Neurology Reviews

Boil ‘em, mash ‘em, include ‘em in a balanced diet

It’s kind of funny that, even though potatoes are vegetables and vegetables are generally considered to be healthy foods, not many people think of potatoes as being particularly good for you. And that’s hardly surprising since we usually either consume them in the form of French fries or potato chips, neither of which are known for their healthiness.

PxHere

In fact, some previous research shows that potatoes are a food to avoid, particularly for people with insulin resistance. However, a new study from England goes against the grain and asserts that the potato is perfectly fine for insulin-resistant individuals and filled with valuable nutrients and health benefits. Which is great news for the state of Idaho and the potato organization funding the research. Of course there’s a potato organization.

For the study, a group of obese, overweight, or insulin-resistant individuals received a diet of either beans, peas, and meat or fish or white potatoes with meat or fish for 8 weeks; both diets were heavy in fruits and vegetables and both diets replaced about 40% of typical meat consumption with either beans and peas or potatoes. By the end of the study, those on the potato diet experienced health benefits equivalent to those on the bean and pea diet, including losing roughly equivalent amounts of weight and similarly reducing the body’s insulin response.

The researchers noted that, because people tend to eat the same amount of food no matter what, replacing something like meat with dense, low-calorie potatoes meant study participants could eat normally yet consume much fewer calories. So you could make a delicious, healthy stew without the brace of conies and the nice fish, which would make Smeagol very happy.
 

You won’t have ‘monkeypox’ to kick around anymore

It’s true. No more monkeypox. It’s gone. It’s history. Adios. The World Health Organization said that the disease formerly known as monkeypox will now be called mpox. What? You didn’t think it had been cured, did you? You did? Really? Silly readers.

NIAID

“Mpox will become a preferred term, replacing monkeypox, after a transition period of 1 year. This serves to mitigate the concerns raised by experts about confusion caused by a name change in the midst of a global outbreak,” WHO said in a statement announcing the change.

The stigma attached to the name was the main problem. New York City Health Commissioner Dr. Ashwin Vasan had sent a letter to WHO earlier this year, according to CNN, saying that there was “growing concern for the potentially devastating and stigmatizing effects that the messaging around the ‘monkeypox’ virus can have on … vulnerable communities.”

We here at LOTME applaud the fight against stigmas of any sort, but we sensed there was more to this name change business, so our dedicated team of investigative journalists went into action. Sure enough, while rooting through WHO Director-General Tedros Adhanom Ghebreyesus’s garbage, we found a list of the names that had been rejected in favor of mpox:

• K-pop (already taken)
• Keeping up with the Kardashi-pox
• Trumpox
• Pox the magic dragon
• Monkey plague (didn’t really solve the problem)
• Hockey pox
• Mission mpoxible
• Jurassic Pox
• The pox that refreshes
• Debbie

Feet catch what the ears miss

The spectrum of frequencies that can be heard by human ears varies from person to person. Then there’s the matter of personal taste in music and volume level. But what really gets people moving? A new study shows that it’s more about the frequency of the sound than the volume.

PxHere

For the study, participants at a concert by electronic music duo Orphx at LIVELab – a research performance center on the McMaster University campus in Hamilton, Ont., that was specifically designed to study music and dance – filled out questionnaires before and after the show. They also wore motion-capture headbands to detect their movement throughout the concert. During the show the researchers turned very-low-frequency (VLF) sounds (8-37 Hz) on and off every 2.5 minutes. Movement speed was calculated during on and off periods.

Although the effects of subliminal messaging aren’t new, past studies have shown that participants were mostly aware of the messaging. In this study, the researchers found that the subjects’ movements increased by 11.8% when the VLF sounds were on, but without their awareness. The researchers and the participants attributed movement to the bass, as lower pitches tend to elicit stronger neural responses and thus movement, compared with higher pitches.

“Our whole sense of the beat is mediated by the vestibular system but nobody’s really, I think, effectively confirmed that,” Jonathan Cannon, an assistant professor of psychology, neuroscience, and behavior at McMaster who not involved in the study, told Live Science.

Not to say this study didn’t have its limitations, such as the effect of the surrounding crowd or vibrations of the floor influencing the need to dance. But it definitely makes you wonder about what’s actually playing in your favorite song.
 

Uncle Leonid wants you

Do you like to travel? Are you a bit of a thrill seeker? Do you have any extra socks? If you’re a physician who answered yes to those three questions, then we’ve got an opportunity for you.

Bicanski/Pixnio

Leonid Slutsky, leader of Russia’s populist Liberal Democratic Party and chairman of the foreign relations committee in the lower house of Russia’s parliament – yes, that Leonid Slutsky – recently made a bit of a recruiting pitch, although that’s not how ABC News described it.

Mr. Slutsky, a strong supporter of his country’s war against Ukraine, recently told the mothers of Russian soldiers “that the whole world is watching us. We are the largest state and when we do not have socks, shorts, doctors, intelligence, communications, or simply care for our children, questions arise that will be very difficult to answer.”

It’s probably not what he meant, but the lack of intelligence is pretty clear.

Boil ‘em, mash ‘em, include ‘em in a balanced diet

It’s kind of funny that, even though potatoes are vegetables and vegetables are generally considered to be healthy foods, not many people think of potatoes as being particularly good for you. And that’s hardly surprising since we usually either consume them in the form of French fries or potato chips, neither of which are known for their healthiness.

PxHere

In fact, some previous research shows that potatoes are a food to avoid, particularly for people with insulin resistance. However, a new study from England goes against the grain and asserts that the potato is perfectly fine for insulin-resistant individuals and filled with valuable nutrients and health benefits. Which is great news for the state of Idaho and the potato organization funding the research. Of course there’s a potato organization.

For the study, a group of obese, overweight, or insulin-resistant individuals received a diet of either beans, peas, and meat or fish or white potatoes with meat or fish for 8 weeks; both diets were heavy in fruits and vegetables and both diets replaced about 40% of typical meat consumption with either beans and peas or potatoes. By the end of the study, those on the potato diet experienced health benefits equivalent to those on the bean and pea diet, including losing roughly equivalent amounts of weight and similarly reducing the body’s insulin response.

The researchers noted that, because people tend to eat the same amount of food no matter what, replacing something like meat with dense, low-calorie potatoes meant study participants could eat normally yet consume much fewer calories. So you could make a delicious, healthy stew without the brace of conies and the nice fish, which would make Smeagol very happy.
 

You won’t have ‘monkeypox’ to kick around anymore

It’s true. No more monkeypox. It’s gone. It’s history. Adios. The World Health Organization said that the disease formerly known as monkeypox will now be called mpox. What? You didn’t think it had been cured, did you? You did? Really? Silly readers.

NIAID

“Mpox will become a preferred term, replacing monkeypox, after a transition period of 1 year. This serves to mitigate the concerns raised by experts about confusion caused by a name change in the midst of a global outbreak,” WHO said in a statement announcing the change.

The stigma attached to the name was the main problem. New York City Health Commissioner Dr. Ashwin Vasan had sent a letter to WHO earlier this year, according to CNN, saying that there was “growing concern for the potentially devastating and stigmatizing effects that the messaging around the ‘monkeypox’ virus can have on … vulnerable communities.”

We here at LOTME applaud the fight against stigmas of any sort, but we sensed there was more to this name change business, so our dedicated team of investigative journalists went into action. Sure enough, while rooting through WHO Director-General Tedros Adhanom Ghebreyesus’s garbage, we found a list of the names that had been rejected in favor of mpox:

• K-pop (already taken)
• Keeping up with the Kardashi-pox
• Trumpox
• Pox the magic dragon
• Monkey plague (didn’t really solve the problem)
• Hockey pox
• Mission mpoxible
• Jurassic Pox
• The pox that refreshes
• Debbie

Feet catch what the ears miss

The spectrum of frequencies that can be heard by human ears varies from person to person. Then there’s the matter of personal taste in music and volume level. But what really gets people moving? A new study shows that it’s more about the frequency of the sound than the volume.

PxHere

For the study, participants at a concert by electronic music duo Orphx at LIVELab – a research performance center on the McMaster University campus in Hamilton, Ont., that was specifically designed to study music and dance – filled out questionnaires before and after the show. They also wore motion-capture headbands to detect their movement throughout the concert. During the show the researchers turned very-low-frequency (VLF) sounds (8-37 Hz) on and off every 2.5 minutes. Movement speed was calculated during on and off periods.

Although the effects of subliminal messaging aren’t new, past studies have shown that participants were mostly aware of the messaging. In this study, the researchers found that the subjects’ movements increased by 11.8% when the VLF sounds were on, but without their awareness. The researchers and the participants attributed movement to the bass, as lower pitches tend to elicit stronger neural responses and thus movement, compared with higher pitches.

“Our whole sense of the beat is mediated by the vestibular system but nobody’s really, I think, effectively confirmed that,” Jonathan Cannon, an assistant professor of psychology, neuroscience, and behavior at McMaster who not involved in the study, told Live Science.

Not to say this study didn’t have its limitations, such as the effect of the surrounding crowd or vibrations of the floor influencing the need to dance. But it definitely makes you wonder about what’s actually playing in your favorite song.
 

Uncle Leonid wants you

Do you like to travel? Are you a bit of a thrill seeker? Do you have any extra socks? If you’re a physician who answered yes to those three questions, then we’ve got an opportunity for you.

Bicanski/Pixnio

Leonid Slutsky, leader of Russia’s populist Liberal Democratic Party and chairman of the foreign relations committee in the lower house of Russia’s parliament – yes, that Leonid Slutsky – recently made a bit of a recruiting pitch, although that’s not how ABC News described it.

Mr. Slutsky, a strong supporter of his country’s war against Ukraine, recently told the mothers of Russian soldiers “that the whole world is watching us. We are the largest state and when we do not have socks, shorts, doctors, intelligence, communications, or simply care for our children, questions arise that will be very difficult to answer.”

It’s probably not what he meant, but the lack of intelligence is pretty clear.

Boil ‘em, mash ‘em, include ‘em in a balanced diet

It’s kind of funny that, even though potatoes are vegetables and vegetables are generally considered to be healthy foods, not many people think of potatoes as being particularly good for you. And that’s hardly surprising since we usually either consume them in the form of French fries or potato chips, neither of which are known for their healthiness.

PxHere

In fact, some previous research shows that potatoes are a food to avoid, particularly for people with insulin resistance. However, a new study from England goes against the grain and asserts that the potato is perfectly fine for insulin-resistant individuals and filled with valuable nutrients and health benefits. Which is great news for the state of Idaho and the potato organization funding the research. Of course there’s a potato organization.

For the study, a group of obese, overweight, or insulin-resistant individuals received a diet of either beans, peas, and meat or fish or white potatoes with meat or fish for 8 weeks; both diets were heavy in fruits and vegetables and both diets replaced about 40% of typical meat consumption with either beans and peas or potatoes. By the end of the study, those on the potato diet experienced health benefits equivalent to those on the bean and pea diet, including losing roughly equivalent amounts of weight and similarly reducing the body’s insulin response.

The researchers noted that, because people tend to eat the same amount of food no matter what, replacing something like meat with dense, low-calorie potatoes meant study participants could eat normally yet consume much fewer calories. So you could make a delicious, healthy stew without the brace of conies and the nice fish, which would make Smeagol very happy.
 

You won’t have ‘monkeypox’ to kick around anymore

It’s true. No more monkeypox. It’s gone. It’s history. Adios. The World Health Organization said that the disease formerly known as monkeypox will now be called mpox. What? You didn’t think it had been cured, did you? You did? Really? Silly readers.

NIAID

“Mpox will become a preferred term, replacing monkeypox, after a transition period of 1 year. This serves to mitigate the concerns raised by experts about confusion caused by a name change in the midst of a global outbreak,” WHO said in a statement announcing the change.

The stigma attached to the name was the main problem. New York City Health Commissioner Dr. Ashwin Vasan had sent a letter to WHO earlier this year, according to CNN, saying that there was “growing concern for the potentially devastating and stigmatizing effects that the messaging around the ‘monkeypox’ virus can have on … vulnerable communities.”

We here at LOTME applaud the fight against stigmas of any sort, but we sensed there was more to this name change business, so our dedicated team of investigative journalists went into action. Sure enough, while rooting through WHO Director-General Tedros Adhanom Ghebreyesus’s garbage, we found a list of the names that had been rejected in favor of mpox:

• K-pop (already taken)
• Keeping up with the Kardashi-pox
• Trumpox
• Pox the magic dragon
• Monkey plague (didn’t really solve the problem)
• Hockey pox
• Mission mpoxible
• Jurassic Pox
• The pox that refreshes
• Debbie

Feet catch what the ears miss

The spectrum of frequencies that can be heard by human ears varies from person to person. Then there’s the matter of personal taste in music and volume level. But what really gets people moving? A new study shows that it’s more about the frequency of the sound than the volume.

PxHere

For the study, participants at a concert by electronic music duo Orphx at LIVELab – a research performance center on the McMaster University campus in Hamilton, Ont., that was specifically designed to study music and dance – filled out questionnaires before and after the show. They also wore motion-capture headbands to detect their movement throughout the concert. During the show the researchers turned very-low-frequency (VLF) sounds (8-37 Hz) on and off every 2.5 minutes. Movement speed was calculated during on and off periods.

Although the effects of subliminal messaging aren’t new, past studies have shown that participants were mostly aware of the messaging. In this study, the researchers found that the subjects’ movements increased by 11.8% when the VLF sounds were on, but without their awareness. The researchers and the participants attributed movement to the bass, as lower pitches tend to elicit stronger neural responses and thus movement, compared with higher pitches.

“Our whole sense of the beat is mediated by the vestibular system but nobody’s really, I think, effectively confirmed that,” Jonathan Cannon, an assistant professor of psychology, neuroscience, and behavior at McMaster who not involved in the study, told Live Science.

Not to say this study didn’t have its limitations, such as the effect of the surrounding crowd or vibrations of the floor influencing the need to dance. But it definitely makes you wonder about what’s actually playing in your favorite song.
 

Uncle Leonid wants you

Do you like to travel? Are you a bit of a thrill seeker? Do you have any extra socks? If you’re a physician who answered yes to those three questions, then we’ve got an opportunity for you.

Bicanski/Pixnio

Leonid Slutsky, leader of Russia’s populist Liberal Democratic Party and chairman of the foreign relations committee in the lower house of Russia’s parliament – yes, that Leonid Slutsky – recently made a bit of a recruiting pitch, although that’s not how ABC News described it.

Mr. Slutsky, a strong supporter of his country’s war against Ukraine, recently told the mothers of Russian soldiers “that the whole world is watching us. We are the largest state and when we do not have socks, shorts, doctors, intelligence, communications, or simply care for our children, questions arise that will be very difficult to answer.”

It’s probably not what he meant, but the lack of intelligence is pretty clear.

By the time Mira Halker started high school, hardly a day passed that she wasn’t either getting a migraine attack or recovering from one. She missed volleyball team practice. She missed classes. She missed social events. And few people understood. After all, she looked healthy.

“A lot of times, people think I’m faking it,” said Mira, now 16, who lives in Phoenix. Friends called her flaky; her volleyball coaches questioned her dedication to the team. “I’m like, ‘I’m not trying to get out of this. This is not what this is about,’ ” she said.

Her mother, Rashmi B. Halker Singh, MD, is a neurologist at Mayo Clinic who happens to specialize in migraine. Even so, finding a solution was not easy. Neither ibuprofen nor triptans, nor various preventive measures such as a daily prescription for topiramate controlled the pain and associated symptoms. Mira was barely making it through her school day and had to quit volleyball. Then, in the spring of 10th grade, Mira told her mother that she couldn’t go to prom because the loud noises and lights could give her a migraine attack.

Mother and daughter decided it was time to get even more aggressive. “There are these key moments in life that you can’t get back,” Dr. Singh said. “Migraine steals so much from you.”
 

Diagnosis

One of the challenges Mira’s physicians faced was deciding which medications and other therapies to prescribe to a teenager. Drug companies have been releasing a steady stream of new treatments for migraine headaches, and researchers promise more are on the way soon. Here’s what works for children, what hasn’t yet been approved for use with minors, and how to diagnose migraines in the first place, from experts at some of the nation’s leading pediatric headache centers.

Migraine affects about 10% of children, according to the American Migraine Foundation. The headaches can strike children as early as age 3 or 4 years, said Robert Little, MD, a pediatric neurologist at Phoenix Children’s Hospital.

Before puberty, boys report more migraine attacks than girls, according to the American Academy of Pediatrics. But that reverses in adolescence: By age 17, as many as 8% of boys and 23% of girls have had migraine. To diagnose migraine, Juliana H. VanderPluym, MD, associate professor of neurology at Mayo Clinic in Phoenix, said she uses the criteria published in the latest edition of the International Classification of Headache Disorders (ICHD): A patient must have had at least five attacks in their life; and in children and adolescents, the attacks must last no less than 2 hours.

In addition, the headaches should exhibit at least two out of four features:

1. Occur more on one side of the head than the other (although Dr. VanderPluym said in children and adolescents headaches often are bilateral).

2. Be of moderate to severe intensity.

3. Have a pounding or throbbing quality.

4. Grow worse with activity or cause an avoidance of activity.

If the attacks meet those criteria, clinicians should check to see if they meet at least one out of the two following:

1. Are sensitive to light and sounds.

2. Are associated with nausea and/or vomiting.

A clinician should consider whether the headaches are not better accounted for by another diagnosis, according to the ICHD criteria. But, Dr. VanderPluym warned that does not necessarily mean running a slew of tests.

“In the absence of red flag features, it is more than likely going to be migraine headache,” she said. That’s especially true if a child has a family history of migraine, as the condition is often passed down from parent to child.

Ultimately, the diagnosis is fairly simple and can be made in a minute or less, said Jack Gladstein, MD, a pediatrician at the University of Maryland whose research focuses on the clinical care of children and adolescents with headache.

“Migraine is acute,” Dr. Gladstein said. “It’s really bad. And it’s recurrent.”
 

First line of treatment

Whatever a patient takes to treat a migraine, they should hit it early and hard, Dr. Gladstein said.

“The first thing you say, as a primary care physician, is treat your migraine at first twinge, whatever you use. Don’t wait, don’t wish it away,” he said. “The longer you wait, the less chance anything will work.”

The second piece of advice, Dr. Gladstein said, is that whatever drug a patient is taking, they should be on the highest feasible dose. “Work as fast as you can to treat them. You want the brain to reset as quickly as you can,” he said.

Patients should begin with over-the-counter pain relievers, Dr. Little said. If those prove insufficient, they can try a triptan. Rizatriptan is the only such agent that the Food and Drug Administration has approved for children aged 6-17 years. Other drugs in the class – sumatriptan/naproxen, almotriptan, and zolmitriptan – are approved for children 12 and older.

Another migraine therapy recently approved for children aged 12 and older is the use of neurostimulators. “It’s helpful to be aware of them,” Dr. VanderPluym said.

However, if neurostimulators and acute medications prove insufficient, clinicians should warn patients not to up their doses of triptans. Rebound headaches can occur if patients take triptans more than twice a week, or a maximum 10 days per month.

Another possibility is to add a preventive therapy. One mild, first option is nutraceuticals, like riboflavin (vitamin B₂) or magnesium, said Anisa F. Kelley, MD, a neurologist and associate director of the headache program at the Ann and Robert H. Lurie Children’s Hospital of Chicago.

“We don’t have definitive evidence, but they’re probably doing more benefit than they are harm,” Dr. Kelley said of these therapies. “In patients who have anywhere from 4 to 8 migraine days a month, where you’re in that in-between period where you don’t necessarily need a [prescription] prophylactic, I will often start with a nutraceutical,” Dr. Kelley said.

For those patients who don’t respond to nutraceuticals, or who need more support, clinicians can prescribe amitriptyline or topiramate. Dr. VanderPluym said.

A 2017 study found such prophylactics to be no more effective than placebo in pediatric migraine patients, but experts caution the results should not be considered definitive.

For one thing, the study enrolled a highly selective group of participants, with milder forms of migraine who may have improved anyway, Dr. VanderPluym said. All participants also received lifestyle counseling.

Every time participants came in for a follow-up, they were asked questions such as how much water were they drinking and how much sleep were they getting, Dr. Kelley noted. The takeaway, she said: “Pediatric and adolescent migraine [management] is very, very much reliant on lifestyle factors.”
 

Lifestyle triggers

Clinicians should counsel their migraine patients about lifestyle changes, experts said. Getting adequate sleep, staying hydrated, and managing stress can help reduce the intensity and frequency of attacks.

Migraine patients should also be mindful of their screen time, Dr. Kelley added.

“I’ve had lots and lots of patients who find excessive screen time will trigger or worsen migraine,” she said.

As for other potential triggers of attacks, the evidence is mixed.

“There’s clearly an association with disrupted sleep and migraine, and that has been very well established,” Dr. Little said. “And there is some modest amount of evidence that regular exercise can be helpful.” But for reported food triggers, he said, there have been very inconclusive results.

Commonly reported triggers include MSG, red wine, chocolate, and aged cheese. When Dr. Little’s patients keep headache diaries, tracking their meals alongside when they got migraine attacks, they often discover individualized triggers – strawberries, for instance, in one case, he said.

Scientists believe migraines result from the inappropriate activation of the trigeminal ganglion. “The question is, what causes it to get triggered? And how does it get triggered?” Dr. Gladstein said. “And that’s where there’s a lot of difference of opinion and no conclusive evidence.” Clinicians also should make sure that something else – usually depression, anxiety, insomnia, and dizziness – is not hindering effective migraine management. “If someone has terrible insomnia, until you treat the insomnia, the headaches aren’t going to get better,” he said.

As for Mira, her migraine attacks did not significantly improve, despite trying triptans, prophylactics, lifestyle changes, and shots to block nerve pain. When the headaches threatened Mira’s chance to go to her prom, her neurologist suggested trying something different. The physician persuaded the family’s insurance to cover a calcitonin gene-related peptide antagonist, an injectable monoclonal antibody treatment for migraine that the FDA has currently approved only for use in adults.

The difference for Mira has been extraordinary.

“I can do so much more than I was able to do,” said Mira, who attended the dance migraine free. “I feel liberated.”

It’s only migraine

One of the greatest challenges in diagnosing migraine can be reassuring the patient, the parents, even clinicians themselves that migraine really is the cause of all this pain and discomfort, experts said.

“A lot of migraine treatment actually comes down to migraine education,” Dr. VanderPluym said.

Patients and their parents often wonder how they can be sure that this pain is not resulting from something more dangerous than migraine, Dr. Little said. In these cases, he cites practice guidelines published by the American Academy of Neurology.

“The gist of those guidelines is that most pediatric patients do not need further workup,” he said. “But I think that there’s always a fear that you’re missing something because we don’t have a test that we can do” for migraine.

Some warning signs that further tests might be warranted, Dr. Kelley said, include:

• Headaches that wake a patient up in the middle of the night.
• Headaches that start first thing in the morning, especially those that include vomiting.
• A headache pattern that suddenly gets much worse.
• Certain symptoms that accompany the headache, such as tingling, numbness or double vision.

Although all of these signs can still stem from migraines – tingling or numbness, for instance, can be signs of migraine aura – running additional tests can rule out more serious concerns, she said.

By the time Mira Halker started high school, hardly a day passed that she wasn’t either getting a migraine attack or recovering from one. She missed volleyball team practice. She missed classes. She missed social events. And few people understood. After all, she looked healthy.

“A lot of times, people think I’m faking it,” said Mira, now 16, who lives in Phoenix. Friends called her flaky; her volleyball coaches questioned her dedication to the team. “I’m like, ‘I’m not trying to get out of this. This is not what this is about,’ ” she said.

Her mother, Rashmi B. Halker Singh, MD, is a neurologist at Mayo Clinic who happens to specialize in migraine. Even so, finding a solution was not easy. Neither ibuprofen nor triptans, nor various preventive measures such as a daily prescription for topiramate controlled the pain and associated symptoms. Mira was barely making it through her school day and had to quit volleyball. Then, in the spring of 10th grade, Mira told her mother that she couldn’t go to prom because the loud noises and lights could give her a migraine attack.

Mother and daughter decided it was time to get even more aggressive. “There are these key moments in life that you can’t get back,” Dr. Singh said. “Migraine steals so much from you.”
 

Diagnosis

One of the challenges Mira’s physicians faced was deciding which medications and other therapies to prescribe to a teenager. Drug companies have been releasing a steady stream of new treatments for migraine headaches, and researchers promise more are on the way soon. Here’s what works for children, what hasn’t yet been approved for use with minors, and how to diagnose migraines in the first place, from experts at some of the nation’s leading pediatric headache centers.

Migraine affects about 10% of children, according to the American Migraine Foundation. The headaches can strike children as early as age 3 or 4 years, said Robert Little, MD, a pediatric neurologist at Phoenix Children’s Hospital.

Before puberty, boys report more migraine attacks than girls, according to the American Academy of Pediatrics. But that reverses in adolescence: By age 17, as many as 8% of boys and 23% of girls have had migraine. To diagnose migraine, Juliana H. VanderPluym, MD, associate professor of neurology at Mayo Clinic in Phoenix, said she uses the criteria published in the latest edition of the International Classification of Headache Disorders (ICHD): A patient must have had at least five attacks in their life; and in children and adolescents, the attacks must last no less than 2 hours.

In addition, the headaches should exhibit at least two out of four features:

1. Occur more on one side of the head than the other (although Dr. VanderPluym said in children and adolescents headaches often are bilateral).

2. Be of moderate to severe intensity.

3. Have a pounding or throbbing quality.

4. Grow worse with activity or cause an avoidance of activity.

If the attacks meet those criteria, clinicians should check to see if they meet at least one out of the two following:

1. Are sensitive to light and sounds.

2. Are associated with nausea and/or vomiting.

A clinician should consider whether the headaches are not better accounted for by another diagnosis, according to the ICHD criteria. But, Dr. VanderPluym warned that does not necessarily mean running a slew of tests.

“In the absence of red flag features, it is more than likely going to be migraine headache,” she said. That’s especially true if a child has a family history of migraine, as the condition is often passed down from parent to child.

Ultimately, the diagnosis is fairly simple and can be made in a minute or less, said Jack Gladstein, MD, a pediatrician at the University of Maryland whose research focuses on the clinical care of children and adolescents with headache.

“Migraine is acute,” Dr. Gladstein said. “It’s really bad. And it’s recurrent.”
 

First line of treatment

Whatever a patient takes to treat a migraine, they should hit it early and hard, Dr. Gladstein said.

“The first thing you say, as a primary care physician, is treat your migraine at first twinge, whatever you use. Don’t wait, don’t wish it away,” he said. “The longer you wait, the less chance anything will work.”

The second piece of advice, Dr. Gladstein said, is that whatever drug a patient is taking, they should be on the highest feasible dose. “Work as fast as you can to treat them. You want the brain to reset as quickly as you can,” he said.

Patients should begin with over-the-counter pain relievers, Dr. Little said. If those prove insufficient, they can try a triptan. Rizatriptan is the only such agent that the Food and Drug Administration has approved for children aged 6-17 years. Other drugs in the class – sumatriptan/naproxen, almotriptan, and zolmitriptan – are approved for children 12 and older.

Another migraine therapy recently approved for children aged 12 and older is the use of neurostimulators. “It’s helpful to be aware of them,” Dr. VanderPluym said.

However, if neurostimulators and acute medications prove insufficient, clinicians should warn patients not to up their doses of triptans. Rebound headaches can occur if patients take triptans more than twice a week, or a maximum 10 days per month.

Another possibility is to add a preventive therapy. One mild, first option is nutraceuticals, like riboflavin (vitamin B₂) or magnesium, said Anisa F. Kelley, MD, a neurologist and associate director of the headache program at the Ann and Robert H. Lurie Children’s Hospital of Chicago.

“We don’t have definitive evidence, but they’re probably doing more benefit than they are harm,” Dr. Kelley said of these therapies. “In patients who have anywhere from 4 to 8 migraine days a month, where you’re in that in-between period where you don’t necessarily need a [prescription] prophylactic, I will often start with a nutraceutical,” Dr. Kelley said.

For those patients who don’t respond to nutraceuticals, or who need more support, clinicians can prescribe amitriptyline or topiramate. Dr. VanderPluym said.

A 2017 study found such prophylactics to be no more effective than placebo in pediatric migraine patients, but experts caution the results should not be considered definitive.

For one thing, the study enrolled a highly selective group of participants, with milder forms of migraine who may have improved anyway, Dr. VanderPluym said. All participants also received lifestyle counseling.

Every time participants came in for a follow-up, they were asked questions such as how much water were they drinking and how much sleep were they getting, Dr. Kelley noted. The takeaway, she said: “Pediatric and adolescent migraine [management] is very, very much reliant on lifestyle factors.”
 

Lifestyle triggers

Clinicians should counsel their migraine patients about lifestyle changes, experts said. Getting adequate sleep, staying hydrated, and managing stress can help reduce the intensity and frequency of attacks.

Migraine patients should also be mindful of their screen time, Dr. Kelley added.

“I’ve had lots and lots of patients who find excessive screen time will trigger or worsen migraine,” she said.

As for other potential triggers of attacks, the evidence is mixed.

“There’s clearly an association with disrupted sleep and migraine, and that has been very well established,” Dr. Little said. “And there is some modest amount of evidence that regular exercise can be helpful.” But for reported food triggers, he said, there have been very inconclusive results.

Commonly reported triggers include MSG, red wine, chocolate, and aged cheese. When Dr. Little’s patients keep headache diaries, tracking their meals alongside when they got migraine attacks, they often discover individualized triggers – strawberries, for instance, in one case, he said.

Scientists believe migraines result from the inappropriate activation of the trigeminal ganglion. “The question is, what causes it to get triggered? And how does it get triggered?” Dr. Gladstein said. “And that’s where there’s a lot of difference of opinion and no conclusive evidence.” Clinicians also should make sure that something else – usually depression, anxiety, insomnia, and dizziness – is not hindering effective migraine management. “If someone has terrible insomnia, until you treat the insomnia, the headaches aren’t going to get better,” he said.

As for Mira, her migraine attacks did not significantly improve, despite trying triptans, prophylactics, lifestyle changes, and shots to block nerve pain. When the headaches threatened Mira’s chance to go to her prom, her neurologist suggested trying something different. The physician persuaded the family’s insurance to cover a calcitonin gene-related peptide antagonist, an injectable monoclonal antibody treatment for migraine that the FDA has currently approved only for use in adults.

The difference for Mira has been extraordinary.

“I can do so much more than I was able to do,” said Mira, who attended the dance migraine free. “I feel liberated.”

It’s only migraine

One of the greatest challenges in diagnosing migraine can be reassuring the patient, the parents, even clinicians themselves that migraine really is the cause of all this pain and discomfort, experts said.

“A lot of migraine treatment actually comes down to migraine education,” Dr. VanderPluym said.

Patients and their parents often wonder how they can be sure that this pain is not resulting from something more dangerous than migraine, Dr. Little said. In these cases, he cites practice guidelines published by the American Academy of Neurology.

“The gist of those guidelines is that most pediatric patients do not need further workup,” he said. “But I think that there’s always a fear that you’re missing something because we don’t have a test that we can do” for migraine.

Some warning signs that further tests might be warranted, Dr. Kelley said, include:

• Headaches that wake a patient up in the middle of the night.
• Headaches that start first thing in the morning, especially those that include vomiting.
• A headache pattern that suddenly gets much worse.
• Certain symptoms that accompany the headache, such as tingling, numbness or double vision.

Although all of these signs can still stem from migraines – tingling or numbness, for instance, can be signs of migraine aura – running additional tests can rule out more serious concerns, she said.

By the time Mira Halker started high school, hardly a day passed that she wasn’t either getting a migraine attack or recovering from one. She missed volleyball team practice. She missed classes. She missed social events. And few people understood. After all, she looked healthy.

“A lot of times, people think I’m faking it,” said Mira, now 16, who lives in Phoenix. Friends called her flaky; her volleyball coaches questioned her dedication to the team. “I’m like, ‘I’m not trying to get out of this. This is not what this is about,’ ” she said.

Her mother, Rashmi B. Halker Singh, MD, is a neurologist at Mayo Clinic who happens to specialize in migraine. Even so, finding a solution was not easy. Neither ibuprofen nor triptans, nor various preventive measures such as a daily prescription for topiramate controlled the pain and associated symptoms. Mira was barely making it through her school day and had to quit volleyball. Then, in the spring of 10th grade, Mira told her mother that she couldn’t go to prom because the loud noises and lights could give her a migraine attack.

Mother and daughter decided it was time to get even more aggressive. “There are these key moments in life that you can’t get back,” Dr. Singh said. “Migraine steals so much from you.”
 

Diagnosis

One of the challenges Mira’s physicians faced was deciding which medications and other therapies to prescribe to a teenager. Drug companies have been releasing a steady stream of new treatments for migraine headaches, and researchers promise more are on the way soon. Here’s what works for children, what hasn’t yet been approved for use with minors, and how to diagnose migraines in the first place, from experts at some of the nation’s leading pediatric headache centers.

Migraine affects about 10% of children, according to the American Migraine Foundation. The headaches can strike children as early as age 3 or 4 years, said Robert Little, MD, a pediatric neurologist at Phoenix Children’s Hospital.

Before puberty, boys report more migraine attacks than girls, according to the American Academy of Pediatrics. But that reverses in adolescence: By age 17, as many as 8% of boys and 23% of girls have had migraine. To diagnose migraine, Juliana H. VanderPluym, MD, associate professor of neurology at Mayo Clinic in Phoenix, said she uses the criteria published in the latest edition of the International Classification of Headache Disorders (ICHD): A patient must have had at least five attacks in their life; and in children and adolescents, the attacks must last no less than 2 hours.

In addition, the headaches should exhibit at least two out of four features:

1. Occur more on one side of the head than the other (although Dr. VanderPluym said in children and adolescents headaches often are bilateral).

2. Be of moderate to severe intensity.

3. Have a pounding or throbbing quality.

4. Grow worse with activity or cause an avoidance of activity.

If the attacks meet those criteria, clinicians should check to see if they meet at least one out of the two following:

1. Are sensitive to light and sounds.

2. Are associated with nausea and/or vomiting.

A clinician should consider whether the headaches are not better accounted for by another diagnosis, according to the ICHD criteria. But, Dr. VanderPluym warned that does not necessarily mean running a slew of tests.

“In the absence of red flag features, it is more than likely going to be migraine headache,” she said. That’s especially true if a child has a family history of migraine, as the condition is often passed down from parent to child.

Ultimately, the diagnosis is fairly simple and can be made in a minute or less, said Jack Gladstein, MD, a pediatrician at the University of Maryland whose research focuses on the clinical care of children and adolescents with headache.

“Migraine is acute,” Dr. Gladstein said. “It’s really bad. And it’s recurrent.”
 

First line of treatment

Whatever a patient takes to treat a migraine, they should hit it early and hard, Dr. Gladstein said.

“The first thing you say, as a primary care physician, is treat your migraine at first twinge, whatever you use. Don’t wait, don’t wish it away,” he said. “The longer you wait, the less chance anything will work.”

The second piece of advice, Dr. Gladstein said, is that whatever drug a patient is taking, they should be on the highest feasible dose. “Work as fast as you can to treat them. You want the brain to reset as quickly as you can,” he said.

Patients should begin with over-the-counter pain relievers, Dr. Little said. If those prove insufficient, they can try a triptan. Rizatriptan is the only such agent that the Food and Drug Administration has approved for children aged 6-17 years. Other drugs in the class – sumatriptan/naproxen, almotriptan, and zolmitriptan – are approved for children 12 and older.

Another migraine therapy recently approved for children aged 12 and older is the use of neurostimulators. “It’s helpful to be aware of them,” Dr. VanderPluym said.

However, if neurostimulators and acute medications prove insufficient, clinicians should warn patients not to up their doses of triptans. Rebound headaches can occur if patients take triptans more than twice a week, or a maximum 10 days per month.

Another possibility is to add a preventive therapy. One mild, first option is nutraceuticals, like riboflavin (vitamin B₂) or magnesium, said Anisa F. Kelley, MD, a neurologist and associate director of the headache program at the Ann and Robert H. Lurie Children’s Hospital of Chicago.

“We don’t have definitive evidence, but they’re probably doing more benefit than they are harm,” Dr. Kelley said of these therapies. “In patients who have anywhere from 4 to 8 migraine days a month, where you’re in that in-between period where you don’t necessarily need a [prescription] prophylactic, I will often start with a nutraceutical,” Dr. Kelley said.

For those patients who don’t respond to nutraceuticals, or who need more support, clinicians can prescribe amitriptyline or topiramate. Dr. VanderPluym said.

A 2017 study found such prophylactics to be no more effective than placebo in pediatric migraine patients, but experts caution the results should not be considered definitive.

For one thing, the study enrolled a highly selective group of participants, with milder forms of migraine who may have improved anyway, Dr. VanderPluym said. All participants also received lifestyle counseling.

Every time participants came in for a follow-up, they were asked questions such as how much water were they drinking and how much sleep were they getting, Dr. Kelley noted. The takeaway, she said: “Pediatric and adolescent migraine [management] is very, very much reliant on lifestyle factors.”
 

Lifestyle triggers

Clinicians should counsel their migraine patients about lifestyle changes, experts said. Getting adequate sleep, staying hydrated, and managing stress can help reduce the intensity and frequency of attacks.

Migraine patients should also be mindful of their screen time, Dr. Kelley added.

“I’ve had lots and lots of patients who find excessive screen time will trigger or worsen migraine,” she said.

As for other potential triggers of attacks, the evidence is mixed.

“There’s clearly an association with disrupted sleep and migraine, and that has been very well established,” Dr. Little said. “And there is some modest amount of evidence that regular exercise can be helpful.” But for reported food triggers, he said, there have been very inconclusive results.

Commonly reported triggers include MSG, red wine, chocolate, and aged cheese. When Dr. Little’s patients keep headache diaries, tracking their meals alongside when they got migraine attacks, they often discover individualized triggers – strawberries, for instance, in one case, he said.

Scientists believe migraines result from the inappropriate activation of the trigeminal ganglion. “The question is, what causes it to get triggered? And how does it get triggered?” Dr. Gladstein said. “And that’s where there’s a lot of difference of opinion and no conclusive evidence.” Clinicians also should make sure that something else – usually depression, anxiety, insomnia, and dizziness – is not hindering effective migraine management. “If someone has terrible insomnia, until you treat the insomnia, the headaches aren’t going to get better,” he said.

As for Mira, her migraine attacks did not significantly improve, despite trying triptans, prophylactics, lifestyle changes, and shots to block nerve pain. When the headaches threatened Mira’s chance to go to her prom, her neurologist suggested trying something different. The physician persuaded the family’s insurance to cover a calcitonin gene-related peptide antagonist, an injectable monoclonal antibody treatment for migraine that the FDA has currently approved only for use in adults.

The difference for Mira has been extraordinary.

“I can do so much more than I was able to do,” said Mira, who attended the dance migraine free. “I feel liberated.”

It’s only migraine

One of the greatest challenges in diagnosing migraine can be reassuring the patient, the parents, even clinicians themselves that migraine really is the cause of all this pain and discomfort, experts said.

“A lot of migraine treatment actually comes down to migraine education,” Dr. VanderPluym said.

Patients and their parents often wonder how they can be sure that this pain is not resulting from something more dangerous than migraine, Dr. Little said. In these cases, he cites practice guidelines published by the American Academy of Neurology.

“The gist of those guidelines is that most pediatric patients do not need further workup,” he said. “But I think that there’s always a fear that you’re missing something because we don’t have a test that we can do” for migraine.

Some warning signs that further tests might be warranted, Dr. Kelley said, include:

• Headaches that wake a patient up in the middle of the night.
• Headaches that start first thing in the morning, especially those that include vomiting.
• A headache pattern that suddenly gets much worse.
• Certain symptoms that accompany the headache, such as tingling, numbness or double vision.

Although all of these signs can still stem from migraines – tingling or numbness, for instance, can be signs of migraine aura – running additional tests can rule out more serious concerns, she said.

CHICAGO – Higher weight and body mass index (BMI) in preadolescents are linked with poor brain health, new research suggests.

Poor brain health has been linked with obesity in adults, but little has been known about the link in children.

Lead author Simone Kaltenhauser, a postgraduate research fellow in radiology and biomedical imaging at the Yale School of Medicine, New Haven, Conn., presented her findings at the annual meeting of the Radiological Society of North America.

To represent the national sociodemographic makeup, the researchers used baseline information from the Adolescent Brain Cognitive Development (ABCD) study, which included 11,878 children aged 9 and 10 years from 21 centers across the United States.

This study included 5,169 children (51.9% girls). Children who had had traumatic brain injury, eating disorders, neurodevelopmental problems, and psychiatric diseases were excluded from the final analysis.

The researchers analyzed information from structural MRI and resting-state functional MRI, which allowed them to measure brain activity by detecting changes in blood flow.

“We analyzed the average fractional anisotropy (FA), mean (MD), axial (AD) and radial diffusivity (RD), and neurite density (ND) of 35 white matter (WM) tracts; cortical thickness and surface of 68 regions; and functional connectivity of 91 predefined network correlations,” the authors explained.

They adjusted for age, sex, race/ethnicity, handedness, and socioeconomic status. They used linear models to determine associations between weight and BMI z-scores and the imaging metrics.
 

Loss of white matter integrity

Among children with obesity, there was pervasive loss of white matter integrity and neurite density, cortical gray matter thinning, and decreased connectivity within and between networks that have been associated with impulse control and reward-based decision-making.

“These changes persisted in a similar pattern also 2 years later,” she said.

A member of the audience asked whether a reverse relationship might be at work – that poor brain health might drive obesity rather than the other way around.

Ms. Kaltenhauser agreed that other factors could be driving the link and acknowledged as a limitation that they did not have access to genetic information on the children.

Information on the effects of overweight and obesity is critical, especially in the United States, where an estimated 1 in 5 children are obese.

Ms. Kaltenhauser said she hopes her study raises awareness of potential brain health consequences as well as the physical consequences of childhood obesity.

Senior author Sam Payabvash, MD, a neuroradiologist and assistant professor of radiology and biomedical imaging at the Yale School of Medicine, said in a press release that the study may help explain the findings from previous studies that show an association between higher BMI in children and poor cognitive functioning and academic performance.

“The longitudinal ABCD study gives us the opportunity to observe any changes that occur in children with higher weight and BMI z-scores,” Dr. Payabvash said. “We’ll need to watch over the next 6-10 years.”
 

Avenues for future research

Amit B. Desai, MD, a neuroradiologist with Mayo Clinic in Jacksonville, Fla., who was not part of the study, said that while the research demonstrates an association between brain structure and BMI and obesity, “there may be other lurking variables.”

“What’s happening at an earlier stage in life could be causing both,” he said.

He noted that he would like to see future studies involving children at even earlier ages, along with investigations of the role of genetics or socioeconomic factors.

Including older children would be interesting as well, he said.

“Myelination doesn’t complete until you’re in your late teens or early 20s, so there are structural changes happening in the brain much later on into adolescence and early adulthood,” Dr. Desai said.

It would be premature, he said, to conclude from these findings that if children have obesity, there must be something wrong with their brain.

He would like to see whether there are changes in this link if a child is obese early on and later has normal weight or if a child has normal weight early and then becomes obese.

“It’s definitely an eye-opening study, but [it] needs additional work to expand upon it,” he said.

Ms. Kaltenhauser and Dr. Desai report no relevant financial relationships.

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

CHICAGO – Higher weight and body mass index (BMI) in preadolescents are linked with poor brain health, new research suggests.

Poor brain health has been linked with obesity in adults, but little has been known about the link in children.

Lead author Simone Kaltenhauser, a postgraduate research fellow in radiology and biomedical imaging at the Yale School of Medicine, New Haven, Conn., presented her findings at the annual meeting of the Radiological Society of North America.

To represent the national sociodemographic makeup, the researchers used baseline information from the Adolescent Brain Cognitive Development (ABCD) study, which included 11,878 children aged 9 and 10 years from 21 centers across the United States.

This study included 5,169 children (51.9% girls). Children who had had traumatic brain injury, eating disorders, neurodevelopmental problems, and psychiatric diseases were excluded from the final analysis.

The researchers analyzed information from structural MRI and resting-state functional MRI, which allowed them to measure brain activity by detecting changes in blood flow.

“We analyzed the average fractional anisotropy (FA), mean (MD), axial (AD) and radial diffusivity (RD), and neurite density (ND) of 35 white matter (WM) tracts; cortical thickness and surface of 68 regions; and functional connectivity of 91 predefined network correlations,” the authors explained.

They adjusted for age, sex, race/ethnicity, handedness, and socioeconomic status. They used linear models to determine associations between weight and BMI z-scores and the imaging metrics.
 

Loss of white matter integrity

Among children with obesity, there was pervasive loss of white matter integrity and neurite density, cortical gray matter thinning, and decreased connectivity within and between networks that have been associated with impulse control and reward-based decision-making.

“These changes persisted in a similar pattern also 2 years later,” she said.

A member of the audience asked whether a reverse relationship might be at work – that poor brain health might drive obesity rather than the other way around.

Ms. Kaltenhauser agreed that other factors could be driving the link and acknowledged as a limitation that they did not have access to genetic information on the children.

Information on the effects of overweight and obesity is critical, especially in the United States, where an estimated 1 in 5 children are obese.

Ms. Kaltenhauser said she hopes her study raises awareness of potential brain health consequences as well as the physical consequences of childhood obesity.

Senior author Sam Payabvash, MD, a neuroradiologist and assistant professor of radiology and biomedical imaging at the Yale School of Medicine, said in a press release that the study may help explain the findings from previous studies that show an association between higher BMI in children and poor cognitive functioning and academic performance.

“The longitudinal ABCD study gives us the opportunity to observe any changes that occur in children with higher weight and BMI z-scores,” Dr. Payabvash said. “We’ll need to watch over the next 6-10 years.”
 

Avenues for future research

Amit B. Desai, MD, a neuroradiologist with Mayo Clinic in Jacksonville, Fla., who was not part of the study, said that while the research demonstrates an association between brain structure and BMI and obesity, “there may be other lurking variables.”

“What’s happening at an earlier stage in life could be causing both,” he said.

He noted that he would like to see future studies involving children at even earlier ages, along with investigations of the role of genetics or socioeconomic factors.

Including older children would be interesting as well, he said.

“Myelination doesn’t complete until you’re in your late teens or early 20s, so there are structural changes happening in the brain much later on into adolescence and early adulthood,” Dr. Desai said.

It would be premature, he said, to conclude from these findings that if children have obesity, there must be something wrong with their brain.

He would like to see whether there are changes in this link if a child is obese early on and later has normal weight or if a child has normal weight early and then becomes obese.

“It’s definitely an eye-opening study, but [it] needs additional work to expand upon it,” he said.

Ms. Kaltenhauser and Dr. Desai report no relevant financial relationships.

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

CHICAGO – Higher weight and body mass index (BMI) in preadolescents are linked with poor brain health, new research suggests.

Poor brain health has been linked with obesity in adults, but little has been known about the link in children.

Lead author Simone Kaltenhauser, a postgraduate research fellow in radiology and biomedical imaging at the Yale School of Medicine, New Haven, Conn., presented her findings at the annual meeting of the Radiological Society of North America.

To represent the national sociodemographic makeup, the researchers used baseline information from the Adolescent Brain Cognitive Development (ABCD) study, which included 11,878 children aged 9 and 10 years from 21 centers across the United States.

This study included 5,169 children (51.9% girls). Children who had had traumatic brain injury, eating disorders, neurodevelopmental problems, and psychiatric diseases were excluded from the final analysis.

The researchers analyzed information from structural MRI and resting-state functional MRI, which allowed them to measure brain activity by detecting changes in blood flow.

“We analyzed the average fractional anisotropy (FA), mean (MD), axial (AD) and radial diffusivity (RD), and neurite density (ND) of 35 white matter (WM) tracts; cortical thickness and surface of 68 regions; and functional connectivity of 91 predefined network correlations,” the authors explained.

They adjusted for age, sex, race/ethnicity, handedness, and socioeconomic status. They used linear models to determine associations between weight and BMI z-scores and the imaging metrics.
 

Loss of white matter integrity

Among children with obesity, there was pervasive loss of white matter integrity and neurite density, cortical gray matter thinning, and decreased connectivity within and between networks that have been associated with impulse control and reward-based decision-making.

“These changes persisted in a similar pattern also 2 years later,” she said.

A member of the audience asked whether a reverse relationship might be at work – that poor brain health might drive obesity rather than the other way around.

Ms. Kaltenhauser agreed that other factors could be driving the link and acknowledged as a limitation that they did not have access to genetic information on the children.

Information on the effects of overweight and obesity is critical, especially in the United States, where an estimated 1 in 5 children are obese.

Ms. Kaltenhauser said she hopes her study raises awareness of potential brain health consequences as well as the physical consequences of childhood obesity.

Senior author Sam Payabvash, MD, a neuroradiologist and assistant professor of radiology and biomedical imaging at the Yale School of Medicine, said in a press release that the study may help explain the findings from previous studies that show an association between higher BMI in children and poor cognitive functioning and academic performance.

“The longitudinal ABCD study gives us the opportunity to observe any changes that occur in children with higher weight and BMI z-scores,” Dr. Payabvash said. “We’ll need to watch over the next 6-10 years.”
 

Avenues for future research

Amit B. Desai, MD, a neuroradiologist with Mayo Clinic in Jacksonville, Fla., who was not part of the study, said that while the research demonstrates an association between brain structure and BMI and obesity, “there may be other lurking variables.”

“What’s happening at an earlier stage in life could be causing both,” he said.

He noted that he would like to see future studies involving children at even earlier ages, along with investigations of the role of genetics or socioeconomic factors.

Including older children would be interesting as well, he said.

“Myelination doesn’t complete until you’re in your late teens or early 20s, so there are structural changes happening in the brain much later on into adolescence and early adulthood,” Dr. Desai said.

It would be premature, he said, to conclude from these findings that if children have obesity, there must be something wrong with their brain.

He would like to see whether there are changes in this link if a child is obese early on and later has normal weight or if a child has normal weight early and then becomes obese.

“It’s definitely an eye-opening study, but [it] needs additional work to expand upon it,” he said.

Ms. Kaltenhauser and Dr. Desai report no relevant financial relationships.

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

SAN FRANCISCO – Widely anticipated data from a phase 3 trial of the monoclonal antibody lecanemab suggest the drug “modestly” relieved cognitive impairment in patients with early Alzheimer’s disease (AD) – but at a cost.

In the CLARITY AD trial, adverse events (AEs) were common compared with placebo, including amyloid-related edema and effusions; and a recent news report linked a second death to the drug.

Moving forward, “longer trials are warranted to determine the efficacy and safety of lecanemab in early Alzheimer’s disease,” wrote Christopher H. van Dyck, MD, Yale University, New Haven, Conn., and colleagues.

The full trial findings were presented at the Clinical Trials on Alzheimer’s Disease (CTAD) conference, with simultaneous publication on Nov. 29 in the New England Journal of Medicine.
 

Complications in the field

The phase 3 trial of lecanemab has been closely watched in AD circles, especially considering positive early data released in September and reported by this news organization at that time.

The Food and Drug Administration is expected to make a decision about possible approval of the drug in January 2023. Only one other antiamyloid treatment, the highly controversial and expensive aducanumab (Aduhelm), is currently approved by the FDA.

For the new 18-month, randomized, double-blind CLARITY AD trial, researchers enrolled 1,795 patients aged 50-90 years (average age, 71 years) with early AD. All were randomly assigned to receive either a placebo (n = 898) or intravenous lecanemab, a humanized immunoglobulin G1 (IgG1) monoclonal antibody that selectively targets amyloid beta (A-beta) protofibrils, at 10 mg/kg of body weight every 2 weeks (n = 897).

The study ran from 2019 to 2021. The participants (52% women, 20% non-White) were recruited in North America, Europe, and Asia. Safety data included all participants, and the modified intention-to-treat group included 1,734 participants, with 859 receiving lecanemab and 875 receiving placebo.

The primary endpoint was the Clinical Dementia Rating–Sum of Boxes (CDR-SB). Scores from 0.5 to 6 are signs of early AD, according to the study. The mean baseline score for both groups was 3.2. The adjusted mean change at 18 months was 1.21 for lecanemab versus 1.66 for placebo (difference, –0.45; 95% confidence interval [CI], –0.67 to –0.23; P < .001).

As Dr. van Dyck noted in his presentation at the CTAD meting, this represents a 27% slowing of the decline in the lecanemab group.

The published findings do not speculate about how this difference would affect the day-to-day life of participants who took the drug, although it does refer to “modestly less decline” of cognition/function in the lecanemab group.

Other measurements that suggest cognitive improvements in the lecanemab group versus placebo include the Alzheimer’s Disease Assessment Scale–Cognitive Subscale score (mean difference, –1.44; 95% CI, –2.27 to –0.61), the Alzheimer’s Disease Composite Score (mean difference, –0.05; 95% CI, –.074 to –.027,), and the Alzheimer’s Disease Cooperative Study–Activities of Daily Living Scale for Mild Cognitive Impairment score (mean difference, 2.0; 95% CI, 1.2-2.8; all, P < .001).

Overall, Dr. van Dyck said, “Lecanemab met the primary and secondary endpoints versus placebo at 18 months, with highly significant differences starting at 6 months.”

In a substudy of 698 participants, results showed that amyloid burden fell at a higher rate in the lecanemab group than in the placebo group (difference, –59.1 centiloids; 95% CI, –62.6 to –55.6).

“Lecanemab has high selectivity for soluble aggregated species of A-beta as compared with monomeric amyloid, with moderate selectivity for fibrillar amyloid; this profile is considered to target the most toxic pathologic amyloid species,” the researchers wrote.
 

Concerning AE data

With respect to AEs, deaths occurred in both groups (0.7% in those who took lecanemab and 0.8% in those who took the placebo). The researchers did not attribute any deaths to the drug. However, according to a report in the journal Science published Nov. 27, a 65-year-old woman who was taking the drug as part of a clinical trial “recently died from a massive brain hemorrhage that some researchers link to the drug.”

The woman, the second person “whose death was linked to lecanemab,” died after suffering a stroke. Researchers summarized a case report as saying that the drug “contributed to her brain hemorrhage after biweekly infusions of lecanemab inflamed and weakened the blood vessels.”

Eisai, which sponsored the new trial, told Science that “all the available safety information indicates that lecanemab therapy is not associated with an increased risk of death overall or from any specific cause.”

In a CTAD presentation, study coauthor Marwan Sabbagh, MD, Barrow Neurological Institute, Phoenix, said two hemorrhage-related deaths occurred in an open-label extension. One was in the context of a tissue plasminogen activator treatment for a stroke, which fits with the description of the case in the Science report. “Causality with lecanemab is a little difficult ...,” he said. “Patients on anticoagulation might need further consideration.”

In the CLARITY AD Trial, serious AEs occurred in 14% of the lecanemab group, leading to discontinuation 6.9% of the time, and in 11.3% of the placebo group, leading to discontinuation 2.9% of the time, the investigators reported.

They added that, in the lecanemab group, the most common AEs, defined as affecting more than 10% of participants, were infusion-related reactions (26.4% vs. 7.4% for placebo); amyloid-related imaging abnormalities with cerebral microhemorrhages, cerebral macrohemorrhages, or superficial siderosis (17.3% vs. 9%, respectively); amyloid-related imaging abnormalities with edema or effusions (12.6% vs. 1.7%); headache (11.1% vs. 8.1%); and falls (10.4% vs. 9.6%).

In addition, macrohemorrhage was reported in 0.6% of the lecanemab group and 0.1% of the placebo group.
 

Cautious optimism

In separate interviews, two Alzheimer’s specialists who weren’t involved in the study praised the trial and described the findings as “exciting.” But they also highlighted its limitations.

Alvaro Pascual-Leone, MD, PhD, professor of neurology at Harvard Medical School and chief medical officer of Linus Health, said the study represents impressive progress after 60-plus trials examining anti-amyloid monoclonal antibodies. “This is the first trial that shows a clinical benefit that can be measured,” he said.

However, it’s unclear whether the changes “are really going to make a difference in people’s lives,” he said. The drug is likely to be expensive, owing to the large investment needed for research, he added, and patients will have to undergo costly testing, such as PET scans and spinal taps.

Still, “this could be a valuable adjunct to the armamentarium we have,” which includes interventions such as lifestyle changes, he said.

Howard Fillit, MD, cofounder and chief science officer at the Alzheimer’s Drug Discovery Foundation, noted that the trial reached its primary and secondary endpoints and that the drug had what he called a “modest” effect on cognition.

However, the drugmaker will need to explore the adverse effects, he said, especially among patients with atrial fibrillation who take anticoagulants. And, he said, medicine is still far from the ultimate goal – fully reversing cognitive decline.

Michael Weiner, MD, president of the CTAD22 Scientific Committee, noted in a press release that there is “growing evidence” that some antiamyloid therapies, “especially lecanemab and donanemab” have shown promising results.

“Unfortunately, these treatments are also associated with abnormal differences seen in imaging, including brain swelling and bleeding in the brain,” said Dr. Weiner, professor of radiology, medicine, and neurology at the University of California, San Francisco.

“There is considerable controversy concerning the significance and impact of these findings, including whether or not governments and medical insurance will provide financial coverage for such treatments,” he added.
 

Rave reviews from the Alzheimer’s Association

In a statement, the Alzheimer’s Association raved about lecanemab and declared that the FDA should approve lecanemab on an accelerated basis. The study “confirms this treatment can meaningfully change the course of the disease for people in the earliest stages of Alzheimer’s disease ...” the association said, adding that “it could mean many months more of recognizing their spouse, children and grandchildren.”

The association, which is a staunch supporter of aducanumab, called on the Centers for Medicare & Medicaid Services to cover the drug if the FDA approves it. The association’s statement did not address the drug’s potential high cost, the adverse effects, or the two reported deaths.

The trial was supported by Eisai (regulatory sponsor) with partial funding from Biogen. Dr. van Dyck reports having received research grants from Biogen, Eisai, Biohaven, Cerevel Therapeutics, Eli Lilly, Genentech, Janssen, Novartis, and UCB. He has been a consultant to Cerevel, Eisai, Ono Pharmaceutical, and Roche. Relevant financial relationships for the other investigators are fully listed in the original article.

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

SAN FRANCISCO – Widely anticipated data from a phase 3 trial of the monoclonal antibody lecanemab suggest the drug “modestly” relieved cognitive impairment in patients with early Alzheimer’s disease (AD) – but at a cost.

In the CLARITY AD trial, adverse events (AEs) were common compared with placebo, including amyloid-related edema and effusions; and a recent news report linked a second death to the drug.

Moving forward, “longer trials are warranted to determine the efficacy and safety of lecanemab in early Alzheimer’s disease,” wrote Christopher H. van Dyck, MD, Yale University, New Haven, Conn., and colleagues.

The full trial findings were presented at the Clinical Trials on Alzheimer’s Disease (CTAD) conference, with simultaneous publication on Nov. 29 in the New England Journal of Medicine.
 

Complications in the field

The phase 3 trial of lecanemab has been closely watched in AD circles, especially considering positive early data released in September and reported by this news organization at that time.

The Food and Drug Administration is expected to make a decision about possible approval of the drug in January 2023. Only one other antiamyloid treatment, the highly controversial and expensive aducanumab (Aduhelm), is currently approved by the FDA.

For the new 18-month, randomized, double-blind CLARITY AD trial, researchers enrolled 1,795 patients aged 50-90 years (average age, 71 years) with early AD. All were randomly assigned to receive either a placebo (n = 898) or intravenous lecanemab, a humanized immunoglobulin G1 (IgG1) monoclonal antibody that selectively targets amyloid beta (A-beta) protofibrils, at 10 mg/kg of body weight every 2 weeks (n = 897).

The study ran from 2019 to 2021. The participants (52% women, 20% non-White) were recruited in North America, Europe, and Asia. Safety data included all participants, and the modified intention-to-treat group included 1,734 participants, with 859 receiving lecanemab and 875 receiving placebo.

The primary endpoint was the Clinical Dementia Rating–Sum of Boxes (CDR-SB). Scores from 0.5 to 6 are signs of early AD, according to the study. The mean baseline score for both groups was 3.2. The adjusted mean change at 18 months was 1.21 for lecanemab versus 1.66 for placebo (difference, –0.45; 95% confidence interval [CI], –0.67 to –0.23; P < .001).

As Dr. van Dyck noted in his presentation at the CTAD meting, this represents a 27% slowing of the decline in the lecanemab group.

The published findings do not speculate about how this difference would affect the day-to-day life of participants who took the drug, although it does refer to “modestly less decline” of cognition/function in the lecanemab group.

Other measurements that suggest cognitive improvements in the lecanemab group versus placebo include the Alzheimer’s Disease Assessment Scale–Cognitive Subscale score (mean difference, –1.44; 95% CI, –2.27 to –0.61), the Alzheimer’s Disease Composite Score (mean difference, –0.05; 95% CI, –.074 to –.027,), and the Alzheimer’s Disease Cooperative Study–Activities of Daily Living Scale for Mild Cognitive Impairment score (mean difference, 2.0; 95% CI, 1.2-2.8; all, P < .001).

Overall, Dr. van Dyck said, “Lecanemab met the primary and secondary endpoints versus placebo at 18 months, with highly significant differences starting at 6 months.”

In a substudy of 698 participants, results showed that amyloid burden fell at a higher rate in the lecanemab group than in the placebo group (difference, –59.1 centiloids; 95% CI, –62.6 to –55.6).

“Lecanemab has high selectivity for soluble aggregated species of A-beta as compared with monomeric amyloid, with moderate selectivity for fibrillar amyloid; this profile is considered to target the most toxic pathologic amyloid species,” the researchers wrote.
 

Concerning AE data

With respect to AEs, deaths occurred in both groups (0.7% in those who took lecanemab and 0.8% in those who took the placebo). The researchers did not attribute any deaths to the drug. However, according to a report in the journal Science published Nov. 27, a 65-year-old woman who was taking the drug as part of a clinical trial “recently died from a massive brain hemorrhage that some researchers link to the drug.”

The woman, the second person “whose death was linked to lecanemab,” died after suffering a stroke. Researchers summarized a case report as saying that the drug “contributed to her brain hemorrhage after biweekly infusions of lecanemab inflamed and weakened the blood vessels.”

Eisai, which sponsored the new trial, told Science that “all the available safety information indicates that lecanemab therapy is not associated with an increased risk of death overall or from any specific cause.”

In a CTAD presentation, study coauthor Marwan Sabbagh, MD, Barrow Neurological Institute, Phoenix, said two hemorrhage-related deaths occurred in an open-label extension. One was in the context of a tissue plasminogen activator treatment for a stroke, which fits with the description of the case in the Science report. “Causality with lecanemab is a little difficult ...,” he said. “Patients on anticoagulation might need further consideration.”

In the CLARITY AD Trial, serious AEs occurred in 14% of the lecanemab group, leading to discontinuation 6.9% of the time, and in 11.3% of the placebo group, leading to discontinuation 2.9% of the time, the investigators reported.

They added that, in the lecanemab group, the most common AEs, defined as affecting more than 10% of participants, were infusion-related reactions (26.4% vs. 7.4% for placebo); amyloid-related imaging abnormalities with cerebral microhemorrhages, cerebral macrohemorrhages, or superficial siderosis (17.3% vs. 9%, respectively); amyloid-related imaging abnormalities with edema or effusions (12.6% vs. 1.7%); headache (11.1% vs. 8.1%); and falls (10.4% vs. 9.6%).

In addition, macrohemorrhage was reported in 0.6% of the lecanemab group and 0.1% of the placebo group.
 

Cautious optimism

In separate interviews, two Alzheimer’s specialists who weren’t involved in the study praised the trial and described the findings as “exciting.” But they also highlighted its limitations.

Alvaro Pascual-Leone, MD, PhD, professor of neurology at Harvard Medical School and chief medical officer of Linus Health, said the study represents impressive progress after 60-plus trials examining anti-amyloid monoclonal antibodies. “This is the first trial that shows a clinical benefit that can be measured,” he said.

However, it’s unclear whether the changes “are really going to make a difference in people’s lives,” he said. The drug is likely to be expensive, owing to the large investment needed for research, he added, and patients will have to undergo costly testing, such as PET scans and spinal taps.

Still, “this could be a valuable adjunct to the armamentarium we have,” which includes interventions such as lifestyle changes, he said.

Howard Fillit, MD, cofounder and chief science officer at the Alzheimer’s Drug Discovery Foundation, noted that the trial reached its primary and secondary endpoints and that the drug had what he called a “modest” effect on cognition.

However, the drugmaker will need to explore the adverse effects, he said, especially among patients with atrial fibrillation who take anticoagulants. And, he said, medicine is still far from the ultimate goal – fully reversing cognitive decline.

Michael Weiner, MD, president of the CTAD22 Scientific Committee, noted in a press release that there is “growing evidence” that some antiamyloid therapies, “especially lecanemab and donanemab” have shown promising results.

“Unfortunately, these treatments are also associated with abnormal differences seen in imaging, including brain swelling and bleeding in the brain,” said Dr. Weiner, professor of radiology, medicine, and neurology at the University of California, San Francisco.

“There is considerable controversy concerning the significance and impact of these findings, including whether or not governments and medical insurance will provide financial coverage for such treatments,” he added.
 

Rave reviews from the Alzheimer’s Association

In a statement, the Alzheimer’s Association raved about lecanemab and declared that the FDA should approve lecanemab on an accelerated basis. The study “confirms this treatment can meaningfully change the course of the disease for people in the earliest stages of Alzheimer’s disease ...” the association said, adding that “it could mean many months more of recognizing their spouse, children and grandchildren.”

The association, which is a staunch supporter of aducanumab, called on the Centers for Medicare & Medicaid Services to cover the drug if the FDA approves it. The association’s statement did not address the drug’s potential high cost, the adverse effects, or the two reported deaths.

The trial was supported by Eisai (regulatory sponsor) with partial funding from Biogen. Dr. van Dyck reports having received research grants from Biogen, Eisai, Biohaven, Cerevel Therapeutics, Eli Lilly, Genentech, Janssen, Novartis, and UCB. He has been a consultant to Cerevel, Eisai, Ono Pharmaceutical, and Roche. Relevant financial relationships for the other investigators are fully listed in the original article.

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

SAN FRANCISCO – Widely anticipated data from a phase 3 trial of the monoclonal antibody lecanemab suggest the drug “modestly” relieved cognitive impairment in patients with early Alzheimer’s disease (AD) – but at a cost.

In the CLARITY AD trial, adverse events (AEs) were common compared with placebo, including amyloid-related edema and effusions; and a recent news report linked a second death to the drug.

Moving forward, “longer trials are warranted to determine the efficacy and safety of lecanemab in early Alzheimer’s disease,” wrote Christopher H. van Dyck, MD, Yale University, New Haven, Conn., and colleagues.

The full trial findings were presented at the Clinical Trials on Alzheimer’s Disease (CTAD) conference, with simultaneous publication on Nov. 29 in the New England Journal of Medicine.
 

Complications in the field

The phase 3 trial of lecanemab has been closely watched in AD circles, especially considering positive early data released in September and reported by this news organization at that time.

The Food and Drug Administration is expected to make a decision about possible approval of the drug in January 2023. Only one other antiamyloid treatment, the highly controversial and expensive aducanumab (Aduhelm), is currently approved by the FDA.

For the new 18-month, randomized, double-blind CLARITY AD trial, researchers enrolled 1,795 patients aged 50-90 years (average age, 71 years) with early AD. All were randomly assigned to receive either a placebo (n = 898) or intravenous lecanemab, a humanized immunoglobulin G1 (IgG1) monoclonal antibody that selectively targets amyloid beta (A-beta) protofibrils, at 10 mg/kg of body weight every 2 weeks (n = 897).

The study ran from 2019 to 2021. The participants (52% women, 20% non-White) were recruited in North America, Europe, and Asia. Safety data included all participants, and the modified intention-to-treat group included 1,734 participants, with 859 receiving lecanemab and 875 receiving placebo.

The primary endpoint was the Clinical Dementia Rating–Sum of Boxes (CDR-SB). Scores from 0.5 to 6 are signs of early AD, according to the study. The mean baseline score for both groups was 3.2. The adjusted mean change at 18 months was 1.21 for lecanemab versus 1.66 for placebo (difference, –0.45; 95% confidence interval [CI], –0.67 to –0.23; P < .001).

As Dr. van Dyck noted in his presentation at the CTAD meting, this represents a 27% slowing of the decline in the lecanemab group.

The published findings do not speculate about how this difference would affect the day-to-day life of participants who took the drug, although it does refer to “modestly less decline” of cognition/function in the lecanemab group.

Other measurements that suggest cognitive improvements in the lecanemab group versus placebo include the Alzheimer’s Disease Assessment Scale–Cognitive Subscale score (mean difference, –1.44; 95% CI, –2.27 to –0.61), the Alzheimer’s Disease Composite Score (mean difference, –0.05; 95% CI, –.074 to –.027,), and the Alzheimer’s Disease Cooperative Study–Activities of Daily Living Scale for Mild Cognitive Impairment score (mean difference, 2.0; 95% CI, 1.2-2.8; all, P < .001).

Overall, Dr. van Dyck said, “Lecanemab met the primary and secondary endpoints versus placebo at 18 months, with highly significant differences starting at 6 months.”

In a substudy of 698 participants, results showed that amyloid burden fell at a higher rate in the lecanemab group than in the placebo group (difference, –59.1 centiloids; 95% CI, –62.6 to –55.6).

“Lecanemab has high selectivity for soluble aggregated species of A-beta as compared with monomeric amyloid, with moderate selectivity for fibrillar amyloid; this profile is considered to target the most toxic pathologic amyloid species,” the researchers wrote.
 

Concerning AE data

With respect to AEs, deaths occurred in both groups (0.7% in those who took lecanemab and 0.8% in those who took the placebo). The researchers did not attribute any deaths to the drug. However, according to a report in the journal Science published Nov. 27, a 65-year-old woman who was taking the drug as part of a clinical trial “recently died from a massive brain hemorrhage that some researchers link to the drug.”

The woman, the second person “whose death was linked to lecanemab,” died after suffering a stroke. Researchers summarized a case report as saying that the drug “contributed to her brain hemorrhage after biweekly infusions of lecanemab inflamed and weakened the blood vessels.”

Eisai, which sponsored the new trial, told Science that “all the available safety information indicates that lecanemab therapy is not associated with an increased risk of death overall or from any specific cause.”

In a CTAD presentation, study coauthor Marwan Sabbagh, MD, Barrow Neurological Institute, Phoenix, said two hemorrhage-related deaths occurred in an open-label extension. One was in the context of a tissue plasminogen activator treatment for a stroke, which fits with the description of the case in the Science report. “Causality with lecanemab is a little difficult ...,” he said. “Patients on anticoagulation might need further consideration.”

In the CLARITY AD Trial, serious AEs occurred in 14% of the lecanemab group, leading to discontinuation 6.9% of the time, and in 11.3% of the placebo group, leading to discontinuation 2.9% of the time, the investigators reported.

They added that, in the lecanemab group, the most common AEs, defined as affecting more than 10% of participants, were infusion-related reactions (26.4% vs. 7.4% for placebo); amyloid-related imaging abnormalities with cerebral microhemorrhages, cerebral macrohemorrhages, or superficial siderosis (17.3% vs. 9%, respectively); amyloid-related imaging abnormalities with edema or effusions (12.6% vs. 1.7%); headache (11.1% vs. 8.1%); and falls (10.4% vs. 9.6%).

In addition, macrohemorrhage was reported in 0.6% of the lecanemab group and 0.1% of the placebo group.
 

Cautious optimism

In separate interviews, two Alzheimer’s specialists who weren’t involved in the study praised the trial and described the findings as “exciting.” But they also highlighted its limitations.

Alvaro Pascual-Leone, MD, PhD, professor of neurology at Harvard Medical School and chief medical officer of Linus Health, said the study represents impressive progress after 60-plus trials examining anti-amyloid monoclonal antibodies. “This is the first trial that shows a clinical benefit that can be measured,” he said.

However, it’s unclear whether the changes “are really going to make a difference in people’s lives,” he said. The drug is likely to be expensive, owing to the large investment needed for research, he added, and patients will have to undergo costly testing, such as PET scans and spinal taps.

Still, “this could be a valuable adjunct to the armamentarium we have,” which includes interventions such as lifestyle changes, he said.

Howard Fillit, MD, cofounder and chief science officer at the Alzheimer’s Drug Discovery Foundation, noted that the trial reached its primary and secondary endpoints and that the drug had what he called a “modest” effect on cognition.

However, the drugmaker will need to explore the adverse effects, he said, especially among patients with atrial fibrillation who take anticoagulants. And, he said, medicine is still far from the ultimate goal – fully reversing cognitive decline.

Michael Weiner, MD, president of the CTAD22 Scientific Committee, noted in a press release that there is “growing evidence” that some antiamyloid therapies, “especially lecanemab and donanemab” have shown promising results.

“Unfortunately, these treatments are also associated with abnormal differences seen in imaging, including brain swelling and bleeding in the brain,” said Dr. Weiner, professor of radiology, medicine, and neurology at the University of California, San Francisco.

“There is considerable controversy concerning the significance and impact of these findings, including whether or not governments and medical insurance will provide financial coverage for such treatments,” he added.
 

Rave reviews from the Alzheimer’s Association

In a statement, the Alzheimer’s Association raved about lecanemab and declared that the FDA should approve lecanemab on an accelerated basis. The study “confirms this treatment can meaningfully change the course of the disease for people in the earliest stages of Alzheimer’s disease ...” the association said, adding that “it could mean many months more of recognizing their spouse, children and grandchildren.”

The association, which is a staunch supporter of aducanumab, called on the Centers for Medicare & Medicaid Services to cover the drug if the FDA approves it. The association’s statement did not address the drug’s potential high cost, the adverse effects, or the two reported deaths.

The trial was supported by Eisai (regulatory sponsor) with partial funding from Biogen. Dr. van Dyck reports having received research grants from Biogen, Eisai, Biohaven, Cerevel Therapeutics, Eli Lilly, Genentech, Janssen, Novartis, and UCB. He has been a consultant to Cerevel, Eisai, Ono Pharmaceutical, and Roche. Relevant financial relationships for the other investigators are fully listed in the original article.

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

Black and Latinx older adults are up to three times as likely to develop Alzheimer’s disease than non-Latinx White adults and tend to experience onset at a younger age with more severe symptoms, according to Monica Rivera-Mindt, PhD, a professor of psychology at Fordham University and the Icahn School of Medicine at Mount Sinai, New York. Looking ahead, that means by 2030, nearly 40% of the 8.4 million Americans affected by Alzheimer’s disease will be Black and/or Latinx, she said. These facts were among the stark disparities in health care outcomes Dr. Rivera-Mindt discussed in her presentation on brain health equity at the 2022 annual meeting of the American Neurological Association.

Dr. Rivera-Mindt’s presentation opened the ANA’s plenary session on health disparities and inequities. The plenary, “Advancing Neurologic Equity: Challenges and Paths Forward,” did not simply enumerate racial and ethnic disparities that exist with various neurological conditions. Rather it went beyond the discussion of what disparities exist into understanding the roots of them as well as tips, tools, and resources that can aid clinicians in addressing or ameliorating them.

“Our most prevalent, most burdensome diseases in neurology disproportionately affect persons from minoritized and marginalized backgrounds,” Roy Hamilton, MD, an associate professor of neurology and physical medicine and rehabilitation at the University of Pennsylvania, Philadelphia, said. “If clinicians are unaware of these disparities or don’t have any sense of how to start to address or think about them, then they’re really missing out on an important component of their education as persons who take care of patients with brain disorders.”

Dr. Hamilton, who organized the plenary, noted that awareness of these disparities is crucial to comprehensively caring for patients.
 

Missed opportunities

“We’re talking about disadvantages that are structural and large scale, but those disadvantages play themselves out in the individual encounter,” Dr. Hamilton said. “When physicians see patients, they have to treat the whole patient in front of them,” which means being aware of the risks and factors that could affect a patient’s clinical presentation. “Being aware of disparities has practical impacts on physician judgment,” he said.

For example, recent research in multiple sclerosis (MS) has highlighted how clinicians may be missing diagnosis of this condition in non-White populations because the condition has been regarded for so long as a “White person’s” disease, Dr. Hamilton said. In non-White patients exhibiting MS symptoms, then, clinicians may have been less likely to consider MS as a possibility, thereby delaying diagnosis and treatment.

Those patterns may partly explain why the mortality rate for MS is greater in Black patients, who also show more rapid neurodegeneration than White patients with MS, Lilyana Amezcua, MD, an associate professor of neurology at the University of Southern California, Los Angeles, reported in the plenary’s second presentation.
 

Transgender issues

The third session, presented by Nicole Rosendale, MD, an assistant professor of neurology at the University of California, San Francisco, and director of the San Francisco General Hospital neurology inpatient services, examined disparities in neurology within the LGBTQ+ community through representative case studies and then offered specific ways that neurologists could make their practices more inclusive and equitable for sexual and gender minorities.

Her first case study was a 52-year-old man who presented with new-onset seizures, right hemiparesis, and aphasia. A brain biopsy consistent with adenocarcinoma eventually led his physician to discover he had metastatic breast cancer. It turned out the man was transgender and, despite a family history of breast cancer, hadn’t been advised to get breast cancer screenings.

“Breast cancer was not initially on the differential as no one had identified that the patient was transmasculine,” Dr. Rosendale said. A major challenge to providing care to transgender patients is a dearth of data on risks and screening recommendations. Another barrier is low knowledge of LGBTQ+ health among neurologists, Dr. Rosendale said while sharing findings from her 2019 study on the topic and calling for more research in LGBTQ+ populations.

Dr. Rosendale’s second case study dealt with a nonbinary patient who suffered from debilitating headaches for decades, first because they lacked access to health insurance and then because negative experiences with providers dissuaded them from seeking care. In data from the Center for American Progress she shared, 8% of LGB respondents and 22% of transgender respondents said they had avoided or delayed care because of fear of discrimination or mistreatment.

“So it’s not only access but also what experiences people are having when they go in and whether they’re actually even getting access to care or being taken care of,” Dr. Rosendale said. Other findings from the CAP found that:

• 8% of LGB patients and 29% of transgender patients reported having a clinician refuse to see them.
• 6% of LGB patients and 12% of transgender patients reported that a clinician refused to give them health care.
• 9% of LGB patients and 21% of transgender patients experienced harsh or abusive language during a health care experience.
• 7% of LGB patients and nearly a third (29%) of transgender patients experienced unwanted physical contact, such as fondling or sexual assault.

Reducing the disparities

Adys Mendizabal, MD, an assistant professor of neurology at the Institute of Society and Genetics at the University of California, Los Angeles, who attended the presentation, was grateful to see how the various lectures enriched the discussion beyond stating the fact of racial/ethnic disparities and dug into the nuances on how to think about and address these disparities. She particularly appreciated discussion about the need to go out of the way to recruit diverse patient populations for clinical trials while also providing them care.

“It is definitely complicated, but it’s not impossible for an individual neurologist or an individual department to do something to reduce some of the disparities,” Dr. Mendizabal said. “It starts with just knowing that they exist and being aware of some of the things that may be impacting care for a particular patient.”
 

Tools to counter disparity

In the final presentation, Amy Kind, MD, PhD, the associate dean for social health sciences and programs at the University of Wisconsin–Madison, rounded out the discussion by exploring social determinants of health and their influence on outcomes.

“Social determinants impact brain health, and brain health is not distributed equally,” Dr. Kind told attendees. “We have known this for decades, yet disparities persist.”

Dr. Kind described the “exposome,” a “measure of all the exposures of an individual in a lifetime and how those exposures relate to health,” according to the CDC, and then introduced a tool clinicians can use to better understand social determinants of health in specific geographic areas. The Neighborhood Atlas, which Dr. Kind described in the New England Journal of Medicine in 2018, measures 17 social determinants across small population-sensitive areas and provides an area deprivation index. A high area deprivation index is linked to a range of negative outcomes, including reshopitalization, later diagnoses, less comprehensive diagnostic evaluation, increased risk of postsurgical complications, and decreased life expectancy.

“One of the things that really stood out to me about Dr. Kind’s discussion of the use of the area deprivation index was the fact that understanding and quantifying these kinds of risks and exposures is the vehicle for creating the kinds of social changes, including policy changes, that will actually lead to addressing and mitigating some of these lifelong risks and exposures,” Dr. Hamilton said. “It is implausible to think that a specific group of people would be genetically more susceptible to basically every disease that we know,” he added. “It makes much more sense to think that groups of individuals have been subjected systematically to conditions that impair health in a variety of ways.”
 

Not just race, ethnicity, sex, and gender

Following the four presentations from researchers in health inequities was an Emerging Scholar presentation in which Jay B. Lusk, an MD/MBA candidate at Duke University, Durham, N.C., shared new research findings on the role of neighborhood disadvantage in predicting mortality from coma, stroke, and other neurologic conditions. His findings revealed that living in a neighborhood with greater deprivation substantially increased risk of mortality even after accounting for individual wealth and demographics.

Maria Eugenia Diaz-Ortiz, PhD, of the department of neurology, University of Pennsylvania, Philadelphia, said she found the five presentations to be an excellent introduction to people like herself who are in the earlier stages of learning about health equity research.

“I think they introduced various important concepts and frameworks and provided tools for people who don’t know about them,” Dr. Diaz-Ortiz said. “Then they asked important questions and provided some solutions to them.”

Dr. Diaz-Ortiz also appreciated seemingly minor but actually important details in how the speakers presented themselves, such as Dr. Rivera-Mindt opening with a land acknowledgment and her disclosures of “positionality.” The former recognized the traditional Native American custodians of the land on which she lives and works, and the latter revealed details about her as an individual – such as being the Afro-Latinx daughter of immigrants yet being cisgender, able-bodied, and U.S.-born – that show where she falls on the axis of adversity and axis of privilege.
 

Implications for research

The biggest takeaway for Dr. Diaz-Ortiz, however, came from the first Q&A session when someone asked how to increase underrepresented populations in dementia research. Dr. Rivera-Mindt described her experience engaging these communities by employing “community-based participatory research practices, which involves making yourself a part of the community and making the community active participants in the research,” Dr. Diaz-Ortiz said. “It’s an evidence-based approach that has been shown to increase participation in research not only in her work but in the work of others.”

Preaching to the choir

Dr. Diaz-Ortiz was pleased overall with the plenary but disappointed in its placement at the end of the meeting, when attendance is always lower as attendees head home.

“The people who stayed were people who already know and recognize the value of health equity work, so I think that was a missed opportunity where the session could have been included on day one or two to boost attendance and also to educate like a broader group of neurologists,” Dr. Diaz-Ortiz said in an interview.

Dr. Mendizabal felt similarly, appreciating the plenary but noting it was “definitely overdue” and that it should not be the last session. Instead, sessions on health equity should be as easy as possible to attend to bring in larger audiences. “Perhaps having that session on a Saturday or Sunday would have a higher likelihood of greater attendance than on a Tuesday,” she said. That said, Dr. Mendizabal also noticed that greater attention to health care disparities was woven into many other sessions throughout the conference, which is “the best way of addressing health equity instead of trying to just designate a session,” she said.

Dr. Mendizabal hopes that plenaries like this one and the weaving of health equity issues into presentations throughout neurology conferences continue.

“After the racial reckoning in 2020, there was a big impetus and a big wave of energy in addressing health disparities in the field, and I hope that that momentum is not starting to wane,” Dr. Mendizabal said. “It’s important because not talking about is not going to make this issue go away.”

Dr. Hamilton agreed that it is important that the conversation continue and that physicians recognize the importance of understanding health care disparities and determinants of health, regardless of where they fall on the political spectrum or whether they choose to get involved in policy or advocacy.

“Irrespective of whether you think race or ethnicity or socioeconomic status are political issues or not, it is the case that you’re obligated to have an objective understanding of the factors that contribute to your patient’s health and as points of intervention,” Dr. Hamilton said. “So even if you don’t want to sit down and jot off that email to your senator, you still have to take these factors into account when you’re treating the person who’s sitting right in front of you, and that’s not political. That’s the promise of being a physician.”

Dr. Amezcua has received personal compensation for consulting, speaking, or serving on steering committees or advisory boards for Biogen Idec, Novartis, Genentech, and EMD Serono, and she has received research support from Biogen Idec and Bristol Myers Squibb Foundation. Dr. Kind reported support from the Alzheimer’s Association. Dr. Diaz-Ortiz is coinventor of a provisional patent submitted by the University of Pennsylvania that relates to a potential therapeutic in Parkinson’s disease. Mr. Lusk reported fellowship support from American Heart Association and travel support from the American Neurological Association. No other speakers or sources had relevant disclosures.
 

Black and Latinx older adults are up to three times as likely to develop Alzheimer’s disease than non-Latinx White adults and tend to experience onset at a younger age with more severe symptoms, according to Monica Rivera-Mindt, PhD, a professor of psychology at Fordham University and the Icahn School of Medicine at Mount Sinai, New York. Looking ahead, that means by 2030, nearly 40% of the 8.4 million Americans affected by Alzheimer’s disease will be Black and/or Latinx, she said. These facts were among the stark disparities in health care outcomes Dr. Rivera-Mindt discussed in her presentation on brain health equity at the 2022 annual meeting of the American Neurological Association.

Dr. Rivera-Mindt’s presentation opened the ANA’s plenary session on health disparities and inequities. The plenary, “Advancing Neurologic Equity: Challenges and Paths Forward,” did not simply enumerate racial and ethnic disparities that exist with various neurological conditions. Rather it went beyond the discussion of what disparities exist into understanding the roots of them as well as tips, tools, and resources that can aid clinicians in addressing or ameliorating them.

“Our most prevalent, most burdensome diseases in neurology disproportionately affect persons from minoritized and marginalized backgrounds,” Roy Hamilton, MD, an associate professor of neurology and physical medicine and rehabilitation at the University of Pennsylvania, Philadelphia, said. “If clinicians are unaware of these disparities or don’t have any sense of how to start to address or think about them, then they’re really missing out on an important component of their education as persons who take care of patients with brain disorders.”

Dr. Hamilton, who organized the plenary, noted that awareness of these disparities is crucial to comprehensively caring for patients.
 

Missed opportunities

“We’re talking about disadvantages that are structural and large scale, but those disadvantages play themselves out in the individual encounter,” Dr. Hamilton said. “When physicians see patients, they have to treat the whole patient in front of them,” which means being aware of the risks and factors that could affect a patient’s clinical presentation. “Being aware of disparities has practical impacts on physician judgment,” he said.

For example, recent research in multiple sclerosis (MS) has highlighted how clinicians may be missing diagnosis of this condition in non-White populations because the condition has been regarded for so long as a “White person’s” disease, Dr. Hamilton said. In non-White patients exhibiting MS symptoms, then, clinicians may have been less likely to consider MS as a possibility, thereby delaying diagnosis and treatment.

Those patterns may partly explain why the mortality rate for MS is greater in Black patients, who also show more rapid neurodegeneration than White patients with MS, Lilyana Amezcua, MD, an associate professor of neurology at the University of Southern California, Los Angeles, reported in the plenary’s second presentation.
 

Transgender issues

The third session, presented by Nicole Rosendale, MD, an assistant professor of neurology at the University of California, San Francisco, and director of the San Francisco General Hospital neurology inpatient services, examined disparities in neurology within the LGBTQ+ community through representative case studies and then offered specific ways that neurologists could make their practices more inclusive and equitable for sexual and gender minorities.

Her first case study was a 52-year-old man who presented with new-onset seizures, right hemiparesis, and aphasia. A brain biopsy consistent with adenocarcinoma eventually led his physician to discover he had metastatic breast cancer. It turned out the man was transgender and, despite a family history of breast cancer, hadn’t been advised to get breast cancer screenings.

“Breast cancer was not initially on the differential as no one had identified that the patient was transmasculine,” Dr. Rosendale said. A major challenge to providing care to transgender patients is a dearth of data on risks and screening recommendations. Another barrier is low knowledge of LGBTQ+ health among neurologists, Dr. Rosendale said while sharing findings from her 2019 study on the topic and calling for more research in LGBTQ+ populations.

Dr. Rosendale’s second case study dealt with a nonbinary patient who suffered from debilitating headaches for decades, first because they lacked access to health insurance and then because negative experiences with providers dissuaded them from seeking care. In data from the Center for American Progress she shared, 8% of LGB respondents and 22% of transgender respondents said they had avoided or delayed care because of fear of discrimination or mistreatment.

“So it’s not only access but also what experiences people are having when they go in and whether they’re actually even getting access to care or being taken care of,” Dr. Rosendale said. Other findings from the CAP found that:

• 8% of LGB patients and 29% of transgender patients reported having a clinician refuse to see them.
• 6% of LGB patients and 12% of transgender patients reported that a clinician refused to give them health care.
• 9% of LGB patients and 21% of transgender patients experienced harsh or abusive language during a health care experience.
• 7% of LGB patients and nearly a third (29%) of transgender patients experienced unwanted physical contact, such as fondling or sexual assault.

Reducing the disparities

Adys Mendizabal, MD, an assistant professor of neurology at the Institute of Society and Genetics at the University of California, Los Angeles, who attended the presentation, was grateful to see how the various lectures enriched the discussion beyond stating the fact of racial/ethnic disparities and dug into the nuances on how to think about and address these disparities. She particularly appreciated discussion about the need to go out of the way to recruit diverse patient populations for clinical trials while also providing them care.

“It is definitely complicated, but it’s not impossible for an individual neurologist or an individual department to do something to reduce some of the disparities,” Dr. Mendizabal said. “It starts with just knowing that they exist and being aware of some of the things that may be impacting care for a particular patient.”
 

Tools to counter disparity

In the final presentation, Amy Kind, MD, PhD, the associate dean for social health sciences and programs at the University of Wisconsin–Madison, rounded out the discussion by exploring social determinants of health and their influence on outcomes.

“Social determinants impact brain health, and brain health is not distributed equally,” Dr. Kind told attendees. “We have known this for decades, yet disparities persist.”

Dr. Kind described the “exposome,” a “measure of all the exposures of an individual in a lifetime and how those exposures relate to health,” according to the CDC, and then introduced a tool clinicians can use to better understand social determinants of health in specific geographic areas. The Neighborhood Atlas, which Dr. Kind described in the New England Journal of Medicine in 2018, measures 17 social determinants across small population-sensitive areas and provides an area deprivation index. A high area deprivation index is linked to a range of negative outcomes, including reshopitalization, later diagnoses, less comprehensive diagnostic evaluation, increased risk of postsurgical complications, and decreased life expectancy.

“One of the things that really stood out to me about Dr. Kind’s discussion of the use of the area deprivation index was the fact that understanding and quantifying these kinds of risks and exposures is the vehicle for creating the kinds of social changes, including policy changes, that will actually lead to addressing and mitigating some of these lifelong risks and exposures,” Dr. Hamilton said. “It is implausible to think that a specific group of people would be genetically more susceptible to basically every disease that we know,” he added. “It makes much more sense to think that groups of individuals have been subjected systematically to conditions that impair health in a variety of ways.”
 

Not just race, ethnicity, sex, and gender

Following the four presentations from researchers in health inequities was an Emerging Scholar presentation in which Jay B. Lusk, an MD/MBA candidate at Duke University, Durham, N.C., shared new research findings on the role of neighborhood disadvantage in predicting mortality from coma, stroke, and other neurologic conditions. His findings revealed that living in a neighborhood with greater deprivation substantially increased risk of mortality even after accounting for individual wealth and demographics.

Maria Eugenia Diaz-Ortiz, PhD, of the department of neurology, University of Pennsylvania, Philadelphia, said she found the five presentations to be an excellent introduction to people like herself who are in the earlier stages of learning about health equity research.

“I think they introduced various important concepts and frameworks and provided tools for people who don’t know about them,” Dr. Diaz-Ortiz said. “Then they asked important questions and provided some solutions to them.”

Dr. Diaz-Ortiz also appreciated seemingly minor but actually important details in how the speakers presented themselves, such as Dr. Rivera-Mindt opening with a land acknowledgment and her disclosures of “positionality.” The former recognized the traditional Native American custodians of the land on which she lives and works, and the latter revealed details about her as an individual – such as being the Afro-Latinx daughter of immigrants yet being cisgender, able-bodied, and U.S.-born – that show where she falls on the axis of adversity and axis of privilege.
 

Implications for research

The biggest takeaway for Dr. Diaz-Ortiz, however, came from the first Q&A session when someone asked how to increase underrepresented populations in dementia research. Dr. Rivera-Mindt described her experience engaging these communities by employing “community-based participatory research practices, which involves making yourself a part of the community and making the community active participants in the research,” Dr. Diaz-Ortiz said. “It’s an evidence-based approach that has been shown to increase participation in research not only in her work but in the work of others.”

Preaching to the choir

Dr. Diaz-Ortiz was pleased overall with the plenary but disappointed in its placement at the end of the meeting, when attendance is always lower as attendees head home.

“The people who stayed were people who already know and recognize the value of health equity work, so I think that was a missed opportunity where the session could have been included on day one or two to boost attendance and also to educate like a broader group of neurologists,” Dr. Diaz-Ortiz said in an interview.

Dr. Mendizabal felt similarly, appreciating the plenary but noting it was “definitely overdue” and that it should not be the last session. Instead, sessions on health equity should be as easy as possible to attend to bring in larger audiences. “Perhaps having that session on a Saturday or Sunday would have a higher likelihood of greater attendance than on a Tuesday,” she said. That said, Dr. Mendizabal also noticed that greater attention to health care disparities was woven into many other sessions throughout the conference, which is “the best way of addressing health equity instead of trying to just designate a session,” she said.

Dr. Mendizabal hopes that plenaries like this one and the weaving of health equity issues into presentations throughout neurology conferences continue.

“After the racial reckoning in 2020, there was a big impetus and a big wave of energy in addressing health disparities in the field, and I hope that that momentum is not starting to wane,” Dr. Mendizabal said. “It’s important because not talking about is not going to make this issue go away.”

Dr. Hamilton agreed that it is important that the conversation continue and that physicians recognize the importance of understanding health care disparities and determinants of health, regardless of where they fall on the political spectrum or whether they choose to get involved in policy or advocacy.

“Irrespective of whether you think race or ethnicity or socioeconomic status are political issues or not, it is the case that you’re obligated to have an objective understanding of the factors that contribute to your patient’s health and as points of intervention,” Dr. Hamilton said. “So even if you don’t want to sit down and jot off that email to your senator, you still have to take these factors into account when you’re treating the person who’s sitting right in front of you, and that’s not political. That’s the promise of being a physician.”

Dr. Amezcua has received personal compensation for consulting, speaking, or serving on steering committees or advisory boards for Biogen Idec, Novartis, Genentech, and EMD Serono, and she has received research support from Biogen Idec and Bristol Myers Squibb Foundation. Dr. Kind reported support from the Alzheimer’s Association. Dr. Diaz-Ortiz is coinventor of a provisional patent submitted by the University of Pennsylvania that relates to a potential therapeutic in Parkinson’s disease. Mr. Lusk reported fellowship support from American Heart Association and travel support from the American Neurological Association. No other speakers or sources had relevant disclosures.
 

Black and Latinx older adults are up to three times as likely to develop Alzheimer’s disease than non-Latinx White adults and tend to experience onset at a younger age with more severe symptoms, according to Monica Rivera-Mindt, PhD, a professor of psychology at Fordham University and the Icahn School of Medicine at Mount Sinai, New York. Looking ahead, that means by 2030, nearly 40% of the 8.4 million Americans affected by Alzheimer’s disease will be Black and/or Latinx, she said. These facts were among the stark disparities in health care outcomes Dr. Rivera-Mindt discussed in her presentation on brain health equity at the 2022 annual meeting of the American Neurological Association.

Dr. Rivera-Mindt’s presentation opened the ANA’s plenary session on health disparities and inequities. The plenary, “Advancing Neurologic Equity: Challenges and Paths Forward,” did not simply enumerate racial and ethnic disparities that exist with various neurological conditions. Rather it went beyond the discussion of what disparities exist into understanding the roots of them as well as tips, tools, and resources that can aid clinicians in addressing or ameliorating them.

“Our most prevalent, most burdensome diseases in neurology disproportionately affect persons from minoritized and marginalized backgrounds,” Roy Hamilton, MD, an associate professor of neurology and physical medicine and rehabilitation at the University of Pennsylvania, Philadelphia, said. “If clinicians are unaware of these disparities or don’t have any sense of how to start to address or think about them, then they’re really missing out on an important component of their education as persons who take care of patients with brain disorders.”

Dr. Hamilton, who organized the plenary, noted that awareness of these disparities is crucial to comprehensively caring for patients.
 

Missed opportunities

“We’re talking about disadvantages that are structural and large scale, but those disadvantages play themselves out in the individual encounter,” Dr. Hamilton said. “When physicians see patients, they have to treat the whole patient in front of them,” which means being aware of the risks and factors that could affect a patient’s clinical presentation. “Being aware of disparities has practical impacts on physician judgment,” he said.

For example, recent research in multiple sclerosis (MS) has highlighted how clinicians may be missing diagnosis of this condition in non-White populations because the condition has been regarded for so long as a “White person’s” disease, Dr. Hamilton said. In non-White patients exhibiting MS symptoms, then, clinicians may have been less likely to consider MS as a possibility, thereby delaying diagnosis and treatment.

Those patterns may partly explain why the mortality rate for MS is greater in Black patients, who also show more rapid neurodegeneration than White patients with MS, Lilyana Amezcua, MD, an associate professor of neurology at the University of Southern California, Los Angeles, reported in the plenary’s second presentation.
 

Transgender issues

The third session, presented by Nicole Rosendale, MD, an assistant professor of neurology at the University of California, San Francisco, and director of the San Francisco General Hospital neurology inpatient services, examined disparities in neurology within the LGBTQ+ community through representative case studies and then offered specific ways that neurologists could make their practices more inclusive and equitable for sexual and gender minorities.

Her first case study was a 52-year-old man who presented with new-onset seizures, right hemiparesis, and aphasia. A brain biopsy consistent with adenocarcinoma eventually led his physician to discover he had metastatic breast cancer. It turned out the man was transgender and, despite a family history of breast cancer, hadn’t been advised to get breast cancer screenings.

“Breast cancer was not initially on the differential as no one had identified that the patient was transmasculine,” Dr. Rosendale said. A major challenge to providing care to transgender patients is a dearth of data on risks and screening recommendations. Another barrier is low knowledge of LGBTQ+ health among neurologists, Dr. Rosendale said while sharing findings from her 2019 study on the topic and calling for more research in LGBTQ+ populations.

Dr. Rosendale’s second case study dealt with a nonbinary patient who suffered from debilitating headaches for decades, first because they lacked access to health insurance and then because negative experiences with providers dissuaded them from seeking care. In data from the Center for American Progress she shared, 8% of LGB respondents and 22% of transgender respondents said they had avoided or delayed care because of fear of discrimination or mistreatment.

“So it’s not only access but also what experiences people are having when they go in and whether they’re actually even getting access to care or being taken care of,” Dr. Rosendale said. Other findings from the CAP found that:

• 8% of LGB patients and 29% of transgender patients reported having a clinician refuse to see them.
• 6% of LGB patients and 12% of transgender patients reported that a clinician refused to give them health care.
• 9% of LGB patients and 21% of transgender patients experienced harsh or abusive language during a health care experience.
• 7% of LGB patients and nearly a third (29%) of transgender patients experienced unwanted physical contact, such as fondling or sexual assault.

Reducing the disparities

Adys Mendizabal, MD, an assistant professor of neurology at the Institute of Society and Genetics at the University of California, Los Angeles, who attended the presentation, was grateful to see how the various lectures enriched the discussion beyond stating the fact of racial/ethnic disparities and dug into the nuances on how to think about and address these disparities. She particularly appreciated discussion about the need to go out of the way to recruit diverse patient populations for clinical trials while also providing them care.

“It is definitely complicated, but it’s not impossible for an individual neurologist or an individual department to do something to reduce some of the disparities,” Dr. Mendizabal said. “It starts with just knowing that they exist and being aware of some of the things that may be impacting care for a particular patient.”
 

Tools to counter disparity

In the final presentation, Amy Kind, MD, PhD, the associate dean for social health sciences and programs at the University of Wisconsin–Madison, rounded out the discussion by exploring social determinants of health and their influence on outcomes.

“Social determinants impact brain health, and brain health is not distributed equally,” Dr. Kind told attendees. “We have known this for decades, yet disparities persist.”

Dr. Kind described the “exposome,” a “measure of all the exposures of an individual in a lifetime and how those exposures relate to health,” according to the CDC, and then introduced a tool clinicians can use to better understand social determinants of health in specific geographic areas. The Neighborhood Atlas, which Dr. Kind described in the New England Journal of Medicine in 2018, measures 17 social determinants across small population-sensitive areas and provides an area deprivation index. A high area deprivation index is linked to a range of negative outcomes, including reshopitalization, later diagnoses, less comprehensive diagnostic evaluation, increased risk of postsurgical complications, and decreased life expectancy.

“One of the things that really stood out to me about Dr. Kind’s discussion of the use of the area deprivation index was the fact that understanding and quantifying these kinds of risks and exposures is the vehicle for creating the kinds of social changes, including policy changes, that will actually lead to addressing and mitigating some of these lifelong risks and exposures,” Dr. Hamilton said. “It is implausible to think that a specific group of people would be genetically more susceptible to basically every disease that we know,” he added. “It makes much more sense to think that groups of individuals have been subjected systematically to conditions that impair health in a variety of ways.”
 

Not just race, ethnicity, sex, and gender

Following the four presentations from researchers in health inequities was an Emerging Scholar presentation in which Jay B. Lusk, an MD/MBA candidate at Duke University, Durham, N.C., shared new research findings on the role of neighborhood disadvantage in predicting mortality from coma, stroke, and other neurologic conditions. His findings revealed that living in a neighborhood with greater deprivation substantially increased risk of mortality even after accounting for individual wealth and demographics.

Maria Eugenia Diaz-Ortiz, PhD, of the department of neurology, University of Pennsylvania, Philadelphia, said she found the five presentations to be an excellent introduction to people like herself who are in the earlier stages of learning about health equity research.

“I think they introduced various important concepts and frameworks and provided tools for people who don’t know about them,” Dr. Diaz-Ortiz said. “Then they asked important questions and provided some solutions to them.”

Dr. Diaz-Ortiz also appreciated seemingly minor but actually important details in how the speakers presented themselves, such as Dr. Rivera-Mindt opening with a land acknowledgment and her disclosures of “positionality.” The former recognized the traditional Native American custodians of the land on which she lives and works, and the latter revealed details about her as an individual – such as being the Afro-Latinx daughter of immigrants yet being cisgender, able-bodied, and U.S.-born – that show where she falls on the axis of adversity and axis of privilege.
 

Implications for research

The biggest takeaway for Dr. Diaz-Ortiz, however, came from the first Q&A session when someone asked how to increase underrepresented populations in dementia research. Dr. Rivera-Mindt described her experience engaging these communities by employing “community-based participatory research practices, which involves making yourself a part of the community and making the community active participants in the research,” Dr. Diaz-Ortiz said. “It’s an evidence-based approach that has been shown to increase participation in research not only in her work but in the work of others.”

Preaching to the choir

Dr. Diaz-Ortiz was pleased overall with the plenary but disappointed in its placement at the end of the meeting, when attendance is always lower as attendees head home.

“The people who stayed were people who already know and recognize the value of health equity work, so I think that was a missed opportunity where the session could have been included on day one or two to boost attendance and also to educate like a broader group of neurologists,” Dr. Diaz-Ortiz said in an interview.

Dr. Mendizabal felt similarly, appreciating the plenary but noting it was “definitely overdue” and that it should not be the last session. Instead, sessions on health equity should be as easy as possible to attend to bring in larger audiences. “Perhaps having that session on a Saturday or Sunday would have a higher likelihood of greater attendance than on a Tuesday,” she said. That said, Dr. Mendizabal also noticed that greater attention to health care disparities was woven into many other sessions throughout the conference, which is “the best way of addressing health equity instead of trying to just designate a session,” she said.

Dr. Mendizabal hopes that plenaries like this one and the weaving of health equity issues into presentations throughout neurology conferences continue.

“After the racial reckoning in 2020, there was a big impetus and a big wave of energy in addressing health disparities in the field, and I hope that that momentum is not starting to wane,” Dr. Mendizabal said. “It’s important because not talking about is not going to make this issue go away.”

Dr. Hamilton agreed that it is important that the conversation continue and that physicians recognize the importance of understanding health care disparities and determinants of health, regardless of where they fall on the political spectrum or whether they choose to get involved in policy or advocacy.

“Irrespective of whether you think race or ethnicity or socioeconomic status are political issues or not, it is the case that you’re obligated to have an objective understanding of the factors that contribute to your patient’s health and as points of intervention,” Dr. Hamilton said. “So even if you don’t want to sit down and jot off that email to your senator, you still have to take these factors into account when you’re treating the person who’s sitting right in front of you, and that’s not political. That’s the promise of being a physician.”

Dr. Amezcua has received personal compensation for consulting, speaking, or serving on steering committees or advisory boards for Biogen Idec, Novartis, Genentech, and EMD Serono, and she has received research support from Biogen Idec and Bristol Myers Squibb Foundation. Dr. Kind reported support from the Alzheimer’s Association. Dr. Diaz-Ortiz is coinventor of a provisional patent submitted by the University of Pennsylvania that relates to a potential therapeutic in Parkinson’s disease. Mr. Lusk reported fellowship support from American Heart Association and travel support from the American Neurological Association. No other speakers or sources had relevant disclosures.
 

In early September, about a week after recovering from COVID-19, Barri Sanders went to the bank to pay a bill. But by mistake, she transferred a large amount of money from the wrong account.

“I’m talking about $20,000,” she said. “I had to go back [later] and fix it.”

Ms. Sanders, 83, had not had confusion like that before. Suddenly, the Albuquerque, N.M., resident found herself looking up from a book and not remembering what she had just read. She would stand up from her chair and forget what she meant to do.

“I kind of thought it was just the aging process,” she said. Combined with sudden balance issues, insomnia, and a nagging postnasal drip, the overall effect was “subtle, but scary,” she said.

After 5 days of this, she went to bed and slept the whole night through. She woke up in the morning to find her balanced restored, her sinuses clear, and the mental fog gone. What she’d had, she realized, wasn’t a rapid start of dementia, but rather a mercifully short form of long COVID.

Somewhere between 22% and 32% of people who recover from COVID-19 get “brain fog,” a nonscientific term used to describe slow or sluggish thinking. While this is disturbing at any age, it can be particularly upsetting to older patients and their caregivers, who fear they’re having or witnessing not just an after-effect of a disease, but the start of a permanent loss of thinking skills. And some scientists are starting to confirm what doctors, patients, and their families can already see: Older patients who have had COVID-19 have a higher risk of getting dementia or, if they already have mental confusion, the illness may worsen their condition.

British scientists who studied medical records from around the world reported in the journal The Lancet Psychiatry that people who recovered from COVID-19 had a higher risk of problems with their thinking and dementia even after 2 years had passed.

Another 2022 study, published in JAMA Neurology, looked at older COVID-19 patients for a year after they were discharged from hospitals in Wuhan, China. Compared with uninfected people, those who survived a severe case of COVID-19 were at higher risk for early onset, late-onset, and progressive decline in their thinking skills. Those who survived a mild infection were at a higher risk for early onset decline, the study found.

Eran Metzger, MD, assistant professor of psychiatry at Beth Israel Deaconess Medical Center in Boston, said he’s noticed that COVID-19 makes some older patients confused, and their brains don’t regain their former clarity.

“We see a stepwise decline in their cognition during the COVID episode, and then they never get back up to their baseline,” said Dr. Metzger, medical director at Hebrew SeniorLife.

New research is beginning to back up such findings.

People who got COVID-19 were twice as likely to receive a diagnosis of Alzheimer’s disease in the 12 months after infection, compared to those who didn’t get COVID, according to a study published in the journal Nature Medicine , which analyzed the health care databases of the U.S. Department of Veterans Affairs.

Joshua Cahan, MD, a cognitive neurologist at Northwestern University, Chicago, advises caution about applying such a specific label simply from a patient’s medical chart. After all, he noted, few patients get tested to confirm that they have the proteins linked to Alzheimer’s.

“Probably the most appropriate conclusion from that is that there’s an increased risk of dementia after a COVID infection,” he said, “but we don’t know whether it’s truly Alzheimer’s disease or not.”

There could be a number of reasons why COVID-19 triggers a decline in thinking skills, says Michelle Monje, MD, a neuroscientist and neuro-oncologist at Stanford (Calif.) University.

In a paper published in the journal Neuron, Dr. Monje and her coauthor, Akiko Iwasaki, PhD, professor of immunobiology at Yale University, New Haven, Conn., propose possible triggers for brain fog caused by COVID: inflammation in the lungs and respiratory passages that leads to inflammation and dysregulation of the central nervous system; autoimmune reactions that damage the central nervous system; brain infection directly caused by the coronavirus (though, they note, this appears rare); a reactivation of an Epstein-Barr virus, which can lead to neuroinflammation; triggered by the coronavirus; and/or complications from severe cases of COVID-19, possibly involving periods of low blood oxygen and multi-organ failure.

Scientific understanding of brain fog is “part of an emerging picture that inflammation elsewhere in the body can be transmitted to become inflammation in the brain,” Dr. Monje said. “And once there’s inflammation in the brain … that can dysregulate other cell types that normally support healthy cognitive function.”

One issue with the concept of brain fog is that, like the term itself, the condition can be tough to define for doctors and patients alike and difficult, if not impossible, to capture on common cognition tests.

These days, patients often arrive at the Center of Excellence for Alzheimer’s Disease, in Syracuse, N.Y., complaining that they “don’t feel the same” as they did before contracting COVID-19, said Sharon Brangman, MD, the center’s director and the chair of the geriatrics department at Upstate Medical University.

But the evidence of diminished cognition just isn’t there.

“There’s nothing that we can find, objectively, that’s wrong with them,” she said. “They’re not severe enough to score low on mental status testing.”

But specialized, directed testing can find some probable signs, said Dr. Cahan, who evaluates patient cognition in a long COVID clinic at Northwestern University.

He often finds that his long COVID patients score in the low normal range on cognitive testing.

“Patients do have a complaint that something’s changed, and we don’t have prior testing,” he said. “So it’s possible that they were maybe in the high normal range or the superior range, but you just don’t know.”

He said he has seen very high-performing people, such as lawyers, executives, PhDs, and other professionals, who have tests that might be interpreted as normal, but given their level of achievement, “you would expect [higher scores].”

Like Ms. Sanders, many of those who do have muddled thinking after a COVID infection return to their former mental status. A study published in the journal Brain Communications  found that people who had recovered from COVID-19, even if they had a mild illness, were significantly more likely to have memory and other cognition issues in the months after infection. But after 9 months, the former COVID patients had returned to their normal level of cognition, the team at Britain’s University of Oxford reported.

Notably, though, the average age of the people in the study was 28.6.

At the Northwestern clinic, Dr. Cahan treats patients who have struggled with COVID-induced cognition issues for months or even years. A rehabilitation program involves working with patients to come up with ways to compensate for cognitive deficits – such as making lists – as well as brain exercises, Dr. Cahan said. Over time, patients may achieve a 75% to 85% improvement, he said.

Dr. Monje hopes that one day, science will come up with ways to fully reverse the decline.

“I think what is likely the most common contributor to brain fog is this neuroinflammation, causing dysfunction of other cell types,” she said. “And, at least in the laboratory, we can rescue that in mouse models of chemotherapy brain fog, which gives me hope that we can rescue that for people.”
 

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

In early September, about a week after recovering from COVID-19, Barri Sanders went to the bank to pay a bill. But by mistake, she transferred a large amount of money from the wrong account.

“I’m talking about $20,000,” she said. “I had to go back [later] and fix it.”

Ms. Sanders, 83, had not had confusion like that before. Suddenly, the Albuquerque, N.M., resident found herself looking up from a book and not remembering what she had just read. She would stand up from her chair and forget what she meant to do.

“I kind of thought it was just the aging process,” she said. Combined with sudden balance issues, insomnia, and a nagging postnasal drip, the overall effect was “subtle, but scary,” she said.

After 5 days of this, she went to bed and slept the whole night through. She woke up in the morning to find her balanced restored, her sinuses clear, and the mental fog gone. What she’d had, she realized, wasn’t a rapid start of dementia, but rather a mercifully short form of long COVID.

Somewhere between 22% and 32% of people who recover from COVID-19 get “brain fog,” a nonscientific term used to describe slow or sluggish thinking. While this is disturbing at any age, it can be particularly upsetting to older patients and their caregivers, who fear they’re having or witnessing not just an after-effect of a disease, but the start of a permanent loss of thinking skills. And some scientists are starting to confirm what doctors, patients, and their families can already see: Older patients who have had COVID-19 have a higher risk of getting dementia or, if they already have mental confusion, the illness may worsen their condition.

British scientists who studied medical records from around the world reported in the journal The Lancet Psychiatry that people who recovered from COVID-19 had a higher risk of problems with their thinking and dementia even after 2 years had passed.

Another 2022 study, published in JAMA Neurology, looked at older COVID-19 patients for a year after they were discharged from hospitals in Wuhan, China. Compared with uninfected people, those who survived a severe case of COVID-19 were at higher risk for early onset, late-onset, and progressive decline in their thinking skills. Those who survived a mild infection were at a higher risk for early onset decline, the study found.

Eran Metzger, MD, assistant professor of psychiatry at Beth Israel Deaconess Medical Center in Boston, said he’s noticed that COVID-19 makes some older patients confused, and their brains don’t regain their former clarity.

“We see a stepwise decline in their cognition during the COVID episode, and then they never get back up to their baseline,” said Dr. Metzger, medical director at Hebrew SeniorLife.

New research is beginning to back up such findings.

People who got COVID-19 were twice as likely to receive a diagnosis of Alzheimer’s disease in the 12 months after infection, compared to those who didn’t get COVID, according to a study published in the journal Nature Medicine , which analyzed the health care databases of the U.S. Department of Veterans Affairs.

Joshua Cahan, MD, a cognitive neurologist at Northwestern University, Chicago, advises caution about applying such a specific label simply from a patient’s medical chart. After all, he noted, few patients get tested to confirm that they have the proteins linked to Alzheimer’s.

“Probably the most appropriate conclusion from that is that there’s an increased risk of dementia after a COVID infection,” he said, “but we don’t know whether it’s truly Alzheimer’s disease or not.”

There could be a number of reasons why COVID-19 triggers a decline in thinking skills, says Michelle Monje, MD, a neuroscientist and neuro-oncologist at Stanford (Calif.) University.

In a paper published in the journal Neuron, Dr. Monje and her coauthor, Akiko Iwasaki, PhD, professor of immunobiology at Yale University, New Haven, Conn., propose possible triggers for brain fog caused by COVID: inflammation in the lungs and respiratory passages that leads to inflammation and dysregulation of the central nervous system; autoimmune reactions that damage the central nervous system; brain infection directly caused by the coronavirus (though, they note, this appears rare); a reactivation of an Epstein-Barr virus, which can lead to neuroinflammation; triggered by the coronavirus; and/or complications from severe cases of COVID-19, possibly involving periods of low blood oxygen and multi-organ failure.

Scientific understanding of brain fog is “part of an emerging picture that inflammation elsewhere in the body can be transmitted to become inflammation in the brain,” Dr. Monje said. “And once there’s inflammation in the brain … that can dysregulate other cell types that normally support healthy cognitive function.”

One issue with the concept of brain fog is that, like the term itself, the condition can be tough to define for doctors and patients alike and difficult, if not impossible, to capture on common cognition tests.

These days, patients often arrive at the Center of Excellence for Alzheimer’s Disease, in Syracuse, N.Y., complaining that they “don’t feel the same” as they did before contracting COVID-19, said Sharon Brangman, MD, the center’s director and the chair of the geriatrics department at Upstate Medical University.

But the evidence of diminished cognition just isn’t there.

“There’s nothing that we can find, objectively, that’s wrong with them,” she said. “They’re not severe enough to score low on mental status testing.”

But specialized, directed testing can find some probable signs, said Dr. Cahan, who evaluates patient cognition in a long COVID clinic at Northwestern University.

He often finds that his long COVID patients score in the low normal range on cognitive testing.

“Patients do have a complaint that something’s changed, and we don’t have prior testing,” he said. “So it’s possible that they were maybe in the high normal range or the superior range, but you just don’t know.”

He said he has seen very high-performing people, such as lawyers, executives, PhDs, and other professionals, who have tests that might be interpreted as normal, but given their level of achievement, “you would expect [higher scores].”

Like Ms. Sanders, many of those who do have muddled thinking after a COVID infection return to their former mental status. A study published in the journal Brain Communications  found that people who had recovered from COVID-19, even if they had a mild illness, were significantly more likely to have memory and other cognition issues in the months after infection. But after 9 months, the former COVID patients had returned to their normal level of cognition, the team at Britain’s University of Oxford reported.

Notably, though, the average age of the people in the study was 28.6.

At the Northwestern clinic, Dr. Cahan treats patients who have struggled with COVID-induced cognition issues for months or even years. A rehabilitation program involves working with patients to come up with ways to compensate for cognitive deficits – such as making lists – as well as brain exercises, Dr. Cahan said. Over time, patients may achieve a 75% to 85% improvement, he said.

Dr. Monje hopes that one day, science will come up with ways to fully reverse the decline.

“I think what is likely the most common contributor to brain fog is this neuroinflammation, causing dysfunction of other cell types,” she said. “And, at least in the laboratory, we can rescue that in mouse models of chemotherapy brain fog, which gives me hope that we can rescue that for people.”
 

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

In early September, about a week after recovering from COVID-19, Barri Sanders went to the bank to pay a bill. But by mistake, she transferred a large amount of money from the wrong account.

“I’m talking about $20,000,” she said. “I had to go back [later] and fix it.”

Ms. Sanders, 83, had not had confusion like that before. Suddenly, the Albuquerque, N.M., resident found herself looking up from a book and not remembering what she had just read. She would stand up from her chair and forget what she meant to do.

“I kind of thought it was just the aging process,” she said. Combined with sudden balance issues, insomnia, and a nagging postnasal drip, the overall effect was “subtle, but scary,” she said.

After 5 days of this, she went to bed and slept the whole night through. She woke up in the morning to find her balanced restored, her sinuses clear, and the mental fog gone. What she’d had, she realized, wasn’t a rapid start of dementia, but rather a mercifully short form of long COVID.

Somewhere between 22% and 32% of people who recover from COVID-19 get “brain fog,” a nonscientific term used to describe slow or sluggish thinking. While this is disturbing at any age, it can be particularly upsetting to older patients and their caregivers, who fear they’re having or witnessing not just an after-effect of a disease, but the start of a permanent loss of thinking skills. And some scientists are starting to confirm what doctors, patients, and their families can already see: Older patients who have had COVID-19 have a higher risk of getting dementia or, if they already have mental confusion, the illness may worsen their condition.

British scientists who studied medical records from around the world reported in the journal The Lancet Psychiatry that people who recovered from COVID-19 had a higher risk of problems with their thinking and dementia even after 2 years had passed.

Another 2022 study, published in JAMA Neurology, looked at older COVID-19 patients for a year after they were discharged from hospitals in Wuhan, China. Compared with uninfected people, those who survived a severe case of COVID-19 were at higher risk for early onset, late-onset, and progressive decline in their thinking skills. Those who survived a mild infection were at a higher risk for early onset decline, the study found.

Eran Metzger, MD, assistant professor of psychiatry at Beth Israel Deaconess Medical Center in Boston, said he’s noticed that COVID-19 makes some older patients confused, and their brains don’t regain their former clarity.

“We see a stepwise decline in their cognition during the COVID episode, and then they never get back up to their baseline,” said Dr. Metzger, medical director at Hebrew SeniorLife.

New research is beginning to back up such findings.

People who got COVID-19 were twice as likely to receive a diagnosis of Alzheimer’s disease in the 12 months after infection, compared to those who didn’t get COVID, according to a study published in the journal Nature Medicine , which analyzed the health care databases of the U.S. Department of Veterans Affairs.

Joshua Cahan, MD, a cognitive neurologist at Northwestern University, Chicago, advises caution about applying such a specific label simply from a patient’s medical chart. After all, he noted, few patients get tested to confirm that they have the proteins linked to Alzheimer’s.

“Probably the most appropriate conclusion from that is that there’s an increased risk of dementia after a COVID infection,” he said, “but we don’t know whether it’s truly Alzheimer’s disease or not.”

There could be a number of reasons why COVID-19 triggers a decline in thinking skills, says Michelle Monje, MD, a neuroscientist and neuro-oncologist at Stanford (Calif.) University.

In a paper published in the journal Neuron, Dr. Monje and her coauthor, Akiko Iwasaki, PhD, professor of immunobiology at Yale University, New Haven, Conn., propose possible triggers for brain fog caused by COVID: inflammation in the lungs and respiratory passages that leads to inflammation and dysregulation of the central nervous system; autoimmune reactions that damage the central nervous system; brain infection directly caused by the coronavirus (though, they note, this appears rare); a reactivation of an Epstein-Barr virus, which can lead to neuroinflammation; triggered by the coronavirus; and/or complications from severe cases of COVID-19, possibly involving periods of low blood oxygen and multi-organ failure.

Scientific understanding of brain fog is “part of an emerging picture that inflammation elsewhere in the body can be transmitted to become inflammation in the brain,” Dr. Monje said. “And once there’s inflammation in the brain … that can dysregulate other cell types that normally support healthy cognitive function.”

One issue with the concept of brain fog is that, like the term itself, the condition can be tough to define for doctors and patients alike and difficult, if not impossible, to capture on common cognition tests.

These days, patients often arrive at the Center of Excellence for Alzheimer’s Disease, in Syracuse, N.Y., complaining that they “don’t feel the same” as they did before contracting COVID-19, said Sharon Brangman, MD, the center’s director and the chair of the geriatrics department at Upstate Medical University.

But the evidence of diminished cognition just isn’t there.

“There’s nothing that we can find, objectively, that’s wrong with them,” she said. “They’re not severe enough to score low on mental status testing.”

But specialized, directed testing can find some probable signs, said Dr. Cahan, who evaluates patient cognition in a long COVID clinic at Northwestern University.

He often finds that his long COVID patients score in the low normal range on cognitive testing.

“Patients do have a complaint that something’s changed, and we don’t have prior testing,” he said. “So it’s possible that they were maybe in the high normal range or the superior range, but you just don’t know.”

He said he has seen very high-performing people, such as lawyers, executives, PhDs, and other professionals, who have tests that might be interpreted as normal, but given their level of achievement, “you would expect [higher scores].”

Like Ms. Sanders, many of those who do have muddled thinking after a COVID infection return to their former mental status. A study published in the journal Brain Communications  found that people who had recovered from COVID-19, even if they had a mild illness, were significantly more likely to have memory and other cognition issues in the months after infection. But after 9 months, the former COVID patients had returned to their normal level of cognition, the team at Britain’s University of Oxford reported.

Notably, though, the average age of the people in the study was 28.6.

At the Northwestern clinic, Dr. Cahan treats patients who have struggled with COVID-induced cognition issues for months or even years. A rehabilitation program involves working with patients to come up with ways to compensate for cognitive deficits – such as making lists – as well as brain exercises, Dr. Cahan said. Over time, patients may achieve a 75% to 85% improvement, he said.

Dr. Monje hopes that one day, science will come up with ways to fully reverse the decline.

“I think what is likely the most common contributor to brain fog is this neuroinflammation, causing dysfunction of other cell types,” she said. “And, at least in the laboratory, we can rescue that in mouse models of chemotherapy brain fog, which gives me hope that we can rescue that for people.”
 

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

One night, at the beginning of Thanksgiving week, my son called from his place across town. His car was having trouble starting, so I went to see what was up.

I got to his place to find his car wouldn’t start, even though the battery was only a few months old. I used my car to jump his, left him mine, and headed back. My plan was to leave it at our usual repair place and walk home.

Easier said than done.

I’d just gotten on the 101, the main loop freeway for the Phoenix metro area, when his car completely died. The lights flickered, the gauges stopped working, and then the engine cut out. Mercifully I was able to pull over into the right emergency lane as it did so. I was nowhere near an exit.

Not even the emergency flashers worked. It was dark. I was on a major freeway. I couldn’t make myself visible. Cars and trucks were whizzing by 2-3 feet to my left, and I was hoping they’d see me.

I called AAA and explained the situation. They were sending a tow truck, but it could take up to another 3 hours. I sent some quick texts to family to let them know what was up. I called the AZ highway patrol to let them know my predicament, in case they wanted to come put a flare or two behind me (they didn’t).

And then I settled in. Seatbelt on, staring at the road in front of me ... and had nothing to do.

When was the last time you had absolutely nothing to do?

It’s pretty rare these days. I mean, we all have breaks in the action, so we watch a cute animal video, or play a round of Wordle, or whatever.

But I had none of that. No books, iPad, or computer. Sure, I had my phone, but it was less than 50% charged with no way to charge it, and so I wanted to conserve that in case I needed it.

I don’t think I’ve ever had a moment like this since I began carrying a phone in 1998. There was, literally, nothing to do but wait. I couldn’t even try to nod off with the seat unadjustable and cars whizzing by.

So my mind wandered, and I thought. I turned over office cases. I went through year-end finances. I thought about my current predicament. I stared endlessly at the road ahead and cars passing me.

At some point I began to realize that I’m actually pretty lucky, and that nothing was nearly as bad as it had seemed earlier in the day. As the initial adrenaline rush drained out of me I calmed down and the things I’d been worrying about that afternoon seemed workable.

The tow truck pulled in front of me, ending my reverie. Mercifully, it had only taken them an hour. I was home 45 minutes later.

I was thankful to be home and I was thankful that nothing more serious had happened in a potentially bad situation.

And, somewhere in there, I was glad to be reminded that having nothing to do but think for a while can be a good thing.

In today’s world of endless screens and texts and calls and notifications, it’s easy to lose track of that.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

One night, at the beginning of Thanksgiving week, my son called from his place across town. His car was having trouble starting, so I went to see what was up.

I got to his place to find his car wouldn’t start, even though the battery was only a few months old. I used my car to jump his, left him mine, and headed back. My plan was to leave it at our usual repair place and walk home.

Easier said than done.

I’d just gotten on the 101, the main loop freeway for the Phoenix metro area, when his car completely died. The lights flickered, the gauges stopped working, and then the engine cut out. Mercifully I was able to pull over into the right emergency lane as it did so. I was nowhere near an exit.

Not even the emergency flashers worked. It was dark. I was on a major freeway. I couldn’t make myself visible. Cars and trucks were whizzing by 2-3 feet to my left, and I was hoping they’d see me.

I called AAA and explained the situation. They were sending a tow truck, but it could take up to another 3 hours. I sent some quick texts to family to let them know what was up. I called the AZ highway patrol to let them know my predicament, in case they wanted to come put a flare or two behind me (they didn’t).

And then I settled in. Seatbelt on, staring at the road in front of me ... and had nothing to do.

When was the last time you had absolutely nothing to do?

It’s pretty rare these days. I mean, we all have breaks in the action, so we watch a cute animal video, or play a round of Wordle, or whatever.

But I had none of that. No books, iPad, or computer. Sure, I had my phone, but it was less than 50% charged with no way to charge it, and so I wanted to conserve that in case I needed it.

I don’t think I’ve ever had a moment like this since I began carrying a phone in 1998. There was, literally, nothing to do but wait. I couldn’t even try to nod off with the seat unadjustable and cars whizzing by.

So my mind wandered, and I thought. I turned over office cases. I went through year-end finances. I thought about my current predicament. I stared endlessly at the road ahead and cars passing me.

At some point I began to realize that I’m actually pretty lucky, and that nothing was nearly as bad as it had seemed earlier in the day. As the initial adrenaline rush drained out of me I calmed down and the things I’d been worrying about that afternoon seemed workable.

The tow truck pulled in front of me, ending my reverie. Mercifully, it had only taken them an hour. I was home 45 minutes later.

I was thankful to be home and I was thankful that nothing more serious had happened in a potentially bad situation.

And, somewhere in there, I was glad to be reminded that having nothing to do but think for a while can be a good thing.

In today’s world of endless screens and texts and calls and notifications, it’s easy to lose track of that.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

One night, at the beginning of Thanksgiving week, my son called from his place across town. His car was having trouble starting, so I went to see what was up.

I got to his place to find his car wouldn’t start, even though the battery was only a few months old. I used my car to jump his, left him mine, and headed back. My plan was to leave it at our usual repair place and walk home.

Easier said than done.

I’d just gotten on the 101, the main loop freeway for the Phoenix metro area, when his car completely died. The lights flickered, the gauges stopped working, and then the engine cut out. Mercifully I was able to pull over into the right emergency lane as it did so. I was nowhere near an exit.

Not even the emergency flashers worked. It was dark. I was on a major freeway. I couldn’t make myself visible. Cars and trucks were whizzing by 2-3 feet to my left, and I was hoping they’d see me.

I called AAA and explained the situation. They were sending a tow truck, but it could take up to another 3 hours. I sent some quick texts to family to let them know what was up. I called the AZ highway patrol to let them know my predicament, in case they wanted to come put a flare or two behind me (they didn’t).

And then I settled in. Seatbelt on, staring at the road in front of me ... and had nothing to do.

When was the last time you had absolutely nothing to do?

It’s pretty rare these days. I mean, we all have breaks in the action, so we watch a cute animal video, or play a round of Wordle, or whatever.

But I had none of that. No books, iPad, or computer. Sure, I had my phone, but it was less than 50% charged with no way to charge it, and so I wanted to conserve that in case I needed it.

I don’t think I’ve ever had a moment like this since I began carrying a phone in 1998. There was, literally, nothing to do but wait. I couldn’t even try to nod off with the seat unadjustable and cars whizzing by.

So my mind wandered, and I thought. I turned over office cases. I went through year-end finances. I thought about my current predicament. I stared endlessly at the road ahead and cars passing me.

At some point I began to realize that I’m actually pretty lucky, and that nothing was nearly as bad as it had seemed earlier in the day. As the initial adrenaline rush drained out of me I calmed down and the things I’d been worrying about that afternoon seemed workable.

The tow truck pulled in front of me, ending my reverie. Mercifully, it had only taken them an hour. I was home 45 minutes later.

I was thankful to be home and I was thankful that nothing more serious had happened in a potentially bad situation.

And, somewhere in there, I was glad to be reminded that having nothing to do but think for a while can be a good thing.

In today’s world of endless screens and texts and calls and notifications, it’s easy to lose track of that.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

People living with HIV (PLWH) had a “mistimed circadian phase” and a shorter night’s sleep compared with HIV-negative individuals with a similar lifestyle, according to findings that suggest both a possible mechanism for increased comorbidities in PLWH and potential solutions.

“It is very well known that sleep problems are common in people living with HIV, and many different reasons for this have been proposed,” coauthor Malcolm von Schantz, PhD, professor of chronobiology at Northumbria University in Newcastle upon Tyne, England, said in an interview. “But the novelty of our findings is the observation of delayed circadian rhythms.”

The mistimed circadian phase in PLWH is linked to later sleep onset and earlier waking and has “important potential implications” for the health and well-being of PLWH, wrote senior author Karine Scheuermaier, MD, from the University of the Witwatersrand, in Johannesburg, South Africa, and coauthors.

Until now, research on sleep in HIV has focused primarily on its homeostatic components, such as sleep duration and staging, rather than on circadian-related aspects, they noted.

“If the lifestyle‐independent circadian misalignment observed in the current study is confirmed to be a constant feature of chronic HIV infection, then it may be a mediator both of poorer sleep health and of poorer physical health in PLWH, which could potentially be alleviated through light therapy or chronobiotic medication or supplements,” they suggested.
 

HIV endemic in study population

The study analyzed a random sample of 187 participants (36 with HIV and 151 without) in the HAALSI (Health and Ageing in Africa: A Longitudinal Study of an INDEPTH Community in South Africa) study, which is part of the Agincourt Health and Socio-demographic Surveillance System.

The study population ranged in age from 45 to 93 years, with an average age of 60.6 years in the HIV-positive group and 68.2 years in the HIV-negative group. Demographic data, Pittsburgh Sleep Quality Index score, and valid actigraphy (measured with an accelerometer for 14 consecutive days) were available for 172 participants (18% with HIV). A subgroup of 51 participants (22% with HIV) also had valid dim light melatonin onset (DLMO) data, a sensitive measure of the internal circadian clock. DLMO was measured for a minimum of 5 consecutive days with hourly saliva sampling between 5 p.m. and 11 p.m. while sitting in a dimly lit room.

In 36 participants (16% with HIV) with both valid actigraphy and DLMO data, circadian phase angle of entrainment was calculated by subtracting DLMO time from habitual sleep-onset time obtained from actigraphy.

After adjustment for age and sex, the study found a slightly later sleep onset (adjusted average delay of 10 minutes), earlier awakening (adjusted average advance of 10 minutes), and shorter sleep duration in PLWH compared with HIV-negative participants.

At the same time, melatonin production in PLWH started more than an hour later on average than in HIV-negative participants, “with half of the HIV+ group having an earlier habitual sleep onset than DLMO time” the authors wrote. In a subgroup of 36 participants with both valid actigraphy and DLMO data, the median circadian phase angle of entrainment was smaller in PLWH (–6 minutes vs. +1 hour 25 minutes in the HIV-negative group).

“Collectively, our data suggest that the sleep phase occurred earlier than what would be biologically optimal among the HIV+ participants,” they added.
 

Asynchrony between bedtime and circadian time

“Ideally, with this delayed timing of circadian phase, they should have delayed their sleep phase (sleep timing) by an equal amount to be sleeping at their optimal biological time,” Dr. Scheuermaier explained. “Their sleep onset was delayed by 12 minutes (statistically significant but biologically not that much) while their circadian phase was delayed by more than an hour.”

Possible consequences of a smaller phase angle of entrainment include difficulty in initiating and maintaining sleep, the authors wrote. “The shorter, potentially mistimed sleep relative to the endogenous circadian cycle observed in this study provides objectively measured evidence supporting the abundant previous subjective reports of poor sleep quality and insomnia in PLWH.”

They noted that a strength of their study is that participants were recruited from rural South Africa, where HIV prevalence is not confined to the so-called “high-risk” groups of gay men, other men who have sex with men, people who inject drugs, and sex workers.

“Behavioral factors associated with belonging to one or more of these groups would be strong potential confounders for studies of sleep and circadian phase,” they explained. “By contrast, in rural southern Africa, the epidemic has been less demographically discriminating ... There are no notable differences in lifestyle between the HIV– and HIV+ individuals in this study. The members of this aging population are mostly beyond retirement age, living quiet, rural lives supported by government remittances and subsistence farming.”
 

Direct evidence warrants further study

The study is “unique” in that it provides “the first direct evidence for potential circadian disturbances in PWLH,” agreed Peng Li, PhD, who was not involved in the study.

“The assessment of dim light melatonin onset in PLWH is a strength of the study; together with actigraphy-based sleep onset assessment, it provides a measure for the phase angle of entrainment,” said Dr. Li, who is research director of the medical biodynamics program, division of sleep and circadian disorders, Brigham and Women’s Hospital, Boston.

But actigraphy has limitations that affect the interpretation of the results, he told this news organization.

“Without the help of sleep diaries, low specificity in assessing sleep using actigraphy has been consistently reported,” he said. “The low specificity means a significant overestimation of sleep. This lowers the value of the reported sleep readouts and limits the validity of sleep onset estimation, especially considering that differences in sleep measures between the two groups are relatively small, compromising the clinical meaning.”

Additionally, he explained that it’s not clear whether sleep onset in the study participants was spontaneous or was “forced” to accommodate routines. “This is a limitation in field study as compared with in-lab studies,” he said.

Dr. Li also pointed to the small sample size and younger age of PLWH, suggesting the study might have benefited from a matched design. Finally, he said the study did not examine gender differences.

“In the general population, it is known that females usually have advanced circadian phase compared to males. ... More rigorous design and analyses based on sex/gender especially in this often-marginalized population are warranted to better inform HIV-specific or general clinical guidelines.”

The study was supported by the Academy of Medical Sciences. The authors did not mention any competing interests. Dr. Li reported grant support from the BrightFocus Foundation. The study is not directly related to this paper. He also receives grant support from the NIH through a Departmental Award, Harvard University Center for AIDS Research and a Pilot Project, HIV and Aging Research Consortium. The projects are on circadian disturbances and cognitive performance in PLWH.

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

People living with HIV (PLWH) had a “mistimed circadian phase” and a shorter night’s sleep compared with HIV-negative individuals with a similar lifestyle, according to findings that suggest both a possible mechanism for increased comorbidities in PLWH and potential solutions.

“It is very well known that sleep problems are common in people living with HIV, and many different reasons for this have been proposed,” coauthor Malcolm von Schantz, PhD, professor of chronobiology at Northumbria University in Newcastle upon Tyne, England, said in an interview. “But the novelty of our findings is the observation of delayed circadian rhythms.”

The mistimed circadian phase in PLWH is linked to later sleep onset and earlier waking and has “important potential implications” for the health and well-being of PLWH, wrote senior author Karine Scheuermaier, MD, from the University of the Witwatersrand, in Johannesburg, South Africa, and coauthors.

Until now, research on sleep in HIV has focused primarily on its homeostatic components, such as sleep duration and staging, rather than on circadian-related aspects, they noted.

“If the lifestyle‐independent circadian misalignment observed in the current study is confirmed to be a constant feature of chronic HIV infection, then it may be a mediator both of poorer sleep health and of poorer physical health in PLWH, which could potentially be alleviated through light therapy or chronobiotic medication or supplements,” they suggested.
 

HIV endemic in study population

The study analyzed a random sample of 187 participants (36 with HIV and 151 without) in the HAALSI (Health and Ageing in Africa: A Longitudinal Study of an INDEPTH Community in South Africa) study, which is part of the Agincourt Health and Socio-demographic Surveillance System.

The study population ranged in age from 45 to 93 years, with an average age of 60.6 years in the HIV-positive group and 68.2 years in the HIV-negative group. Demographic data, Pittsburgh Sleep Quality Index score, and valid actigraphy (measured with an accelerometer for 14 consecutive days) were available for 172 participants (18% with HIV). A subgroup of 51 participants (22% with HIV) also had valid dim light melatonin onset (DLMO) data, a sensitive measure of the internal circadian clock. DLMO was measured for a minimum of 5 consecutive days with hourly saliva sampling between 5 p.m. and 11 p.m. while sitting in a dimly lit room.

In 36 participants (16% with HIV) with both valid actigraphy and DLMO data, circadian phase angle of entrainment was calculated by subtracting DLMO time from habitual sleep-onset time obtained from actigraphy.

After adjustment for age and sex, the study found a slightly later sleep onset (adjusted average delay of 10 minutes), earlier awakening (adjusted average advance of 10 minutes), and shorter sleep duration in PLWH compared with HIV-negative participants.

At the same time, melatonin production in PLWH started more than an hour later on average than in HIV-negative participants, “with half of the HIV+ group having an earlier habitual sleep onset than DLMO time” the authors wrote. In a subgroup of 36 participants with both valid actigraphy and DLMO data, the median circadian phase angle of entrainment was smaller in PLWH (–6 minutes vs. +1 hour 25 minutes in the HIV-negative group).

“Collectively, our data suggest that the sleep phase occurred earlier than what would be biologically optimal among the HIV+ participants,” they added.
 

Asynchrony between bedtime and circadian time

“Ideally, with this delayed timing of circadian phase, they should have delayed their sleep phase (sleep timing) by an equal amount to be sleeping at their optimal biological time,” Dr. Scheuermaier explained. “Their sleep onset was delayed by 12 minutes (statistically significant but biologically not that much) while their circadian phase was delayed by more than an hour.”

Possible consequences of a smaller phase angle of entrainment include difficulty in initiating and maintaining sleep, the authors wrote. “The shorter, potentially mistimed sleep relative to the endogenous circadian cycle observed in this study provides objectively measured evidence supporting the abundant previous subjective reports of poor sleep quality and insomnia in PLWH.”

They noted that a strength of their study is that participants were recruited from rural South Africa, where HIV prevalence is not confined to the so-called “high-risk” groups of gay men, other men who have sex with men, people who inject drugs, and sex workers.

“Behavioral factors associated with belonging to one or more of these groups would be strong potential confounders for studies of sleep and circadian phase,” they explained. “By contrast, in rural southern Africa, the epidemic has been less demographically discriminating ... There are no notable differences in lifestyle between the HIV– and HIV+ individuals in this study. The members of this aging population are mostly beyond retirement age, living quiet, rural lives supported by government remittances and subsistence farming.”
 

Direct evidence warrants further study

The study is “unique” in that it provides “the first direct evidence for potential circadian disturbances in PWLH,” agreed Peng Li, PhD, who was not involved in the study.

“The assessment of dim light melatonin onset in PLWH is a strength of the study; together with actigraphy-based sleep onset assessment, it provides a measure for the phase angle of entrainment,” said Dr. Li, who is research director of the medical biodynamics program, division of sleep and circadian disorders, Brigham and Women’s Hospital, Boston.

But actigraphy has limitations that affect the interpretation of the results, he told this news organization.

“Without the help of sleep diaries, low specificity in assessing sleep using actigraphy has been consistently reported,” he said. “The low specificity means a significant overestimation of sleep. This lowers the value of the reported sleep readouts and limits the validity of sleep onset estimation, especially considering that differences in sleep measures between the two groups are relatively small, compromising the clinical meaning.”

Additionally, he explained that it’s not clear whether sleep onset in the study participants was spontaneous or was “forced” to accommodate routines. “This is a limitation in field study as compared with in-lab studies,” he said.

Dr. Li also pointed to the small sample size and younger age of PLWH, suggesting the study might have benefited from a matched design. Finally, he said the study did not examine gender differences.

“In the general population, it is known that females usually have advanced circadian phase compared to males. ... More rigorous design and analyses based on sex/gender especially in this often-marginalized population are warranted to better inform HIV-specific or general clinical guidelines.”

The study was supported by the Academy of Medical Sciences. The authors did not mention any competing interests. Dr. Li reported grant support from the BrightFocus Foundation. The study is not directly related to this paper. He also receives grant support from the NIH through a Departmental Award, Harvard University Center for AIDS Research and a Pilot Project, HIV and Aging Research Consortium. The projects are on circadian disturbances and cognitive performance in PLWH.

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

People living with HIV (PLWH) had a “mistimed circadian phase” and a shorter night’s sleep compared with HIV-negative individuals with a similar lifestyle, according to findings that suggest both a possible mechanism for increased comorbidities in PLWH and potential solutions.

“It is very well known that sleep problems are common in people living with HIV, and many different reasons for this have been proposed,” coauthor Malcolm von Schantz, PhD, professor of chronobiology at Northumbria University in Newcastle upon Tyne, England, said in an interview. “But the novelty of our findings is the observation of delayed circadian rhythms.”

The mistimed circadian phase in PLWH is linked to later sleep onset and earlier waking and has “important potential implications” for the health and well-being of PLWH, wrote senior author Karine Scheuermaier, MD, from the University of the Witwatersrand, in Johannesburg, South Africa, and coauthors.

Until now, research on sleep in HIV has focused primarily on its homeostatic components, such as sleep duration and staging, rather than on circadian-related aspects, they noted.

“If the lifestyle‐independent circadian misalignment observed in the current study is confirmed to be a constant feature of chronic HIV infection, then it may be a mediator both of poorer sleep health and of poorer physical health in PLWH, which could potentially be alleviated through light therapy or chronobiotic medication or supplements,” they suggested.
 

HIV endemic in study population

The study analyzed a random sample of 187 participants (36 with HIV and 151 without) in the HAALSI (Health and Ageing in Africa: A Longitudinal Study of an INDEPTH Community in South Africa) study, which is part of the Agincourt Health and Socio-demographic Surveillance System.

The study population ranged in age from 45 to 93 years, with an average age of 60.6 years in the HIV-positive group and 68.2 years in the HIV-negative group. Demographic data, Pittsburgh Sleep Quality Index score, and valid actigraphy (measured with an accelerometer for 14 consecutive days) were available for 172 participants (18% with HIV). A subgroup of 51 participants (22% with HIV) also had valid dim light melatonin onset (DLMO) data, a sensitive measure of the internal circadian clock. DLMO was measured for a minimum of 5 consecutive days with hourly saliva sampling between 5 p.m. and 11 p.m. while sitting in a dimly lit room.

In 36 participants (16% with HIV) with both valid actigraphy and DLMO data, circadian phase angle of entrainment was calculated by subtracting DLMO time from habitual sleep-onset time obtained from actigraphy.

After adjustment for age and sex, the study found a slightly later sleep onset (adjusted average delay of 10 minutes), earlier awakening (adjusted average advance of 10 minutes), and shorter sleep duration in PLWH compared with HIV-negative participants.

At the same time, melatonin production in PLWH started more than an hour later on average than in HIV-negative participants, “with half of the HIV+ group having an earlier habitual sleep onset than DLMO time” the authors wrote. In a subgroup of 36 participants with both valid actigraphy and DLMO data, the median circadian phase angle of entrainment was smaller in PLWH (–6 minutes vs. +1 hour 25 minutes in the HIV-negative group).

“Collectively, our data suggest that the sleep phase occurred earlier than what would be biologically optimal among the HIV+ participants,” they added.
 

Asynchrony between bedtime and circadian time

“Ideally, with this delayed timing of circadian phase, they should have delayed their sleep phase (sleep timing) by an equal amount to be sleeping at their optimal biological time,” Dr. Scheuermaier explained. “Their sleep onset was delayed by 12 minutes (statistically significant but biologically not that much) while their circadian phase was delayed by more than an hour.”

Possible consequences of a smaller phase angle of entrainment include difficulty in initiating and maintaining sleep, the authors wrote. “The shorter, potentially mistimed sleep relative to the endogenous circadian cycle observed in this study provides objectively measured evidence supporting the abundant previous subjective reports of poor sleep quality and insomnia in PLWH.”

They noted that a strength of their study is that participants were recruited from rural South Africa, where HIV prevalence is not confined to the so-called “high-risk” groups of gay men, other men who have sex with men, people who inject drugs, and sex workers.

“Behavioral factors associated with belonging to one or more of these groups would be strong potential confounders for studies of sleep and circadian phase,” they explained. “By contrast, in rural southern Africa, the epidemic has been less demographically discriminating ... There are no notable differences in lifestyle between the HIV– and HIV+ individuals in this study. The members of this aging population are mostly beyond retirement age, living quiet, rural lives supported by government remittances and subsistence farming.”
 

Direct evidence warrants further study

The study is “unique” in that it provides “the first direct evidence for potential circadian disturbances in PWLH,” agreed Peng Li, PhD, who was not involved in the study.

“The assessment of dim light melatonin onset in PLWH is a strength of the study; together with actigraphy-based sleep onset assessment, it provides a measure for the phase angle of entrainment,” said Dr. Li, who is research director of the medical biodynamics program, division of sleep and circadian disorders, Brigham and Women’s Hospital, Boston.

But actigraphy has limitations that affect the interpretation of the results, he told this news organization.

“Without the help of sleep diaries, low specificity in assessing sleep using actigraphy has been consistently reported,” he said. “The low specificity means a significant overestimation of sleep. This lowers the value of the reported sleep readouts and limits the validity of sleep onset estimation, especially considering that differences in sleep measures between the two groups are relatively small, compromising the clinical meaning.”

Additionally, he explained that it’s not clear whether sleep onset in the study participants was spontaneous or was “forced” to accommodate routines. “This is a limitation in field study as compared with in-lab studies,” he said.

Dr. Li also pointed to the small sample size and younger age of PLWH, suggesting the study might have benefited from a matched design. Finally, he said the study did not examine gender differences.

“In the general population, it is known that females usually have advanced circadian phase compared to males. ... More rigorous design and analyses based on sex/gender especially in this often-marginalized population are warranted to better inform HIV-specific or general clinical guidelines.”

The study was supported by the Academy of Medical Sciences. The authors did not mention any competing interests. Dr. Li reported grant support from the BrightFocus Foundation. The study is not directly related to this paper. He also receives grant support from the NIH through a Departmental Award, Harvard University Center for AIDS Research and a Pilot Project, HIV and Aging Research Consortium. The projects are on circadian disturbances and cognitive performance in PLWH.

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

When Mark Cucuzzella, MD, meets a new patient at the West Virginia Medical School clinic, he introduces himself as “Mark.” For one thing, says Dr. Cucuzzella, his last name is a mouthful. For another, the 56-year-old general practitioner asserts that getting on a first-name basis with his patients is integral to delivering the best care.

“I’m trying to break down the old paternalistic barriers of the doctor/patient relationship,” he says. “Titles create an environment where the doctors are making all the decisions and not involving the patient in any course of action.”

Aniruddh Setya, MD, has a different take on informality between patients and doctors: It’s not OK. “I am not your friend,” says the 35-year-old pediatrician from Florida-based KIDZ Medical Services. “There has to be a level of respect for the education and accomplishment of being a physician.”

The issue of “untitling” a doctor and failing to use their honorific is becoming increasingly common, according to a recent study published in JAMA Network Open. But that doesn’t mean most physicians support the practice. In fact, some doctors contend that it can be harmful, particularly to female physicians.

“My concern is that untitling (so termed by Amy Diehl, PhD, and Leanne Dzubinski, PhD) intrudes upon important professional boundaries and might be correlated with diminishing the value of someone’s time,” says Leah Witt, MD, a geriatrician at UCSF Health, San Francisco. Dr. Witt, along with colleague Lekshmi Santhosh, MD, a pulmonologist, offered commentary on the study results. “Studies have shown that women physicians get more patient portal messages, spend more time in the electronic health record, and have longer visits,” Dr. Witt said. “Dr. Santhosh and I wonder if untitling is a signifier of this diminished value of our time, and an assumption of increased ease of access leading to this higher workload.”

To compile the results reported in JAMA Network Open, Mayo Clinic researchers analyzed more than 90,000 emails from patients to doctors over the course of 3 years, beginning in 2018. Of those emails, more than 32% included the physician’s first name in greeting or salutation. For women physicians, the odds were twice as high that their titles would be omitted in the correspondence. The same holds true for doctors of osteopathic medicine (DOs) compared with MDs, and primary care physicians had similar odds for a title drop compared with specialists.

Dr. Witt says the findings are not surprising. “They match my experience as a woman in medicine, as Dr. Santhosh and I write in our commentary,” she says. “We think the findings could easily be replicated at other centers.”

Indeed, research on 321 speaker introductions at a medical rounds found that when female physicians introduced other physicians, they usually applied the doctor title. When the job of introducing colleagues fell to male physicians, however, the stats fell to 72.4% for male peers and only 49.2% when introducing female peers.

The Mayo Clinic study authors identified the pitfalls of patients who informally address their doctors. They wrote, “Untitling may have a negative impact on physicians, demonstrate lack of respect, and can lead to reduction in formality of the physician/patient relationship or workplace.”
 

Physician preferences vary

Although the results of the Mayo Clinic analysis didn’t and couldn’t address physician sentiments on patient informality, Dr. Setya observes that American culture is becoming less formal. “I’ve been practicing for over 10 years, and the number of people who consider doctors as equals is growing,” he says. “This has been particularly true over the last couple of years.”

This change was documented in 2015. Add in the pandemic and an entire society that is now accustomed to working from home in sweats, and it’s not a stretch to understand why some patients have become less formal in many settings. The 2015 article noted, however, that most physicians prefer to keep titles in the mix.

Perhaps most troublesome, says Dr. Setya, is that patients forgo asking whether it’s OK to use his first name and simply assume it’s acceptable. “It bothers me,” he says. “I became a doctor for more than the money.”

He suspects that his cultural background (Dr. Setya is of Indian descent) plays a role in how strongly he feels about patient-doctor informality. “As a British colony, Indian culture dictates that you pay respect to elders and to accomplishment,” he points out. “America is far looser when it comes to salutations.”

Dr. Cucuzzella largely agrees with Dr. Setya, but has a different view of the role culture plays in how physicians prefer to be addressed. “If your last name is difficult to pronounce, it can put the patient at ease if you give them an option,” he says. “I like my patients to feel comfortable and have a friendly conversation, so I don’t ask them to try to manage my last name.”

When patients revert to using Dr. Cucuzzella’s last name and title, this often breaks down along generational lines, Dr. Cucuzzella has found: Older patients might drop his title, whereas younger patients might keep it as a sign of respect. In some cases, Dr. Cucuzzella tries to bridge this gap, and offers the option of “Dr. Mark.” In his small West Virginia community, this is how people often refer to him.

Dr. Setya says that most of the older physicians he works with still prefer that patients and younger colleagues use their title, but he has witnessed exceptions to this. “My boss in residence hated to be called ‘Sir’ or ‘Doctor,’ ” he says. “In a situation like that, it is reasonable to ask, ‘How can I address you?’ But it has to be mutually agreed upon.”

Dr. Cucuzzella cites informality as the preferred mode for older patients. “If I have a 70-year-old patient, it seems natural they shouldn’t use my title,” he says. “They are worthy of equality in the community. If I’m talking to a retired CEO or state delegate, it’s uncomfortable if they call me doctor.”

Moreover, Dr. Cucuzzella maintains that establishing a less formal environment with patients leads to better outcomes. “Shared decision-making is a basic human right,” he says. “In 2022, doctors shouldn’t make decisions without patient input, unless it’s an emergency situation. Removing the title barriers makes that easier.”
 

How to handle informality

If you fall more in line with Dr. Setya, there are strategies you can use to try to keep formality in your doctor-patient relationships. Dr. Setya’s approach is indirect. “I don’t correct a patient if they use my first name, because that might seem hostile,” he says. “But I alert them in the way I address them back. A Sir, a Mrs., or a Mr. needs to go both ways.”

This particularly holds true in pediatrics, Dr. Setya has found. He has witnessed many colleagues addressing parents as “Mommy and Daddy,” something he says lacks respect and sets too informal a tone. “It’s almost universal that parents don’t like that, and we need to act accordingly.”

Dr. Witt also avoids directly correcting patients, but struggles when they drop her title. “The standard signature I use to sign every patient portal message I respond to includes my first and last name and credentials,” she says. “I maintain formality in most circumstances with that standard reply.”

Beneath the surface, however, Dr. Witt wishes it were easier. “I have struggled with answering the question, ‘Is it OK if I call you Leah?’ she says. “I want to keep our interaction anchored in professionalism without sacrificing the warmth I think is important to a productive patient-physician relationship. For this reason, I tend to say yes to this request, even though I’d rather patients didn’t make such requests.”

In the Fast Company article by Amy Diehl, PhD, and Leanne Dzubinski, PhD, on the topic of untitling professional women, the authors suggest several actions, beginning with leadership that sets expectations on the topic. They also suggest that physicians use polite corrections if patients untitle them. Supplying positive reinforcement when patients include your title can help, too. If all else fails, you can call out the offensive untitling. More often than not, especially with female physicians, the patient is demonstrating an unconscious bias rather than something deliberate.

Opinions vary on the topic of untitling, and ultimately each physician must make the decision for themselves. But creating informal cultures in an organization can have unintended consequences, especially for female peers.

Says Dr. Witt, “We all want to give our patients the best care we can, but professional boundaries are critical to time management, equitable care, and maintaining work-life balance. I would love to see a study that examines untitling by self-reported race and/or ethnicity of physicians, because we know that women of color experience higher rates of burnout and depression, and I wonder if untitling may be part of this.”

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

When Mark Cucuzzella, MD, meets a new patient at the West Virginia Medical School clinic, he introduces himself as “Mark.” For one thing, says Dr. Cucuzzella, his last name is a mouthful. For another, the 56-year-old general practitioner asserts that getting on a first-name basis with his patients is integral to delivering the best care.

“I’m trying to break down the old paternalistic barriers of the doctor/patient relationship,” he says. “Titles create an environment where the doctors are making all the decisions and not involving the patient in any course of action.”

Aniruddh Setya, MD, has a different take on informality between patients and doctors: It’s not OK. “I am not your friend,” says the 35-year-old pediatrician from Florida-based KIDZ Medical Services. “There has to be a level of respect for the education and accomplishment of being a physician.”

The issue of “untitling” a doctor and failing to use their honorific is becoming increasingly common, according to a recent study published in JAMA Network Open. But that doesn’t mean most physicians support the practice. In fact, some doctors contend that it can be harmful, particularly to female physicians.

“My concern is that untitling (so termed by Amy Diehl, PhD, and Leanne Dzubinski, PhD) intrudes upon important professional boundaries and might be correlated with diminishing the value of someone’s time,” says Leah Witt, MD, a geriatrician at UCSF Health, San Francisco. Dr. Witt, along with colleague Lekshmi Santhosh, MD, a pulmonologist, offered commentary on the study results. “Studies have shown that women physicians get more patient portal messages, spend more time in the electronic health record, and have longer visits,” Dr. Witt said. “Dr. Santhosh and I wonder if untitling is a signifier of this diminished value of our time, and an assumption of increased ease of access leading to this higher workload.”

To compile the results reported in JAMA Network Open, Mayo Clinic researchers analyzed more than 90,000 emails from patients to doctors over the course of 3 years, beginning in 2018. Of those emails, more than 32% included the physician’s first name in greeting or salutation. For women physicians, the odds were twice as high that their titles would be omitted in the correspondence. The same holds true for doctors of osteopathic medicine (DOs) compared with MDs, and primary care physicians had similar odds for a title drop compared with specialists.

Dr. Witt says the findings are not surprising. “They match my experience as a woman in medicine, as Dr. Santhosh and I write in our commentary,” she says. “We think the findings could easily be replicated at other centers.”

Indeed, research on 321 speaker introductions at a medical rounds found that when female physicians introduced other physicians, they usually applied the doctor title. When the job of introducing colleagues fell to male physicians, however, the stats fell to 72.4% for male peers and only 49.2% when introducing female peers.

The Mayo Clinic study authors identified the pitfalls of patients who informally address their doctors. They wrote, “Untitling may have a negative impact on physicians, demonstrate lack of respect, and can lead to reduction in formality of the physician/patient relationship or workplace.”
 

Physician preferences vary

Although the results of the Mayo Clinic analysis didn’t and couldn’t address physician sentiments on patient informality, Dr. Setya observes that American culture is becoming less formal. “I’ve been practicing for over 10 years, and the number of people who consider doctors as equals is growing,” he says. “This has been particularly true over the last couple of years.”

This change was documented in 2015. Add in the pandemic and an entire society that is now accustomed to working from home in sweats, and it’s not a stretch to understand why some patients have become less formal in many settings. The 2015 article noted, however, that most physicians prefer to keep titles in the mix.

Perhaps most troublesome, says Dr. Setya, is that patients forgo asking whether it’s OK to use his first name and simply assume it’s acceptable. “It bothers me,” he says. “I became a doctor for more than the money.”

He suspects that his cultural background (Dr. Setya is of Indian descent) plays a role in how strongly he feels about patient-doctor informality. “As a British colony, Indian culture dictates that you pay respect to elders and to accomplishment,” he points out. “America is far looser when it comes to salutations.”

Dr. Cucuzzella largely agrees with Dr. Setya, but has a different view of the role culture plays in how physicians prefer to be addressed. “If your last name is difficult to pronounce, it can put the patient at ease if you give them an option,” he says. “I like my patients to feel comfortable and have a friendly conversation, so I don’t ask them to try to manage my last name.”

When patients revert to using Dr. Cucuzzella’s last name and title, this often breaks down along generational lines, Dr. Cucuzzella has found: Older patients might drop his title, whereas younger patients might keep it as a sign of respect. In some cases, Dr. Cucuzzella tries to bridge this gap, and offers the option of “Dr. Mark.” In his small West Virginia community, this is how people often refer to him.

Dr. Setya says that most of the older physicians he works with still prefer that patients and younger colleagues use their title, but he has witnessed exceptions to this. “My boss in residence hated to be called ‘Sir’ or ‘Doctor,’ ” he says. “In a situation like that, it is reasonable to ask, ‘How can I address you?’ But it has to be mutually agreed upon.”

Dr. Cucuzzella cites informality as the preferred mode for older patients. “If I have a 70-year-old patient, it seems natural they shouldn’t use my title,” he says. “They are worthy of equality in the community. If I’m talking to a retired CEO or state delegate, it’s uncomfortable if they call me doctor.”

Moreover, Dr. Cucuzzella maintains that establishing a less formal environment with patients leads to better outcomes. “Shared decision-making is a basic human right,” he says. “In 2022, doctors shouldn’t make decisions without patient input, unless it’s an emergency situation. Removing the title barriers makes that easier.”
 

How to handle informality

If you fall more in line with Dr. Setya, there are strategies you can use to try to keep formality in your doctor-patient relationships. Dr. Setya’s approach is indirect. “I don’t correct a patient if they use my first name, because that might seem hostile,” he says. “But I alert them in the way I address them back. A Sir, a Mrs., or a Mr. needs to go both ways.”

This particularly holds true in pediatrics, Dr. Setya has found. He has witnessed many colleagues addressing parents as “Mommy and Daddy,” something he says lacks respect and sets too informal a tone. “It’s almost universal that parents don’t like that, and we need to act accordingly.”

Dr. Witt also avoids directly correcting patients, but struggles when they drop her title. “The standard signature I use to sign every patient portal message I respond to includes my first and last name and credentials,” she says. “I maintain formality in most circumstances with that standard reply.”

Beneath the surface, however, Dr. Witt wishes it were easier. “I have struggled with answering the question, ‘Is it OK if I call you Leah?’ she says. “I want to keep our interaction anchored in professionalism without sacrificing the warmth I think is important to a productive patient-physician relationship. For this reason, I tend to say yes to this request, even though I’d rather patients didn’t make such requests.”

In the Fast Company article by Amy Diehl, PhD, and Leanne Dzubinski, PhD, on the topic of untitling professional women, the authors suggest several actions, beginning with leadership that sets expectations on the topic. They also suggest that physicians use polite corrections if patients untitle them. Supplying positive reinforcement when patients include your title can help, too. If all else fails, you can call out the offensive untitling. More often than not, especially with female physicians, the patient is demonstrating an unconscious bias rather than something deliberate.

Opinions vary on the topic of untitling, and ultimately each physician must make the decision for themselves. But creating informal cultures in an organization can have unintended consequences, especially for female peers.

Says Dr. Witt, “We all want to give our patients the best care we can, but professional boundaries are critical to time management, equitable care, and maintaining work-life balance. I would love to see a study that examines untitling by self-reported race and/or ethnicity of physicians, because we know that women of color experience higher rates of burnout and depression, and I wonder if untitling may be part of this.”

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

When Mark Cucuzzella, MD, meets a new patient at the West Virginia Medical School clinic, he introduces himself as “Mark.” For one thing, says Dr. Cucuzzella, his last name is a mouthful. For another, the 56-year-old general practitioner asserts that getting on a first-name basis with his patients is integral to delivering the best care.

“I’m trying to break down the old paternalistic barriers of the doctor/patient relationship,” he says. “Titles create an environment where the doctors are making all the decisions and not involving the patient in any course of action.”

Aniruddh Setya, MD, has a different take on informality between patients and doctors: It’s not OK. “I am not your friend,” says the 35-year-old pediatrician from Florida-based KIDZ Medical Services. “There has to be a level of respect for the education and accomplishment of being a physician.”

The issue of “untitling” a doctor and failing to use their honorific is becoming increasingly common, according to a recent study published in JAMA Network Open. But that doesn’t mean most physicians support the practice. In fact, some doctors contend that it can be harmful, particularly to female physicians.

“My concern is that untitling (so termed by Amy Diehl, PhD, and Leanne Dzubinski, PhD) intrudes upon important professional boundaries and might be correlated with diminishing the value of someone’s time,” says Leah Witt, MD, a geriatrician at UCSF Health, San Francisco. Dr. Witt, along with colleague Lekshmi Santhosh, MD, a pulmonologist, offered commentary on the study results. “Studies have shown that women physicians get more patient portal messages, spend more time in the electronic health record, and have longer visits,” Dr. Witt said. “Dr. Santhosh and I wonder if untitling is a signifier of this diminished value of our time, and an assumption of increased ease of access leading to this higher workload.”

To compile the results reported in JAMA Network Open, Mayo Clinic researchers analyzed more than 90,000 emails from patients to doctors over the course of 3 years, beginning in 2018. Of those emails, more than 32% included the physician’s first name in greeting or salutation. For women physicians, the odds were twice as high that their titles would be omitted in the correspondence. The same holds true for doctors of osteopathic medicine (DOs) compared with MDs, and primary care physicians had similar odds for a title drop compared with specialists.

Dr. Witt says the findings are not surprising. “They match my experience as a woman in medicine, as Dr. Santhosh and I write in our commentary,” she says. “We think the findings could easily be replicated at other centers.”

Indeed, research on 321 speaker introductions at a medical rounds found that when female physicians introduced other physicians, they usually applied the doctor title. When the job of introducing colleagues fell to male physicians, however, the stats fell to 72.4% for male peers and only 49.2% when introducing female peers.

The Mayo Clinic study authors identified the pitfalls of patients who informally address their doctors. They wrote, “Untitling may have a negative impact on physicians, demonstrate lack of respect, and can lead to reduction in formality of the physician/patient relationship or workplace.”
 

Physician preferences vary

Although the results of the Mayo Clinic analysis didn’t and couldn’t address physician sentiments on patient informality, Dr. Setya observes that American culture is becoming less formal. “I’ve been practicing for over 10 years, and the number of people who consider doctors as equals is growing,” he says. “This has been particularly true over the last couple of years.”

This change was documented in 2015. Add in the pandemic and an entire society that is now accustomed to working from home in sweats, and it’s not a stretch to understand why some patients have become less formal in many settings. The 2015 article noted, however, that most physicians prefer to keep titles in the mix.

Perhaps most troublesome, says Dr. Setya, is that patients forgo asking whether it’s OK to use his first name and simply assume it’s acceptable. “It bothers me,” he says. “I became a doctor for more than the money.”

He suspects that his cultural background (Dr. Setya is of Indian descent) plays a role in how strongly he feels about patient-doctor informality. “As a British colony, Indian culture dictates that you pay respect to elders and to accomplishment,” he points out. “America is far looser when it comes to salutations.”

Dr. Cucuzzella largely agrees with Dr. Setya, but has a different view of the role culture plays in how physicians prefer to be addressed. “If your last name is difficult to pronounce, it can put the patient at ease if you give them an option,” he says. “I like my patients to feel comfortable and have a friendly conversation, so I don’t ask them to try to manage my last name.”

When patients revert to using Dr. Cucuzzella’s last name and title, this often breaks down along generational lines, Dr. Cucuzzella has found: Older patients might drop his title, whereas younger patients might keep it as a sign of respect. In some cases, Dr. Cucuzzella tries to bridge this gap, and offers the option of “Dr. Mark.” In his small West Virginia community, this is how people often refer to him.

Dr. Setya says that most of the older physicians he works with still prefer that patients and younger colleagues use their title, but he has witnessed exceptions to this. “My boss in residence hated to be called ‘Sir’ or ‘Doctor,’ ” he says. “In a situation like that, it is reasonable to ask, ‘How can I address you?’ But it has to be mutually agreed upon.”

Dr. Cucuzzella cites informality as the preferred mode for older patients. “If I have a 70-year-old patient, it seems natural they shouldn’t use my title,” he says. “They are worthy of equality in the community. If I’m talking to a retired CEO or state delegate, it’s uncomfortable if they call me doctor.”

Moreover, Dr. Cucuzzella maintains that establishing a less formal environment with patients leads to better outcomes. “Shared decision-making is a basic human right,” he says. “In 2022, doctors shouldn’t make decisions without patient input, unless it’s an emergency situation. Removing the title barriers makes that easier.”
 

How to handle informality

If you fall more in line with Dr. Setya, there are strategies you can use to try to keep formality in your doctor-patient relationships. Dr. Setya’s approach is indirect. “I don’t correct a patient if they use my first name, because that might seem hostile,” he says. “But I alert them in the way I address them back. A Sir, a Mrs., or a Mr. needs to go both ways.”

This particularly holds true in pediatrics, Dr. Setya has found. He has witnessed many colleagues addressing parents as “Mommy and Daddy,” something he says lacks respect and sets too informal a tone. “It’s almost universal that parents don’t like that, and we need to act accordingly.”

Dr. Witt also avoids directly correcting patients, but struggles when they drop her title. “The standard signature I use to sign every patient portal message I respond to includes my first and last name and credentials,” she says. “I maintain formality in most circumstances with that standard reply.”

Beneath the surface, however, Dr. Witt wishes it were easier. “I have struggled with answering the question, ‘Is it OK if I call you Leah?’ she says. “I want to keep our interaction anchored in professionalism without sacrificing the warmth I think is important to a productive patient-physician relationship. For this reason, I tend to say yes to this request, even though I’d rather patients didn’t make such requests.”

In the Fast Company article by Amy Diehl, PhD, and Leanne Dzubinski, PhD, on the topic of untitling professional women, the authors suggest several actions, beginning with leadership that sets expectations on the topic. They also suggest that physicians use polite corrections if patients untitle them. Supplying positive reinforcement when patients include your title can help, too. If all else fails, you can call out the offensive untitling. More often than not, especially with female physicians, the patient is demonstrating an unconscious bias rather than something deliberate.

Opinions vary on the topic of untitling, and ultimately each physician must make the decision for themselves. But creating informal cultures in an organization can have unintended consequences, especially for female peers.

Says Dr. Witt, “We all want to give our patients the best care we can, but professional boundaries are critical to time management, equitable care, and maintaining work-life balance. I would love to see a study that examines untitling by self-reported race and/or ethnicity of physicians, because we know that women of color experience higher rates of burnout and depression, and I wonder if untitling may be part of this.”

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

Strength training is the most effective form of exercise for reducing migraine, with high-intensity aerobics coming in second, and both beating top-line migraine medications topiramate and amitriptyline, new research suggests.

The new results should encourage clinicians to recommend patients with migraine engage in strength-training exercise whenever possible, study investigator Yohannes W. Woldeamanuel, MD, a physician-scientist and instructor, department of neurology and neurological sciences, Stanford (Calif.) University, told this news organization.

“Exercise is something patients can do all their lives and use it to prevent migraine attacks instead of taking daily medications or repetitive injections that have several adverse effects.”

The findings were published online in the Journal of Headache and Pain.
 

Head-to-head comparison

Several clinical trials have shown exercise is effective for migraine management, but to date, there have been no head-to-head comparisons of strength training and aerobic exercise, said Dr. Woldeamanuel.

This new study used a systematic review with network meta-analysis (NMA), which compares multiple interventions and ranks the efficacy of each one.

After a literature search, researchers included 21 clinical trials with an exercise regimen arm and a comparison control arm. All study data reported monthly frequency of migraine at baseline and at the end of the intervention.

The total combined sample size was 1,195 patients with migraine, who were a mean age of 35.5 years, with a female-to-male ratio of 6.7:1. All studies used International Classification of Headache Disorders (ICHD) criteria for migraine diagnosis.

The NMA provided 27 pairwise comparisons and 8 indirect comparisons. The pairwise comparisons provided direct evidence between the different interventions.

Researchers combined strength training, including weightlifting, with resistance training. Both modalities target muscles, while aerobic exercise targets cardiovascular health.

The average number of weeks was 9.3, 9.3, and 10.7, and the average number of hours per session for strength/resistance training, high-intensity aerobic exercise, and moderate-intensity aerobic exercise interventions was 50, 56, and 45.3, respectively.

The analysis showed all exercise interventions were more effective than the placebo groups in reducing the frequency of migraine. In terms of ranking, strength training came out on top, with a mean difference in monthly migraine days of −3.55 (95% confidence interval, −6.15 to −0.95) between the active and placebo groups.

Next was high-intensity aerobic exercise (−3.13; 95% CI, −5.28 to −0.97) and moderate-intensity aerobic exercise (−2.18; 95% CI, −3.25 to −1.11), followed by topiramate, placebo, and then amitriptyline.

Strength/resistance training was superior possibly because it targets muscle strengthening, particularly major muscles in the neck and shoulder area, which can be a source of the pain trigger, said Dr. Woldeamanuel. He added neck pain is highly comorbid with migraine.

Interestingly, patients doing exercises that focus on unaffected muscles – for example, squats – still get the benefits of less migraine burden, said Dr. Woldeamanuel.
 

Training recommendations

Strength training also increases or preserves lean muscle mass, which is associated with reduced migraine frequency. Research shows preservation of lean body mass combats central sensitization in various pain syndromes, said Dr. Woldeamanuel.

The superior effects of high- versus moderate-intensity aerobic exercise may be due to recruitment of endogenous molecules involved in exercise-mediated hypoalgesia (pain reduction).

The most common pathways are the opioid and endocannabinoid systems, although other systems are also likely involved, said Dr. Woldeamanuel. He noted migraine has been linked to a deficiency of both opioidergic and endocannabinoidergic signaling.

Dr. Woldeamanuel commented on the difficulty of comparing exercise interventions for patients with chronic versus episodic migraine, as many studies include both.

However, the two studies with moderate-intensity aerobic exercise exclusively involving patients with chronic migraine showed large effect sizes (Cohen’s d) of 0.80 and 1.10 in reducing monthly headache frequency.

Based on these new results and their own experience, the researchers recommend strength training start with 50% of repetition maximum (RM) with 2-3 sets of 12-15 repetitions three times a week along with 10 minutes of warm-up, stretching, and cool-down, totaling 45-60 minutes per session. Weight/resistance load can then be increased weekly by 5% of RM if the patient is capable of successfully completing three sets.

They also recommend including active recovery days (low-intensity exercise) between training days. All major muscles, including neck, shoulder, and upper limb muscles, should be trained in a rotation.

For high-intensity aerobic exercise, the authors recommend starting with interval training at 55% VO_2max (maximum respiratory capacity), or 50% HRmax (maximal heart rate) for 45-60 minutes per session, including 10 minutes of warm-up and cool-down, three times per week. The intensity can then be increased by 5%-10% each week to reach a maximum target of 80%-90% by week 12.

It is best for patients to start with a trainer for guidance and supervision, but once they master the routines, they can do the exercises independently, said Dr. Woldeamanuel.
 

Managing flare-ups

Headache flare-ups are normal during exercise, which may be caused by “boom and bust cycles” – exercising excessively when feeling good then completely stopping when feeling bad, said Dr. Woldeamanuel. He noted these flare-ups don’t mean “there’s something wrong with the brain or there’s some injury to muscles.”

The best way to manage such flare-ups is to use a pacing strategy that involves “not going overboard on good days and avoiding excessive rest on bad days,” the investigators note.

Dr. Woldeamanuel noted exercise is a lifestyle-based intervention; it not only helps reduce migraine attacks but also helps control other known comorbidities such as obesity and hypertension.

In a comment, Elizabeth Loder, MD, vice-chair, academic affairs, department of neurology, Brigham and Women’s Hospital, and professor of neurology, Harvard Medical School, both in Boston, said, “It’s useful to collect and summarize all of these studies, and to focus on helping patients and doctors understand the possible value of different kinds of exercise.”

The review was “well done,” said Dr. Loder, adding the researchers “have looked carefully at the quality of included studies.”

The study received support from the National Institute of Neurological Disorders and Stroke of the National Institutes of Health. Dr. Woldeamanuel has reported no relevant financial relationships.

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

Strength training is the most effective form of exercise for reducing migraine, with high-intensity aerobics coming in second, and both beating top-line migraine medications topiramate and amitriptyline, new research suggests.

The new results should encourage clinicians to recommend patients with migraine engage in strength-training exercise whenever possible, study investigator Yohannes W. Woldeamanuel, MD, a physician-scientist and instructor, department of neurology and neurological sciences, Stanford (Calif.) University, told this news organization.

“Exercise is something patients can do all their lives and use it to prevent migraine attacks instead of taking daily medications or repetitive injections that have several adverse effects.”

The findings were published online in the Journal of Headache and Pain.
 

Head-to-head comparison

Several clinical trials have shown exercise is effective for migraine management, but to date, there have been no head-to-head comparisons of strength training and aerobic exercise, said Dr. Woldeamanuel.

This new study used a systematic review with network meta-analysis (NMA), which compares multiple interventions and ranks the efficacy of each one.

After a literature search, researchers included 21 clinical trials with an exercise regimen arm and a comparison control arm. All study data reported monthly frequency of migraine at baseline and at the end of the intervention.

The total combined sample size was 1,195 patients with migraine, who were a mean age of 35.5 years, with a female-to-male ratio of 6.7:1. All studies used International Classification of Headache Disorders (ICHD) criteria for migraine diagnosis.

The NMA provided 27 pairwise comparisons and 8 indirect comparisons. The pairwise comparisons provided direct evidence between the different interventions.

Researchers combined strength training, including weightlifting, with resistance training. Both modalities target muscles, while aerobic exercise targets cardiovascular health.

The average number of weeks was 9.3, 9.3, and 10.7, and the average number of hours per session for strength/resistance training, high-intensity aerobic exercise, and moderate-intensity aerobic exercise interventions was 50, 56, and 45.3, respectively.

The analysis showed all exercise interventions were more effective than the placebo groups in reducing the frequency of migraine. In terms of ranking, strength training came out on top, with a mean difference in monthly migraine days of −3.55 (95% confidence interval, −6.15 to −0.95) between the active and placebo groups.

Next was high-intensity aerobic exercise (−3.13; 95% CI, −5.28 to −0.97) and moderate-intensity aerobic exercise (−2.18; 95% CI, −3.25 to −1.11), followed by topiramate, placebo, and then amitriptyline.

Strength/resistance training was superior possibly because it targets muscle strengthening, particularly major muscles in the neck and shoulder area, which can be a source of the pain trigger, said Dr. Woldeamanuel. He added neck pain is highly comorbid with migraine.

Interestingly, patients doing exercises that focus on unaffected muscles – for example, squats – still get the benefits of less migraine burden, said Dr. Woldeamanuel.
 

Training recommendations

Strength training also increases or preserves lean muscle mass, which is associated with reduced migraine frequency. Research shows preservation of lean body mass combats central sensitization in various pain syndromes, said Dr. Woldeamanuel.

The superior effects of high- versus moderate-intensity aerobic exercise may be due to recruitment of endogenous molecules involved in exercise-mediated hypoalgesia (pain reduction).

The most common pathways are the opioid and endocannabinoid systems, although other systems are also likely involved, said Dr. Woldeamanuel. He noted migraine has been linked to a deficiency of both opioidergic and endocannabinoidergic signaling.

Dr. Woldeamanuel commented on the difficulty of comparing exercise interventions for patients with chronic versus episodic migraine, as many studies include both.

However, the two studies with moderate-intensity aerobic exercise exclusively involving patients with chronic migraine showed large effect sizes (Cohen’s d) of 0.80 and 1.10 in reducing monthly headache frequency.

Based on these new results and their own experience, the researchers recommend strength training start with 50% of repetition maximum (RM) with 2-3 sets of 12-15 repetitions three times a week along with 10 minutes of warm-up, stretching, and cool-down, totaling 45-60 minutes per session. Weight/resistance load can then be increased weekly by 5% of RM if the patient is capable of successfully completing three sets.

They also recommend including active recovery days (low-intensity exercise) between training days. All major muscles, including neck, shoulder, and upper limb muscles, should be trained in a rotation.

For high-intensity aerobic exercise, the authors recommend starting with interval training at 55% VO_2max (maximum respiratory capacity), or 50% HRmax (maximal heart rate) for 45-60 minutes per session, including 10 minutes of warm-up and cool-down, three times per week. The intensity can then be increased by 5%-10% each week to reach a maximum target of 80%-90% by week 12.

It is best for patients to start with a trainer for guidance and supervision, but once they master the routines, they can do the exercises independently, said Dr. Woldeamanuel.
 

Managing flare-ups

Headache flare-ups are normal during exercise, which may be caused by “boom and bust cycles” – exercising excessively when feeling good then completely stopping when feeling bad, said Dr. Woldeamanuel. He noted these flare-ups don’t mean “there’s something wrong with the brain or there’s some injury to muscles.”

The best way to manage such flare-ups is to use a pacing strategy that involves “not going overboard on good days and avoiding excessive rest on bad days,” the investigators note.

Dr. Woldeamanuel noted exercise is a lifestyle-based intervention; it not only helps reduce migraine attacks but also helps control other known comorbidities such as obesity and hypertension.

In a comment, Elizabeth Loder, MD, vice-chair, academic affairs, department of neurology, Brigham and Women’s Hospital, and professor of neurology, Harvard Medical School, both in Boston, said, “It’s useful to collect and summarize all of these studies, and to focus on helping patients and doctors understand the possible value of different kinds of exercise.”

The review was “well done,” said Dr. Loder, adding the researchers “have looked carefully at the quality of included studies.”

The study received support from the National Institute of Neurological Disorders and Stroke of the National Institutes of Health. Dr. Woldeamanuel has reported no relevant financial relationships.

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

Strength training is the most effective form of exercise for reducing migraine, with high-intensity aerobics coming in second, and both beating top-line migraine medications topiramate and amitriptyline, new research suggests.

The new results should encourage clinicians to recommend patients with migraine engage in strength-training exercise whenever possible, study investigator Yohannes W. Woldeamanuel, MD, a physician-scientist and instructor, department of neurology and neurological sciences, Stanford (Calif.) University, told this news organization.

“Exercise is something patients can do all their lives and use it to prevent migraine attacks instead of taking daily medications or repetitive injections that have several adverse effects.”

The findings were published online in the Journal of Headache and Pain.
 

Head-to-head comparison

Several clinical trials have shown exercise is effective for migraine management, but to date, there have been no head-to-head comparisons of strength training and aerobic exercise, said Dr. Woldeamanuel.

This new study used a systematic review with network meta-analysis (NMA), which compares multiple interventions and ranks the efficacy of each one.

After a literature search, researchers included 21 clinical trials with an exercise regimen arm and a comparison control arm. All study data reported monthly frequency of migraine at baseline and at the end of the intervention.

The total combined sample size was 1,195 patients with migraine, who were a mean age of 35.5 years, with a female-to-male ratio of 6.7:1. All studies used International Classification of Headache Disorders (ICHD) criteria for migraine diagnosis.

The NMA provided 27 pairwise comparisons and 8 indirect comparisons. The pairwise comparisons provided direct evidence between the different interventions.

Researchers combined strength training, including weightlifting, with resistance training. Both modalities target muscles, while aerobic exercise targets cardiovascular health.

The average number of weeks was 9.3, 9.3, and 10.7, and the average number of hours per session for strength/resistance training, high-intensity aerobic exercise, and moderate-intensity aerobic exercise interventions was 50, 56, and 45.3, respectively.

The analysis showed all exercise interventions were more effective than the placebo groups in reducing the frequency of migraine. In terms of ranking, strength training came out on top, with a mean difference in monthly migraine days of −3.55 (95% confidence interval, −6.15 to −0.95) between the active and placebo groups.

Next was high-intensity aerobic exercise (−3.13; 95% CI, −5.28 to −0.97) and moderate-intensity aerobic exercise (−2.18; 95% CI, −3.25 to −1.11), followed by topiramate, placebo, and then amitriptyline.

Strength/resistance training was superior possibly because it targets muscle strengthening, particularly major muscles in the neck and shoulder area, which can be a source of the pain trigger, said Dr. Woldeamanuel. He added neck pain is highly comorbid with migraine.

Interestingly, patients doing exercises that focus on unaffected muscles – for example, squats – still get the benefits of less migraine burden, said Dr. Woldeamanuel.
 

Training recommendations

Strength training also increases or preserves lean muscle mass, which is associated with reduced migraine frequency. Research shows preservation of lean body mass combats central sensitization in various pain syndromes, said Dr. Woldeamanuel.

The superior effects of high- versus moderate-intensity aerobic exercise may be due to recruitment of endogenous molecules involved in exercise-mediated hypoalgesia (pain reduction).

The most common pathways are the opioid and endocannabinoid systems, although other systems are also likely involved, said Dr. Woldeamanuel. He noted migraine has been linked to a deficiency of both opioidergic and endocannabinoidergic signaling.

Dr. Woldeamanuel commented on the difficulty of comparing exercise interventions for patients with chronic versus episodic migraine, as many studies include both.

However, the two studies with moderate-intensity aerobic exercise exclusively involving patients with chronic migraine showed large effect sizes (Cohen’s d) of 0.80 and 1.10 in reducing monthly headache frequency.

Based on these new results and their own experience, the researchers recommend strength training start with 50% of repetition maximum (RM) with 2-3 sets of 12-15 repetitions three times a week along with 10 minutes of warm-up, stretching, and cool-down, totaling 45-60 minutes per session. Weight/resistance load can then be increased weekly by 5% of RM if the patient is capable of successfully completing three sets.

They also recommend including active recovery days (low-intensity exercise) between training days. All major muscles, including neck, shoulder, and upper limb muscles, should be trained in a rotation.

For high-intensity aerobic exercise, the authors recommend starting with interval training at 55% VO_2max (maximum respiratory capacity), or 50% HRmax (maximal heart rate) for 45-60 minutes per session, including 10 minutes of warm-up and cool-down, three times per week. The intensity can then be increased by 5%-10% each week to reach a maximum target of 80%-90% by week 12.

It is best for patients to start with a trainer for guidance and supervision, but once they master the routines, they can do the exercises independently, said Dr. Woldeamanuel.
 

Managing flare-ups

Headache flare-ups are normal during exercise, which may be caused by “boom and bust cycles” – exercising excessively when feeling good then completely stopping when feeling bad, said Dr. Woldeamanuel. He noted these flare-ups don’t mean “there’s something wrong with the brain or there’s some injury to muscles.”

The best way to manage such flare-ups is to use a pacing strategy that involves “not going overboard on good days and avoiding excessive rest on bad days,” the investigators note.

Dr. Woldeamanuel noted exercise is a lifestyle-based intervention; it not only helps reduce migraine attacks but also helps control other known comorbidities such as obesity and hypertension.

In a comment, Elizabeth Loder, MD, vice-chair, academic affairs, department of neurology, Brigham and Women’s Hospital, and professor of neurology, Harvard Medical School, both in Boston, said, “It’s useful to collect and summarize all of these studies, and to focus on helping patients and doctors understand the possible value of different kinds of exercise.”

The review was “well done,” said Dr. Loder, adding the researchers “have looked carefully at the quality of included studies.”

The study received support from the National Institute of Neurological Disorders and Stroke of the National Institutes of Health. Dr. Woldeamanuel has reported no relevant financial relationships.

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