autism that would differ from [what we saw in typically developing patients and those with DCD], and that diffusivity in ASD would be related to socioemotional differences,” Dr. Aziz-Zadeh said, in an interview.
“What was surprising was that some pathways that had previously been thought to be different in autism were also compromised in DCD, indicating that they were common to motor deficits which both groups shared, not to core autism symptomology,” she noted.
A message for clinicians from the study is that a dual diagnosis of DCD is often missing in ASD practice, said Dr. Aziz-Zadeh. “Given that approximately 80% of children with ASD have DCD, testing for DCD and addressing potential motor issues should be more common practice,” she said.
Dr. Aziz-Zadeh and colleagues are now investigating relationships between the brain, behavior, and the gut microbiome. “We think that understanding autism from a full-body perspective, examining interactions between the brain and the body, will be an important step in this field,” she emphasized.
The study was limited by several factors, including the small sample size, the use of only right-handed participants, and the use of self-reports by children and parents, the researchers noted. Additionally, they noted that white matter develops at different rates in different age groups, and future studies might consider age as a factor, as well as further behavioral assessments, they said.
Small sample size limits conclusions
“Understanding the neuroanatomic differences that may contribute to the core symptoms of ASD is a very important goal for the field, particularly how they relate to other comorbid symptoms and neurodevelopmental disorders,” said Michael Gandal, MD, of the department of psychiatry at the University of Pennsylvania, Philadelphia, and a member of the Lifespan Brain Institute at the Children’s Hospital of Philadelphia, in an interview.
“While this study provides some clues into how structural connectivity may relate to motor coordination in ASD, it will be important to replicate these findings in a much larger sample before we can really appreciate how robust these findings are and how well they generalize to the broader ASD population,” Dr. Gandal emphasized.
The study was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development. The researchers had no financial conflicts to disclose. Dr. Gandal had no financial conflicts to disclose.
Previous research suggests that individuals with ASD overlap in motor impairment with those with DCD. But these two conditions may differ significantly in some areas, as children with ASD tend to show weaker skills in social motor tasks such as imitation, wrote Emil Kilroy, PhD, of the University of Southern California, Los Angeles, and colleagues.
The neurobiological basis of autism remains unknown, despite many research efforts, in part because of the heterogeneity of the disease, said corresponding author Lisa Aziz-Zadeh, PhD, also of the University of Southern California, in an interview.
Comorbidity with other disorders is a strong contributing factor to heterogeneity, and approximately 80% of autistic individuals have motor impairments and meet criteria for a diagnosis of DCD, said Dr. Aziz-Zadeh. “Controlling for other comorbidities, such as developmental coordination disorder, when trying to understand the neural basis of autism is important, so that we can understand which neural circuits are related to [core symptoms of autism] and which ones are related to motor impairments that are comorbid with autism, but not necessarily part of the core symptomology,” she explained. “We focused on white matter pathways here because many researchers now think the underlying basis of autism, besides genetics, is brain connectivity differences.”
In their study published in Scientific Reports, the researchers reviewed data from whole-brain correlational tractography for 22 individuals with autism spectrum disorder, 16 with developmental coordination disorder, and 21 normally developing individuals, who served as the control group. The mean age of the participants was approximately 11 years; the age range was 8-17 years.
Overall, patterns of brain diffusion (movement of fluid, mainly water molecules, in the brain) were significantly different in ASD children, compared with typically developing children.
The ASD group showed significantly reduced diffusivity in the bilateral fronto-parietal cingulum and the left parolfactory cingulum. This finding reflects previous studies suggesting an association between brain patterns in the cingulum area and ASD. But the current study is “the first to identify the fronto-parietal and the parolfactory portions of the cingulum as well as the anterior caudal u-fibers as specific to core ASD symptomatology and not related to motor-related comorbidity,” the researchers wrote.
Differences in brain diffusivity were associated with worse performance on motor skills and behavioral measures for children with ASD and children with DCD, compared with controls.
Motor development was assessed using the Total Movement Assessment Battery for Children-2 (MABC-2) and the Florida Apraxia Battery modified for children (FAB-M). The MABC-2 is among the most common tools for measuring motor skills and identifying clinically relevant motor deficits in children and teens aged 3-16 years. The test includes three subtest scores (manual dexterity, gross-motor aiming and catching, and balance) and a total score. Scores are based on a child’s best performance on each component, and higher scores indicate better functioning. In the new study, The MABC-2 total scores averaged 10.57 for controls, compared with 5.76 in the ASD group, and 4.31 in the DCD group.
Children with ASD differed from the other groups in social measures. Social skills were measured using several tools, including the Social Responsivity Scale (SRS Total), which is a parent-completed survey that includes a total score designed to reflect the severity of social deficits in ASD. It is divided into five subscales for parents to assess a child’s social skill impairment: social awareness, social cognition, social communication, social motivation, and mannerisms. Scores for the SRS are calculated in T-scores, in which a score of 50 represents the mean. T-scores of 59 and below are generally not associated with ASD, and patients with these scores are considered to have low to no symptomatology. Scores on the SRS Total in the new study were 45.95, 77.45, and 55.81 for the controls, ASD group, and DCD group, respectively.
Results should raise awareness
“The results were largely predicted in our hypotheses – that we would find specific white matter pathways in autism that would differ from [what we saw in typically developing patients and those with DCD], and that diffusivity in ASD would be related to socioemotional differences,” Dr. Aziz-Zadeh said, in an interview.
“What was surprising was that some pathways that had previously been thought to be different in autism were also compromised in DCD, indicating that they were common to motor deficits which both groups shared, not to core autism symptomology,” she noted.
A message for clinicians from the study is that a dual diagnosis of DCD is often missing in ASD practice, said Dr. Aziz-Zadeh. “Given that approximately 80% of children with ASD have DCD, testing for DCD and addressing potential motor issues should be more common practice,” she said.
Dr. Aziz-Zadeh and colleagues are now investigating relationships between the brain, behavior, and the gut microbiome. “We think that understanding autism from a full-body perspective, examining interactions between the brain and the body, will be an important step in this field,” she emphasized.
The study was limited by several factors, including the small sample size, the use of only right-handed participants, and the use of self-reports by children and parents, the researchers noted. Additionally, they noted that white matter develops at different rates in different age groups, and future studies might consider age as a factor, as well as further behavioral assessments, they said.
Small sample size limits conclusions
“Understanding the neuroanatomic differences that may contribute to the core symptoms of ASD is a very important goal for the field, particularly how they relate to other comorbid symptoms and neurodevelopmental disorders,” said Michael Gandal, MD, of the department of psychiatry at the University of Pennsylvania, Philadelphia, and a member of the Lifespan Brain Institute at the Children’s Hospital of Philadelphia, in an interview.
“While this study provides some clues into how structural connectivity may relate to motor coordination in ASD, it will be important to replicate these findings in a much larger sample before we can really appreciate how robust these findings are and how well they generalize to the broader ASD population,” Dr. Gandal emphasized.
The study was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development. The researchers had no financial conflicts to disclose. Dr. Gandal had no financial conflicts to disclose.
FROM SCIENTIFIC REPORTS
Research fails to justify post-COVID-19 wave of new-onset parkinsonism
, a multinational team of researchers reported at the International Congress of Parkinson’s Disease and Movement Disorders.
SARS-CoV-2 led to numerous discussions about a potential post–COVID-19 emergence of new-onset parkinsonism in susceptible individuals, often referred to in the literature as a “perfect storm” or a “wave” of parkinsonism, according to lead study author Iro Boura, MD.
Postviral precedence
“Although pathogens have been associated both with parkinsonism cases and Parkinson’s disease pathogenesis, the main concern of a potential connection between COVID-19 and new-onset parkinsonism arose from the historically documented parkinsonism cases appearing with encephalitis lethargica,” said Dr. Boura, a PhD candidate with the University of Crete in Greece and ex-fellow at King’s College London.
Encephalitis lethargica appeared between 1916 and 1930 and has been epidemiologically related to the Spanish influenza pandemic, “although this link has been strongly debated by other researchers,” she added.
Because the connection of COVID-19 and parkinsonism seemed highly speculative, Dr. Boura and movement disorder specialist Kallol Ray Chaudhuri DSc, FRCP, MD, decided to search for any data supporting this notion. “Such a possibility would have a significant impact on everyday practice, including long follow-up neurological assessments of COVID-19 patients, along with greater vigilance in recognizing potential symptoms,” said Dr. Boura.
They found no organized research exploring this link, aside from published case reports.
Scant evidence of a parkinsonism wave
The investigators conducted a review of the literature up to February 2022 to identify and analyze published cases of new-onset parkinsonism following a confirmed SARS-CoV-2 infection in otherwise healthy individuals. They ended up with 20 such cases.
Although some cases presented during or shortly after a COVID-19 infection, “the numbers are currently quite low to draw safe conclusions and generalize these findings as a risk of parkinsonism for the general population,” said Dr. Boura. Overall, parkinsonism appeared in the context of encephalopathy in 11 patients. Four patients developed postinfectious parkinsonism without encephalopathy. Another four had phenotypic similarities to idiopathic Parkinson’s disease.
Nine patients were responsive to levodopa, while four required immunomodulatory treatment.
Although cases have already been reported, current data do not yet justify the concept of a post–COVID-19 parkinsonism wave. However, long-term surveillance is crucial to ensure that reports of further cases are carefully documented and analyzed.
Dr. Chaudhuri’s research team recently wrote a book exploring the numerous aspects of COVID-19 and parkinsonism, including Parkinson’s disease, said Dr. Boura.
“Moreover, the COVID-19 Clinical Neuroscience Study (COVID-CNS), with serial follow-up visits for COVID-19 patients, including imaging, is currently running in the United Kingdom with the active participation of Prof Chaudhuri’s team, aiming at revealing any potential parkinsonism cases after a COVID-19 infection,” she said.
, a multinational team of researchers reported at the International Congress of Parkinson’s Disease and Movement Disorders.
SARS-CoV-2 led to numerous discussions about a potential post–COVID-19 emergence of new-onset parkinsonism in susceptible individuals, often referred to in the literature as a “perfect storm” or a “wave” of parkinsonism, according to lead study author Iro Boura, MD.
Postviral precedence
“Although pathogens have been associated both with parkinsonism cases and Parkinson’s disease pathogenesis, the main concern of a potential connection between COVID-19 and new-onset parkinsonism arose from the historically documented parkinsonism cases appearing with encephalitis lethargica,” said Dr. Boura, a PhD candidate with the University of Crete in Greece and ex-fellow at King’s College London.
Encephalitis lethargica appeared between 1916 and 1930 and has been epidemiologically related to the Spanish influenza pandemic, “although this link has been strongly debated by other researchers,” she added.
Because the connection of COVID-19 and parkinsonism seemed highly speculative, Dr. Boura and movement disorder specialist Kallol Ray Chaudhuri DSc, FRCP, MD, decided to search for any data supporting this notion. “Such a possibility would have a significant impact on everyday practice, including long follow-up neurological assessments of COVID-19 patients, along with greater vigilance in recognizing potential symptoms,” said Dr. Boura.
They found no organized research exploring this link, aside from published case reports.
Scant evidence of a parkinsonism wave
The investigators conducted a review of the literature up to February 2022 to identify and analyze published cases of new-onset parkinsonism following a confirmed SARS-CoV-2 infection in otherwise healthy individuals. They ended up with 20 such cases.
Although some cases presented during or shortly after a COVID-19 infection, “the numbers are currently quite low to draw safe conclusions and generalize these findings as a risk of parkinsonism for the general population,” said Dr. Boura. Overall, parkinsonism appeared in the context of encephalopathy in 11 patients. Four patients developed postinfectious parkinsonism without encephalopathy. Another four had phenotypic similarities to idiopathic Parkinson’s disease.
Nine patients were responsive to levodopa, while four required immunomodulatory treatment.
Although cases have already been reported, current data do not yet justify the concept of a post–COVID-19 parkinsonism wave. However, long-term surveillance is crucial to ensure that reports of further cases are carefully documented and analyzed.
Dr. Chaudhuri’s research team recently wrote a book exploring the numerous aspects of COVID-19 and parkinsonism, including Parkinson’s disease, said Dr. Boura.
“Moreover, the COVID-19 Clinical Neuroscience Study (COVID-CNS), with serial follow-up visits for COVID-19 patients, including imaging, is currently running in the United Kingdom with the active participation of Prof Chaudhuri’s team, aiming at revealing any potential parkinsonism cases after a COVID-19 infection,” she said.
, a multinational team of researchers reported at the International Congress of Parkinson’s Disease and Movement Disorders.
SARS-CoV-2 led to numerous discussions about a potential post–COVID-19 emergence of new-onset parkinsonism in susceptible individuals, often referred to in the literature as a “perfect storm” or a “wave” of parkinsonism, according to lead study author Iro Boura, MD.
Postviral precedence
“Although pathogens have been associated both with parkinsonism cases and Parkinson’s disease pathogenesis, the main concern of a potential connection between COVID-19 and new-onset parkinsonism arose from the historically documented parkinsonism cases appearing with encephalitis lethargica,” said Dr. Boura, a PhD candidate with the University of Crete in Greece and ex-fellow at King’s College London.
Encephalitis lethargica appeared between 1916 and 1930 and has been epidemiologically related to the Spanish influenza pandemic, “although this link has been strongly debated by other researchers,” she added.
Because the connection of COVID-19 and parkinsonism seemed highly speculative, Dr. Boura and movement disorder specialist Kallol Ray Chaudhuri DSc, FRCP, MD, decided to search for any data supporting this notion. “Such a possibility would have a significant impact on everyday practice, including long follow-up neurological assessments of COVID-19 patients, along with greater vigilance in recognizing potential symptoms,” said Dr. Boura.
They found no organized research exploring this link, aside from published case reports.
Scant evidence of a parkinsonism wave
The investigators conducted a review of the literature up to February 2022 to identify and analyze published cases of new-onset parkinsonism following a confirmed SARS-CoV-2 infection in otherwise healthy individuals. They ended up with 20 such cases.
Although some cases presented during or shortly after a COVID-19 infection, “the numbers are currently quite low to draw safe conclusions and generalize these findings as a risk of parkinsonism for the general population,” said Dr. Boura. Overall, parkinsonism appeared in the context of encephalopathy in 11 patients. Four patients developed postinfectious parkinsonism without encephalopathy. Another four had phenotypic similarities to idiopathic Parkinson’s disease.
Nine patients were responsive to levodopa, while four required immunomodulatory treatment.
Although cases have already been reported, current data do not yet justify the concept of a post–COVID-19 parkinsonism wave. However, long-term surveillance is crucial to ensure that reports of further cases are carefully documented and analyzed.
Dr. Chaudhuri’s research team recently wrote a book exploring the numerous aspects of COVID-19 and parkinsonism, including Parkinson’s disease, said Dr. Boura.
“Moreover, the COVID-19 Clinical Neuroscience Study (COVID-CNS), with serial follow-up visits for COVID-19 patients, including imaging, is currently running in the United Kingdom with the active participation of Prof Chaudhuri’s team, aiming at revealing any potential parkinsonism cases after a COVID-19 infection,” she said.
FROM MDS 2022
Epidemic of brain fog? Long COVID’s effects worry experts
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,
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,
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,
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.
The truth about the ‘happy hormone’: Why we shouldn’t mess with dopamine
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 tied to improvements in Parkinson’s disease symptoms
, 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.
, 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.
, 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.
FROM MDS 2022
Sport climbing tied to improved posture in Parkinson’s disease
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.
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.
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.
FROM MDS 2022
Is vitamin B12 protective against Parkinson’s disease?
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.
FROM MDS 2022
COVID vaccination does not appear to worsen symptoms of 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.
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.
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.
FROM MDS 2022
Telehealth effective in managing patients with 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.
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.
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.
From MDS 2022
Medical cannabis appears safe for 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.
, 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.
, 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.
FROM MDS 2022