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Positive top-line results for cannabinoid-based med for nerve pain
, new top-line results released by Zelira Therapeutics suggest.
“The implications of these results for patients are incredibly promising,” principal investigator Bryan Doner, DO, medical director of HealthyWays Integrated Wellness Solutions, Gibsonia, Pa., said in a news release.
“Through this rigorously designed study, we have demonstrated that ZLT-L-007 is a safe, effective, and well-tolerated alternative for patients who would typically seek a Lyrica-level of pain relief,” he added.
The observational, nonblinded trial tested the efficacy, safety, and tolerability of ZLT-L-007 against pregabalin in 60 adults with diabetic nerve pain.
The study had three groups with 20 patients each (pregabalin alone, pregabalin plus ZLT-L-007, and ZLT-L-007 alone).
Top-line results show the study met its primary endpoint for change in daily pain severity as measured by the percent change from baseline at 30, 60, and 90 days on the Numerical Rating Scale.
For the pregabalin-only group, there was a reduction in symptom severity at all follow-up points, ranging from 20% to 35% (median percent change from baseline), the company said.
For the ZLT-L-007 only group, there was about a 33% reduction in symptom severity at 30 days, and 71% and 78% reduction, respectively, at 60 and 90 days, suggesting a larger improvement in symptom severity than with pregabalin alone, the company said.
For the pregabalin plus ZLT-L-007 group, there was a moderate 20% reduction in symptom severity at 30 days, but a larger reduction at 60 and 90 days (50% and 72%, respectively), which indicates substantially greater improvement in symptom severity than with pregabalin alone, the company said.
The study also met secondary endpoints, including significant decreases in daily pain severity as measured by the Visual Analog Scale and measurable changes in the short-form McGill Pain Questionnaire and Neuropathic Pain Symptom Inventory.
Dr. Doner noted that the top-line data showed “no serious adverse events, and participants’ blood pressure and other safety vitals remained unaffected throughout. This confirms that ZLT-L-007 is a well-tolerated product that delivers statistically significant pain relief, surpassing the levels achieved by Lyrica.”
The company plans to report additional insights from the full study, as they become available, during fiscal year 2023-2024.
A version of this article first appeared on Medscape.com.
, new top-line results released by Zelira Therapeutics suggest.
“The implications of these results for patients are incredibly promising,” principal investigator Bryan Doner, DO, medical director of HealthyWays Integrated Wellness Solutions, Gibsonia, Pa., said in a news release.
“Through this rigorously designed study, we have demonstrated that ZLT-L-007 is a safe, effective, and well-tolerated alternative for patients who would typically seek a Lyrica-level of pain relief,” he added.
The observational, nonblinded trial tested the efficacy, safety, and tolerability of ZLT-L-007 against pregabalin in 60 adults with diabetic nerve pain.
The study had three groups with 20 patients each (pregabalin alone, pregabalin plus ZLT-L-007, and ZLT-L-007 alone).
Top-line results show the study met its primary endpoint for change in daily pain severity as measured by the percent change from baseline at 30, 60, and 90 days on the Numerical Rating Scale.
For the pregabalin-only group, there was a reduction in symptom severity at all follow-up points, ranging from 20% to 35% (median percent change from baseline), the company said.
For the ZLT-L-007 only group, there was about a 33% reduction in symptom severity at 30 days, and 71% and 78% reduction, respectively, at 60 and 90 days, suggesting a larger improvement in symptom severity than with pregabalin alone, the company said.
For the pregabalin plus ZLT-L-007 group, there was a moderate 20% reduction in symptom severity at 30 days, but a larger reduction at 60 and 90 days (50% and 72%, respectively), which indicates substantially greater improvement in symptom severity than with pregabalin alone, the company said.
The study also met secondary endpoints, including significant decreases in daily pain severity as measured by the Visual Analog Scale and measurable changes in the short-form McGill Pain Questionnaire and Neuropathic Pain Symptom Inventory.
Dr. Doner noted that the top-line data showed “no serious adverse events, and participants’ blood pressure and other safety vitals remained unaffected throughout. This confirms that ZLT-L-007 is a well-tolerated product that delivers statistically significant pain relief, surpassing the levels achieved by Lyrica.”
The company plans to report additional insights from the full study, as they become available, during fiscal year 2023-2024.
A version of this article first appeared on Medscape.com.
, new top-line results released by Zelira Therapeutics suggest.
“The implications of these results for patients are incredibly promising,” principal investigator Bryan Doner, DO, medical director of HealthyWays Integrated Wellness Solutions, Gibsonia, Pa., said in a news release.
“Through this rigorously designed study, we have demonstrated that ZLT-L-007 is a safe, effective, and well-tolerated alternative for patients who would typically seek a Lyrica-level of pain relief,” he added.
The observational, nonblinded trial tested the efficacy, safety, and tolerability of ZLT-L-007 against pregabalin in 60 adults with diabetic nerve pain.
The study had three groups with 20 patients each (pregabalin alone, pregabalin plus ZLT-L-007, and ZLT-L-007 alone).
Top-line results show the study met its primary endpoint for change in daily pain severity as measured by the percent change from baseline at 30, 60, and 90 days on the Numerical Rating Scale.
For the pregabalin-only group, there was a reduction in symptom severity at all follow-up points, ranging from 20% to 35% (median percent change from baseline), the company said.
For the ZLT-L-007 only group, there was about a 33% reduction in symptom severity at 30 days, and 71% and 78% reduction, respectively, at 60 and 90 days, suggesting a larger improvement in symptom severity than with pregabalin alone, the company said.
For the pregabalin plus ZLT-L-007 group, there was a moderate 20% reduction in symptom severity at 30 days, but a larger reduction at 60 and 90 days (50% and 72%, respectively), which indicates substantially greater improvement in symptom severity than with pregabalin alone, the company said.
The study also met secondary endpoints, including significant decreases in daily pain severity as measured by the Visual Analog Scale and measurable changes in the short-form McGill Pain Questionnaire and Neuropathic Pain Symptom Inventory.
Dr. Doner noted that the top-line data showed “no serious adverse events, and participants’ blood pressure and other safety vitals remained unaffected throughout. This confirms that ZLT-L-007 is a well-tolerated product that delivers statistically significant pain relief, surpassing the levels achieved by Lyrica.”
The company plans to report additional insights from the full study, as they become available, during fiscal year 2023-2024.
A version of this article first appeared on Medscape.com.
Ancient plague, cyclical pandemics … history lesson?
Even the plague wanted to visit Stonehenge
We’re about to blow your mind: The history you learned in school was often inaccurate. Shocking, we know, so we’ll give you a minute to process this incredible news.
Better? Good. Now, let’s look back at high school European history. The Black Death, specifically. The common narrative is that the Mongols, while besieging a Crimean city belonging to the Genoese, catapulted dead bodies infected with some mystery disease that turned out to be the plague. The Genoese then brought the plague back to Italy, and from there, we all know the rest of the story.
The Black Death was certainly extremely important to the development of modern Europe as we know it, but the history books gloss over the much longer history of the plague. Yersinia pestis did not suddenly appear unbidden in a Mongol war camp in 1347. The Black Death wasn’t even the first horrific, continent-wide pandemic caused by the plague; the Plague of Justinian 800 years earlier crippled the Byzantine Empire during an expansionist phase and killed anywhere between 15 million and 100 million.
Today, though, LOTME looks even deeper into history, nearly beyond even history itself, back into the depths of early Bronze Age northern Europe. Specifically, to two ancient burial sites in England, where researchers have identified three 4,000-year-old cases of Y. pestis, the first recorded incidence of the disease in Britain.
Two of the individuals, identified through analysis of dental pulp, were young children buried at a mass grave in Somerset, while the third, a middle-aged woman, was found in a ring cairn in Cumbria. These sites are hundreds of miles apart, yet carbon dating suggests all three people lived and died at roughly the same time. The strain found is very similar to other samples of plague found across central and western Europe starting around 3,000 BCE, suggesting a single, easily spread disease affecting a large area in a relatively small period of time. In other words, a pandemic. Even in these ancient times, the world was connected. Not even the island of Britain could escape.
Beyond that though, the research helps confirm the cyclical nature of the plague; over time, it loses its effectiveness and goes into hiding, only to mutate and come roaring back. This is a story with absolutely no relevance at all to the modern world. Nope, no plagues or pandemics going around right now, no viruses fading into the background in any way. What a ridiculous inference to make.
Uncovering the invisible with artificial intelligence
This week in “What Else Can AI Do?” new research shows that a computer program can reveal brain injury that couldn’t be seen before with typical MRI.
The hot new AI, birthed by researchers at New York University, could potentially be a game changer by linking repeated head impacts with tiny, structural changes in the brains of athletes who have not been diagnosed with a concussion. By using machine learning to train the AI, the researchers were, for the first time, able to distinguish the brain of athletes who played contact sports (football, soccer, lacrosse) from those participating in noncontact sports such as baseball, basketball, and cross-country.
How did they do it? The investigators “designed statistical techniques that gave their computer program the ability to ‘learn’ how to predict exposure to repeated head impacts using mathematical models,” they explained in a written statement. Adding in data from the MRI scans of 81 male athletes with no known concussion diagnosis and the ability to identify unusual brain features between athletes with and without head trauma allowed the AI to predict results with accuracy even Miss Cleo would envy.
“This method may provide an important diagnostic tool not only for concussion, but also for detecting the damage that stems from subtler and more frequent head impacts,” said lead author Junbo Chen, an engineering doctoral candidate at NYU. That could make this new AI a valuable asset to science and medicine.
There are many things the human brain can do that AI can’t, and delegation could be one of them. Examining the data that represent the human brain in minute detail? Maybe we leave that to the machine.
Talk about your field promotions
If you’re a surgeon doing an amputation, the list of possible assistants pretty much starts and ends in only one place: Not the closest available janitor.
That may seem like an oddly obvious thing for us to say, but there’s at least one former Mainz (Germany) University Hospital physician who really needed to get this bit of advice before he attempted an unassisted toe amputation back in October of 2020. Yes, that does seem like kind of a long time ago for us to be reporting it now, but the details of the incident only just came to light a few days ago, thanks to German public broadcaster SWR.
Since it was just a toe, the surgeon thought he could perform the operation without any help. The toe, unfortunately, had other plans. The partially anesthetized patient got restless in the operating room, but with no actual trained nurse in the vicinity, the surgeon asked the closest available person – that would be the janitor – to lend a hand.
The surgical manager heard about these goings-on and got to the operating room too late to stop the procedure but soon enough to see the cleaning staffer “at the operating table with a bloody suction cup and a bloody compress in their hands,” SWR recently reported.
The incident was reported to the hospital’s medical director and the surgeon was fired, but since the patient experienced no complications not much fuss was made about it at the time.
Well, guess what? It’s toe-tally our job to make a fuss about these kinds of things. Or could it be that our job, much like the surgeon’s employment and the patient’s digit, is here toe-day and gone toe-morrow?
Even the plague wanted to visit Stonehenge
We’re about to blow your mind: The history you learned in school was often inaccurate. Shocking, we know, so we’ll give you a minute to process this incredible news.
Better? Good. Now, let’s look back at high school European history. The Black Death, specifically. The common narrative is that the Mongols, while besieging a Crimean city belonging to the Genoese, catapulted dead bodies infected with some mystery disease that turned out to be the plague. The Genoese then brought the plague back to Italy, and from there, we all know the rest of the story.
The Black Death was certainly extremely important to the development of modern Europe as we know it, but the history books gloss over the much longer history of the plague. Yersinia pestis did not suddenly appear unbidden in a Mongol war camp in 1347. The Black Death wasn’t even the first horrific, continent-wide pandemic caused by the plague; the Plague of Justinian 800 years earlier crippled the Byzantine Empire during an expansionist phase and killed anywhere between 15 million and 100 million.
Today, though, LOTME looks even deeper into history, nearly beyond even history itself, back into the depths of early Bronze Age northern Europe. Specifically, to two ancient burial sites in England, where researchers have identified three 4,000-year-old cases of Y. pestis, the first recorded incidence of the disease in Britain.
Two of the individuals, identified through analysis of dental pulp, were young children buried at a mass grave in Somerset, while the third, a middle-aged woman, was found in a ring cairn in Cumbria. These sites are hundreds of miles apart, yet carbon dating suggests all three people lived and died at roughly the same time. The strain found is very similar to other samples of plague found across central and western Europe starting around 3,000 BCE, suggesting a single, easily spread disease affecting a large area in a relatively small period of time. In other words, a pandemic. Even in these ancient times, the world was connected. Not even the island of Britain could escape.
Beyond that though, the research helps confirm the cyclical nature of the plague; over time, it loses its effectiveness and goes into hiding, only to mutate and come roaring back. This is a story with absolutely no relevance at all to the modern world. Nope, no plagues or pandemics going around right now, no viruses fading into the background in any way. What a ridiculous inference to make.
Uncovering the invisible with artificial intelligence
This week in “What Else Can AI Do?” new research shows that a computer program can reveal brain injury that couldn’t be seen before with typical MRI.
The hot new AI, birthed by researchers at New York University, could potentially be a game changer by linking repeated head impacts with tiny, structural changes in the brains of athletes who have not been diagnosed with a concussion. By using machine learning to train the AI, the researchers were, for the first time, able to distinguish the brain of athletes who played contact sports (football, soccer, lacrosse) from those participating in noncontact sports such as baseball, basketball, and cross-country.
How did they do it? The investigators “designed statistical techniques that gave their computer program the ability to ‘learn’ how to predict exposure to repeated head impacts using mathematical models,” they explained in a written statement. Adding in data from the MRI scans of 81 male athletes with no known concussion diagnosis and the ability to identify unusual brain features between athletes with and without head trauma allowed the AI to predict results with accuracy even Miss Cleo would envy.
“This method may provide an important diagnostic tool not only for concussion, but also for detecting the damage that stems from subtler and more frequent head impacts,” said lead author Junbo Chen, an engineering doctoral candidate at NYU. That could make this new AI a valuable asset to science and medicine.
There are many things the human brain can do that AI can’t, and delegation could be one of them. Examining the data that represent the human brain in minute detail? Maybe we leave that to the machine.
Talk about your field promotions
If you’re a surgeon doing an amputation, the list of possible assistants pretty much starts and ends in only one place: Not the closest available janitor.
That may seem like an oddly obvious thing for us to say, but there’s at least one former Mainz (Germany) University Hospital physician who really needed to get this bit of advice before he attempted an unassisted toe amputation back in October of 2020. Yes, that does seem like kind of a long time ago for us to be reporting it now, but the details of the incident only just came to light a few days ago, thanks to German public broadcaster SWR.
Since it was just a toe, the surgeon thought he could perform the operation without any help. The toe, unfortunately, had other plans. The partially anesthetized patient got restless in the operating room, but with no actual trained nurse in the vicinity, the surgeon asked the closest available person – that would be the janitor – to lend a hand.
The surgical manager heard about these goings-on and got to the operating room too late to stop the procedure but soon enough to see the cleaning staffer “at the operating table with a bloody suction cup and a bloody compress in their hands,” SWR recently reported.
The incident was reported to the hospital’s medical director and the surgeon was fired, but since the patient experienced no complications not much fuss was made about it at the time.
Well, guess what? It’s toe-tally our job to make a fuss about these kinds of things. Or could it be that our job, much like the surgeon’s employment and the patient’s digit, is here toe-day and gone toe-morrow?
Even the plague wanted to visit Stonehenge
We’re about to blow your mind: The history you learned in school was often inaccurate. Shocking, we know, so we’ll give you a minute to process this incredible news.
Better? Good. Now, let’s look back at high school European history. The Black Death, specifically. The common narrative is that the Mongols, while besieging a Crimean city belonging to the Genoese, catapulted dead bodies infected with some mystery disease that turned out to be the plague. The Genoese then brought the plague back to Italy, and from there, we all know the rest of the story.
The Black Death was certainly extremely important to the development of modern Europe as we know it, but the history books gloss over the much longer history of the plague. Yersinia pestis did not suddenly appear unbidden in a Mongol war camp in 1347. The Black Death wasn’t even the first horrific, continent-wide pandemic caused by the plague; the Plague of Justinian 800 years earlier crippled the Byzantine Empire during an expansionist phase and killed anywhere between 15 million and 100 million.
Today, though, LOTME looks even deeper into history, nearly beyond even history itself, back into the depths of early Bronze Age northern Europe. Specifically, to two ancient burial sites in England, where researchers have identified three 4,000-year-old cases of Y. pestis, the first recorded incidence of the disease in Britain.
Two of the individuals, identified through analysis of dental pulp, were young children buried at a mass grave in Somerset, while the third, a middle-aged woman, was found in a ring cairn in Cumbria. These sites are hundreds of miles apart, yet carbon dating suggests all three people lived and died at roughly the same time. The strain found is very similar to other samples of plague found across central and western Europe starting around 3,000 BCE, suggesting a single, easily spread disease affecting a large area in a relatively small period of time. In other words, a pandemic. Even in these ancient times, the world was connected. Not even the island of Britain could escape.
Beyond that though, the research helps confirm the cyclical nature of the plague; over time, it loses its effectiveness and goes into hiding, only to mutate and come roaring back. This is a story with absolutely no relevance at all to the modern world. Nope, no plagues or pandemics going around right now, no viruses fading into the background in any way. What a ridiculous inference to make.
Uncovering the invisible with artificial intelligence
This week in “What Else Can AI Do?” new research shows that a computer program can reveal brain injury that couldn’t be seen before with typical MRI.
The hot new AI, birthed by researchers at New York University, could potentially be a game changer by linking repeated head impacts with tiny, structural changes in the brains of athletes who have not been diagnosed with a concussion. By using machine learning to train the AI, the researchers were, for the first time, able to distinguish the brain of athletes who played contact sports (football, soccer, lacrosse) from those participating in noncontact sports such as baseball, basketball, and cross-country.
How did they do it? The investigators “designed statistical techniques that gave their computer program the ability to ‘learn’ how to predict exposure to repeated head impacts using mathematical models,” they explained in a written statement. Adding in data from the MRI scans of 81 male athletes with no known concussion diagnosis and the ability to identify unusual brain features between athletes with and without head trauma allowed the AI to predict results with accuracy even Miss Cleo would envy.
“This method may provide an important diagnostic tool not only for concussion, but also for detecting the damage that stems from subtler and more frequent head impacts,” said lead author Junbo Chen, an engineering doctoral candidate at NYU. That could make this new AI a valuable asset to science and medicine.
There are many things the human brain can do that AI can’t, and delegation could be one of them. Examining the data that represent the human brain in minute detail? Maybe we leave that to the machine.
Talk about your field promotions
If you’re a surgeon doing an amputation, the list of possible assistants pretty much starts and ends in only one place: Not the closest available janitor.
That may seem like an oddly obvious thing for us to say, but there’s at least one former Mainz (Germany) University Hospital physician who really needed to get this bit of advice before he attempted an unassisted toe amputation back in October of 2020. Yes, that does seem like kind of a long time ago for us to be reporting it now, but the details of the incident only just came to light a few days ago, thanks to German public broadcaster SWR.
Since it was just a toe, the surgeon thought he could perform the operation without any help. The toe, unfortunately, had other plans. The partially anesthetized patient got restless in the operating room, but with no actual trained nurse in the vicinity, the surgeon asked the closest available person – that would be the janitor – to lend a hand.
The surgical manager heard about these goings-on and got to the operating room too late to stop the procedure but soon enough to see the cleaning staffer “at the operating table with a bloody suction cup and a bloody compress in their hands,” SWR recently reported.
The incident was reported to the hospital’s medical director and the surgeon was fired, but since the patient experienced no complications not much fuss was made about it at the time.
Well, guess what? It’s toe-tally our job to make a fuss about these kinds of things. Or could it be that our job, much like the surgeon’s employment and the patient’s digit, is here toe-day and gone toe-morrow?
Researchers discover brain abnormalities in babies who had SIDS
For decades, researchers have been trying to understand why some otherwise healthy babies under 1 year old mysteriously die during their sleep. SIDS is the leading cause of infant death in the U.S., affecting 103 out of every 100,000 babies.
The new study found that babies who died of SIDS had abnormalities in certain brain receptors responsible for waking and restoring breathing. The scientists decided to look at the babies’ brains at the molecular level because previous research showed that the same kind of brain receptors in rodents are responsible for protective breathing functions during sleep.
The study was published in the Journal of Neuropathology & Experimental Neurology. The researchers compared brain stems from 70 babies, some of whom died of SIDS and some who died of other causes.
Despite discovering the differences in the babies’ brains, the lead author of the paper said more study is needed.
Robin Haynes, PhD, who studies SIDS at Boston Children’s Hospital, said in a statement that “the relationship between the abnormalities and cause of death remains unknown.”
She said there is no way to identify babies with the brain abnormalities, and “thus, adherence to safe-sleep practices remains critical.”
The American Academy of Pediatrics recommends numerous steps for creating a safe sleeping environment for babies, including placing babies on their backs on a firm surface. Education campaigns targeting parents and caregivers in the 1990s are largely considered successful, but SIDS rates have remained steady since the practices became widely used.
A version of this article first appeared on WebMD.com.
For decades, researchers have been trying to understand why some otherwise healthy babies under 1 year old mysteriously die during their sleep. SIDS is the leading cause of infant death in the U.S., affecting 103 out of every 100,000 babies.
The new study found that babies who died of SIDS had abnormalities in certain brain receptors responsible for waking and restoring breathing. The scientists decided to look at the babies’ brains at the molecular level because previous research showed that the same kind of brain receptors in rodents are responsible for protective breathing functions during sleep.
The study was published in the Journal of Neuropathology & Experimental Neurology. The researchers compared brain stems from 70 babies, some of whom died of SIDS and some who died of other causes.
Despite discovering the differences in the babies’ brains, the lead author of the paper said more study is needed.
Robin Haynes, PhD, who studies SIDS at Boston Children’s Hospital, said in a statement that “the relationship between the abnormalities and cause of death remains unknown.”
She said there is no way to identify babies with the brain abnormalities, and “thus, adherence to safe-sleep practices remains critical.”
The American Academy of Pediatrics recommends numerous steps for creating a safe sleeping environment for babies, including placing babies on their backs on a firm surface. Education campaigns targeting parents and caregivers in the 1990s are largely considered successful, but SIDS rates have remained steady since the practices became widely used.
A version of this article first appeared on WebMD.com.
For decades, researchers have been trying to understand why some otherwise healthy babies under 1 year old mysteriously die during their sleep. SIDS is the leading cause of infant death in the U.S., affecting 103 out of every 100,000 babies.
The new study found that babies who died of SIDS had abnormalities in certain brain receptors responsible for waking and restoring breathing. The scientists decided to look at the babies’ brains at the molecular level because previous research showed that the same kind of brain receptors in rodents are responsible for protective breathing functions during sleep.
The study was published in the Journal of Neuropathology & Experimental Neurology. The researchers compared brain stems from 70 babies, some of whom died of SIDS and some who died of other causes.
Despite discovering the differences in the babies’ brains, the lead author of the paper said more study is needed.
Robin Haynes, PhD, who studies SIDS at Boston Children’s Hospital, said in a statement that “the relationship between the abnormalities and cause of death remains unknown.”
She said there is no way to identify babies with the brain abnormalities, and “thus, adherence to safe-sleep practices remains critical.”
The American Academy of Pediatrics recommends numerous steps for creating a safe sleeping environment for babies, including placing babies on their backs on a firm surface. Education campaigns targeting parents and caregivers in the 1990s are largely considered successful, but SIDS rates have remained steady since the practices became widely used.
A version of this article first appeared on WebMD.com.
FROM THE JOURNAL OF NEUROPATHY & EXPERIMENTAL NEUROLOGY
Younger age of type 2 diabetes onset linked to dementia risk
, new findings suggest.
Moreover, the new data from the prospective Atherosclerosis Risk in Communities (ARIC) cohort also suggest that the previously identified increased risk for dementia among people with prediabetes appears to be entirely explained by the subset who go on to develop type 2 diabetes.
“Our findings suggest that preventing prediabetes progression, especially in younger individuals, may be an important way to reduce the dementia burden,” wrote PhD student Jiaqi Hu of Johns Hopkins University, Baltimore, and colleagues. Their article was published online in Diabetologia.
The result builds on previous findings linking dysglycemia and cognitive decline, the study’s lead author, Elizabeth Selvin, PhD, of the Bloomberg School of Public Health at Johns Hopkins, said in an interview.
“Our prior work in the ARIC study suggests that improving glucose control could help prevent dementia in later life,” she said.
Other studies have also linked higher A1c levels and diabetes in midlife to increased rates of cognitive decline. In addition, Dr. Selvin noted, “There is growing evidence that focusing on vascular health, especially focusing on diabetes and blood pressure, in midlife can stave off dementia in later life.”
This new study is the first to examine the effect of diabetes in the relationship between prediabetes and dementia, as well as the age of diabetes onset on subsequent dementia.
Prediabetes linked to dementia via diabetes development
Of the 11,656 ARIC participants without diabetes at baseline during 1990-1992 (age 46-70 years), 20.0% had prediabetes (defined as A1c 5.7%-6.4% or 39-46 mmol/mol). During a median follow-up of 15.9 years, 3,143 participants developed diabetes. The proportions of patients who developed diabetes were 44.6% among those with prediabetes at baseline versus 22.5% of those without.
Dementia developed in 2,247 participants over a median follow-up of 24.7 years. The cumulative incidence of dementia was 23.9% among those who developed diabetes versus 20.5% among those who did not.
After adjustment for demographics and for the Alzheimer’s disease–linked apolipoprotein E (APOE) gene, prediabetes was significantly associated with incident dementia (hazard ratio [HR], 1.19). However, significance disappeared after adjustment for incident diabetes (HR, 1.09), the researchers reported.
Younger age at diabetes diagnosis raises dementia risk
Age at diabetes diagnosis made a difference in dementia risk. With adjustments for lifestyle, demographic, and clinical factors, those diagnosed with diabetes before age 60 years had a nearly threefold increased risk for dementia compared with those who never developed diabetes (HR, 2.92; P < .001).
The dementia risk was also significantly increased, although to a lesser degree, among those aged 60-69 years at diabetes diagnosis (HR, 1.73; P < .001) and age 70-79 years at diabetes diagnosis (HR, 1.23; P < .001). The relationship was not significant for those aged 80 years and older (HR, 1.13).
“Prevention efforts in people with diabetes diagnosed younger than 65 years should be a high priority,” the authors urged.
Taken together, the data suggest that prolonged exposure to hyperglycemia plays a major role in dementia development.
“Putative mechanisms include acute and chronic hyperglycemia, glucose toxicity, insulin resistance, and microvascular dysfunction of the central nervous system. ... Glucose toxicity and microvascular dysfunction are associated with increased inflammatory and oxidative stress, leading to increased blood–brain permeability,” the researchers wrote.
Dr. Selvin said that her group is pursuing further work in this area using continuous glucose monitoring. “We plan to look at ... how glycemic control and different patterns of glucose in older adults may be linked to cognitive decline and other neurocognitive outcomes.”
The researchers reported no relevant financial relationships. Dr. Selvin has reported being on the advisory board for Diabetologia; she had no role in peer review of the manuscript.
A version of this article first appeared on Medscape.com.
, new findings suggest.
Moreover, the new data from the prospective Atherosclerosis Risk in Communities (ARIC) cohort also suggest that the previously identified increased risk for dementia among people with prediabetes appears to be entirely explained by the subset who go on to develop type 2 diabetes.
“Our findings suggest that preventing prediabetes progression, especially in younger individuals, may be an important way to reduce the dementia burden,” wrote PhD student Jiaqi Hu of Johns Hopkins University, Baltimore, and colleagues. Their article was published online in Diabetologia.
The result builds on previous findings linking dysglycemia and cognitive decline, the study’s lead author, Elizabeth Selvin, PhD, of the Bloomberg School of Public Health at Johns Hopkins, said in an interview.
“Our prior work in the ARIC study suggests that improving glucose control could help prevent dementia in later life,” she said.
Other studies have also linked higher A1c levels and diabetes in midlife to increased rates of cognitive decline. In addition, Dr. Selvin noted, “There is growing evidence that focusing on vascular health, especially focusing on diabetes and blood pressure, in midlife can stave off dementia in later life.”
This new study is the first to examine the effect of diabetes in the relationship between prediabetes and dementia, as well as the age of diabetes onset on subsequent dementia.
Prediabetes linked to dementia via diabetes development
Of the 11,656 ARIC participants without diabetes at baseline during 1990-1992 (age 46-70 years), 20.0% had prediabetes (defined as A1c 5.7%-6.4% or 39-46 mmol/mol). During a median follow-up of 15.9 years, 3,143 participants developed diabetes. The proportions of patients who developed diabetes were 44.6% among those with prediabetes at baseline versus 22.5% of those without.
Dementia developed in 2,247 participants over a median follow-up of 24.7 years. The cumulative incidence of dementia was 23.9% among those who developed diabetes versus 20.5% among those who did not.
After adjustment for demographics and for the Alzheimer’s disease–linked apolipoprotein E (APOE) gene, prediabetes was significantly associated with incident dementia (hazard ratio [HR], 1.19). However, significance disappeared after adjustment for incident diabetes (HR, 1.09), the researchers reported.
Younger age at diabetes diagnosis raises dementia risk
Age at diabetes diagnosis made a difference in dementia risk. With adjustments for lifestyle, demographic, and clinical factors, those diagnosed with diabetes before age 60 years had a nearly threefold increased risk for dementia compared with those who never developed diabetes (HR, 2.92; P < .001).
The dementia risk was also significantly increased, although to a lesser degree, among those aged 60-69 years at diabetes diagnosis (HR, 1.73; P < .001) and age 70-79 years at diabetes diagnosis (HR, 1.23; P < .001). The relationship was not significant for those aged 80 years and older (HR, 1.13).
“Prevention efforts in people with diabetes diagnosed younger than 65 years should be a high priority,” the authors urged.
Taken together, the data suggest that prolonged exposure to hyperglycemia plays a major role in dementia development.
“Putative mechanisms include acute and chronic hyperglycemia, glucose toxicity, insulin resistance, and microvascular dysfunction of the central nervous system. ... Glucose toxicity and microvascular dysfunction are associated with increased inflammatory and oxidative stress, leading to increased blood–brain permeability,” the researchers wrote.
Dr. Selvin said that her group is pursuing further work in this area using continuous glucose monitoring. “We plan to look at ... how glycemic control and different patterns of glucose in older adults may be linked to cognitive decline and other neurocognitive outcomes.”
The researchers reported no relevant financial relationships. Dr. Selvin has reported being on the advisory board for Diabetologia; she had no role in peer review of the manuscript.
A version of this article first appeared on Medscape.com.
, new findings suggest.
Moreover, the new data from the prospective Atherosclerosis Risk in Communities (ARIC) cohort also suggest that the previously identified increased risk for dementia among people with prediabetes appears to be entirely explained by the subset who go on to develop type 2 diabetes.
“Our findings suggest that preventing prediabetes progression, especially in younger individuals, may be an important way to reduce the dementia burden,” wrote PhD student Jiaqi Hu of Johns Hopkins University, Baltimore, and colleagues. Their article was published online in Diabetologia.
The result builds on previous findings linking dysglycemia and cognitive decline, the study’s lead author, Elizabeth Selvin, PhD, of the Bloomberg School of Public Health at Johns Hopkins, said in an interview.
“Our prior work in the ARIC study suggests that improving glucose control could help prevent dementia in later life,” she said.
Other studies have also linked higher A1c levels and diabetes in midlife to increased rates of cognitive decline. In addition, Dr. Selvin noted, “There is growing evidence that focusing on vascular health, especially focusing on diabetes and blood pressure, in midlife can stave off dementia in later life.”
This new study is the first to examine the effect of diabetes in the relationship between prediabetes and dementia, as well as the age of diabetes onset on subsequent dementia.
Prediabetes linked to dementia via diabetes development
Of the 11,656 ARIC participants without diabetes at baseline during 1990-1992 (age 46-70 years), 20.0% had prediabetes (defined as A1c 5.7%-6.4% or 39-46 mmol/mol). During a median follow-up of 15.9 years, 3,143 participants developed diabetes. The proportions of patients who developed diabetes were 44.6% among those with prediabetes at baseline versus 22.5% of those without.
Dementia developed in 2,247 participants over a median follow-up of 24.7 years. The cumulative incidence of dementia was 23.9% among those who developed diabetes versus 20.5% among those who did not.
After adjustment for demographics and for the Alzheimer’s disease–linked apolipoprotein E (APOE) gene, prediabetes was significantly associated with incident dementia (hazard ratio [HR], 1.19). However, significance disappeared after adjustment for incident diabetes (HR, 1.09), the researchers reported.
Younger age at diabetes diagnosis raises dementia risk
Age at diabetes diagnosis made a difference in dementia risk. With adjustments for lifestyle, demographic, and clinical factors, those diagnosed with diabetes before age 60 years had a nearly threefold increased risk for dementia compared with those who never developed diabetes (HR, 2.92; P < .001).
The dementia risk was also significantly increased, although to a lesser degree, among those aged 60-69 years at diabetes diagnosis (HR, 1.73; P < .001) and age 70-79 years at diabetes diagnosis (HR, 1.23; P < .001). The relationship was not significant for those aged 80 years and older (HR, 1.13).
“Prevention efforts in people with diabetes diagnosed younger than 65 years should be a high priority,” the authors urged.
Taken together, the data suggest that prolonged exposure to hyperglycemia plays a major role in dementia development.
“Putative mechanisms include acute and chronic hyperglycemia, glucose toxicity, insulin resistance, and microvascular dysfunction of the central nervous system. ... Glucose toxicity and microvascular dysfunction are associated with increased inflammatory and oxidative stress, leading to increased blood–brain permeability,” the researchers wrote.
Dr. Selvin said that her group is pursuing further work in this area using continuous glucose monitoring. “We plan to look at ... how glycemic control and different patterns of glucose in older adults may be linked to cognitive decline and other neurocognitive outcomes.”
The researchers reported no relevant financial relationships. Dr. Selvin has reported being on the advisory board for Diabetologia; she had no role in peer review of the manuscript.
A version of this article first appeared on Medscape.com.
FROM DIABETOLOGIA
People still want their medical intelligence in human form
Doctors or AI? Lukewarm vote of confidence goes to …
Well, we’ve got some good news for the physicians out there, and we’ve got some bad news. Which do you want first? Okay, we’re mostly hearing good news, so here goes: Most people would choose a human doctor over artificial intelligence for the diagnosis and treatment of their medical conditions.
And the bad news? In the survey we’re talking about, “most” was 53%, so not exactly a huge victory for the carbon-based life forms. Yup, about 47% of the 2,472 respondents said they would prefer an AI-based clinic over a human specialist, and that number went up if individuals were told that their primary care physicians were on board with AI, “or otherwise nudged to consider AI as good,” the research team said in a written statement released by the University of Arizona, Tucson.
They went on to add that “this signaled the significance of the human physician in guiding a patient’s decision.” So patients will still need their doctors in the future to … um … this is a bit awkward … tell them how good the AI is?
And yes, we know that ChatGPT is already doing the same thing to journalists, but could it write a medical-humor column? Not a chance. Probably can’t even tell a joke.
How do ghosts get rid of wrinkles? Boo-tox. There, let’s see ChatGPT do that.
Explaining the joke makes it funnier, right?
Here at LOTME headquarters, we live by one simple rule, passed down directly from the Buddha himself: “Never let a good presurgical assessment of refractory epilepsy go to waste. Also, don’t believe everything you read on the Internet.”
This human-created joke has been brought to you by the leading theory of humor, which states that comedy stems from our brain reacting to an incongruous part of reality in a positive way. These positive emotions light up our neurons in a specific fashion, and boom, comedy is achieved.
Previous studies into the science of comedy have typically used functional MRI to analyze the brain while it was gripped in the throes of a comedic reaction. Unfortunately, fMRI cannot detect the entirety of the electromagnetic spectrum generated by the brain during these moments, so observing scientists have been, quite literally, missing out on some of the joke. And that’s where a new study from France comes in.
In the study, the researchers showed a group of patients with epilepsy who were hooked up to deep brain electrodes and a high-tech neuroimaging machine – part of the aforementioned presurgical assessment – a 3-minute excerpt from a Charlie Chaplin movie and analyzed their brain activity. Why Charlie Chaplin? Simple. Slapstick is perhaps the most accessible form of comedy across cultures. We can all appreciate a man getting hit in the head with a coconut. The world’s oldest bar joke or whatever this is? Not so much.
During the funniest scenes, all study participants showed increased high-frequency gamma waves (indicating high cognitive engagement) and a decrease in low-frequency waves (indicating reduced inattention and introspection). During unfunny scenes, such as transition moments, the opposite occurred. Importantly, this inverse relationship occurred in the temporal lobe but not in other regions, supporting previous research that indicated humor was mainly processed in the temporal lobe.
The investigators suggested future research should focus on longer videos with more complex forms of comedy, such as jokes, irony, sarcasm, or reference humor. So, uh, a guy getting hit in the head with two coconuts? That’s high-brow stuff right there.
Hot take: Humans aren’t that special
We humans have always prided ourselves on being different from “the animals” in an exceptional way. News flash! We aren’t. We may be the apex predator, but new research shows that humans, as part of the animal kingdom, just aren’t special.
Not special? How can they say that? Are gorillas doing open-heart surgery? Do wolverines tell jokes? At a more basic level, though, the way we operate as mammals in societies is not unique or even new. Elephants are known to mourn their deceased and to have funeral-like practices, ants invented agriculture, and we’re certainly not the only species that has figured out how to use tools.
This new research just demonstrates another way we aren’t exceptional, and that’s in our mating practices and outcomes.
“Humans appear to resemble mammals that live in monogamous partnerships and to some extent, those classified as cooperative breeders, where breeding individuals have to rely on the help of others to raise their offspring,” Monique Borgerhoff Mulder, PhD, professor emerita of anthropology at the University of California, Davis, said in a written statement.
The research team, which consisted of over 100 investigators, looked at 90 human populations based on data from over 80,000 people globally and compared the human data with 49 different nonhuman mammal species. In polygynous societies in which men take several wives, they found, women have more access to resources like food, shelter, and parenting help. Monogamy, on the other hand, “can drive significant inequalities among women,” Dr. Borgerhoff Mulder said, by promoting large differences in the number of children couples produce.
Human day-to-day behavior and child-rearing habits – one parent taking a daughter to ballet class and fixing dinner so the other parent can get to exercise class before picking up the son from soccer practice – may have us thinking that we are part of an evolved society, but really we are not much different than other mammals that hunt, forage for food, and rear and teach their children, the researchers suggested.
So, yes, humans can travel to the moon, create a vaccine for smallpox, and hit other humans with coconuts, but when it comes to simply having offspring or raising them, we’re not all that special. Get over it.
Doctors or AI? Lukewarm vote of confidence goes to …
Well, we’ve got some good news for the physicians out there, and we’ve got some bad news. Which do you want first? Okay, we’re mostly hearing good news, so here goes: Most people would choose a human doctor over artificial intelligence for the diagnosis and treatment of their medical conditions.
And the bad news? In the survey we’re talking about, “most” was 53%, so not exactly a huge victory for the carbon-based life forms. Yup, about 47% of the 2,472 respondents said they would prefer an AI-based clinic over a human specialist, and that number went up if individuals were told that their primary care physicians were on board with AI, “or otherwise nudged to consider AI as good,” the research team said in a written statement released by the University of Arizona, Tucson.
They went on to add that “this signaled the significance of the human physician in guiding a patient’s decision.” So patients will still need their doctors in the future to … um … this is a bit awkward … tell them how good the AI is?
And yes, we know that ChatGPT is already doing the same thing to journalists, but could it write a medical-humor column? Not a chance. Probably can’t even tell a joke.
How do ghosts get rid of wrinkles? Boo-tox. There, let’s see ChatGPT do that.
Explaining the joke makes it funnier, right?
Here at LOTME headquarters, we live by one simple rule, passed down directly from the Buddha himself: “Never let a good presurgical assessment of refractory epilepsy go to waste. Also, don’t believe everything you read on the Internet.”
This human-created joke has been brought to you by the leading theory of humor, which states that comedy stems from our brain reacting to an incongruous part of reality in a positive way. These positive emotions light up our neurons in a specific fashion, and boom, comedy is achieved.
Previous studies into the science of comedy have typically used functional MRI to analyze the brain while it was gripped in the throes of a comedic reaction. Unfortunately, fMRI cannot detect the entirety of the electromagnetic spectrum generated by the brain during these moments, so observing scientists have been, quite literally, missing out on some of the joke. And that’s where a new study from France comes in.
In the study, the researchers showed a group of patients with epilepsy who were hooked up to deep brain electrodes and a high-tech neuroimaging machine – part of the aforementioned presurgical assessment – a 3-minute excerpt from a Charlie Chaplin movie and analyzed their brain activity. Why Charlie Chaplin? Simple. Slapstick is perhaps the most accessible form of comedy across cultures. We can all appreciate a man getting hit in the head with a coconut. The world’s oldest bar joke or whatever this is? Not so much.
During the funniest scenes, all study participants showed increased high-frequency gamma waves (indicating high cognitive engagement) and a decrease in low-frequency waves (indicating reduced inattention and introspection). During unfunny scenes, such as transition moments, the opposite occurred. Importantly, this inverse relationship occurred in the temporal lobe but not in other regions, supporting previous research that indicated humor was mainly processed in the temporal lobe.
The investigators suggested future research should focus on longer videos with more complex forms of comedy, such as jokes, irony, sarcasm, or reference humor. So, uh, a guy getting hit in the head with two coconuts? That’s high-brow stuff right there.
Hot take: Humans aren’t that special
We humans have always prided ourselves on being different from “the animals” in an exceptional way. News flash! We aren’t. We may be the apex predator, but new research shows that humans, as part of the animal kingdom, just aren’t special.
Not special? How can they say that? Are gorillas doing open-heart surgery? Do wolverines tell jokes? At a more basic level, though, the way we operate as mammals in societies is not unique or even new. Elephants are known to mourn their deceased and to have funeral-like practices, ants invented agriculture, and we’re certainly not the only species that has figured out how to use tools.
This new research just demonstrates another way we aren’t exceptional, and that’s in our mating practices and outcomes.
“Humans appear to resemble mammals that live in monogamous partnerships and to some extent, those classified as cooperative breeders, where breeding individuals have to rely on the help of others to raise their offspring,” Monique Borgerhoff Mulder, PhD, professor emerita of anthropology at the University of California, Davis, said in a written statement.
The research team, which consisted of over 100 investigators, looked at 90 human populations based on data from over 80,000 people globally and compared the human data with 49 different nonhuman mammal species. In polygynous societies in which men take several wives, they found, women have more access to resources like food, shelter, and parenting help. Monogamy, on the other hand, “can drive significant inequalities among women,” Dr. Borgerhoff Mulder said, by promoting large differences in the number of children couples produce.
Human day-to-day behavior and child-rearing habits – one parent taking a daughter to ballet class and fixing dinner so the other parent can get to exercise class before picking up the son from soccer practice – may have us thinking that we are part of an evolved society, but really we are not much different than other mammals that hunt, forage for food, and rear and teach their children, the researchers suggested.
So, yes, humans can travel to the moon, create a vaccine for smallpox, and hit other humans with coconuts, but when it comes to simply having offspring or raising them, we’re not all that special. Get over it.
Doctors or AI? Lukewarm vote of confidence goes to …
Well, we’ve got some good news for the physicians out there, and we’ve got some bad news. Which do you want first? Okay, we’re mostly hearing good news, so here goes: Most people would choose a human doctor over artificial intelligence for the diagnosis and treatment of their medical conditions.
And the bad news? In the survey we’re talking about, “most” was 53%, so not exactly a huge victory for the carbon-based life forms. Yup, about 47% of the 2,472 respondents said they would prefer an AI-based clinic over a human specialist, and that number went up if individuals were told that their primary care physicians were on board with AI, “or otherwise nudged to consider AI as good,” the research team said in a written statement released by the University of Arizona, Tucson.
They went on to add that “this signaled the significance of the human physician in guiding a patient’s decision.” So patients will still need their doctors in the future to … um … this is a bit awkward … tell them how good the AI is?
And yes, we know that ChatGPT is already doing the same thing to journalists, but could it write a medical-humor column? Not a chance. Probably can’t even tell a joke.
How do ghosts get rid of wrinkles? Boo-tox. There, let’s see ChatGPT do that.
Explaining the joke makes it funnier, right?
Here at LOTME headquarters, we live by one simple rule, passed down directly from the Buddha himself: “Never let a good presurgical assessment of refractory epilepsy go to waste. Also, don’t believe everything you read on the Internet.”
This human-created joke has been brought to you by the leading theory of humor, which states that comedy stems from our brain reacting to an incongruous part of reality in a positive way. These positive emotions light up our neurons in a specific fashion, and boom, comedy is achieved.
Previous studies into the science of comedy have typically used functional MRI to analyze the brain while it was gripped in the throes of a comedic reaction. Unfortunately, fMRI cannot detect the entirety of the electromagnetic spectrum generated by the brain during these moments, so observing scientists have been, quite literally, missing out on some of the joke. And that’s where a new study from France comes in.
In the study, the researchers showed a group of patients with epilepsy who were hooked up to deep brain electrodes and a high-tech neuroimaging machine – part of the aforementioned presurgical assessment – a 3-minute excerpt from a Charlie Chaplin movie and analyzed their brain activity. Why Charlie Chaplin? Simple. Slapstick is perhaps the most accessible form of comedy across cultures. We can all appreciate a man getting hit in the head with a coconut. The world’s oldest bar joke or whatever this is? Not so much.
During the funniest scenes, all study participants showed increased high-frequency gamma waves (indicating high cognitive engagement) and a decrease in low-frequency waves (indicating reduced inattention and introspection). During unfunny scenes, such as transition moments, the opposite occurred. Importantly, this inverse relationship occurred in the temporal lobe but not in other regions, supporting previous research that indicated humor was mainly processed in the temporal lobe.
The investigators suggested future research should focus on longer videos with more complex forms of comedy, such as jokes, irony, sarcasm, or reference humor. So, uh, a guy getting hit in the head with two coconuts? That’s high-brow stuff right there.
Hot take: Humans aren’t that special
We humans have always prided ourselves on being different from “the animals” in an exceptional way. News flash! We aren’t. We may be the apex predator, but new research shows that humans, as part of the animal kingdom, just aren’t special.
Not special? How can they say that? Are gorillas doing open-heart surgery? Do wolverines tell jokes? At a more basic level, though, the way we operate as mammals in societies is not unique or even new. Elephants are known to mourn their deceased and to have funeral-like practices, ants invented agriculture, and we’re certainly not the only species that has figured out how to use tools.
This new research just demonstrates another way we aren’t exceptional, and that’s in our mating practices and outcomes.
“Humans appear to resemble mammals that live in monogamous partnerships and to some extent, those classified as cooperative breeders, where breeding individuals have to rely on the help of others to raise their offspring,” Monique Borgerhoff Mulder, PhD, professor emerita of anthropology at the University of California, Davis, said in a written statement.
The research team, which consisted of over 100 investigators, looked at 90 human populations based on data from over 80,000 people globally and compared the human data with 49 different nonhuman mammal species. In polygynous societies in which men take several wives, they found, women have more access to resources like food, shelter, and parenting help. Monogamy, on the other hand, “can drive significant inequalities among women,” Dr. Borgerhoff Mulder said, by promoting large differences in the number of children couples produce.
Human day-to-day behavior and child-rearing habits – one parent taking a daughter to ballet class and fixing dinner so the other parent can get to exercise class before picking up the son from soccer practice – may have us thinking that we are part of an evolved society, but really we are not much different than other mammals that hunt, forage for food, and rear and teach their children, the researchers suggested.
So, yes, humans can travel to the moon, create a vaccine for smallpox, and hit other humans with coconuts, but when it comes to simply having offspring or raising them, we’re not all that special. Get over it.
Which interventions could lessen the burden of dementia?
Using a microsimulation algorithm that accounts for the effect on mortality, a team from Marseille, France, has shown that interventions targeting the three main vascular risk factors for dementia – hypertension, diabetes, and physical inactivity – could significantly reduce the burden of dementia by 2040.
Although these modeling results could appear too optimistic, since total disappearance of the risk factors was assumed, the authors say the results do show that targeted interventions for these factors could be effective in reducing the future burden of dementia.
Increasing prevalence
According to the World Alzheimer Report 2018, 50 million people around the world were living with dementia; a population roughly around the size of South Korea or Spain. That community is likely to rise to about 152 million people by 2050, which is similar to the size of Russia or Bangladesh, the result of an aging population.
Among modifiable risk factors, many studies support a deleterious effect of hypertension, diabetes, and physical inactivity on the risk of dementia. However, since the distribution of these risk factors could have a direct impact on mortality, reducing it should increase life expectancy and the number of cases of dementia.
The team, headed by Hélène Jacqmin-Gadda, PhD, research director at the University of Bordeaux (France), has developed a microsimulation model capable of predicting the burden of dementia while accounting for the impact on mortality. The team used this approach to assess the impact of interventions targeting these three main risk factors on the burden of dementia in France by 2040.
Removing risk factors
The researchers estimated the incidence of dementia for men and women using data from the 2020 PAQUID cohort, and these data were combined with the projections forecast by the French National Institute of Statistics and Economic Studies to account for mortality with and without dementia.
Without intervention, the prevalence rate of dementia in 2040 would be 9.6% among men and 14% among women older than 65 years.
These figures would decrease to 6.4% (−33%) and 10.4% (−26%), respectively, under the intervention scenario whereby the three modifiable vascular risk factors (hypertension, diabetes, and physical inactivity) would be removed simultaneously beginning in 2020. The prevalence rates are significantly reduced for men and women from age 75 years. In this scenario, life expectancy without dementia would increase by 3.4 years in men and 2.6 years in women, the result of men being more exposed to these three risk factors.
Other scenarios have estimated dementia prevalence with the disappearance of just one of these risk factors. For example, the disappearance of hypertension alone from 2020 could decrease dementia prevalence by 21% in men and 16% in women (because this risk factor is less common in women than in men) by 2040. This reduction would be associated with a decrease in the lifelong probability of dementia among men and women and a gain in life expectancy without dementia of 2 years in men and 1.4 years in women.
Among the three factors, hypertension has the largest impact on dementia burden in the French population, since this is, by far, the most prevalent (69% in men and 49% in women), while intervention targeting only diabetes or physical inactivity would lead to a reduction in dementia prevalence of only 4%-7%.
The authors reported no conflicts of interest.
This article was translated from Univadis France. A version appeared on Medscape.com.
Using a microsimulation algorithm that accounts for the effect on mortality, a team from Marseille, France, has shown that interventions targeting the three main vascular risk factors for dementia – hypertension, diabetes, and physical inactivity – could significantly reduce the burden of dementia by 2040.
Although these modeling results could appear too optimistic, since total disappearance of the risk factors was assumed, the authors say the results do show that targeted interventions for these factors could be effective in reducing the future burden of dementia.
Increasing prevalence
According to the World Alzheimer Report 2018, 50 million people around the world were living with dementia; a population roughly around the size of South Korea or Spain. That community is likely to rise to about 152 million people by 2050, which is similar to the size of Russia or Bangladesh, the result of an aging population.
Among modifiable risk factors, many studies support a deleterious effect of hypertension, diabetes, and physical inactivity on the risk of dementia. However, since the distribution of these risk factors could have a direct impact on mortality, reducing it should increase life expectancy and the number of cases of dementia.
The team, headed by Hélène Jacqmin-Gadda, PhD, research director at the University of Bordeaux (France), has developed a microsimulation model capable of predicting the burden of dementia while accounting for the impact on mortality. The team used this approach to assess the impact of interventions targeting these three main risk factors on the burden of dementia in France by 2040.
Removing risk factors
The researchers estimated the incidence of dementia for men and women using data from the 2020 PAQUID cohort, and these data were combined with the projections forecast by the French National Institute of Statistics and Economic Studies to account for mortality with and without dementia.
Without intervention, the prevalence rate of dementia in 2040 would be 9.6% among men and 14% among women older than 65 years.
These figures would decrease to 6.4% (−33%) and 10.4% (−26%), respectively, under the intervention scenario whereby the three modifiable vascular risk factors (hypertension, diabetes, and physical inactivity) would be removed simultaneously beginning in 2020. The prevalence rates are significantly reduced for men and women from age 75 years. In this scenario, life expectancy without dementia would increase by 3.4 years in men and 2.6 years in women, the result of men being more exposed to these three risk factors.
Other scenarios have estimated dementia prevalence with the disappearance of just one of these risk factors. For example, the disappearance of hypertension alone from 2020 could decrease dementia prevalence by 21% in men and 16% in women (because this risk factor is less common in women than in men) by 2040. This reduction would be associated with a decrease in the lifelong probability of dementia among men and women and a gain in life expectancy without dementia of 2 years in men and 1.4 years in women.
Among the three factors, hypertension has the largest impact on dementia burden in the French population, since this is, by far, the most prevalent (69% in men and 49% in women), while intervention targeting only diabetes or physical inactivity would lead to a reduction in dementia prevalence of only 4%-7%.
The authors reported no conflicts of interest.
This article was translated from Univadis France. A version appeared on Medscape.com.
Using a microsimulation algorithm that accounts for the effect on mortality, a team from Marseille, France, has shown that interventions targeting the three main vascular risk factors for dementia – hypertension, diabetes, and physical inactivity – could significantly reduce the burden of dementia by 2040.
Although these modeling results could appear too optimistic, since total disappearance of the risk factors was assumed, the authors say the results do show that targeted interventions for these factors could be effective in reducing the future burden of dementia.
Increasing prevalence
According to the World Alzheimer Report 2018, 50 million people around the world were living with dementia; a population roughly around the size of South Korea or Spain. That community is likely to rise to about 152 million people by 2050, which is similar to the size of Russia or Bangladesh, the result of an aging population.
Among modifiable risk factors, many studies support a deleterious effect of hypertension, diabetes, and physical inactivity on the risk of dementia. However, since the distribution of these risk factors could have a direct impact on mortality, reducing it should increase life expectancy and the number of cases of dementia.
The team, headed by Hélène Jacqmin-Gadda, PhD, research director at the University of Bordeaux (France), has developed a microsimulation model capable of predicting the burden of dementia while accounting for the impact on mortality. The team used this approach to assess the impact of interventions targeting these three main risk factors on the burden of dementia in France by 2040.
Removing risk factors
The researchers estimated the incidence of dementia for men and women using data from the 2020 PAQUID cohort, and these data were combined with the projections forecast by the French National Institute of Statistics and Economic Studies to account for mortality with and without dementia.
Without intervention, the prevalence rate of dementia in 2040 would be 9.6% among men and 14% among women older than 65 years.
These figures would decrease to 6.4% (−33%) and 10.4% (−26%), respectively, under the intervention scenario whereby the three modifiable vascular risk factors (hypertension, diabetes, and physical inactivity) would be removed simultaneously beginning in 2020. The prevalence rates are significantly reduced for men and women from age 75 years. In this scenario, life expectancy without dementia would increase by 3.4 years in men and 2.6 years in women, the result of men being more exposed to these three risk factors.
Other scenarios have estimated dementia prevalence with the disappearance of just one of these risk factors. For example, the disappearance of hypertension alone from 2020 could decrease dementia prevalence by 21% in men and 16% in women (because this risk factor is less common in women than in men) by 2040. This reduction would be associated with a decrease in the lifelong probability of dementia among men and women and a gain in life expectancy without dementia of 2 years in men and 1.4 years in women.
Among the three factors, hypertension has the largest impact on dementia burden in the French population, since this is, by far, the most prevalent (69% in men and 49% in women), while intervention targeting only diabetes or physical inactivity would lead to a reduction in dementia prevalence of only 4%-7%.
The authors reported no conflicts of interest.
This article was translated from Univadis France. A version appeared on Medscape.com.
FROM THE EUROPEAN JOURNAL OF EPIDEMIOLOGY
Differences in 30-Day Readmission Rates in Older Adults With Dementia
Study 1 Overview (Park et al)
Objective: To compare rates of adverse events and 30-day readmission among patients with dementia who undergo percutaneous coronary intervention (PCI) with those without dementia.
Design: This cohort study used a national database of hospital readmissions developed by the Agency for Healthcare Research and Quality.
Setting and participants: Data from State Inpatient Databases were used to derive this national readmissions database representing 80% of hospitals from 28 states that contribute data. The study included all individuals aged 18 years and older who were identified to have had a PCI procedure in the years 2017 and 2018. International Classification of Diseases, Tenth Revision (ICD-10) codes were used to identify PCI procedures, including drug-eluting stent placement, bare-metal stent placement, and balloon angioplasty, performed in patients who presented with myocardial infarction and unstable angina and those with stable ischemic heart disease. Patients were stratified into those with or without dementia, also defined using ICD-10 codes. A total of 755,406 index hospitalizations were included; 2.3% of the patients had dementia.
Main outcome measures: The primary study outcome was 30-day all-cause readmission, with the cause classified as cardiovascular or noncardiovascular. Secondary outcome measures examined were delirium, in-hospital mortality, cardiac arrest, blood transfusion, acute kidney injury, fall in hospital, length of hospital stay, and other adverse outcomes. Location at discharge was also examined. Other covariates included in the analysis were age, sex, comorbidities, hospital characteristics, primary payer, and median income. For analysis, a propensity score matching algorithm was applied to match patients with and without dementia. Kaplan-Meier curves were used to examine 30-day readmission rates, and a Cox proportional hazards model was used to calculate hazard ratios (HR) for those with and without dementia. For secondary outcomes, logistic regression models were used to calculate odds ratios (OR) of outcomes between those with and without dementia.
Main results: The average age of those with dementia was 78.8 years vs 64.9 years in those without dementia. Women made up 42.8% of those with dementia and 31.3% of those without dementia. Those with dementia also had higher rates of comorbidities, such as heart failure, renal failure, and depression. After propensity score matching, 17,309 and 17,187 patients with and without dementia, respectively, were included. Covariates were balanced between the 2 groups after matching. For the primary outcome, patients with dementia were more likely to be readmitted at 30 days (HR, 1.11; 95% CI, 1.05-1.18; P < .01) when compared to those without dementia. For other adverse outcomes, delirium was significantly more likely to occur for those with dementia (OR, 4.37; 95% CI, 3.69-5.16; P < .01). Patients with dementia were also more likely to die in hospital (OR, 1.15; 95% CI, 1.01-1.30; P = .03), have cardiac arrest (OR, 1.19; 95% CI, 1.01-1.39; P = .04), receive a blood transfusion (OR, 1.17; 95% CI, 1.00-1.36; P = .05), experience acute kidney injury (OR, 1.30; 95% CI, 1.21-1.39; P < .01), and fall in hospital (OR, 2.51; 95% CI, 2.06-3.07; P < .01). Hospital length of stay was higher for those with dementia, with a mean difference of 1.43 days. For discharge location, patients with dementia were more likely to be sent to a skilled nursing facility (30.1% vs 12.2%) and less likely to be discharged home.
Conclusion: Patients with dementia are more likely to experience adverse events, including delirium, mortality, kidney injury, and falls after PCI, and are more likely to be readmitted to the hospital in 30 days compared to those without dementia.
Study 2 Overview (Gilmore-Bykovskyi et al)
Objective: To examine the association between race and 30-day readmissions in Black and non-Hispanic White Medicare beneficiaries with dementia.
Design: This was a retrospective cohort study that used 100% Medicare fee-for service claims data from all hospitalizations between January 1, 2014, and November 30, 2014, for all enrollees with a dementia diagnosis. The claims data were linked to the patient, hospital stay, and hospital factors. Patients with dementia were identified using a validated algorithm that requires an inpatient, skilled nursing facility, home health, or Part B institutional or noninstitutional claim with a qualifying diagnostic code during a 3-year period. Persons enrolled in a health maintenance organization plan were excluded.
Main outcome measures: The primary outcome examined in this study was 30-day all-cause readmission. Self-reported race and ethnic identity was a baseline covariate. Persons who self-reported Black or non-Hispanic White race were included in the study; other categories of race and ethnicity were excluded because of prior evidence suggesting low accuracy of these categories in Medicare claims data. Other covariates included neighborhood disadvantage, measured using the Area Deprivation Index (ADI), and rurality; hospital-level and hospital stay–level characteristics such as for-profit status and number of annual discharges; and individual demographic characteristics and comorbidities. The ADI is constructed using variables of poverty, education, housing, and employment and is represented as a percentile ranking of level of disadvantage. Unadjusted and adjusted analyses of 30-day hospital readmission were conducted. Models using various levels of adjustment were constructed to examine the contributions of the identified covariates to the estimated association between 30-day readmission and race.
Main results: A total of 1,523,142 index hospital stays among 945,481 beneficiaries were included; 215,815 episodes were among Black beneficiaries and 1,307,327 episodes were among non-Hispanic White beneficiaries. Mean age was 81.5 years, and approximately 61% of beneficiaries were female. Black beneficiaries were younger but had higher rates of dual Medicare/Medicaid eligibility and disability; they were also more likely to reside in disadvantaged neighborhoods. Black beneficiaries had a 30-day readmission rate of 24.1% compared with 18.5% in non-Hispanic White beneficiaries (unadjusted OR, 1.37; 95% CI, 1.35-1.39). The differences in outcomes persisted after adjusting for geographic factors, social factors, hospital characteristics, hospital stay factors, demographics, and comorbidities, suggesting that unmeasured underlying racial disparities not included in this model accounted for the differences. The effects of certain variables, such as neighborhood, differed by race; for example, the protective effect of living in a less disadvantaged neighborhood was observed among White beneficiaries but not Black beneficiaries.
Conclusion: Racial and geographic disparities in 30-day readmission rates were observed among Medicare beneficiaries with dementia. Protective effects associated with neighborhood advantage may confer different levels of benefit for people of different race.
Commentary
Adults living with dementia are at higher risk of adverse outcomes across settings. In the first study, by Park et al, among adults who underwent a cardiac procedure (PCI), those with dementia were more likely to experience adverse events compared to those without dementia. These outcomes include increased rates of 30-day readmissions, delirium, cardiac arrest, and falls. These findings are consistent with other studies that found a similar association among patients who underwent other cardiac procedures, such as transcatheter aortic valve replacement.1 Because dementia is a strong predisposing factor for delirium, it is not surprising that delirium is observed across patients who underwent different procedures or hospitalization episodes.2 Because of the potential hazards for inpatients with dementia, hospitals have developed risk-reduction programs, such as those that promote recognition of dementia, and management strategies that reduce the risk of delirium.3 Delirium prevention may also impact other adverse outcomes, such as falls, discharge to institutional care, and readmissions.
Racial disparities in care outcomes have been documented across settings, including hospital4 and hospice care settings.5 In study 2, by Gilmore-Bykovskyi et al, the findings of higher rates of hospital readmission among Black patients when compared to non-Hispanic White patients were not surprising. The central finding of this study is that even when accounting for various levels of factors, including hospital-level, hospital stay–level, individual (demographics, comorbidities), and neighborhood characteristics (disadvantage), the observed disparity diminished but persisted, suggesting that while these various levels of factors contributed to the observed disparity, other unmeasured factors also contributed. Another key finding is that the effect of the various factors examined in this study may affect different subgroups in different ways, suggesting underlying factors, and thus potential solutions to reduce disparities in care outcomes, could differ among subgroups.
Applications for Clinical Practice and System Implementation
These 2 studies add to the literature on factors that can affect 30-day hospital readmission rates in patients with dementia. These data could allow for more robust discussions of what to anticipate when adults with dementia undergo specific procedures, and also further build the case that improvements in care, such as delirium prevention programs, could offer benefits. The observation about racial and ethnic disparities in care outcomes among patients with dementia highlights the continued need to better understand the drivers of these disparities so that hospital systems and policy makers can consider and test possible solutions. Future studies should further disentangle the relationships among the various levels of factors and observed disparities in outcomes, especially for this vulnerable population of adults living with dementia.
Practice Points
- Clinicians should be aware of the additional risks for poor outcomes that dementia confers.
- Awareness of this increased risk will inform discussions of risks and benefits for older adults considered for procedures.
–William W. Hung, MD, MPH
1. Park DY, Sana MK, Shoura S, et al. Readmission and in-hospital outcomes after transcatheter aortic valve replacement in patients with dementia. Cardiovasc Revasc Med. 2023;46:70-77. doi:10.1016/j.carrev.2022.08.016
2. McNicoll L, Pisani MA, Zhang Y, et al. Delirium in the intensive care unit: occurrence and clinical course in older patients. J Am Geriatr Soc. 2003;51(5):591-598. doi:10.1034/j.1600-0579.2003.00201.x
3. Weldingh NM, Mellingsæter MR, Hegna BW, et al. Impact of a dementia-friendly program on detection and management of patients with cognitive impairment and delirium in acute-care hospital units: a controlled clinical trial design. BMC Geriatr. 2022;22(1):266. doi:10.1186/s12877-022-02949-0
4. Hermosura AH, Noonan CJ, Fyfe-Johnson AL, et al. Hospital disparities between native Hawaiian and other pacific islanders and non-Hispanic whites with Alzheimer’s disease and related dementias. J Aging Health. 2020;32(10):1579-1590. doi:10.1177/0898264320945177
5. Zhang Y, Shao H, Zhang M, Li J. Healthcare utilization and mortality after hospice live discharge among Medicare patients with and without Alzheimer’s disease and related dementias. J Gen Intern Med. 2023 Jan 17. doi:10.1007/s11606-023-08031-8
Study 1 Overview (Park et al)
Objective: To compare rates of adverse events and 30-day readmission among patients with dementia who undergo percutaneous coronary intervention (PCI) with those without dementia.
Design: This cohort study used a national database of hospital readmissions developed by the Agency for Healthcare Research and Quality.
Setting and participants: Data from State Inpatient Databases were used to derive this national readmissions database representing 80% of hospitals from 28 states that contribute data. The study included all individuals aged 18 years and older who were identified to have had a PCI procedure in the years 2017 and 2018. International Classification of Diseases, Tenth Revision (ICD-10) codes were used to identify PCI procedures, including drug-eluting stent placement, bare-metal stent placement, and balloon angioplasty, performed in patients who presented with myocardial infarction and unstable angina and those with stable ischemic heart disease. Patients were stratified into those with or without dementia, also defined using ICD-10 codes. A total of 755,406 index hospitalizations were included; 2.3% of the patients had dementia.
Main outcome measures: The primary study outcome was 30-day all-cause readmission, with the cause classified as cardiovascular or noncardiovascular. Secondary outcome measures examined were delirium, in-hospital mortality, cardiac arrest, blood transfusion, acute kidney injury, fall in hospital, length of hospital stay, and other adverse outcomes. Location at discharge was also examined. Other covariates included in the analysis were age, sex, comorbidities, hospital characteristics, primary payer, and median income. For analysis, a propensity score matching algorithm was applied to match patients with and without dementia. Kaplan-Meier curves were used to examine 30-day readmission rates, and a Cox proportional hazards model was used to calculate hazard ratios (HR) for those with and without dementia. For secondary outcomes, logistic regression models were used to calculate odds ratios (OR) of outcomes between those with and without dementia.
Main results: The average age of those with dementia was 78.8 years vs 64.9 years in those without dementia. Women made up 42.8% of those with dementia and 31.3% of those without dementia. Those with dementia also had higher rates of comorbidities, such as heart failure, renal failure, and depression. After propensity score matching, 17,309 and 17,187 patients with and without dementia, respectively, were included. Covariates were balanced between the 2 groups after matching. For the primary outcome, patients with dementia were more likely to be readmitted at 30 days (HR, 1.11; 95% CI, 1.05-1.18; P < .01) when compared to those without dementia. For other adverse outcomes, delirium was significantly more likely to occur for those with dementia (OR, 4.37; 95% CI, 3.69-5.16; P < .01). Patients with dementia were also more likely to die in hospital (OR, 1.15; 95% CI, 1.01-1.30; P = .03), have cardiac arrest (OR, 1.19; 95% CI, 1.01-1.39; P = .04), receive a blood transfusion (OR, 1.17; 95% CI, 1.00-1.36; P = .05), experience acute kidney injury (OR, 1.30; 95% CI, 1.21-1.39; P < .01), and fall in hospital (OR, 2.51; 95% CI, 2.06-3.07; P < .01). Hospital length of stay was higher for those with dementia, with a mean difference of 1.43 days. For discharge location, patients with dementia were more likely to be sent to a skilled nursing facility (30.1% vs 12.2%) and less likely to be discharged home.
Conclusion: Patients with dementia are more likely to experience adverse events, including delirium, mortality, kidney injury, and falls after PCI, and are more likely to be readmitted to the hospital in 30 days compared to those without dementia.
Study 2 Overview (Gilmore-Bykovskyi et al)
Objective: To examine the association between race and 30-day readmissions in Black and non-Hispanic White Medicare beneficiaries with dementia.
Design: This was a retrospective cohort study that used 100% Medicare fee-for service claims data from all hospitalizations between January 1, 2014, and November 30, 2014, for all enrollees with a dementia diagnosis. The claims data were linked to the patient, hospital stay, and hospital factors. Patients with dementia were identified using a validated algorithm that requires an inpatient, skilled nursing facility, home health, or Part B institutional or noninstitutional claim with a qualifying diagnostic code during a 3-year period. Persons enrolled in a health maintenance organization plan were excluded.
Main outcome measures: The primary outcome examined in this study was 30-day all-cause readmission. Self-reported race and ethnic identity was a baseline covariate. Persons who self-reported Black or non-Hispanic White race were included in the study; other categories of race and ethnicity were excluded because of prior evidence suggesting low accuracy of these categories in Medicare claims data. Other covariates included neighborhood disadvantage, measured using the Area Deprivation Index (ADI), and rurality; hospital-level and hospital stay–level characteristics such as for-profit status and number of annual discharges; and individual demographic characteristics and comorbidities. The ADI is constructed using variables of poverty, education, housing, and employment and is represented as a percentile ranking of level of disadvantage. Unadjusted and adjusted analyses of 30-day hospital readmission were conducted. Models using various levels of adjustment were constructed to examine the contributions of the identified covariates to the estimated association between 30-day readmission and race.
Main results: A total of 1,523,142 index hospital stays among 945,481 beneficiaries were included; 215,815 episodes were among Black beneficiaries and 1,307,327 episodes were among non-Hispanic White beneficiaries. Mean age was 81.5 years, and approximately 61% of beneficiaries were female. Black beneficiaries were younger but had higher rates of dual Medicare/Medicaid eligibility and disability; they were also more likely to reside in disadvantaged neighborhoods. Black beneficiaries had a 30-day readmission rate of 24.1% compared with 18.5% in non-Hispanic White beneficiaries (unadjusted OR, 1.37; 95% CI, 1.35-1.39). The differences in outcomes persisted after adjusting for geographic factors, social factors, hospital characteristics, hospital stay factors, demographics, and comorbidities, suggesting that unmeasured underlying racial disparities not included in this model accounted for the differences. The effects of certain variables, such as neighborhood, differed by race; for example, the protective effect of living in a less disadvantaged neighborhood was observed among White beneficiaries but not Black beneficiaries.
Conclusion: Racial and geographic disparities in 30-day readmission rates were observed among Medicare beneficiaries with dementia. Protective effects associated with neighborhood advantage may confer different levels of benefit for people of different race.
Commentary
Adults living with dementia are at higher risk of adverse outcomes across settings. In the first study, by Park et al, among adults who underwent a cardiac procedure (PCI), those with dementia were more likely to experience adverse events compared to those without dementia. These outcomes include increased rates of 30-day readmissions, delirium, cardiac arrest, and falls. These findings are consistent with other studies that found a similar association among patients who underwent other cardiac procedures, such as transcatheter aortic valve replacement.1 Because dementia is a strong predisposing factor for delirium, it is not surprising that delirium is observed across patients who underwent different procedures or hospitalization episodes.2 Because of the potential hazards for inpatients with dementia, hospitals have developed risk-reduction programs, such as those that promote recognition of dementia, and management strategies that reduce the risk of delirium.3 Delirium prevention may also impact other adverse outcomes, such as falls, discharge to institutional care, and readmissions.
Racial disparities in care outcomes have been documented across settings, including hospital4 and hospice care settings.5 In study 2, by Gilmore-Bykovskyi et al, the findings of higher rates of hospital readmission among Black patients when compared to non-Hispanic White patients were not surprising. The central finding of this study is that even when accounting for various levels of factors, including hospital-level, hospital stay–level, individual (demographics, comorbidities), and neighborhood characteristics (disadvantage), the observed disparity diminished but persisted, suggesting that while these various levels of factors contributed to the observed disparity, other unmeasured factors also contributed. Another key finding is that the effect of the various factors examined in this study may affect different subgroups in different ways, suggesting underlying factors, and thus potential solutions to reduce disparities in care outcomes, could differ among subgroups.
Applications for Clinical Practice and System Implementation
These 2 studies add to the literature on factors that can affect 30-day hospital readmission rates in patients with dementia. These data could allow for more robust discussions of what to anticipate when adults with dementia undergo specific procedures, and also further build the case that improvements in care, such as delirium prevention programs, could offer benefits. The observation about racial and ethnic disparities in care outcomes among patients with dementia highlights the continued need to better understand the drivers of these disparities so that hospital systems and policy makers can consider and test possible solutions. Future studies should further disentangle the relationships among the various levels of factors and observed disparities in outcomes, especially for this vulnerable population of adults living with dementia.
Practice Points
- Clinicians should be aware of the additional risks for poor outcomes that dementia confers.
- Awareness of this increased risk will inform discussions of risks and benefits for older adults considered for procedures.
–William W. Hung, MD, MPH
Study 1 Overview (Park et al)
Objective: To compare rates of adverse events and 30-day readmission among patients with dementia who undergo percutaneous coronary intervention (PCI) with those without dementia.
Design: This cohort study used a national database of hospital readmissions developed by the Agency for Healthcare Research and Quality.
Setting and participants: Data from State Inpatient Databases were used to derive this national readmissions database representing 80% of hospitals from 28 states that contribute data. The study included all individuals aged 18 years and older who were identified to have had a PCI procedure in the years 2017 and 2018. International Classification of Diseases, Tenth Revision (ICD-10) codes were used to identify PCI procedures, including drug-eluting stent placement, bare-metal stent placement, and balloon angioplasty, performed in patients who presented with myocardial infarction and unstable angina and those with stable ischemic heart disease. Patients were stratified into those with or without dementia, also defined using ICD-10 codes. A total of 755,406 index hospitalizations were included; 2.3% of the patients had dementia.
Main outcome measures: The primary study outcome was 30-day all-cause readmission, with the cause classified as cardiovascular or noncardiovascular. Secondary outcome measures examined were delirium, in-hospital mortality, cardiac arrest, blood transfusion, acute kidney injury, fall in hospital, length of hospital stay, and other adverse outcomes. Location at discharge was also examined. Other covariates included in the analysis were age, sex, comorbidities, hospital characteristics, primary payer, and median income. For analysis, a propensity score matching algorithm was applied to match patients with and without dementia. Kaplan-Meier curves were used to examine 30-day readmission rates, and a Cox proportional hazards model was used to calculate hazard ratios (HR) for those with and without dementia. For secondary outcomes, logistic regression models were used to calculate odds ratios (OR) of outcomes between those with and without dementia.
Main results: The average age of those with dementia was 78.8 years vs 64.9 years in those without dementia. Women made up 42.8% of those with dementia and 31.3% of those without dementia. Those with dementia also had higher rates of comorbidities, such as heart failure, renal failure, and depression. After propensity score matching, 17,309 and 17,187 patients with and without dementia, respectively, were included. Covariates were balanced between the 2 groups after matching. For the primary outcome, patients with dementia were more likely to be readmitted at 30 days (HR, 1.11; 95% CI, 1.05-1.18; P < .01) when compared to those without dementia. For other adverse outcomes, delirium was significantly more likely to occur for those with dementia (OR, 4.37; 95% CI, 3.69-5.16; P < .01). Patients with dementia were also more likely to die in hospital (OR, 1.15; 95% CI, 1.01-1.30; P = .03), have cardiac arrest (OR, 1.19; 95% CI, 1.01-1.39; P = .04), receive a blood transfusion (OR, 1.17; 95% CI, 1.00-1.36; P = .05), experience acute kidney injury (OR, 1.30; 95% CI, 1.21-1.39; P < .01), and fall in hospital (OR, 2.51; 95% CI, 2.06-3.07; P < .01). Hospital length of stay was higher for those with dementia, with a mean difference of 1.43 days. For discharge location, patients with dementia were more likely to be sent to a skilled nursing facility (30.1% vs 12.2%) and less likely to be discharged home.
Conclusion: Patients with dementia are more likely to experience adverse events, including delirium, mortality, kidney injury, and falls after PCI, and are more likely to be readmitted to the hospital in 30 days compared to those without dementia.
Study 2 Overview (Gilmore-Bykovskyi et al)
Objective: To examine the association between race and 30-day readmissions in Black and non-Hispanic White Medicare beneficiaries with dementia.
Design: This was a retrospective cohort study that used 100% Medicare fee-for service claims data from all hospitalizations between January 1, 2014, and November 30, 2014, for all enrollees with a dementia diagnosis. The claims data were linked to the patient, hospital stay, and hospital factors. Patients with dementia were identified using a validated algorithm that requires an inpatient, skilled nursing facility, home health, or Part B institutional or noninstitutional claim with a qualifying diagnostic code during a 3-year period. Persons enrolled in a health maintenance organization plan were excluded.
Main outcome measures: The primary outcome examined in this study was 30-day all-cause readmission. Self-reported race and ethnic identity was a baseline covariate. Persons who self-reported Black or non-Hispanic White race were included in the study; other categories of race and ethnicity were excluded because of prior evidence suggesting low accuracy of these categories in Medicare claims data. Other covariates included neighborhood disadvantage, measured using the Area Deprivation Index (ADI), and rurality; hospital-level and hospital stay–level characteristics such as for-profit status and number of annual discharges; and individual demographic characteristics and comorbidities. The ADI is constructed using variables of poverty, education, housing, and employment and is represented as a percentile ranking of level of disadvantage. Unadjusted and adjusted analyses of 30-day hospital readmission were conducted. Models using various levels of adjustment were constructed to examine the contributions of the identified covariates to the estimated association between 30-day readmission and race.
Main results: A total of 1,523,142 index hospital stays among 945,481 beneficiaries were included; 215,815 episodes were among Black beneficiaries and 1,307,327 episodes were among non-Hispanic White beneficiaries. Mean age was 81.5 years, and approximately 61% of beneficiaries were female. Black beneficiaries were younger but had higher rates of dual Medicare/Medicaid eligibility and disability; they were also more likely to reside in disadvantaged neighborhoods. Black beneficiaries had a 30-day readmission rate of 24.1% compared with 18.5% in non-Hispanic White beneficiaries (unadjusted OR, 1.37; 95% CI, 1.35-1.39). The differences in outcomes persisted after adjusting for geographic factors, social factors, hospital characteristics, hospital stay factors, demographics, and comorbidities, suggesting that unmeasured underlying racial disparities not included in this model accounted for the differences. The effects of certain variables, such as neighborhood, differed by race; for example, the protective effect of living in a less disadvantaged neighborhood was observed among White beneficiaries but not Black beneficiaries.
Conclusion: Racial and geographic disparities in 30-day readmission rates were observed among Medicare beneficiaries with dementia. Protective effects associated with neighborhood advantage may confer different levels of benefit for people of different race.
Commentary
Adults living with dementia are at higher risk of adverse outcomes across settings. In the first study, by Park et al, among adults who underwent a cardiac procedure (PCI), those with dementia were more likely to experience adverse events compared to those without dementia. These outcomes include increased rates of 30-day readmissions, delirium, cardiac arrest, and falls. These findings are consistent with other studies that found a similar association among patients who underwent other cardiac procedures, such as transcatheter aortic valve replacement.1 Because dementia is a strong predisposing factor for delirium, it is not surprising that delirium is observed across patients who underwent different procedures or hospitalization episodes.2 Because of the potential hazards for inpatients with dementia, hospitals have developed risk-reduction programs, such as those that promote recognition of dementia, and management strategies that reduce the risk of delirium.3 Delirium prevention may also impact other adverse outcomes, such as falls, discharge to institutional care, and readmissions.
Racial disparities in care outcomes have been documented across settings, including hospital4 and hospice care settings.5 In study 2, by Gilmore-Bykovskyi et al, the findings of higher rates of hospital readmission among Black patients when compared to non-Hispanic White patients were not surprising. The central finding of this study is that even when accounting for various levels of factors, including hospital-level, hospital stay–level, individual (demographics, comorbidities), and neighborhood characteristics (disadvantage), the observed disparity diminished but persisted, suggesting that while these various levels of factors contributed to the observed disparity, other unmeasured factors also contributed. Another key finding is that the effect of the various factors examined in this study may affect different subgroups in different ways, suggesting underlying factors, and thus potential solutions to reduce disparities in care outcomes, could differ among subgroups.
Applications for Clinical Practice and System Implementation
These 2 studies add to the literature on factors that can affect 30-day hospital readmission rates in patients with dementia. These data could allow for more robust discussions of what to anticipate when adults with dementia undergo specific procedures, and also further build the case that improvements in care, such as delirium prevention programs, could offer benefits. The observation about racial and ethnic disparities in care outcomes among patients with dementia highlights the continued need to better understand the drivers of these disparities so that hospital systems and policy makers can consider and test possible solutions. Future studies should further disentangle the relationships among the various levels of factors and observed disparities in outcomes, especially for this vulnerable population of adults living with dementia.
Practice Points
- Clinicians should be aware of the additional risks for poor outcomes that dementia confers.
- Awareness of this increased risk will inform discussions of risks and benefits for older adults considered for procedures.
–William W. Hung, MD, MPH
1. Park DY, Sana MK, Shoura S, et al. Readmission and in-hospital outcomes after transcatheter aortic valve replacement in patients with dementia. Cardiovasc Revasc Med. 2023;46:70-77. doi:10.1016/j.carrev.2022.08.016
2. McNicoll L, Pisani MA, Zhang Y, et al. Delirium in the intensive care unit: occurrence and clinical course in older patients. J Am Geriatr Soc. 2003;51(5):591-598. doi:10.1034/j.1600-0579.2003.00201.x
3. Weldingh NM, Mellingsæter MR, Hegna BW, et al. Impact of a dementia-friendly program on detection and management of patients with cognitive impairment and delirium in acute-care hospital units: a controlled clinical trial design. BMC Geriatr. 2022;22(1):266. doi:10.1186/s12877-022-02949-0
4. Hermosura AH, Noonan CJ, Fyfe-Johnson AL, et al. Hospital disparities between native Hawaiian and other pacific islanders and non-Hispanic whites with Alzheimer’s disease and related dementias. J Aging Health. 2020;32(10):1579-1590. doi:10.1177/0898264320945177
5. Zhang Y, Shao H, Zhang M, Li J. Healthcare utilization and mortality after hospice live discharge among Medicare patients with and without Alzheimer’s disease and related dementias. J Gen Intern Med. 2023 Jan 17. doi:10.1007/s11606-023-08031-8
1. Park DY, Sana MK, Shoura S, et al. Readmission and in-hospital outcomes after transcatheter aortic valve replacement in patients with dementia. Cardiovasc Revasc Med. 2023;46:70-77. doi:10.1016/j.carrev.2022.08.016
2. McNicoll L, Pisani MA, Zhang Y, et al. Delirium in the intensive care unit: occurrence and clinical course in older patients. J Am Geriatr Soc. 2003;51(5):591-598. doi:10.1034/j.1600-0579.2003.00201.x
3. Weldingh NM, Mellingsæter MR, Hegna BW, et al. Impact of a dementia-friendly program on detection and management of patients with cognitive impairment and delirium in acute-care hospital units: a controlled clinical trial design. BMC Geriatr. 2022;22(1):266. doi:10.1186/s12877-022-02949-0
4. Hermosura AH, Noonan CJ, Fyfe-Johnson AL, et al. Hospital disparities between native Hawaiian and other pacific islanders and non-Hispanic whites with Alzheimer’s disease and related dementias. J Aging Health. 2020;32(10):1579-1590. doi:10.1177/0898264320945177
5. Zhang Y, Shao H, Zhang M, Li J. Healthcare utilization and mortality after hospice live discharge among Medicare patients with and without Alzheimer’s disease and related dementias. J Gen Intern Med. 2023 Jan 17. doi:10.1007/s11606-023-08031-8
‘Robust evidence’ that exercise cuts Parkinson’s risk in women
Investigators found that among almost 99,000 women participating in the ongoing E3N study, those who exercised the most frequently had up to a 25% lower risk for PD than their less-active counterparts.
The results highlight the importance of exercising early in mid-life to prevent PD later on, study investigator Alexis Elbaz, MD, PhD, research director, French Institute of Health and Medical Research (Inserm), Paris, said in an interview.
This is especially critical since there is no cure nor disease-modifying treatments. The medications that are available are aimed at symptom reduction.
“Finding ways to prevent or delay the onset of Parkinson’s is really important, and physical activity seems to be one of the possible strategies to reduce the risk,” Dr. Elbaz said.
The study was published online in Neurology.
Direct protective effect?
Results from previous research examining the relationship physical activity and PD has been inconsistent. One meta-analysis showed a statistically significant association among men but a nonsignificant link in women.
The investigators noted that some of the findings from previous studies may have been affected by reverse causation. As nonmotor symptoms such as constipation and subtle motor signs such as tremor and balance issues can present years before a PD diagnosis, patients may reduce their physical activity because of such symptoms.
To address this potential confounder, the researchers used “lag” analyses, where data on physical activity levels in the years close to a PD diagnosis are omitted.
The study relied on data from the E3N, an ongoing cohort study of 98,995 women, born between 1925 and 1950 and recruited in 1990, who were affiliated with a French national health insurance plan that primarily covers teachers. Participants completed a questionnaire on lifestyle and medical history at baseline and follow-up questionnaires every 2-3 years.
In six of the questionnaires, participants provided details about various recreational, sports, and household activities – for example, walking, climbing stairs, gardening, and cleaning. The authors attributed metabolic equivalent of task (MET) values to each activity and multiplied METs by their frequency and duration to obtain a physical activity score.
Definite and probable PD cases were determined through self-reported physician diagnoses, anti-parkinsonian drug claims, and medical records, with diagnoses verified by an expert panel.
Researchers investigated the relationship between physical activity and PD onset in a nested-case control study that included 25,075 women (1,196 PD cases and 23,879 controls) with a mean age of 71.9 years. They found physical activity was significantly lower in cases than in controls throughout follow-up.
The difference between cases and controls began to increase at 10 years before diagnosis (P-interaction = .003). “When we looked at the trajectories of physical activity in PD patients and in controls, we saw that in the 10 years before the diagnosis, physical activity declined at a steeper rate in controls. We think this is because those subtle prodromal symptoms cause people to exercise less,” said Dr. Elbaz.
In the main analysis, which had a 10-year lag, 1,074 women developed incident PD during a mean follow-up of 17.2 years. Those in the highest quartile of physical activity had a 25% lower risk for PD vs. those in the lowest quartile (adjusted hazard ratio [HR], 0.75, 95% confidence interval [CI], 0.63-0.89).
The risk for PD decreased with increasing levels of physical activity in a linear fashion, noted Dr. Elbaz. “So doing even a little bit of physical activity is better than doing nothing at all.”
Analyses that included 15-year and 20-year lag times had similar findings.
Sensitivity analyses that adjusted for the Mediterranean diet and caffeine and dairy intake also yielded comparable results. This was also true for analyses that adjusted for comorbidities such as body mass index, hypertension, hypercholesterolemia, diabetes, and cardiovascular disease, all of which can affect PD risk.
“This gives weight to the idea that diabetes or cardiovascular diseases do not explain the relationship between physical activity and PD, which means the most likely hypothesis is that physical activity has a direct protective effect on the brain,” said Dr. Elbaz.
Studies have shown that physical activity affects brain plasticity and can reduce oxidative stress in the brain – a key mechanism involved in PD, he added.
Physical activity is a low-risk, inexpensive, and accessible intervention. But the study was not designed to determine the types of physical activity that are most protective against PD.
The study’s main limitation is that it used self-reported physical activity rather than objective measures such as accelerometers. In addition, the participants were not necessarily representative of the general population.
Robust evidence
In an accompanying editorial, Lana M. Chahine, MD, associate professor in the department of neurology at the University of Pittsburgh, and Sirwan K. L. Darweesh, MD, PhD, Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Center of Expertise for Parkinson and Movement Disorders, Nijmegen, the Netherlands, said the study “provides robust evidence” that physical activity reduces risk for PD in women.
“These results show that the field is moving in the right direction and provide a clear rationale for exercise trials to prevent or delay the onset of manifest PD in at-risk individuals” they wrote.
The study highlights “gaps” in knowledge that merit closer attention and that “further insight is warranted on how much the effects on PD vary by type, intensity, frequency, and duration of physical activity,” the editorialists noted.
Another gap is how the accuracy of assessment of physical activity can be improved beyond self-report. “Wearable sensor technology now offers the potential to assess physical activity remotely and objectively in prevention trials,” they added.
Other areas that need exploring relate to mechanisms by which physical activity reduces PD risk, and to what extent effects of physical activity vary between individuals, Dr. Chahine and Dr. Darweesh noted.
Commenting for this article, Michael S. Okun, MD, executive director of the Fixel Institute for Neurological Diseases at University of Florida Health, and medical adviser for the Parkinson’s Foundation, said the findings are “significant and important.”
Based on only a handful of previous studies, it was assumed that physical activity was associated with reduced Parkinson’s diagnosis only in men, said Dr. Okun. “The current dataset was larger and included longer-term outcomes, and it informs the field that exercise may be important for reducing the risk of Parkinson’s disease in men as well as in women.”
The investigators, the editorialists, and Dr. Okun reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Investigators found that among almost 99,000 women participating in the ongoing E3N study, those who exercised the most frequently had up to a 25% lower risk for PD than their less-active counterparts.
The results highlight the importance of exercising early in mid-life to prevent PD later on, study investigator Alexis Elbaz, MD, PhD, research director, French Institute of Health and Medical Research (Inserm), Paris, said in an interview.
This is especially critical since there is no cure nor disease-modifying treatments. The medications that are available are aimed at symptom reduction.
“Finding ways to prevent or delay the onset of Parkinson’s is really important, and physical activity seems to be one of the possible strategies to reduce the risk,” Dr. Elbaz said.
The study was published online in Neurology.
Direct protective effect?
Results from previous research examining the relationship physical activity and PD has been inconsistent. One meta-analysis showed a statistically significant association among men but a nonsignificant link in women.
The investigators noted that some of the findings from previous studies may have been affected by reverse causation. As nonmotor symptoms such as constipation and subtle motor signs such as tremor and balance issues can present years before a PD diagnosis, patients may reduce their physical activity because of such symptoms.
To address this potential confounder, the researchers used “lag” analyses, where data on physical activity levels in the years close to a PD diagnosis are omitted.
The study relied on data from the E3N, an ongoing cohort study of 98,995 women, born between 1925 and 1950 and recruited in 1990, who were affiliated with a French national health insurance plan that primarily covers teachers. Participants completed a questionnaire on lifestyle and medical history at baseline and follow-up questionnaires every 2-3 years.
In six of the questionnaires, participants provided details about various recreational, sports, and household activities – for example, walking, climbing stairs, gardening, and cleaning. The authors attributed metabolic equivalent of task (MET) values to each activity and multiplied METs by their frequency and duration to obtain a physical activity score.
Definite and probable PD cases were determined through self-reported physician diagnoses, anti-parkinsonian drug claims, and medical records, with diagnoses verified by an expert panel.
Researchers investigated the relationship between physical activity and PD onset in a nested-case control study that included 25,075 women (1,196 PD cases and 23,879 controls) with a mean age of 71.9 years. They found physical activity was significantly lower in cases than in controls throughout follow-up.
The difference between cases and controls began to increase at 10 years before diagnosis (P-interaction = .003). “When we looked at the trajectories of physical activity in PD patients and in controls, we saw that in the 10 years before the diagnosis, physical activity declined at a steeper rate in controls. We think this is because those subtle prodromal symptoms cause people to exercise less,” said Dr. Elbaz.
In the main analysis, which had a 10-year lag, 1,074 women developed incident PD during a mean follow-up of 17.2 years. Those in the highest quartile of physical activity had a 25% lower risk for PD vs. those in the lowest quartile (adjusted hazard ratio [HR], 0.75, 95% confidence interval [CI], 0.63-0.89).
The risk for PD decreased with increasing levels of physical activity in a linear fashion, noted Dr. Elbaz. “So doing even a little bit of physical activity is better than doing nothing at all.”
Analyses that included 15-year and 20-year lag times had similar findings.
Sensitivity analyses that adjusted for the Mediterranean diet and caffeine and dairy intake also yielded comparable results. This was also true for analyses that adjusted for comorbidities such as body mass index, hypertension, hypercholesterolemia, diabetes, and cardiovascular disease, all of which can affect PD risk.
“This gives weight to the idea that diabetes or cardiovascular diseases do not explain the relationship between physical activity and PD, which means the most likely hypothesis is that physical activity has a direct protective effect on the brain,” said Dr. Elbaz.
Studies have shown that physical activity affects brain plasticity and can reduce oxidative stress in the brain – a key mechanism involved in PD, he added.
Physical activity is a low-risk, inexpensive, and accessible intervention. But the study was not designed to determine the types of physical activity that are most protective against PD.
The study’s main limitation is that it used self-reported physical activity rather than objective measures such as accelerometers. In addition, the participants were not necessarily representative of the general population.
Robust evidence
In an accompanying editorial, Lana M. Chahine, MD, associate professor in the department of neurology at the University of Pittsburgh, and Sirwan K. L. Darweesh, MD, PhD, Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Center of Expertise for Parkinson and Movement Disorders, Nijmegen, the Netherlands, said the study “provides robust evidence” that physical activity reduces risk for PD in women.
“These results show that the field is moving in the right direction and provide a clear rationale for exercise trials to prevent or delay the onset of manifest PD in at-risk individuals” they wrote.
The study highlights “gaps” in knowledge that merit closer attention and that “further insight is warranted on how much the effects on PD vary by type, intensity, frequency, and duration of physical activity,” the editorialists noted.
Another gap is how the accuracy of assessment of physical activity can be improved beyond self-report. “Wearable sensor technology now offers the potential to assess physical activity remotely and objectively in prevention trials,” they added.
Other areas that need exploring relate to mechanisms by which physical activity reduces PD risk, and to what extent effects of physical activity vary between individuals, Dr. Chahine and Dr. Darweesh noted.
Commenting for this article, Michael S. Okun, MD, executive director of the Fixel Institute for Neurological Diseases at University of Florida Health, and medical adviser for the Parkinson’s Foundation, said the findings are “significant and important.”
Based on only a handful of previous studies, it was assumed that physical activity was associated with reduced Parkinson’s diagnosis only in men, said Dr. Okun. “The current dataset was larger and included longer-term outcomes, and it informs the field that exercise may be important for reducing the risk of Parkinson’s disease in men as well as in women.”
The investigators, the editorialists, and Dr. Okun reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Investigators found that among almost 99,000 women participating in the ongoing E3N study, those who exercised the most frequently had up to a 25% lower risk for PD than their less-active counterparts.
The results highlight the importance of exercising early in mid-life to prevent PD later on, study investigator Alexis Elbaz, MD, PhD, research director, French Institute of Health and Medical Research (Inserm), Paris, said in an interview.
This is especially critical since there is no cure nor disease-modifying treatments. The medications that are available are aimed at symptom reduction.
“Finding ways to prevent or delay the onset of Parkinson’s is really important, and physical activity seems to be one of the possible strategies to reduce the risk,” Dr. Elbaz said.
The study was published online in Neurology.
Direct protective effect?
Results from previous research examining the relationship physical activity and PD has been inconsistent. One meta-analysis showed a statistically significant association among men but a nonsignificant link in women.
The investigators noted that some of the findings from previous studies may have been affected by reverse causation. As nonmotor symptoms such as constipation and subtle motor signs such as tremor and balance issues can present years before a PD diagnosis, patients may reduce their physical activity because of such symptoms.
To address this potential confounder, the researchers used “lag” analyses, where data on physical activity levels in the years close to a PD diagnosis are omitted.
The study relied on data from the E3N, an ongoing cohort study of 98,995 women, born between 1925 and 1950 and recruited in 1990, who were affiliated with a French national health insurance plan that primarily covers teachers. Participants completed a questionnaire on lifestyle and medical history at baseline and follow-up questionnaires every 2-3 years.
In six of the questionnaires, participants provided details about various recreational, sports, and household activities – for example, walking, climbing stairs, gardening, and cleaning. The authors attributed metabolic equivalent of task (MET) values to each activity and multiplied METs by their frequency and duration to obtain a physical activity score.
Definite and probable PD cases were determined through self-reported physician diagnoses, anti-parkinsonian drug claims, and medical records, with diagnoses verified by an expert panel.
Researchers investigated the relationship between physical activity and PD onset in a nested-case control study that included 25,075 women (1,196 PD cases and 23,879 controls) with a mean age of 71.9 years. They found physical activity was significantly lower in cases than in controls throughout follow-up.
The difference between cases and controls began to increase at 10 years before diagnosis (P-interaction = .003). “When we looked at the trajectories of physical activity in PD patients and in controls, we saw that in the 10 years before the diagnosis, physical activity declined at a steeper rate in controls. We think this is because those subtle prodromal symptoms cause people to exercise less,” said Dr. Elbaz.
In the main analysis, which had a 10-year lag, 1,074 women developed incident PD during a mean follow-up of 17.2 years. Those in the highest quartile of physical activity had a 25% lower risk for PD vs. those in the lowest quartile (adjusted hazard ratio [HR], 0.75, 95% confidence interval [CI], 0.63-0.89).
The risk for PD decreased with increasing levels of physical activity in a linear fashion, noted Dr. Elbaz. “So doing even a little bit of physical activity is better than doing nothing at all.”
Analyses that included 15-year and 20-year lag times had similar findings.
Sensitivity analyses that adjusted for the Mediterranean diet and caffeine and dairy intake also yielded comparable results. This was also true for analyses that adjusted for comorbidities such as body mass index, hypertension, hypercholesterolemia, diabetes, and cardiovascular disease, all of which can affect PD risk.
“This gives weight to the idea that diabetes or cardiovascular diseases do not explain the relationship between physical activity and PD, which means the most likely hypothesis is that physical activity has a direct protective effect on the brain,” said Dr. Elbaz.
Studies have shown that physical activity affects brain plasticity and can reduce oxidative stress in the brain – a key mechanism involved in PD, he added.
Physical activity is a low-risk, inexpensive, and accessible intervention. But the study was not designed to determine the types of physical activity that are most protective against PD.
The study’s main limitation is that it used self-reported physical activity rather than objective measures such as accelerometers. In addition, the participants were not necessarily representative of the general population.
Robust evidence
In an accompanying editorial, Lana M. Chahine, MD, associate professor in the department of neurology at the University of Pittsburgh, and Sirwan K. L. Darweesh, MD, PhD, Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Center of Expertise for Parkinson and Movement Disorders, Nijmegen, the Netherlands, said the study “provides robust evidence” that physical activity reduces risk for PD in women.
“These results show that the field is moving in the right direction and provide a clear rationale for exercise trials to prevent or delay the onset of manifest PD in at-risk individuals” they wrote.
The study highlights “gaps” in knowledge that merit closer attention and that “further insight is warranted on how much the effects on PD vary by type, intensity, frequency, and duration of physical activity,” the editorialists noted.
Another gap is how the accuracy of assessment of physical activity can be improved beyond self-report. “Wearable sensor technology now offers the potential to assess physical activity remotely and objectively in prevention trials,” they added.
Other areas that need exploring relate to mechanisms by which physical activity reduces PD risk, and to what extent effects of physical activity vary between individuals, Dr. Chahine and Dr. Darweesh noted.
Commenting for this article, Michael S. Okun, MD, executive director of the Fixel Institute for Neurological Diseases at University of Florida Health, and medical adviser for the Parkinson’s Foundation, said the findings are “significant and important.”
Based on only a handful of previous studies, it was assumed that physical activity was associated with reduced Parkinson’s diagnosis only in men, said Dr. Okun. “The current dataset was larger and included longer-term outcomes, and it informs the field that exercise may be important for reducing the risk of Parkinson’s disease in men as well as in women.”
The investigators, the editorialists, and Dr. Okun reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
FROM NEUROLOGY
Internet use a modifiable dementia risk factor in older adults?
Investigators followed more than 18,000 older individuals and found that regular Internet use was associated with about a 50% reduction in dementia risk, compared with their counterparts who did not use the Internet regularly.
They also found that longer duration of regular Internet use was associated with a reduced risk of dementia, although excessive daily Internet usage appeared to adversely affect dementia risk.
“Online engagement can develop and maintain cognitive reserve – resiliency against physiological damage to the brain – and increased cognitive reserve can, in turn, compensate for brain aging and reduce the risk of dementia,” study investigator Gawon Cho, a doctoral candidate at New York University School of Global Public Health, said in an interview.
The study was published online in the Journal of the American Geriatrics Society.
Unexamined benefits
Prior research has shown that older adult Internet users have “better overall cognitive performance, verbal reasoning, and memory,” compared with nonusers, the authors note.
However, because this body of research consists of cross-sectional analyses and longitudinal studies with brief follow-up periods, the long-term cognitive benefits of Internet usage remain “unexamined.”
In addition, despite “extensive evidence of a disproportionately high burden of dementia in people of color, individuals without higher education, and adults who experienced other socioeconomic hardships, little is known about whether the Internet has exacerbated population-level disparities in cognitive health,” the investigators add.
Another question concerns whether excessive Internet usage may actually be detrimental to neurocognitive outcomes. However, “existing evidence on the adverse effects of Internet usage is concentrated in younger populations whose brains are still undergoing maturation.”
Ms. Cho said the motivation for the study was the lack of longitudinal studies on this topic, especially those with sufficient follow-up periods. In addition, she said, there is insufficient evidence about how changes in Internet usage in older age are associated with prospective dementia risk.
For the study, investigators turned to participants in the Health and Retirement Study, an ongoing longitudinal survey of a nationally representative sample of U.S.-based older adults (aged ≥ 50 years).
All participants (n = 18,154; 47.36% male; median age, 55.17 years) were dementia-free, community-dwelling older adults who completed a 2002 baseline cognitive assessment and were asked about Internet usage every 2 years thereafter.
Participants were followed from 2002 to 2018 for a maximum of 17.1 years (median, 7.9 years), which is the longest follow-up period to date. Of the total sample, 64.76% were regular Internet users.
The study’s primary outcome was incident dementia, based on performance on the Modified Telephone Interview for Cognitive Status (TICS-M), which was administered every 2 years.
The exposure examined in the study was cumulative Internet usage in late adulthood, defined as “the number of biennial waves where participants used the Internet regularly during the first three waves.”
In addition, participants were asked how many hours they spent using the Internet during the past week for activities other than viewing television shows or movies.
The researchers also investigated whether the link between Internet usage and dementia risk varied by educational attainment, race-ethnicity, sex, and generational cohort.
Covariates included baseline TICS-M score, health, age, household income, marital status, and region of residence.
U-shaped curve
More than half of the sample (52.96%) showed no changes in Internet use from baseline during the study period, while one-fifth (20.54%) did show changes in use.
Investigators found a robust link between Internet usage and lower dementia risk (cause-specific hazard ratio, 0.57 [95% CI, 0.46-0.71]) – a finding that remained even after adjusting for self-selection into baseline usage (csHR, 0.54 [0.41-0.72]) and signs of cognitive decline at baseline (csHR, 0.62 [0.46-0.85]).
Each additional wave of regular Internet usage was associated with a 21% decrease in the risk of dementia (95% CI, 13%-29%), wherein additional regular periods were associated with reduced dementia risk (csHR, 0.80 [95% CI, 0.68-0.95]).
“The difference in risk between regular and nonregular users did not vary by educational attainment, race-ethnicity, sex, and generation,” the investigators note.
A U-shaped association was found between daily hours of online engagement, wherein the lowest risk was observed in those with 0.1-2 hours of usage (compared with 0 hours of usage). The risk increased in a “monotonic fashion” after 2 hours, with 6.1-8 hours of usage showing the highest risk.
This finding was not considered statistically significant, but the “consistent U-shaped trend offers a preliminary suggestion that excessive online engagement may have adverse cognitive effects on older adults,” the investigators note.
“Among older adults, regular Internet users may experience a lower risk of dementia compared to nonregular users, and longer periods of regular Internet usage in late adulthood may help reduce the risks of subsequent dementia incidence,” said Ms. Cho. “Nonetheless, using the Internet excessively daily may negatively affect the risk of dementia in older adults.”
Bidirectional relationship?
Commenting for this article, Claire Sexton, DPhil, Alzheimer’s Association senior director of scientific programs and outreach, noted that some risk factors for Alzheimer’s or other dementias can’t be changed, while others are modifiable, “either at a personal or a population level.”
She called the current research “important” because it “identifies a potentially modifiable factor that may influence dementia risk.”
However, cautioned Dr. Sexton, who was not involved with the study, the findings cannot establish cause and effect. In fact, the relationship may be bidirectional.
“It may be that regular Internet usage is associated with increased cognitive stimulation, and in turn reduced risk of dementia; or it may be that individuals with lower risk of dementia are more likely to engage in regular Internet usage,” she said. Thus, “interventional studies are able to shed more light on causation.”
The Health and Retirement Study is sponsored by the National Institute on Aging and is conducted by the University of Michigan, Ann Arbor. Ms. Cho, her coauthors, and Dr. Sexton have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Investigators followed more than 18,000 older individuals and found that regular Internet use was associated with about a 50% reduction in dementia risk, compared with their counterparts who did not use the Internet regularly.
They also found that longer duration of regular Internet use was associated with a reduced risk of dementia, although excessive daily Internet usage appeared to adversely affect dementia risk.
“Online engagement can develop and maintain cognitive reserve – resiliency against physiological damage to the brain – and increased cognitive reserve can, in turn, compensate for brain aging and reduce the risk of dementia,” study investigator Gawon Cho, a doctoral candidate at New York University School of Global Public Health, said in an interview.
The study was published online in the Journal of the American Geriatrics Society.
Unexamined benefits
Prior research has shown that older adult Internet users have “better overall cognitive performance, verbal reasoning, and memory,” compared with nonusers, the authors note.
However, because this body of research consists of cross-sectional analyses and longitudinal studies with brief follow-up periods, the long-term cognitive benefits of Internet usage remain “unexamined.”
In addition, despite “extensive evidence of a disproportionately high burden of dementia in people of color, individuals without higher education, and adults who experienced other socioeconomic hardships, little is known about whether the Internet has exacerbated population-level disparities in cognitive health,” the investigators add.
Another question concerns whether excessive Internet usage may actually be detrimental to neurocognitive outcomes. However, “existing evidence on the adverse effects of Internet usage is concentrated in younger populations whose brains are still undergoing maturation.”
Ms. Cho said the motivation for the study was the lack of longitudinal studies on this topic, especially those with sufficient follow-up periods. In addition, she said, there is insufficient evidence about how changes in Internet usage in older age are associated with prospective dementia risk.
For the study, investigators turned to participants in the Health and Retirement Study, an ongoing longitudinal survey of a nationally representative sample of U.S.-based older adults (aged ≥ 50 years).
All participants (n = 18,154; 47.36% male; median age, 55.17 years) were dementia-free, community-dwelling older adults who completed a 2002 baseline cognitive assessment and were asked about Internet usage every 2 years thereafter.
Participants were followed from 2002 to 2018 for a maximum of 17.1 years (median, 7.9 years), which is the longest follow-up period to date. Of the total sample, 64.76% were regular Internet users.
The study’s primary outcome was incident dementia, based on performance on the Modified Telephone Interview for Cognitive Status (TICS-M), which was administered every 2 years.
The exposure examined in the study was cumulative Internet usage in late adulthood, defined as “the number of biennial waves where participants used the Internet regularly during the first three waves.”
In addition, participants were asked how many hours they spent using the Internet during the past week for activities other than viewing television shows or movies.
The researchers also investigated whether the link between Internet usage and dementia risk varied by educational attainment, race-ethnicity, sex, and generational cohort.
Covariates included baseline TICS-M score, health, age, household income, marital status, and region of residence.
U-shaped curve
More than half of the sample (52.96%) showed no changes in Internet use from baseline during the study period, while one-fifth (20.54%) did show changes in use.
Investigators found a robust link between Internet usage and lower dementia risk (cause-specific hazard ratio, 0.57 [95% CI, 0.46-0.71]) – a finding that remained even after adjusting for self-selection into baseline usage (csHR, 0.54 [0.41-0.72]) and signs of cognitive decline at baseline (csHR, 0.62 [0.46-0.85]).
Each additional wave of regular Internet usage was associated with a 21% decrease in the risk of dementia (95% CI, 13%-29%), wherein additional regular periods were associated with reduced dementia risk (csHR, 0.80 [95% CI, 0.68-0.95]).
“The difference in risk between regular and nonregular users did not vary by educational attainment, race-ethnicity, sex, and generation,” the investigators note.
A U-shaped association was found between daily hours of online engagement, wherein the lowest risk was observed in those with 0.1-2 hours of usage (compared with 0 hours of usage). The risk increased in a “monotonic fashion” after 2 hours, with 6.1-8 hours of usage showing the highest risk.
This finding was not considered statistically significant, but the “consistent U-shaped trend offers a preliminary suggestion that excessive online engagement may have adverse cognitive effects on older adults,” the investigators note.
“Among older adults, regular Internet users may experience a lower risk of dementia compared to nonregular users, and longer periods of regular Internet usage in late adulthood may help reduce the risks of subsequent dementia incidence,” said Ms. Cho. “Nonetheless, using the Internet excessively daily may negatively affect the risk of dementia in older adults.”
Bidirectional relationship?
Commenting for this article, Claire Sexton, DPhil, Alzheimer’s Association senior director of scientific programs and outreach, noted that some risk factors for Alzheimer’s or other dementias can’t be changed, while others are modifiable, “either at a personal or a population level.”
She called the current research “important” because it “identifies a potentially modifiable factor that may influence dementia risk.”
However, cautioned Dr. Sexton, who was not involved with the study, the findings cannot establish cause and effect. In fact, the relationship may be bidirectional.
“It may be that regular Internet usage is associated with increased cognitive stimulation, and in turn reduced risk of dementia; or it may be that individuals with lower risk of dementia are more likely to engage in regular Internet usage,” she said. Thus, “interventional studies are able to shed more light on causation.”
The Health and Retirement Study is sponsored by the National Institute on Aging and is conducted by the University of Michigan, Ann Arbor. Ms. Cho, her coauthors, and Dr. Sexton have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Investigators followed more than 18,000 older individuals and found that regular Internet use was associated with about a 50% reduction in dementia risk, compared with their counterparts who did not use the Internet regularly.
They also found that longer duration of regular Internet use was associated with a reduced risk of dementia, although excessive daily Internet usage appeared to adversely affect dementia risk.
“Online engagement can develop and maintain cognitive reserve – resiliency against physiological damage to the brain – and increased cognitive reserve can, in turn, compensate for brain aging and reduce the risk of dementia,” study investigator Gawon Cho, a doctoral candidate at New York University School of Global Public Health, said in an interview.
The study was published online in the Journal of the American Geriatrics Society.
Unexamined benefits
Prior research has shown that older adult Internet users have “better overall cognitive performance, verbal reasoning, and memory,” compared with nonusers, the authors note.
However, because this body of research consists of cross-sectional analyses and longitudinal studies with brief follow-up periods, the long-term cognitive benefits of Internet usage remain “unexamined.”
In addition, despite “extensive evidence of a disproportionately high burden of dementia in people of color, individuals without higher education, and adults who experienced other socioeconomic hardships, little is known about whether the Internet has exacerbated population-level disparities in cognitive health,” the investigators add.
Another question concerns whether excessive Internet usage may actually be detrimental to neurocognitive outcomes. However, “existing evidence on the adverse effects of Internet usage is concentrated in younger populations whose brains are still undergoing maturation.”
Ms. Cho said the motivation for the study was the lack of longitudinal studies on this topic, especially those with sufficient follow-up periods. In addition, she said, there is insufficient evidence about how changes in Internet usage in older age are associated with prospective dementia risk.
For the study, investigators turned to participants in the Health and Retirement Study, an ongoing longitudinal survey of a nationally representative sample of U.S.-based older adults (aged ≥ 50 years).
All participants (n = 18,154; 47.36% male; median age, 55.17 years) were dementia-free, community-dwelling older adults who completed a 2002 baseline cognitive assessment and were asked about Internet usage every 2 years thereafter.
Participants were followed from 2002 to 2018 for a maximum of 17.1 years (median, 7.9 years), which is the longest follow-up period to date. Of the total sample, 64.76% were regular Internet users.
The study’s primary outcome was incident dementia, based on performance on the Modified Telephone Interview for Cognitive Status (TICS-M), which was administered every 2 years.
The exposure examined in the study was cumulative Internet usage in late adulthood, defined as “the number of biennial waves where participants used the Internet regularly during the first three waves.”
In addition, participants were asked how many hours they spent using the Internet during the past week for activities other than viewing television shows or movies.
The researchers also investigated whether the link between Internet usage and dementia risk varied by educational attainment, race-ethnicity, sex, and generational cohort.
Covariates included baseline TICS-M score, health, age, household income, marital status, and region of residence.
U-shaped curve
More than half of the sample (52.96%) showed no changes in Internet use from baseline during the study period, while one-fifth (20.54%) did show changes in use.
Investigators found a robust link between Internet usage and lower dementia risk (cause-specific hazard ratio, 0.57 [95% CI, 0.46-0.71]) – a finding that remained even after adjusting for self-selection into baseline usage (csHR, 0.54 [0.41-0.72]) and signs of cognitive decline at baseline (csHR, 0.62 [0.46-0.85]).
Each additional wave of regular Internet usage was associated with a 21% decrease in the risk of dementia (95% CI, 13%-29%), wherein additional regular periods were associated with reduced dementia risk (csHR, 0.80 [95% CI, 0.68-0.95]).
“The difference in risk between regular and nonregular users did not vary by educational attainment, race-ethnicity, sex, and generation,” the investigators note.
A U-shaped association was found between daily hours of online engagement, wherein the lowest risk was observed in those with 0.1-2 hours of usage (compared with 0 hours of usage). The risk increased in a “monotonic fashion” after 2 hours, with 6.1-8 hours of usage showing the highest risk.
This finding was not considered statistically significant, but the “consistent U-shaped trend offers a preliminary suggestion that excessive online engagement may have adverse cognitive effects on older adults,” the investigators note.
“Among older adults, regular Internet users may experience a lower risk of dementia compared to nonregular users, and longer periods of regular Internet usage in late adulthood may help reduce the risks of subsequent dementia incidence,” said Ms. Cho. “Nonetheless, using the Internet excessively daily may negatively affect the risk of dementia in older adults.”
Bidirectional relationship?
Commenting for this article, Claire Sexton, DPhil, Alzheimer’s Association senior director of scientific programs and outreach, noted that some risk factors for Alzheimer’s or other dementias can’t be changed, while others are modifiable, “either at a personal or a population level.”
She called the current research “important” because it “identifies a potentially modifiable factor that may influence dementia risk.”
However, cautioned Dr. Sexton, who was not involved with the study, the findings cannot establish cause and effect. In fact, the relationship may be bidirectional.
“It may be that regular Internet usage is associated with increased cognitive stimulation, and in turn reduced risk of dementia; or it may be that individuals with lower risk of dementia are more likely to engage in regular Internet usage,” she said. Thus, “interventional studies are able to shed more light on causation.”
The Health and Retirement Study is sponsored by the National Institute on Aging and is conducted by the University of Michigan, Ann Arbor. Ms. Cho, her coauthors, and Dr. Sexton have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
FROM THE JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
What to expect in the new concussion guidelines
This transcript has been edited for clarity.
Andrew N. Wilner, MD: I’m your host, Dr. Andrew Wilner, reporting virtually from the 2023 American Academy of Neurology meeting in Boston. It’s my pleasure today to speak with Dr. Shae Datta, codirector of the NYU Langone Concussion Center.
She’s also a clinical assistant professor of neurology at NYU School of Medicine. Dr. Datta is chair of the AAN Sports Neurology Section, and she’s leading a panel on concussion at this year’s meeting. She’s going to give us an update. Welcome, Dr. Datta.
Shae Datta, MD: Thank you so much, Andrew. I really love the fact that I’m here speaking to you about all of the new, exciting developments in the field.
Dr. Wilner: Before we get too deep, tell us how you got interested in this topic.
Dr. Datta: I initially thought, when I was in training as a resident, that I wanted to do something like neurocritical care or EEG. It also puzzled me why these seemingly smaller head injuries that didn’t end up in the hospital or ICU were bounced from neurology headache clinic to neuro-ophthalmology headache clinic to neurovestibular headache clinic, and nobody seemed to be able to put together the dots about why they’re having so many different issues — but at the same time, nobody could help them.
At that time, this field was very new. I was on a plane to Paris to a neurocritical care conference as a resident, and I saw the movie Concussion with Will Smith.
It featured one of my current mentors who taught at the fellowship that I graduated from, and it was a fascinating field. I just started looking deeply into it, and I saw that there was a new training fellowship for sports neurology and concussion management, and this is basically why we’re here today.
New concussion consensus guidelines coming
Dr. Wilner: I think this field has really exploded. It used to be that you banged your head, you did a CT scan – remember, I trained about 45 years ago – and if there was nothing on the CT scan, you were done. If you had headaches, you took Tylenol until they went away.
Now, we do MRI, and we realized that it’s really a syndrome. I understand that there are going to be some formal guidelines that have been put together. Is that correct?
Dr. Datta: That’s correct. The 6th International Consensus Conference on Concussion in Sport, in Amsterdam, where I attended and presented a poster, was really a meeting of all the best minds – clinicians and researchers in brain injury – to form a consensus on the newest guidelines that are going to direct our treatment going forward.
Dr. Wilner: I’m going to ask you a trick question because the last time I looked it up I did not get a satisfying answer. What is a concussion?
Dr. Datta: That’s a very good question, and everyone always asks. A concussion is an external force that is emitted upon the head or the neck, or the body, in general, that may cause temporary loss of function. It’s a functional problem.
We don’t see much on CT. We can do MRI. We can do SPECT or we can do these very fancy images, sometimes, of high-velocity head injuries and see small microhemorrhages.
Often, we don’t see anything, but still the patient is loopy. They can’t see straight. They are double-visioned. They have vertigo. Why is that happening? On the cellular level, we have an energy deficit in the sodium-potassium-ATPase pump of the neurons themselves.
Dr. Wilner: Suppose you do see diffuse axonal injury; does that take it out of concussion, or can you have a concussion with visible injury?
Dr. Datta: I think you can have overlap in the symptoms. The diffuse axonal injury would put it into a higher grade of head injury as opposed to a mild traumatic brain injury. Definitely, we would need to work together with our trauma doctors to ensure that patients are not on blood thinners or anything until they heal well enough. Obviously, I would pick them up as an outpatient and follow them until we resolve or rehab them as best as possible.
Concussion assessment tools
Dr. Wilner: There are many sports out there where concussions are fairly frequent, like American football and hockey, for example. Are there any statements in the new guidelines?
Dr. Datta: There are no statements for or against a particular sport because that would really make too much of a bold statement about cause and effect. There is a cause and effect in long-term, repetitive exposure, I would say, in terms of someone being able to play or sustain injury.
Right now, at least at the concussion conference I went to and in the upcoming consensus statement, they will not comment on a specific sport. Obviously, we know that the higher-impact sports are a little more dangerous.
Let’s be honest. At the high school, middle school, or even younger level, some kids are not necessarily the most athletic, right? They play because their friends are playing. If they’re repeatedly getting injured, it’s time for an astute clinician, or a coach, and a whole team to assess them to see if maybe this person is just going to continue to get hurt if they’re not taken out of the game and perhaps they should go to a lower-impact sport.
Dr. Wilner: In schools, often there’s a big size and weight difference. There are 14-year-olds who are 6 fett 2 inches and 200 pounds, and there are 14-year-olds who are 5 feet 2 inches and 110 pounds. Obviously, they’re mismatched on the football field.
You mentioned coaches. Is there anything in the guidelines about training coaches?
Dr. Datta: Specifically, there was nothing in the guidelines about that. There’s a tool for coaches at every level to use, which is called the Sports Concussion Assessment Tool, or SCAT, which is going to be updated to the SCAT6. At the NCAA level, they must receive annual training on concussion management and be given an NCAA concussion handout for coaches.
Obviously, there are more rigorous protocols for national-level coaching. As it stands now, it is not mandatory, but they are given tools to assess someone once they’ve gotten a hit to take them out of the game.
Dr. Wilner: I’ve been following the concussion research through the years. They did some neuropsychological testing on athletes who’ve had this many concussions or that many concussions, and they would find deficits here or subtle deficits there, but they had no baseline.
Then, there was a movement to start testing athletes before the season starts so that they could do a repeat test after concussion and see if there is any difference. Is that something we’re recommending?
Dr. Datta: Most of the time, NCAA-level – certainly where I trained – and national-level sports do testing, but it’s not everywhere. Prior guidelines have indicated that preseason testing is not required. That is largely because there has been no standardized neuropsychological testing established.
There are computerized testing options where the validity and reliability are questionable. Also, let’s say it’s a college student; they didn’t sleep all night and then they took this computer test. They would probably do worse than they would if they had received a head hit.
Just to be on the safe side, most places that have collegiate-level sports that are at a high level do preseason testing. If I were to speak personally, aside from the guidelines, I would say that it’s been helpful for me to look at the before and after, in general, overall, to make a decision about my treatment protocol.
Dr. Wilner: Let’s talk about the patient. You have a 20-year-old guy. He’s playing football. There’s a big play. Bonk, he gets hit on the head. He’s on the ground. He’s dazed, staggers a little bit, gets up, and you ask how he is feeling. He says he’s fine and then he wobbles off to the sideline. What do you do with that kid?
Dr. Datta: Obviously, the first thing is to remove him from the play environment to a quiet space. Second, either an athletic trainer or a coach would administer basic screening neurologic tests, such as “where are you, what’s today’s date, what is your name?” and other orientation questions.
They’ll also go through the SCAT – that’ll be SCAT6 starting in July – the SCAT5 symptom questionnaire to see what symptoms they have. Often, they’re using sideline testing software.
There are two things that can be used on a card to test eye movements, to see if they’re slower. They come out of NYU, coincidentally – the Memory Image Completion (MIC) and the Mobile Universal Lexicon Evaluation System (MULES) – and are used to determine whether eye movements are slower. That way, you can tell whether someone is, compared with before they got their head hit, slower than before.
Based on this composite information, usually the teammates and the head people on the team will know if a player looks different.
They need to be taken out, obviously, if there is nausea or vomiting, any neurologic signs and symptoms, or a neck injury that needs to be stabilized. ABCs first, right? If there’s any vomiting or seizures, they should be taken to the ER right away.
The first thing is to take them out, then do a sideline assessment. Third, see if they need to immediately go to the ED versus follow-up outpatient with me within a day or two.
Dr. Wilner: I think it’s the subtle injuries that are the tough ones. Back to our 20-year-old. He says: “Oh, I’m fine. I want to go back in the game.” Everybody can tell he’s not quite right, even though he passed all the tests. What do you do then?
Dr. Datta: You have to make a judgment call for the safety of the player. They always want to go back, right? This is also an issue when they’re competing for college scholarships and things of that nature. Sometimes they’re sandbagging, where they memorize the answers.
Everything’s on the Internet nowadays, right? We have to make a judgment call as members of the healthcare community and the sports community to keep that player safe.
Just keep them out. Don’t bring them back in the game. Keep them out for a reasonable amount of time. There’s a test called the Buffalo Concussion Treadmill Test; Dr. John Leddy from University of Buffalo has developed a way for us to put athletes through a screening protocol.
This can be part of their vestibular and ocular rehabilitation, where if they don’t have symptoms when we bring their heart rate to certain levels, then we can slowly clear them for return to play as long as they’re nonsymptomatic.
Dr. Wilner: I spoke with your colleague, Dr. Riggins, who is also on your panel, and we were talking about when they can go back. She said they can go back when they don’t have any symptoms. No more headache, no more dizziness, no more lightheadedness, no more trouble concentrating or with memory – all those things have gone away.
Sometimes these symptoms are stubborn. If you have, say, 100 patients like our 20-year-old who got bonked on the head, has some headaches, and doesn’t feel quite right, what usually happens? How many are back to play the next day, the next week, or the next month? How many are out for the season? How does that play out?
Dr. Datta: It depends on a couple of different factors. One, have they had previous head injuries? Two, do they have preexisting symptoms or signs, or diagnoses like migraines, which are likely to get worse after a head injury? Anything that’s preexisting, like a mood disorder, anxiety, depression, or trouble sleeping, is going to get worse.
If they were compensating for untreated ADD or borderline personality or bipolar, I’ve seen many people who’ve developed them. These are not the norm, but I’m saying that you have to be very careful.
Getting back to the question, you treat them. Reasonably, if they’re healthy and they don’t have preexisting signs and symptoms, I would say more than half are back in about 2 weeks.. I would say 60%-70%. It all depends. If they have preexisting issues, then it’s going to take much longer.
From SCAT to SCOAT
Dr. Wilner: This has been very informative. Before we wrap up, tell us what to expect from these guidelines in July. How are they really going to help?
Dr. Datta: We’ve been using the SCAT, which was meant for more sideline assessment because that’s all we had, and it’s worked perfectly well.
This will be better because we often see them within 24-48 hours, when the symptoms are sometimes a little bit better.
We also will see the sport and concussion group come up with added athlete perspectives, ethics discussion, power-sport athlete considerations, and development of this new SCOAT.
Dr. Wilner: Dr. Datta, this is very exciting. I look forward to reading these guidelines in July. I want to thank you for your hard work. I also look forward to talking to you at next year’s meeting. Thank you very much for giving us this update.
Dr. Datta: No problem. It’s my pleasure.
A version of this article originally appeared on Medscape.com.
This transcript has been edited for clarity.
Andrew N. Wilner, MD: I’m your host, Dr. Andrew Wilner, reporting virtually from the 2023 American Academy of Neurology meeting in Boston. It’s my pleasure today to speak with Dr. Shae Datta, codirector of the NYU Langone Concussion Center.
She’s also a clinical assistant professor of neurology at NYU School of Medicine. Dr. Datta is chair of the AAN Sports Neurology Section, and she’s leading a panel on concussion at this year’s meeting. She’s going to give us an update. Welcome, Dr. Datta.
Shae Datta, MD: Thank you so much, Andrew. I really love the fact that I’m here speaking to you about all of the new, exciting developments in the field.
Dr. Wilner: Before we get too deep, tell us how you got interested in this topic.
Dr. Datta: I initially thought, when I was in training as a resident, that I wanted to do something like neurocritical care or EEG. It also puzzled me why these seemingly smaller head injuries that didn’t end up in the hospital or ICU were bounced from neurology headache clinic to neuro-ophthalmology headache clinic to neurovestibular headache clinic, and nobody seemed to be able to put together the dots about why they’re having so many different issues — but at the same time, nobody could help them.
At that time, this field was very new. I was on a plane to Paris to a neurocritical care conference as a resident, and I saw the movie Concussion with Will Smith.
It featured one of my current mentors who taught at the fellowship that I graduated from, and it was a fascinating field. I just started looking deeply into it, and I saw that there was a new training fellowship for sports neurology and concussion management, and this is basically why we’re here today.
New concussion consensus guidelines coming
Dr. Wilner: I think this field has really exploded. It used to be that you banged your head, you did a CT scan – remember, I trained about 45 years ago – and if there was nothing on the CT scan, you were done. If you had headaches, you took Tylenol until they went away.
Now, we do MRI, and we realized that it’s really a syndrome. I understand that there are going to be some formal guidelines that have been put together. Is that correct?
Dr. Datta: That’s correct. The 6th International Consensus Conference on Concussion in Sport, in Amsterdam, where I attended and presented a poster, was really a meeting of all the best minds – clinicians and researchers in brain injury – to form a consensus on the newest guidelines that are going to direct our treatment going forward.
Dr. Wilner: I’m going to ask you a trick question because the last time I looked it up I did not get a satisfying answer. What is a concussion?
Dr. Datta: That’s a very good question, and everyone always asks. A concussion is an external force that is emitted upon the head or the neck, or the body, in general, that may cause temporary loss of function. It’s a functional problem.
We don’t see much on CT. We can do MRI. We can do SPECT or we can do these very fancy images, sometimes, of high-velocity head injuries and see small microhemorrhages.
Often, we don’t see anything, but still the patient is loopy. They can’t see straight. They are double-visioned. They have vertigo. Why is that happening? On the cellular level, we have an energy deficit in the sodium-potassium-ATPase pump of the neurons themselves.
Dr. Wilner: Suppose you do see diffuse axonal injury; does that take it out of concussion, or can you have a concussion with visible injury?
Dr. Datta: I think you can have overlap in the symptoms. The diffuse axonal injury would put it into a higher grade of head injury as opposed to a mild traumatic brain injury. Definitely, we would need to work together with our trauma doctors to ensure that patients are not on blood thinners or anything until they heal well enough. Obviously, I would pick them up as an outpatient and follow them until we resolve or rehab them as best as possible.
Concussion assessment tools
Dr. Wilner: There are many sports out there where concussions are fairly frequent, like American football and hockey, for example. Are there any statements in the new guidelines?
Dr. Datta: There are no statements for or against a particular sport because that would really make too much of a bold statement about cause and effect. There is a cause and effect in long-term, repetitive exposure, I would say, in terms of someone being able to play or sustain injury.
Right now, at least at the concussion conference I went to and in the upcoming consensus statement, they will not comment on a specific sport. Obviously, we know that the higher-impact sports are a little more dangerous.
Let’s be honest. At the high school, middle school, or even younger level, some kids are not necessarily the most athletic, right? They play because their friends are playing. If they’re repeatedly getting injured, it’s time for an astute clinician, or a coach, and a whole team to assess them to see if maybe this person is just going to continue to get hurt if they’re not taken out of the game and perhaps they should go to a lower-impact sport.
Dr. Wilner: In schools, often there’s a big size and weight difference. There are 14-year-olds who are 6 fett 2 inches and 200 pounds, and there are 14-year-olds who are 5 feet 2 inches and 110 pounds. Obviously, they’re mismatched on the football field.
You mentioned coaches. Is there anything in the guidelines about training coaches?
Dr. Datta: Specifically, there was nothing in the guidelines about that. There’s a tool for coaches at every level to use, which is called the Sports Concussion Assessment Tool, or SCAT, which is going to be updated to the SCAT6. At the NCAA level, they must receive annual training on concussion management and be given an NCAA concussion handout for coaches.
Obviously, there are more rigorous protocols for national-level coaching. As it stands now, it is not mandatory, but they are given tools to assess someone once they’ve gotten a hit to take them out of the game.
Dr. Wilner: I’ve been following the concussion research through the years. They did some neuropsychological testing on athletes who’ve had this many concussions or that many concussions, and they would find deficits here or subtle deficits there, but they had no baseline.
Then, there was a movement to start testing athletes before the season starts so that they could do a repeat test after concussion and see if there is any difference. Is that something we’re recommending?
Dr. Datta: Most of the time, NCAA-level – certainly where I trained – and national-level sports do testing, but it’s not everywhere. Prior guidelines have indicated that preseason testing is not required. That is largely because there has been no standardized neuropsychological testing established.
There are computerized testing options where the validity and reliability are questionable. Also, let’s say it’s a college student; they didn’t sleep all night and then they took this computer test. They would probably do worse than they would if they had received a head hit.
Just to be on the safe side, most places that have collegiate-level sports that are at a high level do preseason testing. If I were to speak personally, aside from the guidelines, I would say that it’s been helpful for me to look at the before and after, in general, overall, to make a decision about my treatment protocol.
Dr. Wilner: Let’s talk about the patient. You have a 20-year-old guy. He’s playing football. There’s a big play. Bonk, he gets hit on the head. He’s on the ground. He’s dazed, staggers a little bit, gets up, and you ask how he is feeling. He says he’s fine and then he wobbles off to the sideline. What do you do with that kid?
Dr. Datta: Obviously, the first thing is to remove him from the play environment to a quiet space. Second, either an athletic trainer or a coach would administer basic screening neurologic tests, such as “where are you, what’s today’s date, what is your name?” and other orientation questions.
They’ll also go through the SCAT – that’ll be SCAT6 starting in July – the SCAT5 symptom questionnaire to see what symptoms they have. Often, they’re using sideline testing software.
There are two things that can be used on a card to test eye movements, to see if they’re slower. They come out of NYU, coincidentally – the Memory Image Completion (MIC) and the Mobile Universal Lexicon Evaluation System (MULES) – and are used to determine whether eye movements are slower. That way, you can tell whether someone is, compared with before they got their head hit, slower than before.
Based on this composite information, usually the teammates and the head people on the team will know if a player looks different.
They need to be taken out, obviously, if there is nausea or vomiting, any neurologic signs and symptoms, or a neck injury that needs to be stabilized. ABCs first, right? If there’s any vomiting or seizures, they should be taken to the ER right away.
The first thing is to take them out, then do a sideline assessment. Third, see if they need to immediately go to the ED versus follow-up outpatient with me within a day or two.
Dr. Wilner: I think it’s the subtle injuries that are the tough ones. Back to our 20-year-old. He says: “Oh, I’m fine. I want to go back in the game.” Everybody can tell he’s not quite right, even though he passed all the tests. What do you do then?
Dr. Datta: You have to make a judgment call for the safety of the player. They always want to go back, right? This is also an issue when they’re competing for college scholarships and things of that nature. Sometimes they’re sandbagging, where they memorize the answers.
Everything’s on the Internet nowadays, right? We have to make a judgment call as members of the healthcare community and the sports community to keep that player safe.
Just keep them out. Don’t bring them back in the game. Keep them out for a reasonable amount of time. There’s a test called the Buffalo Concussion Treadmill Test; Dr. John Leddy from University of Buffalo has developed a way for us to put athletes through a screening protocol.
This can be part of their vestibular and ocular rehabilitation, where if they don’t have symptoms when we bring their heart rate to certain levels, then we can slowly clear them for return to play as long as they’re nonsymptomatic.
Dr. Wilner: I spoke with your colleague, Dr. Riggins, who is also on your panel, and we were talking about when they can go back. She said they can go back when they don’t have any symptoms. No more headache, no more dizziness, no more lightheadedness, no more trouble concentrating or with memory – all those things have gone away.
Sometimes these symptoms are stubborn. If you have, say, 100 patients like our 20-year-old who got bonked on the head, has some headaches, and doesn’t feel quite right, what usually happens? How many are back to play the next day, the next week, or the next month? How many are out for the season? How does that play out?
Dr. Datta: It depends on a couple of different factors. One, have they had previous head injuries? Two, do they have preexisting symptoms or signs, or diagnoses like migraines, which are likely to get worse after a head injury? Anything that’s preexisting, like a mood disorder, anxiety, depression, or trouble sleeping, is going to get worse.
If they were compensating for untreated ADD or borderline personality or bipolar, I’ve seen many people who’ve developed them. These are not the norm, but I’m saying that you have to be very careful.
Getting back to the question, you treat them. Reasonably, if they’re healthy and they don’t have preexisting signs and symptoms, I would say more than half are back in about 2 weeks.. I would say 60%-70%. It all depends. If they have preexisting issues, then it’s going to take much longer.
From SCAT to SCOAT
Dr. Wilner: This has been very informative. Before we wrap up, tell us what to expect from these guidelines in July. How are they really going to help?
Dr. Datta: We’ve been using the SCAT, which was meant for more sideline assessment because that’s all we had, and it’s worked perfectly well.
This will be better because we often see them within 24-48 hours, when the symptoms are sometimes a little bit better.
We also will see the sport and concussion group come up with added athlete perspectives, ethics discussion, power-sport athlete considerations, and development of this new SCOAT.
Dr. Wilner: Dr. Datta, this is very exciting. I look forward to reading these guidelines in July. I want to thank you for your hard work. I also look forward to talking to you at next year’s meeting. Thank you very much for giving us this update.
Dr. Datta: No problem. It’s my pleasure.
A version of this article originally appeared on Medscape.com.
This transcript has been edited for clarity.
Andrew N. Wilner, MD: I’m your host, Dr. Andrew Wilner, reporting virtually from the 2023 American Academy of Neurology meeting in Boston. It’s my pleasure today to speak with Dr. Shae Datta, codirector of the NYU Langone Concussion Center.
She’s also a clinical assistant professor of neurology at NYU School of Medicine. Dr. Datta is chair of the AAN Sports Neurology Section, and she’s leading a panel on concussion at this year’s meeting. She’s going to give us an update. Welcome, Dr. Datta.
Shae Datta, MD: Thank you so much, Andrew. I really love the fact that I’m here speaking to you about all of the new, exciting developments in the field.
Dr. Wilner: Before we get too deep, tell us how you got interested in this topic.
Dr. Datta: I initially thought, when I was in training as a resident, that I wanted to do something like neurocritical care or EEG. It also puzzled me why these seemingly smaller head injuries that didn’t end up in the hospital or ICU were bounced from neurology headache clinic to neuro-ophthalmology headache clinic to neurovestibular headache clinic, and nobody seemed to be able to put together the dots about why they’re having so many different issues — but at the same time, nobody could help them.
At that time, this field was very new. I was on a plane to Paris to a neurocritical care conference as a resident, and I saw the movie Concussion with Will Smith.
It featured one of my current mentors who taught at the fellowship that I graduated from, and it was a fascinating field. I just started looking deeply into it, and I saw that there was a new training fellowship for sports neurology and concussion management, and this is basically why we’re here today.
New concussion consensus guidelines coming
Dr. Wilner: I think this field has really exploded. It used to be that you banged your head, you did a CT scan – remember, I trained about 45 years ago – and if there was nothing on the CT scan, you were done. If you had headaches, you took Tylenol until they went away.
Now, we do MRI, and we realized that it’s really a syndrome. I understand that there are going to be some formal guidelines that have been put together. Is that correct?
Dr. Datta: That’s correct. The 6th International Consensus Conference on Concussion in Sport, in Amsterdam, where I attended and presented a poster, was really a meeting of all the best minds – clinicians and researchers in brain injury – to form a consensus on the newest guidelines that are going to direct our treatment going forward.
Dr. Wilner: I’m going to ask you a trick question because the last time I looked it up I did not get a satisfying answer. What is a concussion?
Dr. Datta: That’s a very good question, and everyone always asks. A concussion is an external force that is emitted upon the head or the neck, or the body, in general, that may cause temporary loss of function. It’s a functional problem.
We don’t see much on CT. We can do MRI. We can do SPECT or we can do these very fancy images, sometimes, of high-velocity head injuries and see small microhemorrhages.
Often, we don’t see anything, but still the patient is loopy. They can’t see straight. They are double-visioned. They have vertigo. Why is that happening? On the cellular level, we have an energy deficit in the sodium-potassium-ATPase pump of the neurons themselves.
Dr. Wilner: Suppose you do see diffuse axonal injury; does that take it out of concussion, or can you have a concussion with visible injury?
Dr. Datta: I think you can have overlap in the symptoms. The diffuse axonal injury would put it into a higher grade of head injury as opposed to a mild traumatic brain injury. Definitely, we would need to work together with our trauma doctors to ensure that patients are not on blood thinners or anything until they heal well enough. Obviously, I would pick them up as an outpatient and follow them until we resolve or rehab them as best as possible.
Concussion assessment tools
Dr. Wilner: There are many sports out there where concussions are fairly frequent, like American football and hockey, for example. Are there any statements in the new guidelines?
Dr. Datta: There are no statements for or against a particular sport because that would really make too much of a bold statement about cause and effect. There is a cause and effect in long-term, repetitive exposure, I would say, in terms of someone being able to play or sustain injury.
Right now, at least at the concussion conference I went to and in the upcoming consensus statement, they will not comment on a specific sport. Obviously, we know that the higher-impact sports are a little more dangerous.
Let’s be honest. At the high school, middle school, or even younger level, some kids are not necessarily the most athletic, right? They play because their friends are playing. If they’re repeatedly getting injured, it’s time for an astute clinician, or a coach, and a whole team to assess them to see if maybe this person is just going to continue to get hurt if they’re not taken out of the game and perhaps they should go to a lower-impact sport.
Dr. Wilner: In schools, often there’s a big size and weight difference. There are 14-year-olds who are 6 fett 2 inches and 200 pounds, and there are 14-year-olds who are 5 feet 2 inches and 110 pounds. Obviously, they’re mismatched on the football field.
You mentioned coaches. Is there anything in the guidelines about training coaches?
Dr. Datta: Specifically, there was nothing in the guidelines about that. There’s a tool for coaches at every level to use, which is called the Sports Concussion Assessment Tool, or SCAT, which is going to be updated to the SCAT6. At the NCAA level, they must receive annual training on concussion management and be given an NCAA concussion handout for coaches.
Obviously, there are more rigorous protocols for national-level coaching. As it stands now, it is not mandatory, but they are given tools to assess someone once they’ve gotten a hit to take them out of the game.
Dr. Wilner: I’ve been following the concussion research through the years. They did some neuropsychological testing on athletes who’ve had this many concussions or that many concussions, and they would find deficits here or subtle deficits there, but they had no baseline.
Then, there was a movement to start testing athletes before the season starts so that they could do a repeat test after concussion and see if there is any difference. Is that something we’re recommending?
Dr. Datta: Most of the time, NCAA-level – certainly where I trained – and national-level sports do testing, but it’s not everywhere. Prior guidelines have indicated that preseason testing is not required. That is largely because there has been no standardized neuropsychological testing established.
There are computerized testing options where the validity and reliability are questionable. Also, let’s say it’s a college student; they didn’t sleep all night and then they took this computer test. They would probably do worse than they would if they had received a head hit.
Just to be on the safe side, most places that have collegiate-level sports that are at a high level do preseason testing. If I were to speak personally, aside from the guidelines, I would say that it’s been helpful for me to look at the before and after, in general, overall, to make a decision about my treatment protocol.
Dr. Wilner: Let’s talk about the patient. You have a 20-year-old guy. He’s playing football. There’s a big play. Bonk, he gets hit on the head. He’s on the ground. He’s dazed, staggers a little bit, gets up, and you ask how he is feeling. He says he’s fine and then he wobbles off to the sideline. What do you do with that kid?
Dr. Datta: Obviously, the first thing is to remove him from the play environment to a quiet space. Second, either an athletic trainer or a coach would administer basic screening neurologic tests, such as “where are you, what’s today’s date, what is your name?” and other orientation questions.
They’ll also go through the SCAT – that’ll be SCAT6 starting in July – the SCAT5 symptom questionnaire to see what symptoms they have. Often, they’re using sideline testing software.
There are two things that can be used on a card to test eye movements, to see if they’re slower. They come out of NYU, coincidentally – the Memory Image Completion (MIC) and the Mobile Universal Lexicon Evaluation System (MULES) – and are used to determine whether eye movements are slower. That way, you can tell whether someone is, compared with before they got their head hit, slower than before.
Based on this composite information, usually the teammates and the head people on the team will know if a player looks different.
They need to be taken out, obviously, if there is nausea or vomiting, any neurologic signs and symptoms, or a neck injury that needs to be stabilized. ABCs first, right? If there’s any vomiting or seizures, they should be taken to the ER right away.
The first thing is to take them out, then do a sideline assessment. Third, see if they need to immediately go to the ED versus follow-up outpatient with me within a day or two.
Dr. Wilner: I think it’s the subtle injuries that are the tough ones. Back to our 20-year-old. He says: “Oh, I’m fine. I want to go back in the game.” Everybody can tell he’s not quite right, even though he passed all the tests. What do you do then?
Dr. Datta: You have to make a judgment call for the safety of the player. They always want to go back, right? This is also an issue when they’re competing for college scholarships and things of that nature. Sometimes they’re sandbagging, where they memorize the answers.
Everything’s on the Internet nowadays, right? We have to make a judgment call as members of the healthcare community and the sports community to keep that player safe.
Just keep them out. Don’t bring them back in the game. Keep them out for a reasonable amount of time. There’s a test called the Buffalo Concussion Treadmill Test; Dr. John Leddy from University of Buffalo has developed a way for us to put athletes through a screening protocol.
This can be part of their vestibular and ocular rehabilitation, where if they don’t have symptoms when we bring their heart rate to certain levels, then we can slowly clear them for return to play as long as they’re nonsymptomatic.
Dr. Wilner: I spoke with your colleague, Dr. Riggins, who is also on your panel, and we were talking about when they can go back. She said they can go back when they don’t have any symptoms. No more headache, no more dizziness, no more lightheadedness, no more trouble concentrating or with memory – all those things have gone away.
Sometimes these symptoms are stubborn. If you have, say, 100 patients like our 20-year-old who got bonked on the head, has some headaches, and doesn’t feel quite right, what usually happens? How many are back to play the next day, the next week, or the next month? How many are out for the season? How does that play out?
Dr. Datta: It depends on a couple of different factors. One, have they had previous head injuries? Two, do they have preexisting symptoms or signs, or diagnoses like migraines, which are likely to get worse after a head injury? Anything that’s preexisting, like a mood disorder, anxiety, depression, or trouble sleeping, is going to get worse.
If they were compensating for untreated ADD or borderline personality or bipolar, I’ve seen many people who’ve developed them. These are not the norm, but I’m saying that you have to be very careful.
Getting back to the question, you treat them. Reasonably, if they’re healthy and they don’t have preexisting signs and symptoms, I would say more than half are back in about 2 weeks.. I would say 60%-70%. It all depends. If they have preexisting issues, then it’s going to take much longer.
From SCAT to SCOAT
Dr. Wilner: This has been very informative. Before we wrap up, tell us what to expect from these guidelines in July. How are they really going to help?
Dr. Datta: We’ve been using the SCAT, which was meant for more sideline assessment because that’s all we had, and it’s worked perfectly well.
This will be better because we often see them within 24-48 hours, when the symptoms are sometimes a little bit better.
We also will see the sport and concussion group come up with added athlete perspectives, ethics discussion, power-sport athlete considerations, and development of this new SCOAT.
Dr. Wilner: Dr. Datta, this is very exciting. I look forward to reading these guidelines in July. I want to thank you for your hard work. I also look forward to talking to you at next year’s meeting. Thank you very much for giving us this update.
Dr. Datta: No problem. It’s my pleasure.
A version of this article originally appeared on Medscape.com.