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Top U.S. neurology, neurosurgery hospitals ranked
of best hospitals for neurology and neurosurgery.
NYU Langone also claimed the top spot in last year’s ranking.
In the latest rankings, UCSF Health–UCSF Medical Center, San Francisco, holds the No. 2 spot and New York–Presbyterian Hospital–Columbia and Cornell in New York City holds the No. 3 spot for neurology care, with no change from last year.
This year, Mayo Clinic, Rochester, Minn., is ranked No. 4 in neurology and neurosurgery care, up from No. 6 last year, while Cedars-Sinai Medical Center, Los Angeles, ranks fifth this year, rising two spots from No. 7 last year.
Rounding out the top 10 hospitals for neurology and neurosurgery (in order) are UCLA Medical Center, Los Angeles; Johns Hopkins Hospital, Baltimore; Massachusetts General Hospital, Boston; Mount Sinai Hospital, New York; and Northwestern Medicine–Northwestern Memorial Hospital, Chicago.
U.S. News evaluated 1,245 hospitals and ranked the top 50 that treat patients with challenging neurological issues including stroke, conditions affecting the central nervous system, spinal disorders and injuries, seizures, and degenerative nervous system diagnoses such as multiple sclerosis.
“Consumers want useful resources to help them assess which hospital can best meet their specific care needs,” Ben Harder, chief of health analysis and managing editor at U.S. News, said in a statement.
“The 2023-2024 Best Hospitals rankings offer patients and the physicians with whom they consult a data-driven source for comparing performance in outcomes, patient satisfaction, and other metrics that matter to them,” Mr. Harder said.
Honor roll
This year, as in prior years, U.S. News recognized “honor roll” hospitals that have excelled across multiple areas of care. However, this year, for the first time, there is no ordinal ranking of hospitals making the honor roll. Instead, they are listed in alphabetical order.
In a letter to hospital leaders, U.S. News explained that the major change in format came after months of deliberation, feedback from health care organizations and professionals, and an analysis of how consumers navigate the organization’s website.
Ordinal ranking of hospitals that make the honor roll “obscures the fact that all of the honor roll hospitals have attained the highest standard of care in the nation,” the letter reads.
This year there are 22 honor roll hospitals:
- Barnes-Jewish Hospital, St. Louis
- Brigham and Women’s Hospital, Boston
- Cedars-Sinai Medical Center, Los Angeles
- Cleveland Clinic
- Hospitals of the University of Pennsylvania-Penn Medicine, Philadelphia
- Houston Methodist Hospital
- Johns Hopkins Hospital, Baltimore
- Massachusetts General Hospital, Boston
- Mayo Clinic, Rochester, Minn.
- Mount Sinai Hospital, New York City
- New York–Presbyterian Hospital–Columbia and Cornell, New York City
- North Shore University Hospital at Northwell Health, Manhasset, N.Y.
- Northwestern Memorial Hospital, Chicago
- NYU Langone Hospitals, New York City
- Rush University Medical Center, Chicago
- Stanford (Calif.) Health Care–Stanford Hospital
- UC San Diego Health–La Jolla and Hillcrest Hospitals
- UCLA Medical Center, Los Angeles
- UCSF Health–UCSF Medical Center, San Francisco
- University of Michigan Health–Ann Arbor
- UT Southwestern Medical Center, Dallas
- Vanderbilt University Medical Center, Nashville, Tenn.
U.S. News noted that to keep pace with consumers’ needs and the ever-evolving landscape of health care, “several refinements” are reflected in the latest best hospitals rankings.
These include the introduction of outpatient outcomes in key specialty rankings and surgical ratings, the expanded inclusion of other outpatient data, an increased weight on objective quality measures, and a reduced weight on expert opinion.
In addition, hospital profiles at usnews.com feature refined health equity measures, including a new measure of racial disparities in outcomes.
The full report for best hospitals, best specialty hospitals, and methodology is available online.
A version of this article first appeared on Medscape.com.
of best hospitals for neurology and neurosurgery.
NYU Langone also claimed the top spot in last year’s ranking.
In the latest rankings, UCSF Health–UCSF Medical Center, San Francisco, holds the No. 2 spot and New York–Presbyterian Hospital–Columbia and Cornell in New York City holds the No. 3 spot for neurology care, with no change from last year.
This year, Mayo Clinic, Rochester, Minn., is ranked No. 4 in neurology and neurosurgery care, up from No. 6 last year, while Cedars-Sinai Medical Center, Los Angeles, ranks fifth this year, rising two spots from No. 7 last year.
Rounding out the top 10 hospitals for neurology and neurosurgery (in order) are UCLA Medical Center, Los Angeles; Johns Hopkins Hospital, Baltimore; Massachusetts General Hospital, Boston; Mount Sinai Hospital, New York; and Northwestern Medicine–Northwestern Memorial Hospital, Chicago.
U.S. News evaluated 1,245 hospitals and ranked the top 50 that treat patients with challenging neurological issues including stroke, conditions affecting the central nervous system, spinal disorders and injuries, seizures, and degenerative nervous system diagnoses such as multiple sclerosis.
“Consumers want useful resources to help them assess which hospital can best meet their specific care needs,” Ben Harder, chief of health analysis and managing editor at U.S. News, said in a statement.
“The 2023-2024 Best Hospitals rankings offer patients and the physicians with whom they consult a data-driven source for comparing performance in outcomes, patient satisfaction, and other metrics that matter to them,” Mr. Harder said.
Honor roll
This year, as in prior years, U.S. News recognized “honor roll” hospitals that have excelled across multiple areas of care. However, this year, for the first time, there is no ordinal ranking of hospitals making the honor roll. Instead, they are listed in alphabetical order.
In a letter to hospital leaders, U.S. News explained that the major change in format came after months of deliberation, feedback from health care organizations and professionals, and an analysis of how consumers navigate the organization’s website.
Ordinal ranking of hospitals that make the honor roll “obscures the fact that all of the honor roll hospitals have attained the highest standard of care in the nation,” the letter reads.
This year there are 22 honor roll hospitals:
- Barnes-Jewish Hospital, St. Louis
- Brigham and Women’s Hospital, Boston
- Cedars-Sinai Medical Center, Los Angeles
- Cleveland Clinic
- Hospitals of the University of Pennsylvania-Penn Medicine, Philadelphia
- Houston Methodist Hospital
- Johns Hopkins Hospital, Baltimore
- Massachusetts General Hospital, Boston
- Mayo Clinic, Rochester, Minn.
- Mount Sinai Hospital, New York City
- New York–Presbyterian Hospital–Columbia and Cornell, New York City
- North Shore University Hospital at Northwell Health, Manhasset, N.Y.
- Northwestern Memorial Hospital, Chicago
- NYU Langone Hospitals, New York City
- Rush University Medical Center, Chicago
- Stanford (Calif.) Health Care–Stanford Hospital
- UC San Diego Health–La Jolla and Hillcrest Hospitals
- UCLA Medical Center, Los Angeles
- UCSF Health–UCSF Medical Center, San Francisco
- University of Michigan Health–Ann Arbor
- UT Southwestern Medical Center, Dallas
- Vanderbilt University Medical Center, Nashville, Tenn.
U.S. News noted that to keep pace with consumers’ needs and the ever-evolving landscape of health care, “several refinements” are reflected in the latest best hospitals rankings.
These include the introduction of outpatient outcomes in key specialty rankings and surgical ratings, the expanded inclusion of other outpatient data, an increased weight on objective quality measures, and a reduced weight on expert opinion.
In addition, hospital profiles at usnews.com feature refined health equity measures, including a new measure of racial disparities in outcomes.
The full report for best hospitals, best specialty hospitals, and methodology is available online.
A version of this article first appeared on Medscape.com.
of best hospitals for neurology and neurosurgery.
NYU Langone also claimed the top spot in last year’s ranking.
In the latest rankings, UCSF Health–UCSF Medical Center, San Francisco, holds the No. 2 spot and New York–Presbyterian Hospital–Columbia and Cornell in New York City holds the No. 3 spot for neurology care, with no change from last year.
This year, Mayo Clinic, Rochester, Minn., is ranked No. 4 in neurology and neurosurgery care, up from No. 6 last year, while Cedars-Sinai Medical Center, Los Angeles, ranks fifth this year, rising two spots from No. 7 last year.
Rounding out the top 10 hospitals for neurology and neurosurgery (in order) are UCLA Medical Center, Los Angeles; Johns Hopkins Hospital, Baltimore; Massachusetts General Hospital, Boston; Mount Sinai Hospital, New York; and Northwestern Medicine–Northwestern Memorial Hospital, Chicago.
U.S. News evaluated 1,245 hospitals and ranked the top 50 that treat patients with challenging neurological issues including stroke, conditions affecting the central nervous system, spinal disorders and injuries, seizures, and degenerative nervous system diagnoses such as multiple sclerosis.
“Consumers want useful resources to help them assess which hospital can best meet their specific care needs,” Ben Harder, chief of health analysis and managing editor at U.S. News, said in a statement.
“The 2023-2024 Best Hospitals rankings offer patients and the physicians with whom they consult a data-driven source for comparing performance in outcomes, patient satisfaction, and other metrics that matter to them,” Mr. Harder said.
Honor roll
This year, as in prior years, U.S. News recognized “honor roll” hospitals that have excelled across multiple areas of care. However, this year, for the first time, there is no ordinal ranking of hospitals making the honor roll. Instead, they are listed in alphabetical order.
In a letter to hospital leaders, U.S. News explained that the major change in format came after months of deliberation, feedback from health care organizations and professionals, and an analysis of how consumers navigate the organization’s website.
Ordinal ranking of hospitals that make the honor roll “obscures the fact that all of the honor roll hospitals have attained the highest standard of care in the nation,” the letter reads.
This year there are 22 honor roll hospitals:
- Barnes-Jewish Hospital, St. Louis
- Brigham and Women’s Hospital, Boston
- Cedars-Sinai Medical Center, Los Angeles
- Cleveland Clinic
- Hospitals of the University of Pennsylvania-Penn Medicine, Philadelphia
- Houston Methodist Hospital
- Johns Hopkins Hospital, Baltimore
- Massachusetts General Hospital, Boston
- Mayo Clinic, Rochester, Minn.
- Mount Sinai Hospital, New York City
- New York–Presbyterian Hospital–Columbia and Cornell, New York City
- North Shore University Hospital at Northwell Health, Manhasset, N.Y.
- Northwestern Memorial Hospital, Chicago
- NYU Langone Hospitals, New York City
- Rush University Medical Center, Chicago
- Stanford (Calif.) Health Care–Stanford Hospital
- UC San Diego Health–La Jolla and Hillcrest Hospitals
- UCLA Medical Center, Los Angeles
- UCSF Health–UCSF Medical Center, San Francisco
- University of Michigan Health–Ann Arbor
- UT Southwestern Medical Center, Dallas
- Vanderbilt University Medical Center, Nashville, Tenn.
U.S. News noted that to keep pace with consumers’ needs and the ever-evolving landscape of health care, “several refinements” are reflected in the latest best hospitals rankings.
These include the introduction of outpatient outcomes in key specialty rankings and surgical ratings, the expanded inclusion of other outpatient data, an increased weight on objective quality measures, and a reduced weight on expert opinion.
In addition, hospital profiles at usnews.com feature refined health equity measures, including a new measure of racial disparities in outcomes.
The full report for best hospitals, best specialty hospitals, and methodology is available online.
A version of this article first appeared on Medscape.com.
A new and completely different pain medicine
This transcript has been edited for clarity.
When you stub your toe or get a paper cut on your finger, you feel the pain in that part of your body. It feels like the pain is coming from that place. But, of course, that’s not really what is happening. Pain doesn’t really happen in your toe or your finger. It happens in your brain.
It’s a game of telephone, really. The afferent nerve fiber detects the noxious stimulus, passing that signal to the second-order neuron in the dorsal root ganglia of the spinal cord, which runs it up to the thalamus to be passed to the third-order neuron which brings it to the cortex for localization and conscious perception. It’s not even a very good game of telephone. It takes about 100 ms for a pain signal to get from the hand to the brain – longer from the feet, given the greater distance. You see your foot hit the corner of the coffee table and have just enough time to think: “Oh no!” before the pain hits.
Given the Rube Goldberg nature of the process, it would seem like there are any number of places we could stop pain sensation. And sure, local anesthetics at the site of injury, or even spinal anesthetics, are powerful – if temporary and hard to administer – solutions to acute pain.
But in our everyday armamentarium, let’s be honest – we essentially have three options: opiates and opioids, which activate the mu-receptors in the brain to dull pain (and cause a host of other nasty side effects); NSAIDs, which block prostaglandin synthesis and thus limit the ability for pain-conducting neurons to get excited; and acetaminophen, which, despite being used for a century, is poorly understood.
But
If you were to zoom in on the connection between that first afferent pain fiber and the secondary nerve in the spinal cord dorsal root ganglion, you would see a receptor called Nav1.8, a voltage-gated sodium channel.
This receptor is a key part of the apparatus that passes information from nerve 1 to nerve 2, but only for fibers that transmit pain signals. In fact, humans with mutations in this receptor that leave it always in the “open” state have a severe pain syndrome. Blocking the receptor, therefore, might reduce pain.
In preclinical work, researchers identified VX-548, which doesn’t have a brand name yet, as a potent blocker of that channel even in nanomolar concentrations. Importantly, the compound was highly selective for that particular channel – about 30,000 times more selective than it was for the other sodium channels in that family.
Of course, a highly selective and specific drug does not a blockbuster analgesic make. To determine how this drug would work on humans in pain, they turned to two populations: 303 individuals undergoing abdominoplasty and 274 undergoing bunionectomy, as reported in a new paper in the New England Journal of Medicine.
I know this seems a bit random, but abdominoplasty is quite painful and a good model for soft-tissue pain. Bunionectomy is also quite a painful procedure and a useful model of bone pain. After the surgeries, patients were randomized to several different doses of VX-548, hydrocodone plus acetaminophen, or placebo for 48 hours.
At 19 time points over that 48-hour period, participants were asked to rate their pain on a scale from 0 to 10. The primary outcome was the cumulative pain experienced over the 48 hours. So, higher pain would be worse here, but longer duration of pain would also be worse.
The story of the study is really told in this chart.
Yes, those assigned to the highest dose of VX-548 had a statistically significant lower cumulative amount of pain in the 48 hours after surgery. But the picture is really worth more than the stats here. You can see that the onset of pain relief was fairly quick, and that pain relief was sustained over time. You can also see that this is not a miracle drug. Pain scores were a bit better 48 hours out, but only by about a point and a half.
Placebo isn’t really the fair comparison here; few of us treat our postabdominoplasty patients with placebo, after all. The authors do not formally compare the effect of VX-548 with that of the opioid hydrocodone, for instance. But that doesn’t stop us.
This graph, which I put together from data in the paper, shows pain control across the four randomization categories, with higher numbers indicating more (cumulative) control. While all the active agents do a bit better than placebo, VX-548 at the higher dose appears to do the best. But I should note that 5 mg of hydrocodone may not be an adequate dose for most people.
Yes, I would really have killed for an NSAID arm in this trial. Its absence, given that NSAIDs are a staple of postoperative care, is ... well, let’s just say, notable.
Although not a pain-destroying machine, VX-548 has some other things to recommend it. The receptor is really not found in the brain at all, which suggests that the drug should not carry much risk for dependency, though that has not been formally studied.
The side effects were generally mild – headache was the most common – and less prevalent than what you see even in the placebo arm.
Perhaps most notable is the fact that the rate of discontinuation of the study drug was lowest in the VX-548 arm. Patients could stop taking the pill they were assigned for any reason, ranging from perceived lack of efficacy to side effects. A low discontinuation rate indicates to me a sort of “voting with your feet” that suggests this might be a well-tolerated and reasonably effective drug.
VX-548 isn’t on the market yet; phase 3 trials are ongoing. But whether it is this particular drug or another in this class, I’m happy to see researchers trying to find new ways to target that most primeval form of suffering: pain.
Dr. Wilson is an associate professor of medicine and public health and director of Yale’s Clinical and Translational Research Accelerator, New Haven, Conn. He disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
When you stub your toe or get a paper cut on your finger, you feel the pain in that part of your body. It feels like the pain is coming from that place. But, of course, that’s not really what is happening. Pain doesn’t really happen in your toe or your finger. It happens in your brain.
It’s a game of telephone, really. The afferent nerve fiber detects the noxious stimulus, passing that signal to the second-order neuron in the dorsal root ganglia of the spinal cord, which runs it up to the thalamus to be passed to the third-order neuron which brings it to the cortex for localization and conscious perception. It’s not even a very good game of telephone. It takes about 100 ms for a pain signal to get from the hand to the brain – longer from the feet, given the greater distance. You see your foot hit the corner of the coffee table and have just enough time to think: “Oh no!” before the pain hits.
Given the Rube Goldberg nature of the process, it would seem like there are any number of places we could stop pain sensation. And sure, local anesthetics at the site of injury, or even spinal anesthetics, are powerful – if temporary and hard to administer – solutions to acute pain.
But in our everyday armamentarium, let’s be honest – we essentially have three options: opiates and opioids, which activate the mu-receptors in the brain to dull pain (and cause a host of other nasty side effects); NSAIDs, which block prostaglandin synthesis and thus limit the ability for pain-conducting neurons to get excited; and acetaminophen, which, despite being used for a century, is poorly understood.
But
If you were to zoom in on the connection between that first afferent pain fiber and the secondary nerve in the spinal cord dorsal root ganglion, you would see a receptor called Nav1.8, a voltage-gated sodium channel.
This receptor is a key part of the apparatus that passes information from nerve 1 to nerve 2, but only for fibers that transmit pain signals. In fact, humans with mutations in this receptor that leave it always in the “open” state have a severe pain syndrome. Blocking the receptor, therefore, might reduce pain.
In preclinical work, researchers identified VX-548, which doesn’t have a brand name yet, as a potent blocker of that channel even in nanomolar concentrations. Importantly, the compound was highly selective for that particular channel – about 30,000 times more selective than it was for the other sodium channels in that family.
Of course, a highly selective and specific drug does not a blockbuster analgesic make. To determine how this drug would work on humans in pain, they turned to two populations: 303 individuals undergoing abdominoplasty and 274 undergoing bunionectomy, as reported in a new paper in the New England Journal of Medicine.
I know this seems a bit random, but abdominoplasty is quite painful and a good model for soft-tissue pain. Bunionectomy is also quite a painful procedure and a useful model of bone pain. After the surgeries, patients were randomized to several different doses of VX-548, hydrocodone plus acetaminophen, or placebo for 48 hours.
At 19 time points over that 48-hour period, participants were asked to rate their pain on a scale from 0 to 10. The primary outcome was the cumulative pain experienced over the 48 hours. So, higher pain would be worse here, but longer duration of pain would also be worse.
The story of the study is really told in this chart.
Yes, those assigned to the highest dose of VX-548 had a statistically significant lower cumulative amount of pain in the 48 hours after surgery. But the picture is really worth more than the stats here. You can see that the onset of pain relief was fairly quick, and that pain relief was sustained over time. You can also see that this is not a miracle drug. Pain scores were a bit better 48 hours out, but only by about a point and a half.
Placebo isn’t really the fair comparison here; few of us treat our postabdominoplasty patients with placebo, after all. The authors do not formally compare the effect of VX-548 with that of the opioid hydrocodone, for instance. But that doesn’t stop us.
This graph, which I put together from data in the paper, shows pain control across the four randomization categories, with higher numbers indicating more (cumulative) control. While all the active agents do a bit better than placebo, VX-548 at the higher dose appears to do the best. But I should note that 5 mg of hydrocodone may not be an adequate dose for most people.
Yes, I would really have killed for an NSAID arm in this trial. Its absence, given that NSAIDs are a staple of postoperative care, is ... well, let’s just say, notable.
Although not a pain-destroying machine, VX-548 has some other things to recommend it. The receptor is really not found in the brain at all, which suggests that the drug should not carry much risk for dependency, though that has not been formally studied.
The side effects were generally mild – headache was the most common – and less prevalent than what you see even in the placebo arm.
Perhaps most notable is the fact that the rate of discontinuation of the study drug was lowest in the VX-548 arm. Patients could stop taking the pill they were assigned for any reason, ranging from perceived lack of efficacy to side effects. A low discontinuation rate indicates to me a sort of “voting with your feet” that suggests this might be a well-tolerated and reasonably effective drug.
VX-548 isn’t on the market yet; phase 3 trials are ongoing. But whether it is this particular drug or another in this class, I’m happy to see researchers trying to find new ways to target that most primeval form of suffering: pain.
Dr. Wilson is an associate professor of medicine and public health and director of Yale’s Clinical and Translational Research Accelerator, New Haven, Conn. He disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
When you stub your toe or get a paper cut on your finger, you feel the pain in that part of your body. It feels like the pain is coming from that place. But, of course, that’s not really what is happening. Pain doesn’t really happen in your toe or your finger. It happens in your brain.
It’s a game of telephone, really. The afferent nerve fiber detects the noxious stimulus, passing that signal to the second-order neuron in the dorsal root ganglia of the spinal cord, which runs it up to the thalamus to be passed to the third-order neuron which brings it to the cortex for localization and conscious perception. It’s not even a very good game of telephone. It takes about 100 ms for a pain signal to get from the hand to the brain – longer from the feet, given the greater distance. You see your foot hit the corner of the coffee table and have just enough time to think: “Oh no!” before the pain hits.
Given the Rube Goldberg nature of the process, it would seem like there are any number of places we could stop pain sensation. And sure, local anesthetics at the site of injury, or even spinal anesthetics, are powerful – if temporary and hard to administer – solutions to acute pain.
But in our everyday armamentarium, let’s be honest – we essentially have three options: opiates and opioids, which activate the mu-receptors in the brain to dull pain (and cause a host of other nasty side effects); NSAIDs, which block prostaglandin synthesis and thus limit the ability for pain-conducting neurons to get excited; and acetaminophen, which, despite being used for a century, is poorly understood.
But
If you were to zoom in on the connection between that first afferent pain fiber and the secondary nerve in the spinal cord dorsal root ganglion, you would see a receptor called Nav1.8, a voltage-gated sodium channel.
This receptor is a key part of the apparatus that passes information from nerve 1 to nerve 2, but only for fibers that transmit pain signals. In fact, humans with mutations in this receptor that leave it always in the “open” state have a severe pain syndrome. Blocking the receptor, therefore, might reduce pain.
In preclinical work, researchers identified VX-548, which doesn’t have a brand name yet, as a potent blocker of that channel even in nanomolar concentrations. Importantly, the compound was highly selective for that particular channel – about 30,000 times more selective than it was for the other sodium channels in that family.
Of course, a highly selective and specific drug does not a blockbuster analgesic make. To determine how this drug would work on humans in pain, they turned to two populations: 303 individuals undergoing abdominoplasty and 274 undergoing bunionectomy, as reported in a new paper in the New England Journal of Medicine.
I know this seems a bit random, but abdominoplasty is quite painful and a good model for soft-tissue pain. Bunionectomy is also quite a painful procedure and a useful model of bone pain. After the surgeries, patients were randomized to several different doses of VX-548, hydrocodone plus acetaminophen, or placebo for 48 hours.
At 19 time points over that 48-hour period, participants were asked to rate their pain on a scale from 0 to 10. The primary outcome was the cumulative pain experienced over the 48 hours. So, higher pain would be worse here, but longer duration of pain would also be worse.
The story of the study is really told in this chart.
Yes, those assigned to the highest dose of VX-548 had a statistically significant lower cumulative amount of pain in the 48 hours after surgery. But the picture is really worth more than the stats here. You can see that the onset of pain relief was fairly quick, and that pain relief was sustained over time. You can also see that this is not a miracle drug. Pain scores were a bit better 48 hours out, but only by about a point and a half.
Placebo isn’t really the fair comparison here; few of us treat our postabdominoplasty patients with placebo, after all. The authors do not formally compare the effect of VX-548 with that of the opioid hydrocodone, for instance. But that doesn’t stop us.
This graph, which I put together from data in the paper, shows pain control across the four randomization categories, with higher numbers indicating more (cumulative) control. While all the active agents do a bit better than placebo, VX-548 at the higher dose appears to do the best. But I should note that 5 mg of hydrocodone may not be an adequate dose for most people.
Yes, I would really have killed for an NSAID arm in this trial. Its absence, given that NSAIDs are a staple of postoperative care, is ... well, let’s just say, notable.
Although not a pain-destroying machine, VX-548 has some other things to recommend it. The receptor is really not found in the brain at all, which suggests that the drug should not carry much risk for dependency, though that has not been formally studied.
The side effects were generally mild – headache was the most common – and less prevalent than what you see even in the placebo arm.
Perhaps most notable is the fact that the rate of discontinuation of the study drug was lowest in the VX-548 arm. Patients could stop taking the pill they were assigned for any reason, ranging from perceived lack of efficacy to side effects. A low discontinuation rate indicates to me a sort of “voting with your feet” that suggests this might be a well-tolerated and reasonably effective drug.
VX-548 isn’t on the market yet; phase 3 trials are ongoing. But whether it is this particular drug or another in this class, I’m happy to see researchers trying to find new ways to target that most primeval form of suffering: pain.
Dr. Wilson is an associate professor of medicine and public health and director of Yale’s Clinical and Translational Research Accelerator, New Haven, Conn. He disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Depression at any stage of life tied to increased dementia risk
Adults with depression have more than double the risk of developing dementia and the risk persists regardless of when in life depression is diagnosed, a large population-based study shows.
That the association between depression and dementia persisted even among individuals first diagnosed with depression in early or mid-life provides “strong evidence that depression is not only an early symptom of dementia, but also that depression increases dementia risk,” study investigator Holly Elser, MD, PhD, epidemiologist and resident physician, University of Pennsylvania, Philadelphia, told this news organization.
The study was published online in JAMA Neurology.
Double the risk
Several prior studies that have examined the relationship between depression and dementia over the life course have consistently shown depression later in life is associated with subsequent dementia.
“Late-life depression is generally thought to be an early symptom of dementia or a reaction to subclinical cognitive decline,” said Dr. Elser.
The investigators wanted to examine whether the association between depression and dementia persists even when depression is diagnosed earlier in life, which may suggest it increases the risk of dementia.
“To my knowledge, ours is the largest study on this topic to date, leveraging routinely and prospectively collected data from more than 1.4 million Danish citizens followed from 1977 to 2018,” Dr. Elser noted.
The cohort included 246,499 individuals diagnosed with depression and 1,190,302 individuals without depression.
In both groups, the median age was 50 years and 65% were women. Roughly two-thirds (68%) of those diagnosed with depression were diagnosed before age 60 years.
In Cox proportional hazards regression models, the overall hazard of dementia was more than doubled in those diagnosed with depression (hazard ratio [HR] 2.41). The risk of dementia with depression was more pronounced for men (HR, 2.98) than in women (HR, 2.21).
This association persisted even when the time elapsed from depression diagnosis was between 20 and 39 years (HR, 1.79) and whether depression was diagnosed in early life (18-44 years: HR, 3.08), mid-life (45-59 years: HR, 2.95), or late life (≥ 60 years: HR, 2.31).
It remains unclear whether effective treatment of depression modifies the risk of dementia, as the current study explored the role of antidepressants in a “very limited fashion,” Dr. Elser said.
Specifically, the researchers considered whether an individual was treated with an antidepressant within 6 months of the initial depression diagnosis and found no evidence of a difference in dementia risk between the treated and untreated groups.
“Research that explores implications of the timing and duration of treatment with antidepressants for dementia, treatment with cognitive behavioral therapy, and is able to evaluate the effectiveness of those treatments will be extremely important,” Dr. Elser said.
‘An assault on the brain’
Reached for comment, John Showalter, MD, chief product officer at Linus Health, said one of the most “intriguing” findings of the study is that a depression diagnosis earlier in adulthood conferred a greater risk of developing vascular dementia (HR, 3.28) than did dementia due to Alzheimer’s disease (HR, 1.73).
“The difference in risk for subtypes of dementia is a meaningful addition to our understanding of depression’s connection to dementia,” said Dr. Showalter, who was not involved in the study.
Also weighing in, Shaheen Lakhan, MD, PhD, a neurologist and researcher in Boston, said the findings from this “far-reaching investigation leave little room for doubt – depression unleashes a devastating storm within the brain, wreaking havoc on the lives of those ensnared by its grip.
“This massive, multi-decade, and high-data quality registry study adds another brick to the growing edifice of evidence attesting to the profound connection between psychiatric health and the very essence of brain health,” said Dr. Lakhan, who was not involved in the study.
“In a resounding declaration, this research underscores that psychiatric health should be perceived as an integral component of overall health – a paradigm shift that challenges long-standing misconceptions and stigmas surrounding mental disorders. Depression, once marginalized, now claims its rightful place on the pedestal of health concerns that must be addressed with unwavering resolve,” said Dr. Lakhan.
He noted that depression is “not just a mental battle, it’s a profound assault on the very fabric of the brain, leaving lives in turmoil and hearts in search of hope. No longer shrouded in silence, depression demands society’s attention.”
The study had no specific funding. Dr. Elser, Dr. Showalter, and Dr. Lakhan have reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
Adults with depression have more than double the risk of developing dementia and the risk persists regardless of when in life depression is diagnosed, a large population-based study shows.
That the association between depression and dementia persisted even among individuals first diagnosed with depression in early or mid-life provides “strong evidence that depression is not only an early symptom of dementia, but also that depression increases dementia risk,” study investigator Holly Elser, MD, PhD, epidemiologist and resident physician, University of Pennsylvania, Philadelphia, told this news organization.
The study was published online in JAMA Neurology.
Double the risk
Several prior studies that have examined the relationship between depression and dementia over the life course have consistently shown depression later in life is associated with subsequent dementia.
“Late-life depression is generally thought to be an early symptom of dementia or a reaction to subclinical cognitive decline,” said Dr. Elser.
The investigators wanted to examine whether the association between depression and dementia persists even when depression is diagnosed earlier in life, which may suggest it increases the risk of dementia.
“To my knowledge, ours is the largest study on this topic to date, leveraging routinely and prospectively collected data from more than 1.4 million Danish citizens followed from 1977 to 2018,” Dr. Elser noted.
The cohort included 246,499 individuals diagnosed with depression and 1,190,302 individuals without depression.
In both groups, the median age was 50 years and 65% were women. Roughly two-thirds (68%) of those diagnosed with depression were diagnosed before age 60 years.
In Cox proportional hazards regression models, the overall hazard of dementia was more than doubled in those diagnosed with depression (hazard ratio [HR] 2.41). The risk of dementia with depression was more pronounced for men (HR, 2.98) than in women (HR, 2.21).
This association persisted even when the time elapsed from depression diagnosis was between 20 and 39 years (HR, 1.79) and whether depression was diagnosed in early life (18-44 years: HR, 3.08), mid-life (45-59 years: HR, 2.95), or late life (≥ 60 years: HR, 2.31).
It remains unclear whether effective treatment of depression modifies the risk of dementia, as the current study explored the role of antidepressants in a “very limited fashion,” Dr. Elser said.
Specifically, the researchers considered whether an individual was treated with an antidepressant within 6 months of the initial depression diagnosis and found no evidence of a difference in dementia risk between the treated and untreated groups.
“Research that explores implications of the timing and duration of treatment with antidepressants for dementia, treatment with cognitive behavioral therapy, and is able to evaluate the effectiveness of those treatments will be extremely important,” Dr. Elser said.
‘An assault on the brain’
Reached for comment, John Showalter, MD, chief product officer at Linus Health, said one of the most “intriguing” findings of the study is that a depression diagnosis earlier in adulthood conferred a greater risk of developing vascular dementia (HR, 3.28) than did dementia due to Alzheimer’s disease (HR, 1.73).
“The difference in risk for subtypes of dementia is a meaningful addition to our understanding of depression’s connection to dementia,” said Dr. Showalter, who was not involved in the study.
Also weighing in, Shaheen Lakhan, MD, PhD, a neurologist and researcher in Boston, said the findings from this “far-reaching investigation leave little room for doubt – depression unleashes a devastating storm within the brain, wreaking havoc on the lives of those ensnared by its grip.
“This massive, multi-decade, and high-data quality registry study adds another brick to the growing edifice of evidence attesting to the profound connection between psychiatric health and the very essence of brain health,” said Dr. Lakhan, who was not involved in the study.
“In a resounding declaration, this research underscores that psychiatric health should be perceived as an integral component of overall health – a paradigm shift that challenges long-standing misconceptions and stigmas surrounding mental disorders. Depression, once marginalized, now claims its rightful place on the pedestal of health concerns that must be addressed with unwavering resolve,” said Dr. Lakhan.
He noted that depression is “not just a mental battle, it’s a profound assault on the very fabric of the brain, leaving lives in turmoil and hearts in search of hope. No longer shrouded in silence, depression demands society’s attention.”
The study had no specific funding. Dr. Elser, Dr. Showalter, and Dr. Lakhan have reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
Adults with depression have more than double the risk of developing dementia and the risk persists regardless of when in life depression is diagnosed, a large population-based study shows.
That the association between depression and dementia persisted even among individuals first diagnosed with depression in early or mid-life provides “strong evidence that depression is not only an early symptom of dementia, but also that depression increases dementia risk,” study investigator Holly Elser, MD, PhD, epidemiologist and resident physician, University of Pennsylvania, Philadelphia, told this news organization.
The study was published online in JAMA Neurology.
Double the risk
Several prior studies that have examined the relationship between depression and dementia over the life course have consistently shown depression later in life is associated with subsequent dementia.
“Late-life depression is generally thought to be an early symptom of dementia or a reaction to subclinical cognitive decline,” said Dr. Elser.
The investigators wanted to examine whether the association between depression and dementia persists even when depression is diagnosed earlier in life, which may suggest it increases the risk of dementia.
“To my knowledge, ours is the largest study on this topic to date, leveraging routinely and prospectively collected data from more than 1.4 million Danish citizens followed from 1977 to 2018,” Dr. Elser noted.
The cohort included 246,499 individuals diagnosed with depression and 1,190,302 individuals without depression.
In both groups, the median age was 50 years and 65% were women. Roughly two-thirds (68%) of those diagnosed with depression were diagnosed before age 60 years.
In Cox proportional hazards regression models, the overall hazard of dementia was more than doubled in those diagnosed with depression (hazard ratio [HR] 2.41). The risk of dementia with depression was more pronounced for men (HR, 2.98) than in women (HR, 2.21).
This association persisted even when the time elapsed from depression diagnosis was between 20 and 39 years (HR, 1.79) and whether depression was diagnosed in early life (18-44 years: HR, 3.08), mid-life (45-59 years: HR, 2.95), or late life (≥ 60 years: HR, 2.31).
It remains unclear whether effective treatment of depression modifies the risk of dementia, as the current study explored the role of antidepressants in a “very limited fashion,” Dr. Elser said.
Specifically, the researchers considered whether an individual was treated with an antidepressant within 6 months of the initial depression diagnosis and found no evidence of a difference in dementia risk between the treated and untreated groups.
“Research that explores implications of the timing and duration of treatment with antidepressants for dementia, treatment with cognitive behavioral therapy, and is able to evaluate the effectiveness of those treatments will be extremely important,” Dr. Elser said.
‘An assault on the brain’
Reached for comment, John Showalter, MD, chief product officer at Linus Health, said one of the most “intriguing” findings of the study is that a depression diagnosis earlier in adulthood conferred a greater risk of developing vascular dementia (HR, 3.28) than did dementia due to Alzheimer’s disease (HR, 1.73).
“The difference in risk for subtypes of dementia is a meaningful addition to our understanding of depression’s connection to dementia,” said Dr. Showalter, who was not involved in the study.
Also weighing in, Shaheen Lakhan, MD, PhD, a neurologist and researcher in Boston, said the findings from this “far-reaching investigation leave little room for doubt – depression unleashes a devastating storm within the brain, wreaking havoc on the lives of those ensnared by its grip.
“This massive, multi-decade, and high-data quality registry study adds another brick to the growing edifice of evidence attesting to the profound connection between psychiatric health and the very essence of brain health,” said Dr. Lakhan, who was not involved in the study.
“In a resounding declaration, this research underscores that psychiatric health should be perceived as an integral component of overall health – a paradigm shift that challenges long-standing misconceptions and stigmas surrounding mental disorders. Depression, once marginalized, now claims its rightful place on the pedestal of health concerns that must be addressed with unwavering resolve,” said Dr. Lakhan.
He noted that depression is “not just a mental battle, it’s a profound assault on the very fabric of the brain, leaving lives in turmoil and hearts in search of hope. No longer shrouded in silence, depression demands society’s attention.”
The study had no specific funding. Dr. Elser, Dr. Showalter, and Dr. Lakhan have reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
Medicare to pay for at-home dementia care coordination
Under a new Medicare pilot program that will begin in 2024, the federal government will pay clinicians to coordinate at-home dementia support services, including respite care for family members.
A Department of Health & Human Services initiative, part of the aim of the Guiding an Improved Dementia Experience (GUIDE) program is to help Medicare beneficiaries with dementia stay in the community for as long as possible. It is estimated that there are 6.7 million Americans living with Alzheimer’s disease or some other form of dementia, said HHS.
The program is voluntary and will be open to Medicare-enrolled clinicians and other providers who can assemble an interdisciplinary care team and meet the program’s participation criteria.
“Our new GUIDE Model has the potential to improve the quality of life for people with dementia and alleviate the significant strain on our families,” said HHS Secretary Xavier Becerra, in a statement.
“Not only is dementia care management a proven way to improve the quality of care and quality of life for those living with Alzheimer’s and other dementia, but now we know that it would also save the federal government billions of dollars,” Robert Egge, Alzheimer’s Association chief public policy officer and Alzheimer’s Impact Movement (AIM) executive director, said in a statement.
Mr. Egge cited a recent analysis commissioned by AIM that found that dementia care management would save the federal government nearly $21 billion over 10 years.
“People living with dementia and their caregivers too often struggle to manage their health care and connect with key supports that can allow them to remain in their homes and communities,” said Centers for Medicare & Medicaid Services Administrator Chiquita Brooks-LaSure, in the HHS statement.
“Fragmented care contributes to the mental and physical health strain of caring for someone with dementia, as well as the substantial financial burden,” she said, adding that Black, Hispanic, Asian American, Native Hawaiian, and Pacific Islander populations have been especially disadvantaged.
The GUIDE Model will provide new resources and greater access to specialty care to those communities, said Ms. Brooks-LaSure.
Care teams that seek to participate in the GUIDE model must have a care navigator who has received required training in dementia, assessment, and care planning.
The teams also must have a clinician with dementia proficiency as recognized by experience caring for adults with cognitive impairment; experience caring for patients aged 65 years old or older; or specialty designation in neurology, psychiatry, geriatrics, geriatric psychiatry, behavioral neurology, or geriatric neurology.
Medicare beneficiaries will be eligible if they are not residing in a nursing home; are not enrolled in hospice; and have a confirmed dementia diagnosis.
Beneficiaries who receive care from GUIDE participants will be placed in one of five “tiers,” based on a combination of disease stage and caregiver status. Beneficiary needs, and care intensity and payment, increase by tier.
GUIDE teams will receive a monthly, per-beneficiary amount for providing care management and coordination and caregiver education and support services. They can also bill for respite services – up to an annual cap – for Medicare beneficiaries who have an unpaid caregiver.
Clinicians seeking to participate in GUIDE can apply beginning in the fall. The program will run for 8 years beginning July 1, 2024.
Alzheimer’s Association President and CEO Joanne Pike, DrPH, said in a statement that the organization had “advocated for this approach for years, believing it [to be] the key to addressing systemic challenges faced by those with dementia, their families and those who provide them with care and support.”
The John A. Hartford Foundation noted that it also had long pushed for a comprehensive dementia care program. “Comprehensive dementia care supports both the medical and nonmedical needs of patients and their family caregivers,” said Foundation President Terry Fulmer, PhD, RN, FAAN, in a statement.
“Notably and necessarily, the model will help improve equity in access to care for underserved communities by addressing unpaid caregiver needs, including respite services and screening for health-related social needs,” added Dr. Fulmer.
A version of this article first appeared on Medscape.com.
Under a new Medicare pilot program that will begin in 2024, the federal government will pay clinicians to coordinate at-home dementia support services, including respite care for family members.
A Department of Health & Human Services initiative, part of the aim of the Guiding an Improved Dementia Experience (GUIDE) program is to help Medicare beneficiaries with dementia stay in the community for as long as possible. It is estimated that there are 6.7 million Americans living with Alzheimer’s disease or some other form of dementia, said HHS.
The program is voluntary and will be open to Medicare-enrolled clinicians and other providers who can assemble an interdisciplinary care team and meet the program’s participation criteria.
“Our new GUIDE Model has the potential to improve the quality of life for people with dementia and alleviate the significant strain on our families,” said HHS Secretary Xavier Becerra, in a statement.
“Not only is dementia care management a proven way to improve the quality of care and quality of life for those living with Alzheimer’s and other dementia, but now we know that it would also save the federal government billions of dollars,” Robert Egge, Alzheimer’s Association chief public policy officer and Alzheimer’s Impact Movement (AIM) executive director, said in a statement.
Mr. Egge cited a recent analysis commissioned by AIM that found that dementia care management would save the federal government nearly $21 billion over 10 years.
“People living with dementia and their caregivers too often struggle to manage their health care and connect with key supports that can allow them to remain in their homes and communities,” said Centers for Medicare & Medicaid Services Administrator Chiquita Brooks-LaSure, in the HHS statement.
“Fragmented care contributes to the mental and physical health strain of caring for someone with dementia, as well as the substantial financial burden,” she said, adding that Black, Hispanic, Asian American, Native Hawaiian, and Pacific Islander populations have been especially disadvantaged.
The GUIDE Model will provide new resources and greater access to specialty care to those communities, said Ms. Brooks-LaSure.
Care teams that seek to participate in the GUIDE model must have a care navigator who has received required training in dementia, assessment, and care planning.
The teams also must have a clinician with dementia proficiency as recognized by experience caring for adults with cognitive impairment; experience caring for patients aged 65 years old or older; or specialty designation in neurology, psychiatry, geriatrics, geriatric psychiatry, behavioral neurology, or geriatric neurology.
Medicare beneficiaries will be eligible if they are not residing in a nursing home; are not enrolled in hospice; and have a confirmed dementia diagnosis.
Beneficiaries who receive care from GUIDE participants will be placed in one of five “tiers,” based on a combination of disease stage and caregiver status. Beneficiary needs, and care intensity and payment, increase by tier.
GUIDE teams will receive a monthly, per-beneficiary amount for providing care management and coordination and caregiver education and support services. They can also bill for respite services – up to an annual cap – for Medicare beneficiaries who have an unpaid caregiver.
Clinicians seeking to participate in GUIDE can apply beginning in the fall. The program will run for 8 years beginning July 1, 2024.
Alzheimer’s Association President and CEO Joanne Pike, DrPH, said in a statement that the organization had “advocated for this approach for years, believing it [to be] the key to addressing systemic challenges faced by those with dementia, their families and those who provide them with care and support.”
The John A. Hartford Foundation noted that it also had long pushed for a comprehensive dementia care program. “Comprehensive dementia care supports both the medical and nonmedical needs of patients and their family caregivers,” said Foundation President Terry Fulmer, PhD, RN, FAAN, in a statement.
“Notably and necessarily, the model will help improve equity in access to care for underserved communities by addressing unpaid caregiver needs, including respite services and screening for health-related social needs,” added Dr. Fulmer.
A version of this article first appeared on Medscape.com.
Under a new Medicare pilot program that will begin in 2024, the federal government will pay clinicians to coordinate at-home dementia support services, including respite care for family members.
A Department of Health & Human Services initiative, part of the aim of the Guiding an Improved Dementia Experience (GUIDE) program is to help Medicare beneficiaries with dementia stay in the community for as long as possible. It is estimated that there are 6.7 million Americans living with Alzheimer’s disease or some other form of dementia, said HHS.
The program is voluntary and will be open to Medicare-enrolled clinicians and other providers who can assemble an interdisciplinary care team and meet the program’s participation criteria.
“Our new GUIDE Model has the potential to improve the quality of life for people with dementia and alleviate the significant strain on our families,” said HHS Secretary Xavier Becerra, in a statement.
“Not only is dementia care management a proven way to improve the quality of care and quality of life for those living with Alzheimer’s and other dementia, but now we know that it would also save the federal government billions of dollars,” Robert Egge, Alzheimer’s Association chief public policy officer and Alzheimer’s Impact Movement (AIM) executive director, said in a statement.
Mr. Egge cited a recent analysis commissioned by AIM that found that dementia care management would save the federal government nearly $21 billion over 10 years.
“People living with dementia and their caregivers too often struggle to manage their health care and connect with key supports that can allow them to remain in their homes and communities,” said Centers for Medicare & Medicaid Services Administrator Chiquita Brooks-LaSure, in the HHS statement.
“Fragmented care contributes to the mental and physical health strain of caring for someone with dementia, as well as the substantial financial burden,” she said, adding that Black, Hispanic, Asian American, Native Hawaiian, and Pacific Islander populations have been especially disadvantaged.
The GUIDE Model will provide new resources and greater access to specialty care to those communities, said Ms. Brooks-LaSure.
Care teams that seek to participate in the GUIDE model must have a care navigator who has received required training in dementia, assessment, and care planning.
The teams also must have a clinician with dementia proficiency as recognized by experience caring for adults with cognitive impairment; experience caring for patients aged 65 years old or older; or specialty designation in neurology, psychiatry, geriatrics, geriatric psychiatry, behavioral neurology, or geriatric neurology.
Medicare beneficiaries will be eligible if they are not residing in a nursing home; are not enrolled in hospice; and have a confirmed dementia diagnosis.
Beneficiaries who receive care from GUIDE participants will be placed in one of five “tiers,” based on a combination of disease stage and caregiver status. Beneficiary needs, and care intensity and payment, increase by tier.
GUIDE teams will receive a monthly, per-beneficiary amount for providing care management and coordination and caregiver education and support services. They can also bill for respite services – up to an annual cap – for Medicare beneficiaries who have an unpaid caregiver.
Clinicians seeking to participate in GUIDE can apply beginning in the fall. The program will run for 8 years beginning July 1, 2024.
Alzheimer’s Association President and CEO Joanne Pike, DrPH, said in a statement that the organization had “advocated for this approach for years, believing it [to be] the key to addressing systemic challenges faced by those with dementia, their families and those who provide them with care and support.”
The John A. Hartford Foundation noted that it also had long pushed for a comprehensive dementia care program. “Comprehensive dementia care supports both the medical and nonmedical needs of patients and their family caregivers,” said Foundation President Terry Fulmer, PhD, RN, FAAN, in a statement.
“Notably and necessarily, the model will help improve equity in access to care for underserved communities by addressing unpaid caregiver needs, including respite services and screening for health-related social needs,” added Dr. Fulmer.
A version of this article first appeared on Medscape.com.
Folic acid supplementation for birth defects reaffirmed
Taking folic acid supplements before conception and in the first trimester of pregnancy continues to be a major line of defense against neural tube defects.
In a statement published in JAMA, the U.S. Preventive Services Task Force recommended that all people planning on becoming pregnant or who could become pregnant take a daily supplement of 0.4-0.8 mg (400-800 mcg) of folic acid to prevent neural tube defects.
The task force also found that folic acid is not associated with maternal cancer or autism, which were the concerns of some researchers. The current findings regarding potential harm align with earlier evidence examining possible risks.
The recommendation also aligns with previous recommendations from the USPSTF and is supported by 12 more recent observational studies. Neural tube defects occur in an estimated 3,000 pregnancies per year.
Folic acid deficiency is common due to diet, impaired folate metabolism, and poor nutrient uptake as a result of medications or bariatric surgery.
“As much as we’ve been trying to get the word out there, we still need to get it out there even more,” Wanda Nicholson, MD, MPH, MBA, vice chair of the USPSTF, told this news organization. “It’s so simple and straightforward and can be so impactful for the health of the baby.”
Neural tube formation occurs 26-28 days after fertilization. Folic acid supplementation is essential for all people who may become pregnant, considering half of the pregnancies in the United States are unplanned, according to the USPSTF.
“In many cases, neural tube formation has already occurred, or not occurred appropriately, before someone realizes that they’re pregnant,” Dr. Nicholson said. “That’s why it’s so important to start taking folic acid one month prior to conception if you’re planning on becoming pregnant, and if you’re capable of being pregnant but not planning pregnancy, yes, we’re advocating that you also proceed with folic acid supplementation.”
Primary care physicians play a key role in patient education and ensuring that all patients receive adequate folic acid, according to Spencer McClelland, MD, an obstetrician-gynecologist at Denver Health, who was not involved in the statement. Dr. McClelland advised that clinicians recommend patients who are or could get pregnant take a multivitamin, because most brands will contain the recommended dosage of folic acid.
“There’s some confusion about folic acid,” he said. “Many patients know that they should be on a prenatal vitamin, but most don’t know that the reason we’re recommending a prenatal vitamin is almost entirely because of the value of folic acid, and everything else in the prenatal vitamin is kind of icing on the cake.”
For patients trying to get pregnant, the risk for neural tube defects “is one of many examples of the importance of preconception counseling,” Dr. McClelland said.
Dr. Nicholson noted that the recommended 0.4-0.8 mg of folic acid per day is for patients without heightened deficiency due to medications or bariatric surgery. At-risk patients should receive counseling from their physician to determine the correct amount to take.
The authors report no conflicts of interest, financial or otherwise.
A version of this article first appeared on Medscape.com.
Taking folic acid supplements before conception and in the first trimester of pregnancy continues to be a major line of defense against neural tube defects.
In a statement published in JAMA, the U.S. Preventive Services Task Force recommended that all people planning on becoming pregnant or who could become pregnant take a daily supplement of 0.4-0.8 mg (400-800 mcg) of folic acid to prevent neural tube defects.
The task force also found that folic acid is not associated with maternal cancer or autism, which were the concerns of some researchers. The current findings regarding potential harm align with earlier evidence examining possible risks.
The recommendation also aligns with previous recommendations from the USPSTF and is supported by 12 more recent observational studies. Neural tube defects occur in an estimated 3,000 pregnancies per year.
Folic acid deficiency is common due to diet, impaired folate metabolism, and poor nutrient uptake as a result of medications or bariatric surgery.
“As much as we’ve been trying to get the word out there, we still need to get it out there even more,” Wanda Nicholson, MD, MPH, MBA, vice chair of the USPSTF, told this news organization. “It’s so simple and straightforward and can be so impactful for the health of the baby.”
Neural tube formation occurs 26-28 days after fertilization. Folic acid supplementation is essential for all people who may become pregnant, considering half of the pregnancies in the United States are unplanned, according to the USPSTF.
“In many cases, neural tube formation has already occurred, or not occurred appropriately, before someone realizes that they’re pregnant,” Dr. Nicholson said. “That’s why it’s so important to start taking folic acid one month prior to conception if you’re planning on becoming pregnant, and if you’re capable of being pregnant but not planning pregnancy, yes, we’re advocating that you also proceed with folic acid supplementation.”
Primary care physicians play a key role in patient education and ensuring that all patients receive adequate folic acid, according to Spencer McClelland, MD, an obstetrician-gynecologist at Denver Health, who was not involved in the statement. Dr. McClelland advised that clinicians recommend patients who are or could get pregnant take a multivitamin, because most brands will contain the recommended dosage of folic acid.
“There’s some confusion about folic acid,” he said. “Many patients know that they should be on a prenatal vitamin, but most don’t know that the reason we’re recommending a prenatal vitamin is almost entirely because of the value of folic acid, and everything else in the prenatal vitamin is kind of icing on the cake.”
For patients trying to get pregnant, the risk for neural tube defects “is one of many examples of the importance of preconception counseling,” Dr. McClelland said.
Dr. Nicholson noted that the recommended 0.4-0.8 mg of folic acid per day is for patients without heightened deficiency due to medications or bariatric surgery. At-risk patients should receive counseling from their physician to determine the correct amount to take.
The authors report no conflicts of interest, financial or otherwise.
A version of this article first appeared on Medscape.com.
Taking folic acid supplements before conception and in the first trimester of pregnancy continues to be a major line of defense against neural tube defects.
In a statement published in JAMA, the U.S. Preventive Services Task Force recommended that all people planning on becoming pregnant or who could become pregnant take a daily supplement of 0.4-0.8 mg (400-800 mcg) of folic acid to prevent neural tube defects.
The task force also found that folic acid is not associated with maternal cancer or autism, which were the concerns of some researchers. The current findings regarding potential harm align with earlier evidence examining possible risks.
The recommendation also aligns with previous recommendations from the USPSTF and is supported by 12 more recent observational studies. Neural tube defects occur in an estimated 3,000 pregnancies per year.
Folic acid deficiency is common due to diet, impaired folate metabolism, and poor nutrient uptake as a result of medications or bariatric surgery.
“As much as we’ve been trying to get the word out there, we still need to get it out there even more,” Wanda Nicholson, MD, MPH, MBA, vice chair of the USPSTF, told this news organization. “It’s so simple and straightforward and can be so impactful for the health of the baby.”
Neural tube formation occurs 26-28 days after fertilization. Folic acid supplementation is essential for all people who may become pregnant, considering half of the pregnancies in the United States are unplanned, according to the USPSTF.
“In many cases, neural tube formation has already occurred, or not occurred appropriately, before someone realizes that they’re pregnant,” Dr. Nicholson said. “That’s why it’s so important to start taking folic acid one month prior to conception if you’re planning on becoming pregnant, and if you’re capable of being pregnant but not planning pregnancy, yes, we’re advocating that you also proceed with folic acid supplementation.”
Primary care physicians play a key role in patient education and ensuring that all patients receive adequate folic acid, according to Spencer McClelland, MD, an obstetrician-gynecologist at Denver Health, who was not involved in the statement. Dr. McClelland advised that clinicians recommend patients who are or could get pregnant take a multivitamin, because most brands will contain the recommended dosage of folic acid.
“There’s some confusion about folic acid,” he said. “Many patients know that they should be on a prenatal vitamin, but most don’t know that the reason we’re recommending a prenatal vitamin is almost entirely because of the value of folic acid, and everything else in the prenatal vitamin is kind of icing on the cake.”
For patients trying to get pregnant, the risk for neural tube defects “is one of many examples of the importance of preconception counseling,” Dr. McClelland said.
Dr. Nicholson noted that the recommended 0.4-0.8 mg of folic acid per day is for patients without heightened deficiency due to medications or bariatric surgery. At-risk patients should receive counseling from their physician to determine the correct amount to take.
The authors report no conflicts of interest, financial or otherwise.
A version of this article first appeared on Medscape.com.
FROM JAMA
Daily aspirin for stroke prevention in healthy elderly should be avoided
according to results from a large randomized trial.
The findings, published in JAMA Network Open, bolster recommendations published in 2022 by the U.S. Preventive Services Task Force against daily aspirin for primary prevention of stroke in older adults and add to a mounting consensus that it should be avoided in the healthy elderly, for whom bleeding risks outweigh potential benefits.
Stroke was a preplanned secondary outcome of the Aspirin in Reducing Events in the Elderly (ASPREE) trial, which randomized 19,114 community-living people in Australia and the United States (56% women, 91% White) to 100 mg. daily aspirin or placebo. Participants were aged 70 and older, with the exception of U.S. Black and Hispanic individuals, who could be as young as 65. Participants did not have disability or known cardiovascular disease at baseline, and blood pressure was adequately controlled.
ASPEE findings
In 2018 the ASPREE authors, led by John McNeil, PhD, of Monash University, Melbourne, published their findings that aspirin did not reduce mortality or cardiovascular events (including stroke) in the same large cohort.
The new analysis, led by Geoffrey Cloud, MB, BS, of Monash University, focuses on stroke and intracranial bleeding outcomes. At 5 years’ follow up, the ASPREE investigators saw no significant reduction in ischemic stroke incidence associated with aspirin (hazard ratio, 0.89; 95% confidence interval, 0.71-1.11), while incidence of all types of intracranial bleeding, including hemorrhagic stroke, was significantly increased (HR, 1.38; 95% CI, 1.03-1.84).
Altogether 108 of participants taking aspirin (1.1%) experienced some form of intracranial bleeding (subdural, extradural, and/or subarachnoid), compared with 79 (0.8%) in the placebo group. Aspirin-treated patients also saw more hemorrhagic stroke (0.5% vs. 0.4%). As the ASPREE investigators had reported in an earlier paper, upper gastrointestinal bleeding occurred in significantly more aspirin-treated patients than those on placebo (HR, 1.87; 95% CI, 1.32-2.66).
“These outcomes may alter the balance of risks and benefits of an antiplatelet drug, especially if given to individuals at low risk in a primary prevention setting. This concern is relevant given the high stroke risk in older individuals, worldwide increases in populations of older individuals, and the importance of evaluating preventive strategies in this age group,” the investigators wrote.
The investigators cited the study’s large size as a strength while noting among its weaknesses that fewer stroke and bleeding events occurred during follow-up than expected, and that not all ischemic stroke events among older participants were thoroughly investigated.
Patients need to know their risk
In an interview, Shlee Song, MD, director of the stroke center at Cedars-Sinai, Los Angeles, said that the new ASPREE findings underscore the importance of careful communication with patients and their families, who may be confused about which risk group they belong to and either cease taking aspirin when it is in fact indicated, or take it when it could harm them.
“We need to be clear for our patients whether these results are relevant to them or not,” Dr. Song said. “People with a history of ischemic stroke need to know aspirin therapy is helpful in reducing risk of another stroke.”
Some patients may come to believe that because their stroke occurred a long time ago, they are in a lower-risk group. “But people need to understand that with a history of a heart attack or stroke, you’re always a separate group,” Dr. Song said. “Our job is also surveillance screening – have you had a fall this past year? Have you had a change in bowel movements? The bleeding events seen in ASPREE include bleeding in the head and bleeding in the gut.”
A key issue to stress with patients, Dr. Song said, is blood pressure management. “Patients might take aspirin because a family member had a stroke, without controlling blood pressure first. That could be the perfect storm for a head bleed: uncontrolled hypertension and an antiplatelet agent.”
The ASPREE study was funded by the National Institutes of Health in the United States and Monash University and the Victorian Cancer Agency in Australia. Three coauthors reported receiving funding or fees from drug manufacturers. Dr. Song disclosed no financial conflicts related to her comments.
according to results from a large randomized trial.
The findings, published in JAMA Network Open, bolster recommendations published in 2022 by the U.S. Preventive Services Task Force against daily aspirin for primary prevention of stroke in older adults and add to a mounting consensus that it should be avoided in the healthy elderly, for whom bleeding risks outweigh potential benefits.
Stroke was a preplanned secondary outcome of the Aspirin in Reducing Events in the Elderly (ASPREE) trial, which randomized 19,114 community-living people in Australia and the United States (56% women, 91% White) to 100 mg. daily aspirin or placebo. Participants were aged 70 and older, with the exception of U.S. Black and Hispanic individuals, who could be as young as 65. Participants did not have disability or known cardiovascular disease at baseline, and blood pressure was adequately controlled.
ASPEE findings
In 2018 the ASPREE authors, led by John McNeil, PhD, of Monash University, Melbourne, published their findings that aspirin did not reduce mortality or cardiovascular events (including stroke) in the same large cohort.
The new analysis, led by Geoffrey Cloud, MB, BS, of Monash University, focuses on stroke and intracranial bleeding outcomes. At 5 years’ follow up, the ASPREE investigators saw no significant reduction in ischemic stroke incidence associated with aspirin (hazard ratio, 0.89; 95% confidence interval, 0.71-1.11), while incidence of all types of intracranial bleeding, including hemorrhagic stroke, was significantly increased (HR, 1.38; 95% CI, 1.03-1.84).
Altogether 108 of participants taking aspirin (1.1%) experienced some form of intracranial bleeding (subdural, extradural, and/or subarachnoid), compared with 79 (0.8%) in the placebo group. Aspirin-treated patients also saw more hemorrhagic stroke (0.5% vs. 0.4%). As the ASPREE investigators had reported in an earlier paper, upper gastrointestinal bleeding occurred in significantly more aspirin-treated patients than those on placebo (HR, 1.87; 95% CI, 1.32-2.66).
“These outcomes may alter the balance of risks and benefits of an antiplatelet drug, especially if given to individuals at low risk in a primary prevention setting. This concern is relevant given the high stroke risk in older individuals, worldwide increases in populations of older individuals, and the importance of evaluating preventive strategies in this age group,” the investigators wrote.
The investigators cited the study’s large size as a strength while noting among its weaknesses that fewer stroke and bleeding events occurred during follow-up than expected, and that not all ischemic stroke events among older participants were thoroughly investigated.
Patients need to know their risk
In an interview, Shlee Song, MD, director of the stroke center at Cedars-Sinai, Los Angeles, said that the new ASPREE findings underscore the importance of careful communication with patients and their families, who may be confused about which risk group they belong to and either cease taking aspirin when it is in fact indicated, or take it when it could harm them.
“We need to be clear for our patients whether these results are relevant to them or not,” Dr. Song said. “People with a history of ischemic stroke need to know aspirin therapy is helpful in reducing risk of another stroke.”
Some patients may come to believe that because their stroke occurred a long time ago, they are in a lower-risk group. “But people need to understand that with a history of a heart attack or stroke, you’re always a separate group,” Dr. Song said. “Our job is also surveillance screening – have you had a fall this past year? Have you had a change in bowel movements? The bleeding events seen in ASPREE include bleeding in the head and bleeding in the gut.”
A key issue to stress with patients, Dr. Song said, is blood pressure management. “Patients might take aspirin because a family member had a stroke, without controlling blood pressure first. That could be the perfect storm for a head bleed: uncontrolled hypertension and an antiplatelet agent.”
The ASPREE study was funded by the National Institutes of Health in the United States and Monash University and the Victorian Cancer Agency in Australia. Three coauthors reported receiving funding or fees from drug manufacturers. Dr. Song disclosed no financial conflicts related to her comments.
according to results from a large randomized trial.
The findings, published in JAMA Network Open, bolster recommendations published in 2022 by the U.S. Preventive Services Task Force against daily aspirin for primary prevention of stroke in older adults and add to a mounting consensus that it should be avoided in the healthy elderly, for whom bleeding risks outweigh potential benefits.
Stroke was a preplanned secondary outcome of the Aspirin in Reducing Events in the Elderly (ASPREE) trial, which randomized 19,114 community-living people in Australia and the United States (56% women, 91% White) to 100 mg. daily aspirin or placebo. Participants were aged 70 and older, with the exception of U.S. Black and Hispanic individuals, who could be as young as 65. Participants did not have disability or known cardiovascular disease at baseline, and blood pressure was adequately controlled.
ASPEE findings
In 2018 the ASPREE authors, led by John McNeil, PhD, of Monash University, Melbourne, published their findings that aspirin did not reduce mortality or cardiovascular events (including stroke) in the same large cohort.
The new analysis, led by Geoffrey Cloud, MB, BS, of Monash University, focuses on stroke and intracranial bleeding outcomes. At 5 years’ follow up, the ASPREE investigators saw no significant reduction in ischemic stroke incidence associated with aspirin (hazard ratio, 0.89; 95% confidence interval, 0.71-1.11), while incidence of all types of intracranial bleeding, including hemorrhagic stroke, was significantly increased (HR, 1.38; 95% CI, 1.03-1.84).
Altogether 108 of participants taking aspirin (1.1%) experienced some form of intracranial bleeding (subdural, extradural, and/or subarachnoid), compared with 79 (0.8%) in the placebo group. Aspirin-treated patients also saw more hemorrhagic stroke (0.5% vs. 0.4%). As the ASPREE investigators had reported in an earlier paper, upper gastrointestinal bleeding occurred in significantly more aspirin-treated patients than those on placebo (HR, 1.87; 95% CI, 1.32-2.66).
“These outcomes may alter the balance of risks and benefits of an antiplatelet drug, especially if given to individuals at low risk in a primary prevention setting. This concern is relevant given the high stroke risk in older individuals, worldwide increases in populations of older individuals, and the importance of evaluating preventive strategies in this age group,” the investigators wrote.
The investigators cited the study’s large size as a strength while noting among its weaknesses that fewer stroke and bleeding events occurred during follow-up than expected, and that not all ischemic stroke events among older participants were thoroughly investigated.
Patients need to know their risk
In an interview, Shlee Song, MD, director of the stroke center at Cedars-Sinai, Los Angeles, said that the new ASPREE findings underscore the importance of careful communication with patients and their families, who may be confused about which risk group they belong to and either cease taking aspirin when it is in fact indicated, or take it when it could harm them.
“We need to be clear for our patients whether these results are relevant to them or not,” Dr. Song said. “People with a history of ischemic stroke need to know aspirin therapy is helpful in reducing risk of another stroke.”
Some patients may come to believe that because their stroke occurred a long time ago, they are in a lower-risk group. “But people need to understand that with a history of a heart attack or stroke, you’re always a separate group,” Dr. Song said. “Our job is also surveillance screening – have you had a fall this past year? Have you had a change in bowel movements? The bleeding events seen in ASPREE include bleeding in the head and bleeding in the gut.”
A key issue to stress with patients, Dr. Song said, is blood pressure management. “Patients might take aspirin because a family member had a stroke, without controlling blood pressure first. That could be the perfect storm for a head bleed: uncontrolled hypertension and an antiplatelet agent.”
The ASPREE study was funded by the National Institutes of Health in the United States and Monash University and the Victorian Cancer Agency in Australia. Three coauthors reported receiving funding or fees from drug manufacturers. Dr. Song disclosed no financial conflicts related to her comments.
FROM JAMA NETWORK OPEN
Concussion may not affect IQ in children
data suggest.
In a multicenter study of almost 900 children with concussion or orthopedic injury, differences between groups in full-scale IQ (Cohen’s d = 0.13) and matrix reasoning scores (d = 0.16) were small.
“We draw the inference that IQ scores are unchanged, in the sense that they’re not different from [those of] kids with other types of injuries that don’t involve the brain,” said study author Keith Owen Yeates, PhD, Ronald and Irene Ward Chair in Pediatric Brain Injury and a professor of psychology at the University of Calgary (Alta.).
The study was published in Pediatrics.
A representative sample
The investigators analyzed data from two prospective cohort studies of children who were treated for concussion or mild orthopedic injury at two hospitals in the United States and five in Canada. Participants were aged 8-17 years and were recruited within 24 hours of the index event. Patients in the United States completed IQ and performance validity testing at 3-18 days after injury. Patients in Canada did so at 3 months after injury. The study used the short-form IQ test. The investigators included 866 children in their analysis.
Using linear modeling, Bayesian analysis, and multigroup factor analysis, the researchers found “very small group differences” in full-scale IQ scores between the two groups. Mean IQ was 104.95 for the concussion group and 106.08 for the orthopedic-injury group. Matrix reasoning scores were 52.28 and 53.81 for the concussion and orthopedic-injury groups, respectively.
Vocabulary scores did not differ between the two groups (53.25 for the concussion group and 53.27 for the orthopedic-injury group).
The study population is “pretty representative” from a demographic perspective, although it was predominantly White, said Dr. Yeates. “On the other hand, we did look at socioeconomic status, and that didn’t seem to alter the findings at all.”
The sample size is one of the study’s strengths, said Dr. Yeates. “Having 866 kids is far larger, I think, than just about any other study out there.” Drawing from seven children’s hospitals in North America is another strength. “Previous studies, in addition to having smaller samples, were from a single site and often recruited from a clinic population, not a representative group for a general population of kids with concussion.”
The findings must be interpreted precisely, however. “We don’t have actual preinjury data, so the more precise way of describing the findings is to say they’re not different from kids who are very similar to them demographically, have the same risk factors for injuries, and had a similar experience of a traumatic injury,” said Dr. Yeates. “The IQ scores for both groups are smack dab in the average range.”
Overall, the results are encouraging. “There’s been a lot of bad news in the media and in the science about concussion that worries patients, so it’s nice to be able to provide a little bit of balance,” said Dr. Yeates. “The message I give parents is that most kids recover within 2-4 weeks, and we’re much better now at predicting who’s going to [recover] and who isn’t, and that helps, too, so that we can focus our intervention on kids who are most at risk.”
Some children will have persisting symptoms, but evidence-based treatments are lacking. “I think that’ll be a really important direction for the future,” said Dr. Yeates.
Graduated return
Commenting on the findings, Michael Esser, MD, a pediatric neurologist at Alberta Children’s Hospital, Calgary, and an associate professor in pediatrics at the University of Calgary, said that they can help allay parents’ concerns about concussions. “It can also be of help for clinicians who want to have evidence to reassure families and promote a graduated return to activities. In particular, the study would support the philosophy of a graduated return to school or work, after a brief period of rest, following concussion.” Dr. Esser did not participate in the study.
The research is also noteworthy because it acknowledges that the differences in the design and methodology used in prior studies may explain the apparent disagreement over how concussion may influence cognitive function.
“This is an important message,” said Dr. Esser. “Families struggle with determining the merit of a lot of information due to the myriad of social media comments about concussion and the risk for cognitive impairment. Therefore, it is important that conclusions with a significant implication are evaluated with a variety of approaches.”
The study received funding from the National Institutes of Health and the Canadian Institutes for Health Research. Dr. Yeates disclosed relationships with the American Psychological Association, Guilford Press, and Cambridge University Press. He has received grant funding from the Canadian Institutes of Health Research, the National Institutes of Health, Brain Canada Foundation, and the National Football League Scientific Advisory Board. He also has relationships with the National Institute for Child Health and Human Development, National Institute of Neurologic Disorders and Stroke, National Pediatric Rehabilitation Resource Center, Center for Pediatric Rehabilitation, and Virginia Tech University. Dr. Esser had no relevant relationships to disclose.
A version of this article appeared on Medscape.com.
data suggest.
In a multicenter study of almost 900 children with concussion or orthopedic injury, differences between groups in full-scale IQ (Cohen’s d = 0.13) and matrix reasoning scores (d = 0.16) were small.
“We draw the inference that IQ scores are unchanged, in the sense that they’re not different from [those of] kids with other types of injuries that don’t involve the brain,” said study author Keith Owen Yeates, PhD, Ronald and Irene Ward Chair in Pediatric Brain Injury and a professor of psychology at the University of Calgary (Alta.).
The study was published in Pediatrics.
A representative sample
The investigators analyzed data from two prospective cohort studies of children who were treated for concussion or mild orthopedic injury at two hospitals in the United States and five in Canada. Participants were aged 8-17 years and were recruited within 24 hours of the index event. Patients in the United States completed IQ and performance validity testing at 3-18 days after injury. Patients in Canada did so at 3 months after injury. The study used the short-form IQ test. The investigators included 866 children in their analysis.
Using linear modeling, Bayesian analysis, and multigroup factor analysis, the researchers found “very small group differences” in full-scale IQ scores between the two groups. Mean IQ was 104.95 for the concussion group and 106.08 for the orthopedic-injury group. Matrix reasoning scores were 52.28 and 53.81 for the concussion and orthopedic-injury groups, respectively.
Vocabulary scores did not differ between the two groups (53.25 for the concussion group and 53.27 for the orthopedic-injury group).
The study population is “pretty representative” from a demographic perspective, although it was predominantly White, said Dr. Yeates. “On the other hand, we did look at socioeconomic status, and that didn’t seem to alter the findings at all.”
The sample size is one of the study’s strengths, said Dr. Yeates. “Having 866 kids is far larger, I think, than just about any other study out there.” Drawing from seven children’s hospitals in North America is another strength. “Previous studies, in addition to having smaller samples, were from a single site and often recruited from a clinic population, not a representative group for a general population of kids with concussion.”
The findings must be interpreted precisely, however. “We don’t have actual preinjury data, so the more precise way of describing the findings is to say they’re not different from kids who are very similar to them demographically, have the same risk factors for injuries, and had a similar experience of a traumatic injury,” said Dr. Yeates. “The IQ scores for both groups are smack dab in the average range.”
Overall, the results are encouraging. “There’s been a lot of bad news in the media and in the science about concussion that worries patients, so it’s nice to be able to provide a little bit of balance,” said Dr. Yeates. “The message I give parents is that most kids recover within 2-4 weeks, and we’re much better now at predicting who’s going to [recover] and who isn’t, and that helps, too, so that we can focus our intervention on kids who are most at risk.”
Some children will have persisting symptoms, but evidence-based treatments are lacking. “I think that’ll be a really important direction for the future,” said Dr. Yeates.
Graduated return
Commenting on the findings, Michael Esser, MD, a pediatric neurologist at Alberta Children’s Hospital, Calgary, and an associate professor in pediatrics at the University of Calgary, said that they can help allay parents’ concerns about concussions. “It can also be of help for clinicians who want to have evidence to reassure families and promote a graduated return to activities. In particular, the study would support the philosophy of a graduated return to school or work, after a brief period of rest, following concussion.” Dr. Esser did not participate in the study.
The research is also noteworthy because it acknowledges that the differences in the design and methodology used in prior studies may explain the apparent disagreement over how concussion may influence cognitive function.
“This is an important message,” said Dr. Esser. “Families struggle with determining the merit of a lot of information due to the myriad of social media comments about concussion and the risk for cognitive impairment. Therefore, it is important that conclusions with a significant implication are evaluated with a variety of approaches.”
The study received funding from the National Institutes of Health and the Canadian Institutes for Health Research. Dr. Yeates disclosed relationships with the American Psychological Association, Guilford Press, and Cambridge University Press. He has received grant funding from the Canadian Institutes of Health Research, the National Institutes of Health, Brain Canada Foundation, and the National Football League Scientific Advisory Board. He also has relationships with the National Institute for Child Health and Human Development, National Institute of Neurologic Disorders and Stroke, National Pediatric Rehabilitation Resource Center, Center for Pediatric Rehabilitation, and Virginia Tech University. Dr. Esser had no relevant relationships to disclose.
A version of this article appeared on Medscape.com.
data suggest.
In a multicenter study of almost 900 children with concussion or orthopedic injury, differences between groups in full-scale IQ (Cohen’s d = 0.13) and matrix reasoning scores (d = 0.16) were small.
“We draw the inference that IQ scores are unchanged, in the sense that they’re not different from [those of] kids with other types of injuries that don’t involve the brain,” said study author Keith Owen Yeates, PhD, Ronald and Irene Ward Chair in Pediatric Brain Injury and a professor of psychology at the University of Calgary (Alta.).
The study was published in Pediatrics.
A representative sample
The investigators analyzed data from two prospective cohort studies of children who were treated for concussion or mild orthopedic injury at two hospitals in the United States and five in Canada. Participants were aged 8-17 years and were recruited within 24 hours of the index event. Patients in the United States completed IQ and performance validity testing at 3-18 days after injury. Patients in Canada did so at 3 months after injury. The study used the short-form IQ test. The investigators included 866 children in their analysis.
Using linear modeling, Bayesian analysis, and multigroup factor analysis, the researchers found “very small group differences” in full-scale IQ scores between the two groups. Mean IQ was 104.95 for the concussion group and 106.08 for the orthopedic-injury group. Matrix reasoning scores were 52.28 and 53.81 for the concussion and orthopedic-injury groups, respectively.
Vocabulary scores did not differ between the two groups (53.25 for the concussion group and 53.27 for the orthopedic-injury group).
The study population is “pretty representative” from a demographic perspective, although it was predominantly White, said Dr. Yeates. “On the other hand, we did look at socioeconomic status, and that didn’t seem to alter the findings at all.”
The sample size is one of the study’s strengths, said Dr. Yeates. “Having 866 kids is far larger, I think, than just about any other study out there.” Drawing from seven children’s hospitals in North America is another strength. “Previous studies, in addition to having smaller samples, were from a single site and often recruited from a clinic population, not a representative group for a general population of kids with concussion.”
The findings must be interpreted precisely, however. “We don’t have actual preinjury data, so the more precise way of describing the findings is to say they’re not different from kids who are very similar to them demographically, have the same risk factors for injuries, and had a similar experience of a traumatic injury,” said Dr. Yeates. “The IQ scores for both groups are smack dab in the average range.”
Overall, the results are encouraging. “There’s been a lot of bad news in the media and in the science about concussion that worries patients, so it’s nice to be able to provide a little bit of balance,” said Dr. Yeates. “The message I give parents is that most kids recover within 2-4 weeks, and we’re much better now at predicting who’s going to [recover] and who isn’t, and that helps, too, so that we can focus our intervention on kids who are most at risk.”
Some children will have persisting symptoms, but evidence-based treatments are lacking. “I think that’ll be a really important direction for the future,” said Dr. Yeates.
Graduated return
Commenting on the findings, Michael Esser, MD, a pediatric neurologist at Alberta Children’s Hospital, Calgary, and an associate professor in pediatrics at the University of Calgary, said that they can help allay parents’ concerns about concussions. “It can also be of help for clinicians who want to have evidence to reassure families and promote a graduated return to activities. In particular, the study would support the philosophy of a graduated return to school or work, after a brief period of rest, following concussion.” Dr. Esser did not participate in the study.
The research is also noteworthy because it acknowledges that the differences in the design and methodology used in prior studies may explain the apparent disagreement over how concussion may influence cognitive function.
“This is an important message,” said Dr. Esser. “Families struggle with determining the merit of a lot of information due to the myriad of social media comments about concussion and the risk for cognitive impairment. Therefore, it is important that conclusions with a significant implication are evaluated with a variety of approaches.”
The study received funding from the National Institutes of Health and the Canadian Institutes for Health Research. Dr. Yeates disclosed relationships with the American Psychological Association, Guilford Press, and Cambridge University Press. He has received grant funding from the Canadian Institutes of Health Research, the National Institutes of Health, Brain Canada Foundation, and the National Football League Scientific Advisory Board. He also has relationships with the National Institute for Child Health and Human Development, National Institute of Neurologic Disorders and Stroke, National Pediatric Rehabilitation Resource Center, Center for Pediatric Rehabilitation, and Virginia Tech University. Dr. Esser had no relevant relationships to disclose.
A version of this article appeared on Medscape.com.
FROM PEDIATRICS
Research casts doubt on value of daily aspirin for healthy adults
Daily use of low-dose aspirin offers no significant protection against stroke and was linked to a higher rate of bleeding in the brain, according to new research published in JAMA.
The research matches other evidence advising that healthy older adults without a history of heart conditions or warning signs of stroke should not take low-dose aspirin.
The findings also support the recommendation from the U.S. Preventive Services Task Force that low-dose aspirin should not be prescribed for preventing a first heart attack or stroke in healthy older adults, The New York Times reported.
“We can be very emphatic that healthy people who are not on aspirin and do not have multiple risk factors should not be starting it now,” said Randall Stafford, MD, of Stanford (Calif.) University, who was not involved in the study, in the Times.
It’s not as clear for others, he said.
“The longer you’ve been on aspirin and the more risk factors you have for heart attacks and strokes, the murkier it gets,” he said.
Some cardiac and stroke experts say daily aspirin should remain part of the regimen for people who have had a heart attack or stroke.
The JAMA report was based on data from a randomized control trial of 19,000 people from Australia and America. Participants were over the age of 70 and did not have heart disease.
The data covered an average of almost 4.7 years and revealed that aspirin lowered the rate of ischemic stroke but not significantly. An ischemic stroke happens when a clot forms in a blood vessel that sends blood to the brain.
There was also a 38% higher rate of brain bleeds for people who took aspirin daily, compared with those who took a placebo.
The Times wrote, “In the past, some doctors regarded aspirin as something of a wonder drug, capable of protecting healthy patients against a future heart attack or stroke. But recent studies have shown that the powerful drug has limited protective power among people who have not yet had such an event, and it comes with dangerous side effects.”
A version of this article first appeared on WebMD.com.
Daily use of low-dose aspirin offers no significant protection against stroke and was linked to a higher rate of bleeding in the brain, according to new research published in JAMA.
The research matches other evidence advising that healthy older adults without a history of heart conditions or warning signs of stroke should not take low-dose aspirin.
The findings also support the recommendation from the U.S. Preventive Services Task Force that low-dose aspirin should not be prescribed for preventing a first heart attack or stroke in healthy older adults, The New York Times reported.
“We can be very emphatic that healthy people who are not on aspirin and do not have multiple risk factors should not be starting it now,” said Randall Stafford, MD, of Stanford (Calif.) University, who was not involved in the study, in the Times.
It’s not as clear for others, he said.
“The longer you’ve been on aspirin and the more risk factors you have for heart attacks and strokes, the murkier it gets,” he said.
Some cardiac and stroke experts say daily aspirin should remain part of the regimen for people who have had a heart attack or stroke.
The JAMA report was based on data from a randomized control trial of 19,000 people from Australia and America. Participants were over the age of 70 and did not have heart disease.
The data covered an average of almost 4.7 years and revealed that aspirin lowered the rate of ischemic stroke but not significantly. An ischemic stroke happens when a clot forms in a blood vessel that sends blood to the brain.
There was also a 38% higher rate of brain bleeds for people who took aspirin daily, compared with those who took a placebo.
The Times wrote, “In the past, some doctors regarded aspirin as something of a wonder drug, capable of protecting healthy patients against a future heart attack or stroke. But recent studies have shown that the powerful drug has limited protective power among people who have not yet had such an event, and it comes with dangerous side effects.”
A version of this article first appeared on WebMD.com.
Daily use of low-dose aspirin offers no significant protection against stroke and was linked to a higher rate of bleeding in the brain, according to new research published in JAMA.
The research matches other evidence advising that healthy older adults without a history of heart conditions or warning signs of stroke should not take low-dose aspirin.
The findings also support the recommendation from the U.S. Preventive Services Task Force that low-dose aspirin should not be prescribed for preventing a first heart attack or stroke in healthy older adults, The New York Times reported.
“We can be very emphatic that healthy people who are not on aspirin and do not have multiple risk factors should not be starting it now,” said Randall Stafford, MD, of Stanford (Calif.) University, who was not involved in the study, in the Times.
It’s not as clear for others, he said.
“The longer you’ve been on aspirin and the more risk factors you have for heart attacks and strokes, the murkier it gets,” he said.
Some cardiac and stroke experts say daily aspirin should remain part of the regimen for people who have had a heart attack or stroke.
The JAMA report was based on data from a randomized control trial of 19,000 people from Australia and America. Participants were over the age of 70 and did not have heart disease.
The data covered an average of almost 4.7 years and revealed that aspirin lowered the rate of ischemic stroke but not significantly. An ischemic stroke happens when a clot forms in a blood vessel that sends blood to the brain.
There was also a 38% higher rate of brain bleeds for people who took aspirin daily, compared with those who took a placebo.
The Times wrote, “In the past, some doctors regarded aspirin as something of a wonder drug, capable of protecting healthy patients against a future heart attack or stroke. But recent studies have shown that the powerful drug has limited protective power among people who have not yet had such an event, and it comes with dangerous side effects.”
A version of this article first appeared on WebMD.com.
FROM JAMA
Why scratching is so contagious
If you’ve ever felt an urge to scratch after witnessing someone else relieve their own itch, you’re certainly not alone. Itching can be contagious and the phenomenon is so common it doesn’t just affect humans. Now researchers may understand why.
Some background: In a 2007 study led by Zhou-Feng Chen, PhD, professor of anesthesiology, psychiatry, and developmental biology at the Washington University in St. Louis, researchers discovered a specific gene, the GRPR (gastrin-releasing peptide receptor), in the spinal cord and a corresponding neuropeptide, GRP (gastrin-releasing peptide). Together, the GRP system was found to transmit the “itch information” from one’s skin to the spinal cord.
This discovery was further backed by 2017 findings when Dr. Chen and his colleagues closely observed the molecular and neural basis of contagious itch behavior in mice. “We played a video that showed a mouse scratching at a very high frequency to other mice,” said Dr. Chen. “We found that, indeed, the mice who watched the video also scratched.”
To determine the inner workings at play, the researchers used molecular mapping to reveal increased neuronal activity in the suprachiasmatic nucleus (SCN), a bilateral structure found in the hypothalamus of the mouse’s brain. In other words, this part of the mouse’s brain “lit up” when a mouse displayed contagious scratching behavior.
The researchers then decided to take this one step further by manipulating the amount of GRP in the hypothalamus. “When we deleted the GRP in the SCN, the mice stopped imitating the scratch,” Dr. Chen said. “When we injected more GRP into the SCN, the mice started scratching like crazy.”
Now, after more investigating and research published in 2022 in Cell Reports, Dr. Chen and his team suspect contagious itching may have just as much to do with our eyeballs as our skin and spinal cord. Why? The phenomenon begins with a visual component: Someone seeing another person scratching.
The researchers targeted mice’s retinal ganglion cells, a type of light-capturing neuron found near the inner surface of the retina. When those cells were disabled, all scratching stopped.
This recent study argues that a previously undiscovered visual pathway may exist between the retina and the brain – bypassing the visual cortex – to provide more immediate physical reactions to potential adverse situations.
There’s more (and it could be quite relatable to some people): After the mice watched a video of another mouse scratching for half an hour, the researchers measured the mice’s stress hormone levels, finding a significant increase. This suggested that exposure to impulsive, contagious scratching behavior may have caused heightened anxiety in the mice.
said Dr. Chen. “We humans also scratch a lot, sometimes as a way to unconsciously express our internal anxiety.”
The mice may have interpreted the scratching video as a sudden negative change to their environment that they had to prepare for. “Contagious behavior is actually a very efficient way to inform other animals of what’s coming,” Dr. Chen said. “When we see other people running in a panic, there is no time to think. You just run as fast as you can. This is another example of contagious behavior that is in your own interest to survive.”
As a result, Dr. Chen believes it’s fair to infer that contagious behavior, including yawning and emotional contagion, is merely an expression of a fundamental survival mechanism that has evolved over time. “The human being is just an imitation machine. It’s often very difficult for people to act independently or as a minority because you would be working against evolution,” said Dr. Chen.
Scott Ira Krakower, DO, a child and adolescent psychiatrist at Northwell Health in Glen Oaks, N.Y., (and not party to this research), seconds this sentiment. “In regard to the physical benefits of contagion, it acts as a permanent defense and helps build collective immunity,” he said. “The social benefits when it comes to empathy or social media contagion are also important to our development. It helps us understand, adapt, and connect with others.”
Observing how empathy operates as a socially contagious behavior is something Dr. Chen and his colleagues are interested in looking into in the future.
“The definition of empathy is the sharing of emotions,” Dr. Chen said. “Shared feelings are crucial for social bonding and mental health, and for other animals, like mice, this is also the case.” Previous studies have shown that mice do, in fact, experience empathy and share feelings of pain and fear with one another.
There is still much to be explored in the study of contagious behaviors and the components of the brain that are activated during such behavior. Dr. Chen and his team intend to, ahem, scratch that particular itch.
A version of this article first appeared on Medscape.com.
If you’ve ever felt an urge to scratch after witnessing someone else relieve their own itch, you’re certainly not alone. Itching can be contagious and the phenomenon is so common it doesn’t just affect humans. Now researchers may understand why.
Some background: In a 2007 study led by Zhou-Feng Chen, PhD, professor of anesthesiology, psychiatry, and developmental biology at the Washington University in St. Louis, researchers discovered a specific gene, the GRPR (gastrin-releasing peptide receptor), in the spinal cord and a corresponding neuropeptide, GRP (gastrin-releasing peptide). Together, the GRP system was found to transmit the “itch information” from one’s skin to the spinal cord.
This discovery was further backed by 2017 findings when Dr. Chen and his colleagues closely observed the molecular and neural basis of contagious itch behavior in mice. “We played a video that showed a mouse scratching at a very high frequency to other mice,” said Dr. Chen. “We found that, indeed, the mice who watched the video also scratched.”
To determine the inner workings at play, the researchers used molecular mapping to reveal increased neuronal activity in the suprachiasmatic nucleus (SCN), a bilateral structure found in the hypothalamus of the mouse’s brain. In other words, this part of the mouse’s brain “lit up” when a mouse displayed contagious scratching behavior.
The researchers then decided to take this one step further by manipulating the amount of GRP in the hypothalamus. “When we deleted the GRP in the SCN, the mice stopped imitating the scratch,” Dr. Chen said. “When we injected more GRP into the SCN, the mice started scratching like crazy.”
Now, after more investigating and research published in 2022 in Cell Reports, Dr. Chen and his team suspect contagious itching may have just as much to do with our eyeballs as our skin and spinal cord. Why? The phenomenon begins with a visual component: Someone seeing another person scratching.
The researchers targeted mice’s retinal ganglion cells, a type of light-capturing neuron found near the inner surface of the retina. When those cells were disabled, all scratching stopped.
This recent study argues that a previously undiscovered visual pathway may exist between the retina and the brain – bypassing the visual cortex – to provide more immediate physical reactions to potential adverse situations.
There’s more (and it could be quite relatable to some people): After the mice watched a video of another mouse scratching for half an hour, the researchers measured the mice’s stress hormone levels, finding a significant increase. This suggested that exposure to impulsive, contagious scratching behavior may have caused heightened anxiety in the mice.
said Dr. Chen. “We humans also scratch a lot, sometimes as a way to unconsciously express our internal anxiety.”
The mice may have interpreted the scratching video as a sudden negative change to their environment that they had to prepare for. “Contagious behavior is actually a very efficient way to inform other animals of what’s coming,” Dr. Chen said. “When we see other people running in a panic, there is no time to think. You just run as fast as you can. This is another example of contagious behavior that is in your own interest to survive.”
As a result, Dr. Chen believes it’s fair to infer that contagious behavior, including yawning and emotional contagion, is merely an expression of a fundamental survival mechanism that has evolved over time. “The human being is just an imitation machine. It’s often very difficult for people to act independently or as a minority because you would be working against evolution,” said Dr. Chen.
Scott Ira Krakower, DO, a child and adolescent psychiatrist at Northwell Health in Glen Oaks, N.Y., (and not party to this research), seconds this sentiment. “In regard to the physical benefits of contagion, it acts as a permanent defense and helps build collective immunity,” he said. “The social benefits when it comes to empathy or social media contagion are also important to our development. It helps us understand, adapt, and connect with others.”
Observing how empathy operates as a socially contagious behavior is something Dr. Chen and his colleagues are interested in looking into in the future.
“The definition of empathy is the sharing of emotions,” Dr. Chen said. “Shared feelings are crucial for social bonding and mental health, and for other animals, like mice, this is also the case.” Previous studies have shown that mice do, in fact, experience empathy and share feelings of pain and fear with one another.
There is still much to be explored in the study of contagious behaviors and the components of the brain that are activated during such behavior. Dr. Chen and his team intend to, ahem, scratch that particular itch.
A version of this article first appeared on Medscape.com.
If you’ve ever felt an urge to scratch after witnessing someone else relieve their own itch, you’re certainly not alone. Itching can be contagious and the phenomenon is so common it doesn’t just affect humans. Now researchers may understand why.
Some background: In a 2007 study led by Zhou-Feng Chen, PhD, professor of anesthesiology, psychiatry, and developmental biology at the Washington University in St. Louis, researchers discovered a specific gene, the GRPR (gastrin-releasing peptide receptor), in the spinal cord and a corresponding neuropeptide, GRP (gastrin-releasing peptide). Together, the GRP system was found to transmit the “itch information” from one’s skin to the spinal cord.
This discovery was further backed by 2017 findings when Dr. Chen and his colleagues closely observed the molecular and neural basis of contagious itch behavior in mice. “We played a video that showed a mouse scratching at a very high frequency to other mice,” said Dr. Chen. “We found that, indeed, the mice who watched the video also scratched.”
To determine the inner workings at play, the researchers used molecular mapping to reveal increased neuronal activity in the suprachiasmatic nucleus (SCN), a bilateral structure found in the hypothalamus of the mouse’s brain. In other words, this part of the mouse’s brain “lit up” when a mouse displayed contagious scratching behavior.
The researchers then decided to take this one step further by manipulating the amount of GRP in the hypothalamus. “When we deleted the GRP in the SCN, the mice stopped imitating the scratch,” Dr. Chen said. “When we injected more GRP into the SCN, the mice started scratching like crazy.”
Now, after more investigating and research published in 2022 in Cell Reports, Dr. Chen and his team suspect contagious itching may have just as much to do with our eyeballs as our skin and spinal cord. Why? The phenomenon begins with a visual component: Someone seeing another person scratching.
The researchers targeted mice’s retinal ganglion cells, a type of light-capturing neuron found near the inner surface of the retina. When those cells were disabled, all scratching stopped.
This recent study argues that a previously undiscovered visual pathway may exist between the retina and the brain – bypassing the visual cortex – to provide more immediate physical reactions to potential adverse situations.
There’s more (and it could be quite relatable to some people): After the mice watched a video of another mouse scratching for half an hour, the researchers measured the mice’s stress hormone levels, finding a significant increase. This suggested that exposure to impulsive, contagious scratching behavior may have caused heightened anxiety in the mice.
said Dr. Chen. “We humans also scratch a lot, sometimes as a way to unconsciously express our internal anxiety.”
The mice may have interpreted the scratching video as a sudden negative change to their environment that they had to prepare for. “Contagious behavior is actually a very efficient way to inform other animals of what’s coming,” Dr. Chen said. “When we see other people running in a panic, there is no time to think. You just run as fast as you can. This is another example of contagious behavior that is in your own interest to survive.”
As a result, Dr. Chen believes it’s fair to infer that contagious behavior, including yawning and emotional contagion, is merely an expression of a fundamental survival mechanism that has evolved over time. “The human being is just an imitation machine. It’s often very difficult for people to act independently or as a minority because you would be working against evolution,” said Dr. Chen.
Scott Ira Krakower, DO, a child and adolescent psychiatrist at Northwell Health in Glen Oaks, N.Y., (and not party to this research), seconds this sentiment. “In regard to the physical benefits of contagion, it acts as a permanent defense and helps build collective immunity,” he said. “The social benefits when it comes to empathy or social media contagion are also important to our development. It helps us understand, adapt, and connect with others.”
Observing how empathy operates as a socially contagious behavior is something Dr. Chen and his colleagues are interested in looking into in the future.
“The definition of empathy is the sharing of emotions,” Dr. Chen said. “Shared feelings are crucial for social bonding and mental health, and for other animals, like mice, this is also the case.” Previous studies have shown that mice do, in fact, experience empathy and share feelings of pain and fear with one another.
There is still much to be explored in the study of contagious behaviors and the components of the brain that are activated during such behavior. Dr. Chen and his team intend to, ahem, scratch that particular itch.
A version of this article first appeared on Medscape.com.
FROM CELL REPORTS
Tooth loss, gum disease tied to hippocampal atrophy
Gum disease and tooth loss are linked to hippocampal atrophy and may have a more negative impact on the brain than aging, new research suggests.
Investigators found that in a late middle-aged and older cohort, among patients with mild periodontitis, having fewer teeth was linked to a faster rate of left hippocampal atrophy. For those with severe gum disease, each additional lost tooth was associated with a faster rate of brain shrinkage, equivalent to 1.3 years of brain aging.
“Tooth loss and gum disease, which is inflammation of the tissue around the teeth that can cause shrinkage of the gums and loosening of the teeth, are very common, so evaluating a potential link with dementia is incredibly important,” study investigator Satoshi Yamaguchi, PhD, DDS, of Tohoku University, in Sendai, Japan, said in a release.
“Our study found that these conditions may play a role in the health of the brain area that controls thinking and memory, giving people another reason to take better care of their teeth,” Dr. Yamaguchi noted.
The findings were published online in Neurology.
Greater effect than aging
Although previous research suggests that tooth loss and periodontitis are risk factors for Alzheimer’s disease, longitudinal research has not shown a significant correlation between these conditions and hippocampal atrophy.
To clarify this association, the investigators followed 172 men and women (average age, 67 years) who had undergone two MRI brain scans 4 years apart and had had a dental examination. None of the participants had any signs of cognitive decline at baseline.
At study outset, information on cerebrovascular and cardiovascular disease, alcohol consumption, smoking, depression history, and cognitive function was gathered. The Mini Mental State Exam and dental exams were administered at baseline and at 4-year follow-up.
For each participant, the number of teeth was counted, and all participants were assessed for gum disease via periodontal probing depth (PD).
Healthy gums typically measure between 1 and 3 mm in depth. Mild gum disease is signified by measurements of 3-4 mm in several areas. Severe gum disease involves measurements of 5-6 mm and is accompanied by greater bone loss, leading to potential tooth loss.
Multiple regression analysis was performed, with the annual symmetric percentage change (SPC) of hippocampal volume as the dependent variable. The analysis included an interaction term between the number of teeth present (NTP) and mean PD.
Over the 4-year study period, the investigators found that the qualitative interaction between NTP and mean PD was significant for the annual SPC in the left hippocampus.
Among those with mild periodontitis, having fewer teeth correlated with more rapid atrophy of the left hippocampus, such that every tooth lost was equivalent to nearly 1 year of brain aging.
In contrast, having more teeth was associated with a faster rate of left hippocampal atrophy among those with severe periodontitis and was equivalent to 1.3 years of brain aging.
For those with severe gum disease, each additional lost tooth corresponded to a faster rate of brain shrinkage, equivalent to 1.3 years of brain aging.
“This finding indicates that periodontitis may have a greater association with left hippocampal atrophy than the association exhibited by age. Furthermore, in cases of mild periodontitis, fewer teeth may be associated with a subsequent decline in cognitive function,” the investigators write.
The study’s results, they add, highlight the importance of preserving oral health, not just the retaining of teeth. “These findings suggest that retaining teeth with severe gum disease is associated with brain atrophy,” said Dr. Yamaguchi.
“Controlling the progression of gum disease through regular dental visits is crucial, and teeth with severe gum disease may need to be extracted and replaced with appropriate prosthetic devices,” he added.
The researchers note that further studies are needed to confirm these findings.
The study was supported the Japanese Ministry of Education, Culture, Sports, Science, and Technology; Kelo University; Japan Arteriosclerosis Prevention Fund; Japanese Ministry of Health, Labor, and Welfare; Teiko University; Pfizer Japan; Bayer Yakuhin; Chugai Pharmaceutical; Daiichi Sankyo; Astrellas Pharma; Takeda Pharmaceutical; the Health Care Science Institute; the Health Science Center; and the Takeda Science Foundation. The investigators reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Gum disease and tooth loss are linked to hippocampal atrophy and may have a more negative impact on the brain than aging, new research suggests.
Investigators found that in a late middle-aged and older cohort, among patients with mild periodontitis, having fewer teeth was linked to a faster rate of left hippocampal atrophy. For those with severe gum disease, each additional lost tooth was associated with a faster rate of brain shrinkage, equivalent to 1.3 years of brain aging.
“Tooth loss and gum disease, which is inflammation of the tissue around the teeth that can cause shrinkage of the gums and loosening of the teeth, are very common, so evaluating a potential link with dementia is incredibly important,” study investigator Satoshi Yamaguchi, PhD, DDS, of Tohoku University, in Sendai, Japan, said in a release.
“Our study found that these conditions may play a role in the health of the brain area that controls thinking and memory, giving people another reason to take better care of their teeth,” Dr. Yamaguchi noted.
The findings were published online in Neurology.
Greater effect than aging
Although previous research suggests that tooth loss and periodontitis are risk factors for Alzheimer’s disease, longitudinal research has not shown a significant correlation between these conditions and hippocampal atrophy.
To clarify this association, the investigators followed 172 men and women (average age, 67 years) who had undergone two MRI brain scans 4 years apart and had had a dental examination. None of the participants had any signs of cognitive decline at baseline.
At study outset, information on cerebrovascular and cardiovascular disease, alcohol consumption, smoking, depression history, and cognitive function was gathered. The Mini Mental State Exam and dental exams were administered at baseline and at 4-year follow-up.
For each participant, the number of teeth was counted, and all participants were assessed for gum disease via periodontal probing depth (PD).
Healthy gums typically measure between 1 and 3 mm in depth. Mild gum disease is signified by measurements of 3-4 mm in several areas. Severe gum disease involves measurements of 5-6 mm and is accompanied by greater bone loss, leading to potential tooth loss.
Multiple regression analysis was performed, with the annual symmetric percentage change (SPC) of hippocampal volume as the dependent variable. The analysis included an interaction term between the number of teeth present (NTP) and mean PD.
Over the 4-year study period, the investigators found that the qualitative interaction between NTP and mean PD was significant for the annual SPC in the left hippocampus.
Among those with mild periodontitis, having fewer teeth correlated with more rapid atrophy of the left hippocampus, such that every tooth lost was equivalent to nearly 1 year of brain aging.
In contrast, having more teeth was associated with a faster rate of left hippocampal atrophy among those with severe periodontitis and was equivalent to 1.3 years of brain aging.
For those with severe gum disease, each additional lost tooth corresponded to a faster rate of brain shrinkage, equivalent to 1.3 years of brain aging.
“This finding indicates that periodontitis may have a greater association with left hippocampal atrophy than the association exhibited by age. Furthermore, in cases of mild periodontitis, fewer teeth may be associated with a subsequent decline in cognitive function,” the investigators write.
The study’s results, they add, highlight the importance of preserving oral health, not just the retaining of teeth. “These findings suggest that retaining teeth with severe gum disease is associated with brain atrophy,” said Dr. Yamaguchi.
“Controlling the progression of gum disease through regular dental visits is crucial, and teeth with severe gum disease may need to be extracted and replaced with appropriate prosthetic devices,” he added.
The researchers note that further studies are needed to confirm these findings.
The study was supported the Japanese Ministry of Education, Culture, Sports, Science, and Technology; Kelo University; Japan Arteriosclerosis Prevention Fund; Japanese Ministry of Health, Labor, and Welfare; Teiko University; Pfizer Japan; Bayer Yakuhin; Chugai Pharmaceutical; Daiichi Sankyo; Astrellas Pharma; Takeda Pharmaceutical; the Health Care Science Institute; the Health Science Center; and the Takeda Science Foundation. The investigators reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Gum disease and tooth loss are linked to hippocampal atrophy and may have a more negative impact on the brain than aging, new research suggests.
Investigators found that in a late middle-aged and older cohort, among patients with mild periodontitis, having fewer teeth was linked to a faster rate of left hippocampal atrophy. For those with severe gum disease, each additional lost tooth was associated with a faster rate of brain shrinkage, equivalent to 1.3 years of brain aging.
“Tooth loss and gum disease, which is inflammation of the tissue around the teeth that can cause shrinkage of the gums and loosening of the teeth, are very common, so evaluating a potential link with dementia is incredibly important,” study investigator Satoshi Yamaguchi, PhD, DDS, of Tohoku University, in Sendai, Japan, said in a release.
“Our study found that these conditions may play a role in the health of the brain area that controls thinking and memory, giving people another reason to take better care of their teeth,” Dr. Yamaguchi noted.
The findings were published online in Neurology.
Greater effect than aging
Although previous research suggests that tooth loss and periodontitis are risk factors for Alzheimer’s disease, longitudinal research has not shown a significant correlation between these conditions and hippocampal atrophy.
To clarify this association, the investigators followed 172 men and women (average age, 67 years) who had undergone two MRI brain scans 4 years apart and had had a dental examination. None of the participants had any signs of cognitive decline at baseline.
At study outset, information on cerebrovascular and cardiovascular disease, alcohol consumption, smoking, depression history, and cognitive function was gathered. The Mini Mental State Exam and dental exams were administered at baseline and at 4-year follow-up.
For each participant, the number of teeth was counted, and all participants were assessed for gum disease via periodontal probing depth (PD).
Healthy gums typically measure between 1 and 3 mm in depth. Mild gum disease is signified by measurements of 3-4 mm in several areas. Severe gum disease involves measurements of 5-6 mm and is accompanied by greater bone loss, leading to potential tooth loss.
Multiple regression analysis was performed, with the annual symmetric percentage change (SPC) of hippocampal volume as the dependent variable. The analysis included an interaction term between the number of teeth present (NTP) and mean PD.
Over the 4-year study period, the investigators found that the qualitative interaction between NTP and mean PD was significant for the annual SPC in the left hippocampus.
Among those with mild periodontitis, having fewer teeth correlated with more rapid atrophy of the left hippocampus, such that every tooth lost was equivalent to nearly 1 year of brain aging.
In contrast, having more teeth was associated with a faster rate of left hippocampal atrophy among those with severe periodontitis and was equivalent to 1.3 years of brain aging.
For those with severe gum disease, each additional lost tooth corresponded to a faster rate of brain shrinkage, equivalent to 1.3 years of brain aging.
“This finding indicates that periodontitis may have a greater association with left hippocampal atrophy than the association exhibited by age. Furthermore, in cases of mild periodontitis, fewer teeth may be associated with a subsequent decline in cognitive function,” the investigators write.
The study’s results, they add, highlight the importance of preserving oral health, not just the retaining of teeth. “These findings suggest that retaining teeth with severe gum disease is associated with brain atrophy,” said Dr. Yamaguchi.
“Controlling the progression of gum disease through regular dental visits is crucial, and teeth with severe gum disease may need to be extracted and replaced with appropriate prosthetic devices,” he added.
The researchers note that further studies are needed to confirm these findings.
The study was supported the Japanese Ministry of Education, Culture, Sports, Science, and Technology; Kelo University; Japan Arteriosclerosis Prevention Fund; Japanese Ministry of Health, Labor, and Welfare; Teiko University; Pfizer Japan; Bayer Yakuhin; Chugai Pharmaceutical; Daiichi Sankyo; Astrellas Pharma; Takeda Pharmaceutical; the Health Care Science Institute; the Health Science Center; and the Takeda Science Foundation. The investigators reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM NEUROLOGY