MDedge Neurology

New expert guidance to help clinicians manage the treatment of patients with epilepsy during pregnancy has been released.

Issued by the American Academy of Neurology, the American Epilepsy Society, and the Society for Maternal-Fetal Medicine, the new practice guideline covers the use of antiseizure medications (ASMs) and folic acid supplementation before conception and during pregnancy.

“Most children born to people with epilepsy are healthy, but there is a small risk of pregnancy-related problems, partly due to seizures and partly due to the effects of antiseizure medications,” the guidelines’ lead author Alison M. Pack, MD, MPH, professor of neurology and chief of the Epilepsy and Sleep Division, Columbia University, New York City, said in a news release.

“This guideline provides recommendations regarding the effects of antiseizure medications and folic acid supplementation on malformations at birth and the development of children during pregnancy, so that doctors and people with epilepsy can determine which treatments may be best for them,” she added. 

The guideline was published online in Neurology.
 

Why Now? 

The new guideline updates the 2009 guidance on epilepsy management during pregnancy. Since then, Dr. Pack told this news organization, there has been a wealth of new data on differential effects of different ASMs — notably, lamotrigine and levetiracetam — the most commonly prescribed medications in this population.

“In this guideline, we were able to assess differential effects of different ASMs on outcomes of interest, including major congenital malformations [MCMs], perinatal outcomes, and neurodevelopmental outcomes. In addition, we looked at the effect of folic acid supplementation on each of these outcomes,” she said.

The overarching goals of care for patients are to “optimize health outcomes both for individuals and their future offspring,” the authors wrote. Shared decision-making, they add, leads to better decision-making by providing a better understanding of the available treatment options and their potential risks, resulting in enhanced decision-making that aligns with personal values.

Clinicians should recommend ASMs that optimize seizure control and fetal outcomes, in the event of a pregnancy, at the earliest possible preconception time, the guideline authors note.

“Overall, treating clinicians need to balance treating the person with epilepsy to control convulsive seizures (generalized tonic-clonic seizures and focal-to-bilateral tonic-clonic seizures) to minimize potential risks to the birth parent and the possible risks of certain ASMs on the fetus if pregnancy occurs,” they wrote.

If a patient is already pregnant, the experts recommend that clinicians “exercise caution” in removing or replacing an ASM that controls convulsive seizures, even if it’s “not an optimal choice” for the fetus. 

In addition, they advise that ASM levels should be monitored throughout the pregnancy, guided by individual ASM pharmacokinetics and an individual patient’s clinical presentation. ASM dose, they note, should be adjusted during pregnancy in response to decreasing serum ASM levels or worsening seizure control.

The authors point out that there are limited data on “pregnancy-related outcomes with respect to acetazolamide, eslicarbazepine, ethosuximide, lacosamide, nitrazepam, perampanel, piracetam, pregabalin, rufinamide, stiripentol, tiagabine, and vigabatrin.”

Patients should be informed that the birth prevalence of any major congenital malformation in the general population ranges between 2.4% and 2.9%.
 

If Feasible, Avoid Valproic Acid 

“One of the most important take-home messages is that valproic acid has the highest unadjusted birth prevalence of all major congenital malformations — 9.7% — and the highest unadjusted birth prevalence of neural tube defects at 1.4%,” Dr. Pack said. As a result, the guideline authors advise against using valproic acid, if clinically feasible.

Valproic acid also has the highest prevalence of negative neurodevelopmental outcomes, including a reduction in global IQ and an increased prevalence of autism spectrum disorder (ASD). Patients should be counseled accordingly and advised of the increased risk for ASD and decreased IQ resulting from valproic acid.

Clinicians should consider using lamotrigine, levetiracetam, or oxcarbazepine when appropriate. Serum concentrations of most ASMs have a “defined therapeutic window” for effective seizure control and that concentration may decrease during pregnancy, particularly with lamotrigine and levetiracetam, the authors note.

Phenobarbital, topiramate, and valproic acid should because of the increased risk for cardiac malformations, oral clefts, and urogenital and renal malformations.

Fetal screening for major congenital malformations is recommended to enable early detection and timely intervention in patients treated with any ASM during pregnancy Patients receiving phenobarbital during pregnancy should also undergo fetal cardiac screenings.

Valproic acid and topiramate are also associated with children who are small for their gestational age. To enable early identification of fetal growth restriction, patients taking valproic acid or topiramate should be monitored. In addition, children exposed to these medications in utero should be monitored during childhood to ensure they are meeting age-appropriate developmental milestones. 

Folic acid taken during pregnancy can reduce the prevalence of negative neurodevelopment outcomes, but not major congenital malformations, Dr. Pack noted. 

“Due to limited available data, we were unable to define an optimal dose of folic acid supplementation beyond at least 0.4 mg/d,” Dr. Pack said. “Future studies, preferably randomized clinical trials, are needed to better define the optimal dose.”

She emphasized that epilepsy is one of the most common neurologic disorders, and 1 in 5 of those affected are people of childbearing potential. Understanding the effects of ASMs on pregnancy outcomes is critical for physicians who manage these patients.
 

Uncertainty Remains 

Commenting for this news organization, Kimford Meador, MD, a professor in the Department of Neurology and Neurological Sciences at Stanford University School of Medicine , Stanford Neuroscience Health Center, Palo Alto, California, noted that the new guidelines reflect the gains in knowledge since 2009 and that the recommendations are “reasonable, based on available data.”

However, “one very important point is how much remains unknown,” said Dr. Meador, who was not involved in writing the current guideline. “Many ASMs have no data, and several have estimates based on small samples or a single observational study.” Thus, “the risks for the majority of ASMs are uncertain.”

Given that randomized trials “are not possible in this population, and that all observational studies are subject to residual confounding, a reliable signal across multiple studies in humans is required to be certain of findings,” he stated.

This practice guideline was developed with financial support from the American Academy of Neurology. Dr. Pack serves on the editorial board for the journal Epilepsy Currents, receives royalties from UpToDate, receives funding from the National Institutes of Health for serving as coinvestigator and site principal investigator for the Maternal Outcomes and Neurodevelopmental Effects of Antiepileptic Drugs (MONEAD) study, and receives funding from Bayer for serving as a co-investigator on a study on women with epilepsy initiating a progestin intrauterine device. One of Dr. Pack’s immediate family members has received personal compensation for serving as an employee of REGENEXBIO. The other authors’ disclosures are listed on the original paper. Dr. Meador has received research support from the National Institutes of Health, Veterans Administration, Eisai, Inc, and Suno Medtronic Navigation, Inc, and the Epilepsy Study Consortium pays Dr. Meador’s university for his research on the Human Epilepsy Project and consultant time related to Eisai, UCB Pharma, and Xenon.

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

New expert guidance to help clinicians manage the treatment of patients with epilepsy during pregnancy has been released.

Issued by the American Academy of Neurology, the American Epilepsy Society, and the Society for Maternal-Fetal Medicine, the new practice guideline covers the use of antiseizure medications (ASMs) and folic acid supplementation before conception and during pregnancy.

“Most children born to people with epilepsy are healthy, but there is a small risk of pregnancy-related problems, partly due to seizures and partly due to the effects of antiseizure medications,” the guidelines’ lead author Alison M. Pack, MD, MPH, professor of neurology and chief of the Epilepsy and Sleep Division, Columbia University, New York City, said in a news release.

“This guideline provides recommendations regarding the effects of antiseizure medications and folic acid supplementation on malformations at birth and the development of children during pregnancy, so that doctors and people with epilepsy can determine which treatments may be best for them,” she added. 

The guideline was published online in Neurology.
 

Why Now? 

The new guideline updates the 2009 guidance on epilepsy management during pregnancy. Since then, Dr. Pack told this news organization, there has been a wealth of new data on differential effects of different ASMs — notably, lamotrigine and levetiracetam — the most commonly prescribed medications in this population.

“In this guideline, we were able to assess differential effects of different ASMs on outcomes of interest, including major congenital malformations [MCMs], perinatal outcomes, and neurodevelopmental outcomes. In addition, we looked at the effect of folic acid supplementation on each of these outcomes,” she said.

The overarching goals of care for patients are to “optimize health outcomes both for individuals and their future offspring,” the authors wrote. Shared decision-making, they add, leads to better decision-making by providing a better understanding of the available treatment options and their potential risks, resulting in enhanced decision-making that aligns with personal values.

Clinicians should recommend ASMs that optimize seizure control and fetal outcomes, in the event of a pregnancy, at the earliest possible preconception time, the guideline authors note.

“Overall, treating clinicians need to balance treating the person with epilepsy to control convulsive seizures (generalized tonic-clonic seizures and focal-to-bilateral tonic-clonic seizures) to minimize potential risks to the birth parent and the possible risks of certain ASMs on the fetus if pregnancy occurs,” they wrote.

If a patient is already pregnant, the experts recommend that clinicians “exercise caution” in removing or replacing an ASM that controls convulsive seizures, even if it’s “not an optimal choice” for the fetus. 

In addition, they advise that ASM levels should be monitored throughout the pregnancy, guided by individual ASM pharmacokinetics and an individual patient’s clinical presentation. ASM dose, they note, should be adjusted during pregnancy in response to decreasing serum ASM levels or worsening seizure control.

The authors point out that there are limited data on “pregnancy-related outcomes with respect to acetazolamide, eslicarbazepine, ethosuximide, lacosamide, nitrazepam, perampanel, piracetam, pregabalin, rufinamide, stiripentol, tiagabine, and vigabatrin.”

Patients should be informed that the birth prevalence of any major congenital malformation in the general population ranges between 2.4% and 2.9%.
 

If Feasible, Avoid Valproic Acid 

“One of the most important take-home messages is that valproic acid has the highest unadjusted birth prevalence of all major congenital malformations — 9.7% — and the highest unadjusted birth prevalence of neural tube defects at 1.4%,” Dr. Pack said. As a result, the guideline authors advise against using valproic acid, if clinically feasible.

Valproic acid also has the highest prevalence of negative neurodevelopmental outcomes, including a reduction in global IQ and an increased prevalence of autism spectrum disorder (ASD). Patients should be counseled accordingly and advised of the increased risk for ASD and decreased IQ resulting from valproic acid.

Clinicians should consider using lamotrigine, levetiracetam, or oxcarbazepine when appropriate. Serum concentrations of most ASMs have a “defined therapeutic window” for effective seizure control and that concentration may decrease during pregnancy, particularly with lamotrigine and levetiracetam, the authors note.

Phenobarbital, topiramate, and valproic acid should because of the increased risk for cardiac malformations, oral clefts, and urogenital and renal malformations.

Fetal screening for major congenital malformations is recommended to enable early detection and timely intervention in patients treated with any ASM during pregnancy Patients receiving phenobarbital during pregnancy should also undergo fetal cardiac screenings.

Valproic acid and topiramate are also associated with children who are small for their gestational age. To enable early identification of fetal growth restriction, patients taking valproic acid or topiramate should be monitored. In addition, children exposed to these medications in utero should be monitored during childhood to ensure they are meeting age-appropriate developmental milestones. 

Folic acid taken during pregnancy can reduce the prevalence of negative neurodevelopment outcomes, but not major congenital malformations, Dr. Pack noted. 

“Due to limited available data, we were unable to define an optimal dose of folic acid supplementation beyond at least 0.4 mg/d,” Dr. Pack said. “Future studies, preferably randomized clinical trials, are needed to better define the optimal dose.”

She emphasized that epilepsy is one of the most common neurologic disorders, and 1 in 5 of those affected are people of childbearing potential. Understanding the effects of ASMs on pregnancy outcomes is critical for physicians who manage these patients.
 

Uncertainty Remains 

Commenting for this news organization, Kimford Meador, MD, a professor in the Department of Neurology and Neurological Sciences at Stanford University School of Medicine , Stanford Neuroscience Health Center, Palo Alto, California, noted that the new guidelines reflect the gains in knowledge since 2009 and that the recommendations are “reasonable, based on available data.”

However, “one very important point is how much remains unknown,” said Dr. Meador, who was not involved in writing the current guideline. “Many ASMs have no data, and several have estimates based on small samples or a single observational study.” Thus, “the risks for the majority of ASMs are uncertain.”

Given that randomized trials “are not possible in this population, and that all observational studies are subject to residual confounding, a reliable signal across multiple studies in humans is required to be certain of findings,” he stated.

This practice guideline was developed with financial support from the American Academy of Neurology. Dr. Pack serves on the editorial board for the journal Epilepsy Currents, receives royalties from UpToDate, receives funding from the National Institutes of Health for serving as coinvestigator and site principal investigator for the Maternal Outcomes and Neurodevelopmental Effects of Antiepileptic Drugs (MONEAD) study, and receives funding from Bayer for serving as a co-investigator on a study on women with epilepsy initiating a progestin intrauterine device. One of Dr. Pack’s immediate family members has received personal compensation for serving as an employee of REGENEXBIO. The other authors’ disclosures are listed on the original paper. Dr. Meador has received research support from the National Institutes of Health, Veterans Administration, Eisai, Inc, and Suno Medtronic Navigation, Inc, and the Epilepsy Study Consortium pays Dr. Meador’s university for his research on the Human Epilepsy Project and consultant time related to Eisai, UCB Pharma, and Xenon.

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

New expert guidance to help clinicians manage the treatment of patients with epilepsy during pregnancy has been released.

Issued by the American Academy of Neurology, the American Epilepsy Society, and the Society for Maternal-Fetal Medicine, the new practice guideline covers the use of antiseizure medications (ASMs) and folic acid supplementation before conception and during pregnancy.

“Most children born to people with epilepsy are healthy, but there is a small risk of pregnancy-related problems, partly due to seizures and partly due to the effects of antiseizure medications,” the guidelines’ lead author Alison M. Pack, MD, MPH, professor of neurology and chief of the Epilepsy and Sleep Division, Columbia University, New York City, said in a news release.

“This guideline provides recommendations regarding the effects of antiseizure medications and folic acid supplementation on malformations at birth and the development of children during pregnancy, so that doctors and people with epilepsy can determine which treatments may be best for them,” she added. 

The guideline was published online in Neurology.
 

Why Now? 

The new guideline updates the 2009 guidance on epilepsy management during pregnancy. Since then, Dr. Pack told this news organization, there has been a wealth of new data on differential effects of different ASMs — notably, lamotrigine and levetiracetam — the most commonly prescribed medications in this population.

“In this guideline, we were able to assess differential effects of different ASMs on outcomes of interest, including major congenital malformations [MCMs], perinatal outcomes, and neurodevelopmental outcomes. In addition, we looked at the effect of folic acid supplementation on each of these outcomes,” she said.

The overarching goals of care for patients are to “optimize health outcomes both for individuals and their future offspring,” the authors wrote. Shared decision-making, they add, leads to better decision-making by providing a better understanding of the available treatment options and their potential risks, resulting in enhanced decision-making that aligns with personal values.

Clinicians should recommend ASMs that optimize seizure control and fetal outcomes, in the event of a pregnancy, at the earliest possible preconception time, the guideline authors note.

“Overall, treating clinicians need to balance treating the person with epilepsy to control convulsive seizures (generalized tonic-clonic seizures and focal-to-bilateral tonic-clonic seizures) to minimize potential risks to the birth parent and the possible risks of certain ASMs on the fetus if pregnancy occurs,” they wrote.

If a patient is already pregnant, the experts recommend that clinicians “exercise caution” in removing or replacing an ASM that controls convulsive seizures, even if it’s “not an optimal choice” for the fetus. 

In addition, they advise that ASM levels should be monitored throughout the pregnancy, guided by individual ASM pharmacokinetics and an individual patient’s clinical presentation. ASM dose, they note, should be adjusted during pregnancy in response to decreasing serum ASM levels or worsening seizure control.

The authors point out that there are limited data on “pregnancy-related outcomes with respect to acetazolamide, eslicarbazepine, ethosuximide, lacosamide, nitrazepam, perampanel, piracetam, pregabalin, rufinamide, stiripentol, tiagabine, and vigabatrin.”

Patients should be informed that the birth prevalence of any major congenital malformation in the general population ranges between 2.4% and 2.9%.
 

If Feasible, Avoid Valproic Acid 

“One of the most important take-home messages is that valproic acid has the highest unadjusted birth prevalence of all major congenital malformations — 9.7% — and the highest unadjusted birth prevalence of neural tube defects at 1.4%,” Dr. Pack said. As a result, the guideline authors advise against using valproic acid, if clinically feasible.

Valproic acid also has the highest prevalence of negative neurodevelopmental outcomes, including a reduction in global IQ and an increased prevalence of autism spectrum disorder (ASD). Patients should be counseled accordingly and advised of the increased risk for ASD and decreased IQ resulting from valproic acid.

Clinicians should consider using lamotrigine, levetiracetam, or oxcarbazepine when appropriate. Serum concentrations of most ASMs have a “defined therapeutic window” for effective seizure control and that concentration may decrease during pregnancy, particularly with lamotrigine and levetiracetam, the authors note.

Phenobarbital, topiramate, and valproic acid should because of the increased risk for cardiac malformations, oral clefts, and urogenital and renal malformations.

Fetal screening for major congenital malformations is recommended to enable early detection and timely intervention in patients treated with any ASM during pregnancy Patients receiving phenobarbital during pregnancy should also undergo fetal cardiac screenings.

Valproic acid and topiramate are also associated with children who are small for their gestational age. To enable early identification of fetal growth restriction, patients taking valproic acid or topiramate should be monitored. In addition, children exposed to these medications in utero should be monitored during childhood to ensure they are meeting age-appropriate developmental milestones. 

Folic acid taken during pregnancy can reduce the prevalence of negative neurodevelopment outcomes, but not major congenital malformations, Dr. Pack noted. 

“Due to limited available data, we were unable to define an optimal dose of folic acid supplementation beyond at least 0.4 mg/d,” Dr. Pack said. “Future studies, preferably randomized clinical trials, are needed to better define the optimal dose.”

She emphasized that epilepsy is one of the most common neurologic disorders, and 1 in 5 of those affected are people of childbearing potential. Understanding the effects of ASMs on pregnancy outcomes is critical for physicians who manage these patients.
 

Uncertainty Remains 

Commenting for this news organization, Kimford Meador, MD, a professor in the Department of Neurology and Neurological Sciences at Stanford University School of Medicine , Stanford Neuroscience Health Center, Palo Alto, California, noted that the new guidelines reflect the gains in knowledge since 2009 and that the recommendations are “reasonable, based on available data.”

However, “one very important point is how much remains unknown,” said Dr. Meador, who was not involved in writing the current guideline. “Many ASMs have no data, and several have estimates based on small samples or a single observational study.” Thus, “the risks for the majority of ASMs are uncertain.”

Given that randomized trials “are not possible in this population, and that all observational studies are subject to residual confounding, a reliable signal across multiple studies in humans is required to be certain of findings,” he stated.

This practice guideline was developed with financial support from the American Academy of Neurology. Dr. Pack serves on the editorial board for the journal Epilepsy Currents, receives royalties from UpToDate, receives funding from the National Institutes of Health for serving as coinvestigator and site principal investigator for the Maternal Outcomes and Neurodevelopmental Effects of Antiepileptic Drugs (MONEAD) study, and receives funding from Bayer for serving as a co-investigator on a study on women with epilepsy initiating a progestin intrauterine device. One of Dr. Pack’s immediate family members has received personal compensation for serving as an employee of REGENEXBIO. The other authors’ disclosures are listed on the original paper. Dr. Meador has received research support from the National Institutes of Health, Veterans Administration, Eisai, Inc, and Suno Medtronic Navigation, Inc, and the Epilepsy Study Consortium pays Dr. Meador’s university for his research on the Human Epilepsy Project and consultant time related to Eisai, UCB Pharma, and Xenon.

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

TOPLINE:

Antiepileptic and anti-infectious agents were the most common drugs associated with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) in children in an analysis of a World Health Organization (WHO) database.

METHODOLOGY:

• SJS and TEN are rare, life-threatening mucocutaneous reactions mainly associated with medications, but large pharmacovigilance studies of drugs associated with SJS-TEN in the pediatric population are still lacking.
• Using the WHO’s pharmacovigilance database (VigiBase) containing individual case safety reports from January 1967 to July 2022, researchers identified 7342 adverse drug reaction reports of SJS-TEN in children (younger than 18 years; median age, 9 years) in all six continents. Median onset was 5 days, and 3.2% were fatal.
• They analyzed drugs reported as suspected treatments, and for each molecule, they performed a case–non-case study to assess a potential pharmacovigilance signal by computing the information component (IC).
• A positive IC value suggested more frequent reporting of a specific drug-adverse reaction pair. A positive IC025, a traditional threshold for statistical signal detection, is suggestive of a potential pharmacovigilance signal.

TAKEAWAY:

• Overall, 165 drugs were associated with a diagnosis of SJS-TEN; antiepileptic and anti-infectious drugs were the most common drug classes represented.
• The five most frequently reported drugs were carbamazepine (11.7%), lamotrigine (10.6%), sulfamethoxazole-trimethoprim (9%), acetaminophen (8.4%), and phenytoin (6.6%). The five drugs with the highest IC025 were lamotrigine, carbamazepine, phenobarbital, phenytoin, and nimesulide.
• All antiepileptics, many antibiotic families, dapsone, antiretroviral drugs, some antifungal drugs, and nonsteroidal anti-inflammatory drugs were identified in reports, with penicillins the most frequently reported antibiotic family and sulfonamides having the strongest pharmacovigilance signal.
• Vaccines were not associated with significant signals.

IN PRACTICE:

The study provides an update on “the spectrum of drugs potentially associated with SJS-TEN in the pediatric population,” the authors concluded, and “underlines the importance of reporting to pharmacovigilance the suspicion of this severe side effect of drugs with the most precise and detailed clinical description possible.”

SOURCE:

The study, led by Pauline Bataille, MD, of the Department of Pediatric Dermatology, Hôpital Necker-Enfants Malades, Paris City University, France, was published online in the Journal of the European Academy of Dermatology and Venereology.

LIMITATIONS:

Limitations include the possibility that some cases could have had an infectious or idiopathic cause not related to a drug and the lack of detailed clinical data in the database.

DISCLOSURES:

This study did not receive any funding. The authors declared no conflict of interest.

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

TOPLINE:

Antiepileptic and anti-infectious agents were the most common drugs associated with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) in children in an analysis of a World Health Organization (WHO) database.

METHODOLOGY:

• SJS and TEN are rare, life-threatening mucocutaneous reactions mainly associated with medications, but large pharmacovigilance studies of drugs associated with SJS-TEN in the pediatric population are still lacking.
• Using the WHO’s pharmacovigilance database (VigiBase) containing individual case safety reports from January 1967 to July 2022, researchers identified 7342 adverse drug reaction reports of SJS-TEN in children (younger than 18 years; median age, 9 years) in all six continents. Median onset was 5 days, and 3.2% were fatal.
• They analyzed drugs reported as suspected treatments, and for each molecule, they performed a case–non-case study to assess a potential pharmacovigilance signal by computing the information component (IC).
• A positive IC value suggested more frequent reporting of a specific drug-adverse reaction pair. A positive IC025, a traditional threshold for statistical signal detection, is suggestive of a potential pharmacovigilance signal.

TAKEAWAY:

• Overall, 165 drugs were associated with a diagnosis of SJS-TEN; antiepileptic and anti-infectious drugs were the most common drug classes represented.
• The five most frequently reported drugs were carbamazepine (11.7%), lamotrigine (10.6%), sulfamethoxazole-trimethoprim (9%), acetaminophen (8.4%), and phenytoin (6.6%). The five drugs with the highest IC025 were lamotrigine, carbamazepine, phenobarbital, phenytoin, and nimesulide.
• All antiepileptics, many antibiotic families, dapsone, antiretroviral drugs, some antifungal drugs, and nonsteroidal anti-inflammatory drugs were identified in reports, with penicillins the most frequently reported antibiotic family and sulfonamides having the strongest pharmacovigilance signal.
• Vaccines were not associated with significant signals.

IN PRACTICE:

The study provides an update on “the spectrum of drugs potentially associated with SJS-TEN in the pediatric population,” the authors concluded, and “underlines the importance of reporting to pharmacovigilance the suspicion of this severe side effect of drugs with the most precise and detailed clinical description possible.”

SOURCE:

The study, led by Pauline Bataille, MD, of the Department of Pediatric Dermatology, Hôpital Necker-Enfants Malades, Paris City University, France, was published online in the Journal of the European Academy of Dermatology and Venereology.

LIMITATIONS:

Limitations include the possibility that some cases could have had an infectious or idiopathic cause not related to a drug and the lack of detailed clinical data in the database.

DISCLOSURES:

This study did not receive any funding. The authors declared no conflict of interest.

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

TOPLINE:

Antiepileptic and anti-infectious agents were the most common drugs associated with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) in children in an analysis of a World Health Organization (WHO) database.

METHODOLOGY:

• SJS and TEN are rare, life-threatening mucocutaneous reactions mainly associated with medications, but large pharmacovigilance studies of drugs associated with SJS-TEN in the pediatric population are still lacking.
• Using the WHO’s pharmacovigilance database (VigiBase) containing individual case safety reports from January 1967 to July 2022, researchers identified 7342 adverse drug reaction reports of SJS-TEN in children (younger than 18 years; median age, 9 years) in all six continents. Median onset was 5 days, and 3.2% were fatal.
• They analyzed drugs reported as suspected treatments, and for each molecule, they performed a case–non-case study to assess a potential pharmacovigilance signal by computing the information component (IC).
• A positive IC value suggested more frequent reporting of a specific drug-adverse reaction pair. A positive IC025, a traditional threshold for statistical signal detection, is suggestive of a potential pharmacovigilance signal.

TAKEAWAY:

• Overall, 165 drugs were associated with a diagnosis of SJS-TEN; antiepileptic and anti-infectious drugs were the most common drug classes represented.
• The five most frequently reported drugs were carbamazepine (11.7%), lamotrigine (10.6%), sulfamethoxazole-trimethoprim (9%), acetaminophen (8.4%), and phenytoin (6.6%). The five drugs with the highest IC025 were lamotrigine, carbamazepine, phenobarbital, phenytoin, and nimesulide.
• All antiepileptics, many antibiotic families, dapsone, antiretroviral drugs, some antifungal drugs, and nonsteroidal anti-inflammatory drugs were identified in reports, with penicillins the most frequently reported antibiotic family and sulfonamides having the strongest pharmacovigilance signal.
• Vaccines were not associated with significant signals.

IN PRACTICE:

The study provides an update on “the spectrum of drugs potentially associated with SJS-TEN in the pediatric population,” the authors concluded, and “underlines the importance of reporting to pharmacovigilance the suspicion of this severe side effect of drugs with the most precise and detailed clinical description possible.”

SOURCE:

The study, led by Pauline Bataille, MD, of the Department of Pediatric Dermatology, Hôpital Necker-Enfants Malades, Paris City University, France, was published online in the Journal of the European Academy of Dermatology and Venereology.

LIMITATIONS:

Limitations include the possibility that some cases could have had an infectious or idiopathic cause not related to a drug and the lack of detailed clinical data in the database.

DISCLOSURES:

This study did not receive any funding. The authors declared no conflict of interest.

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

A distant friend and I were recently chatting by email. After years of trying, she’s become a successful author, and decided to leave medicine to focus on the new career.

She’s excited about this, as it’s really what she’s always dreamed of doing, but at the same time feels guilty about it. Leaving medicine for a new career isn’t quite the same as quitting your job as a waitress or insurance salesman. You’ve put a lot of time, and effort, and money, into becoming an attending physician.

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

A distant friend and I were recently chatting by email. After years of trying, she’s become a successful author, and decided to leave medicine to focus on the new career.

She’s excited about this, as it’s really what she’s always dreamed of doing, but at the same time feels guilty about it. Leaving medicine for a new career isn’t quite the same as quitting your job as a waitress or insurance salesman. You’ve put a lot of time, and effort, and money, into becoming an attending physician.

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

A distant friend and I were recently chatting by email. After years of trying, she’s become a successful author, and decided to leave medicine to focus on the new career.

She’s excited about this, as it’s really what she’s always dreamed of doing, but at the same time feels guilty about it. Leaving medicine for a new career isn’t quite the same as quitting your job as a waitress or insurance salesman. You’ve put a lot of time, and effort, and money, into becoming an attending physician.

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

Meningitis has been highlighted as a novel risk factor for trigeminal neuralgia in a nationwide, propensity-matched study of hospital admissions.

In multivariate analysis, the odds of meningitis were threefold higher in patients admitted with trigeminal neuralgia than in matched controls without trigeminal neuralgia.

This is the first nationwide population-based study of the rare, chronic pain disorder to identify the prevalence of trigeminal neuralgia admissions in the United States and risk factors contributing to trigeminal neuralgia development.

“Our results affirm known associations between trigeminal neuralgia and comorbidities like multiple sclerosis, and they also identify meningitis as a novel risk factor for trigeminal neuralgia,” said investigator Megan Tang, BS, a medical student at the Icahn School of Medicine at Mount Sinai, New York City.

The findings were presented at the American Association of Neurological Surgeons (AANS) 2024 annual meeting.
 

Strong Clinical Risk Factors

Trigeminal neuralgia is a rare pain disorder involving neurovascular compression of the trigeminal nerve. Its etiology and risk factors are poorly understood. Current literature is based on limited datasets and reports inconsistent risk factors across studies.

To better understand the disorder, researchers used International Classification of Diseases (ICD)-9 codes to identify trigeminal neuralgia admissions in the National Inpatient Sample from 2016 to 2019, and then propensity matched them 1:1 to non-trigeminal neuralgia admissions based on demographics, socioeconomic status, and Charlson comorbidity index scores.

Univariate analysis identified 136,345 trigeminal neuralgia admissions or an overall prevalence of 0.096%.

Trigeminal neuralgia admissions had lower morbidity than non-trigeminal neuralgia admissions and a higher prevalence of non-White patients, private insurance, and prolonged length of stay, Ms. Tang said.

Patients admitted for trigeminal neuralgia also had a higher prevalence of several chronic conditions, including hypertension, hyperlipidemia, and osteoarthritis; inflammatory conditions like lupus, meningitis, rheumatoid arthritis, and inflammatory bowel disease; and neurologic conditions including multiple sclerosis, epilepsy, stroke, and neurovascular compression disorders.

In multivariate analysis, investigators identified meningitis as a previously unknown risk factor for trigeminal neuralgia (odds ratio [OR], 3.1; P < .001).

Other strong risk factors were neurovascular compression disorders (OR, 39.82; P < .001) and multiple sclerosis (OR, 12.41; P < .001). Non-White race (Black; OR, 1.09; Hispanic; OR, 1.23; Other; OR, 1.24) and use of Medicaid (OR, 1.07) and other insurance (OR, 1.17) were demographic risk factors for trigeminal neuralgia.

“This finding points us toward future work exploring the potential mechanisms of predictors, most notably inflammatory conditions in trigeminal neuralgia development,” Ms. Tang concluded.

She declined to comment further on the findings, noting the investigators are still finalizing the results and interpretation.
 

Ask About Meningitis, Fever

Commenting on the findings, Michael D. Staudt, MD, MSc, University Hospitals Cleveland Medical Center, said that many patients who present with classical trigeminal neuralgia will have a blood vessel on MRI that is pressing on the trigeminal nerve.

“Obviously, the nerve is bathed in cerebrospinal fluid. So, if there’s an inflammatory marker, inflammation, or infection that could be injuring the nerve in a way that we don’t yet understand, that could be something that could cause trigeminal neuralgia without having to see a blood vessel,” said Dr. Staudt, who was not involved in the study. “It makes sense, theoretically. Something that’s inflammatory, something that’s irritating, that’s novel.”

Currently, predictive markers include clinical history, response to classical medications such as carbamazepine, and MRI findings, Dr. Staudt noted.

“Someone shows up with symptoms and MRI, and it’s basically do they have a blood vessel or not,” he said. “Treatments are generally within the same categories, but we don’t think it’s the same sort of success rate as seeing a blood vessel.”

Further research is needed, but, in the meantime, Dr. Staudt said, “We can ask patients who show up with facial pain if they’ve ever had meningitis or some sort of fever that preceded their onset of pain.”

The study had no specific funding. Ms. Tang and coauthor Jack Y. Zhang, MS, reported no relevant financial disclosures. Dr. Staudt reported serving as a consultant for Abbott and as a scientific adviser and consultant for Boston Scientific.

A version of this article appeared on Medscape.com.

Meningitis has been highlighted as a novel risk factor for trigeminal neuralgia in a nationwide, propensity-matched study of hospital admissions.

In multivariate analysis, the odds of meningitis were threefold higher in patients admitted with trigeminal neuralgia than in matched controls without trigeminal neuralgia.

This is the first nationwide population-based study of the rare, chronic pain disorder to identify the prevalence of trigeminal neuralgia admissions in the United States and risk factors contributing to trigeminal neuralgia development.

“Our results affirm known associations between trigeminal neuralgia and comorbidities like multiple sclerosis, and they also identify meningitis as a novel risk factor for trigeminal neuralgia,” said investigator Megan Tang, BS, a medical student at the Icahn School of Medicine at Mount Sinai, New York City.

The findings were presented at the American Association of Neurological Surgeons (AANS) 2024 annual meeting.
 

Strong Clinical Risk Factors

Trigeminal neuralgia is a rare pain disorder involving neurovascular compression of the trigeminal nerve. Its etiology and risk factors are poorly understood. Current literature is based on limited datasets and reports inconsistent risk factors across studies.

To better understand the disorder, researchers used International Classification of Diseases (ICD)-9 codes to identify trigeminal neuralgia admissions in the National Inpatient Sample from 2016 to 2019, and then propensity matched them 1:1 to non-trigeminal neuralgia admissions based on demographics, socioeconomic status, and Charlson comorbidity index scores.

Univariate analysis identified 136,345 trigeminal neuralgia admissions or an overall prevalence of 0.096%.

Trigeminal neuralgia admissions had lower morbidity than non-trigeminal neuralgia admissions and a higher prevalence of non-White patients, private insurance, and prolonged length of stay, Ms. Tang said.

Patients admitted for trigeminal neuralgia also had a higher prevalence of several chronic conditions, including hypertension, hyperlipidemia, and osteoarthritis; inflammatory conditions like lupus, meningitis, rheumatoid arthritis, and inflammatory bowel disease; and neurologic conditions including multiple sclerosis, epilepsy, stroke, and neurovascular compression disorders.

In multivariate analysis, investigators identified meningitis as a previously unknown risk factor for trigeminal neuralgia (odds ratio [OR], 3.1; P < .001).

Other strong risk factors were neurovascular compression disorders (OR, 39.82; P < .001) and multiple sclerosis (OR, 12.41; P < .001). Non-White race (Black; OR, 1.09; Hispanic; OR, 1.23; Other; OR, 1.24) and use of Medicaid (OR, 1.07) and other insurance (OR, 1.17) were demographic risk factors for trigeminal neuralgia.

“This finding points us toward future work exploring the potential mechanisms of predictors, most notably inflammatory conditions in trigeminal neuralgia development,” Ms. Tang concluded.

She declined to comment further on the findings, noting the investigators are still finalizing the results and interpretation.
 

Ask About Meningitis, Fever

Commenting on the findings, Michael D. Staudt, MD, MSc, University Hospitals Cleveland Medical Center, said that many patients who present with classical trigeminal neuralgia will have a blood vessel on MRI that is pressing on the trigeminal nerve.

“Obviously, the nerve is bathed in cerebrospinal fluid. So, if there’s an inflammatory marker, inflammation, or infection that could be injuring the nerve in a way that we don’t yet understand, that could be something that could cause trigeminal neuralgia without having to see a blood vessel,” said Dr. Staudt, who was not involved in the study. “It makes sense, theoretically. Something that’s inflammatory, something that’s irritating, that’s novel.”

Currently, predictive markers include clinical history, response to classical medications such as carbamazepine, and MRI findings, Dr. Staudt noted.

“Someone shows up with symptoms and MRI, and it’s basically do they have a blood vessel or not,” he said. “Treatments are generally within the same categories, but we don’t think it’s the same sort of success rate as seeing a blood vessel.”

Further research is needed, but, in the meantime, Dr. Staudt said, “We can ask patients who show up with facial pain if they’ve ever had meningitis or some sort of fever that preceded their onset of pain.”

The study had no specific funding. Ms. Tang and coauthor Jack Y. Zhang, MS, reported no relevant financial disclosures. Dr. Staudt reported serving as a consultant for Abbott and as a scientific adviser and consultant for Boston Scientific.

A version of this article appeared on Medscape.com.

Meningitis has been highlighted as a novel risk factor for trigeminal neuralgia in a nationwide, propensity-matched study of hospital admissions.

In multivariate analysis, the odds of meningitis were threefold higher in patients admitted with trigeminal neuralgia than in matched controls without trigeminal neuralgia.

This is the first nationwide population-based study of the rare, chronic pain disorder to identify the prevalence of trigeminal neuralgia admissions in the United States and risk factors contributing to trigeminal neuralgia development.

“Our results affirm known associations between trigeminal neuralgia and comorbidities like multiple sclerosis, and they also identify meningitis as a novel risk factor for trigeminal neuralgia,” said investigator Megan Tang, BS, a medical student at the Icahn School of Medicine at Mount Sinai, New York City.

The findings were presented at the American Association of Neurological Surgeons (AANS) 2024 annual meeting.
 

Strong Clinical Risk Factors

Trigeminal neuralgia is a rare pain disorder involving neurovascular compression of the trigeminal nerve. Its etiology and risk factors are poorly understood. Current literature is based on limited datasets and reports inconsistent risk factors across studies.

To better understand the disorder, researchers used International Classification of Diseases (ICD)-9 codes to identify trigeminal neuralgia admissions in the National Inpatient Sample from 2016 to 2019, and then propensity matched them 1:1 to non-trigeminal neuralgia admissions based on demographics, socioeconomic status, and Charlson comorbidity index scores.

Univariate analysis identified 136,345 trigeminal neuralgia admissions or an overall prevalence of 0.096%.

Trigeminal neuralgia admissions had lower morbidity than non-trigeminal neuralgia admissions and a higher prevalence of non-White patients, private insurance, and prolonged length of stay, Ms. Tang said.

Patients admitted for trigeminal neuralgia also had a higher prevalence of several chronic conditions, including hypertension, hyperlipidemia, and osteoarthritis; inflammatory conditions like lupus, meningitis, rheumatoid arthritis, and inflammatory bowel disease; and neurologic conditions including multiple sclerosis, epilepsy, stroke, and neurovascular compression disorders.

In multivariate analysis, investigators identified meningitis as a previously unknown risk factor for trigeminal neuralgia (odds ratio [OR], 3.1; P < .001).

Other strong risk factors were neurovascular compression disorders (OR, 39.82; P < .001) and multiple sclerosis (OR, 12.41; P < .001). Non-White race (Black; OR, 1.09; Hispanic; OR, 1.23; Other; OR, 1.24) and use of Medicaid (OR, 1.07) and other insurance (OR, 1.17) were demographic risk factors for trigeminal neuralgia.

“This finding points us toward future work exploring the potential mechanisms of predictors, most notably inflammatory conditions in trigeminal neuralgia development,” Ms. Tang concluded.

She declined to comment further on the findings, noting the investigators are still finalizing the results and interpretation.
 

Ask About Meningitis, Fever

Commenting on the findings, Michael D. Staudt, MD, MSc, University Hospitals Cleveland Medical Center, said that many patients who present with classical trigeminal neuralgia will have a blood vessel on MRI that is pressing on the trigeminal nerve.

“Obviously, the nerve is bathed in cerebrospinal fluid. So, if there’s an inflammatory marker, inflammation, or infection that could be injuring the nerve in a way that we don’t yet understand, that could be something that could cause trigeminal neuralgia without having to see a blood vessel,” said Dr. Staudt, who was not involved in the study. “It makes sense, theoretically. Something that’s inflammatory, something that’s irritating, that’s novel.”

Currently, predictive markers include clinical history, response to classical medications such as carbamazepine, and MRI findings, Dr. Staudt noted.

“Someone shows up with symptoms and MRI, and it’s basically do they have a blood vessel or not,” he said. “Treatments are generally within the same categories, but we don’t think it’s the same sort of success rate as seeing a blood vessel.”

Further research is needed, but, in the meantime, Dr. Staudt said, “We can ask patients who show up with facial pain if they’ve ever had meningitis or some sort of fever that preceded their onset of pain.”

The study had no specific funding. Ms. Tang and coauthor Jack Y. Zhang, MS, reported no relevant financial disclosures. Dr. Staudt reported serving as a consultant for Abbott and as a scientific adviser and consultant for Boston Scientific.

A version of this article appeared on Medscape.com.

Racial discrimination in Black Americans is associated with an increased risk of developing Alzheimer’s disease (AD) in later life, new findings showed.

Researchers found that Black Americans who experience racism in their 40s and 50s are more likely to have increased serum levels of AD biomarkers p-tau181 and neurofilament light (NfL) more than a decade later.

“We know that Black Americans are at an elevated risk of Alzheimer’s disease and other dementias compared to non-Hispanic White Americans, but we don’t fully understand all the factors that contribute to this disproportionate risk,” Michelle Mielke, PhD, co-author and professor of epidemiology and prevention at Wake Forest University School of Medicine, Winston-Salem, North Carolina, said in a press release.

Recent data show AD is twice as prevalent in Black Americans as in Whites, at 18.6% and 10%, respectively. Dr. Mielke said this level of disparity cannot be attributed solely to genetic differences, and evidence suggests that racism and its related stress may play a role.

The findings were published online in Alzheimer’s and Dementia.
 

AD Biomarker Testing

To further explore a possible link between exposure to racism and AD risk, investigators analyzed data from the Family and Community Health Study, a multisite, longitudinal investigation that included more than 800 families in the United States.

Blood samples and information on racial discrimination were collected from 255 middle-aged Black Americans between 2002 and 2005.

Blood samples were tested for serum phosphorylated tau181 (p-Tau181), a marker of AD pathology; NfL, a nonspecific marker of neurodegeneration; and glial fibrillary acidic protein (GFAP), a marker of brain inflammation.

Participants answered questions about racial discrimination, which included whether they have been subjected to disrespectful treatment including racial slurs, harassment from law enforcement, or if they had ever been excluded from social activities because of their race.

The sample included 212 females and 43 males with a mean age of 46. Most participants (70%) lived in urban areas.
 

Stress-Related?

Investigators found no correlation between racial discrimination and increased levels of AD blood biomarkers in 2008 when participants were a mean age of 46 years. However, 11 years later, when participants were roughly 57 years old, investigators found experiencing racism in middle age was significantly correlated with higher levels of both p-Tau181 (r = 0.158; P ≤ .012) and NfL (r = 0.143; P ≤ .023). There was no significant association between reported discrimination and GFAP.

“These findings support the hypothesis that unique life stressors encountered by Black Americans in midlife become biologically embedded and contribute to AD pathology and neurodegeneration later in life,” the authors wrote.

Investigators speculated based on previous research that the stress related to discrimination may be associated with reductions in hippocampal and prefrontal cortex volumes and neurodegeneration in general.

Dr. Mielke also said it’s clear that future studies should focus on racism experienced by Black Americans to further understand their risk for dementia.

“This research can help inform policies and interventions to reduce racial disparities and reduce dementia risk,” she said.

Study limitations include the absence of amyloid biomarkers. Investigators noted that participants had non-detectable levels of amyloid, likely due to the use of serum vs cerebrospinal fluid.

The study was funded by the National Institute on Aging and the National Heart, Lung, and Blood Institute. Mielke reported serving on scientific advisory boards and/or having consulted for Acadia, Biogen, Eisai, LabCorp, Lilly, Merck, PeerView Institute, Roche, Siemens Healthineers, and Sunbird Bio.

A version of this article appeared on Medscape.com.

Racial discrimination in Black Americans is associated with an increased risk of developing Alzheimer’s disease (AD) in later life, new findings showed.

Researchers found that Black Americans who experience racism in their 40s and 50s are more likely to have increased serum levels of AD biomarkers p-tau181 and neurofilament light (NfL) more than a decade later.

“We know that Black Americans are at an elevated risk of Alzheimer’s disease and other dementias compared to non-Hispanic White Americans, but we don’t fully understand all the factors that contribute to this disproportionate risk,” Michelle Mielke, PhD, co-author and professor of epidemiology and prevention at Wake Forest University School of Medicine, Winston-Salem, North Carolina, said in a press release.

Recent data show AD is twice as prevalent in Black Americans as in Whites, at 18.6% and 10%, respectively. Dr. Mielke said this level of disparity cannot be attributed solely to genetic differences, and evidence suggests that racism and its related stress may play a role.

The findings were published online in Alzheimer’s and Dementia.
 

AD Biomarker Testing

To further explore a possible link between exposure to racism and AD risk, investigators analyzed data from the Family and Community Health Study, a multisite, longitudinal investigation that included more than 800 families in the United States.

Blood samples and information on racial discrimination were collected from 255 middle-aged Black Americans between 2002 and 2005.

Blood samples were tested for serum phosphorylated tau181 (p-Tau181), a marker of AD pathology; NfL, a nonspecific marker of neurodegeneration; and glial fibrillary acidic protein (GFAP), a marker of brain inflammation.

Participants answered questions about racial discrimination, which included whether they have been subjected to disrespectful treatment including racial slurs, harassment from law enforcement, or if they had ever been excluded from social activities because of their race.

The sample included 212 females and 43 males with a mean age of 46. Most participants (70%) lived in urban areas.
 

Stress-Related?

Investigators found no correlation between racial discrimination and increased levels of AD blood biomarkers in 2008 when participants were a mean age of 46 years. However, 11 years later, when participants were roughly 57 years old, investigators found experiencing racism in middle age was significantly correlated with higher levels of both p-Tau181 (r = 0.158; P ≤ .012) and NfL (r = 0.143; P ≤ .023). There was no significant association between reported discrimination and GFAP.

“These findings support the hypothesis that unique life stressors encountered by Black Americans in midlife become biologically embedded and contribute to AD pathology and neurodegeneration later in life,” the authors wrote.

Investigators speculated based on previous research that the stress related to discrimination may be associated with reductions in hippocampal and prefrontal cortex volumes and neurodegeneration in general.

Dr. Mielke also said it’s clear that future studies should focus on racism experienced by Black Americans to further understand their risk for dementia.

“This research can help inform policies and interventions to reduce racial disparities and reduce dementia risk,” she said.

Study limitations include the absence of amyloid biomarkers. Investigators noted that participants had non-detectable levels of amyloid, likely due to the use of serum vs cerebrospinal fluid.

The study was funded by the National Institute on Aging and the National Heart, Lung, and Blood Institute. Mielke reported serving on scientific advisory boards and/or having consulted for Acadia, Biogen, Eisai, LabCorp, Lilly, Merck, PeerView Institute, Roche, Siemens Healthineers, and Sunbird Bio.

A version of this article appeared on Medscape.com.

Racial discrimination in Black Americans is associated with an increased risk of developing Alzheimer’s disease (AD) in later life, new findings showed.

Researchers found that Black Americans who experience racism in their 40s and 50s are more likely to have increased serum levels of AD biomarkers p-tau181 and neurofilament light (NfL) more than a decade later.

“We know that Black Americans are at an elevated risk of Alzheimer’s disease and other dementias compared to non-Hispanic White Americans, but we don’t fully understand all the factors that contribute to this disproportionate risk,” Michelle Mielke, PhD, co-author and professor of epidemiology and prevention at Wake Forest University School of Medicine, Winston-Salem, North Carolina, said in a press release.

Recent data show AD is twice as prevalent in Black Americans as in Whites, at 18.6% and 10%, respectively. Dr. Mielke said this level of disparity cannot be attributed solely to genetic differences, and evidence suggests that racism and its related stress may play a role.

The findings were published online in Alzheimer’s and Dementia.
 

AD Biomarker Testing

To further explore a possible link between exposure to racism and AD risk, investigators analyzed data from the Family and Community Health Study, a multisite, longitudinal investigation that included more than 800 families in the United States.

Blood samples and information on racial discrimination were collected from 255 middle-aged Black Americans between 2002 and 2005.

Blood samples were tested for serum phosphorylated tau181 (p-Tau181), a marker of AD pathology; NfL, a nonspecific marker of neurodegeneration; and glial fibrillary acidic protein (GFAP), a marker of brain inflammation.

Participants answered questions about racial discrimination, which included whether they have been subjected to disrespectful treatment including racial slurs, harassment from law enforcement, or if they had ever been excluded from social activities because of their race.

The sample included 212 females and 43 males with a mean age of 46. Most participants (70%) lived in urban areas.
 

Stress-Related?

Investigators found no correlation between racial discrimination and increased levels of AD blood biomarkers in 2008 when participants were a mean age of 46 years. However, 11 years later, when participants were roughly 57 years old, investigators found experiencing racism in middle age was significantly correlated with higher levels of both p-Tau181 (r = 0.158; P ≤ .012) and NfL (r = 0.143; P ≤ .023). There was no significant association between reported discrimination and GFAP.

“These findings support the hypothesis that unique life stressors encountered by Black Americans in midlife become biologically embedded and contribute to AD pathology and neurodegeneration later in life,” the authors wrote.

Investigators speculated based on previous research that the stress related to discrimination may be associated with reductions in hippocampal and prefrontal cortex volumes and neurodegeneration in general.

Dr. Mielke also said it’s clear that future studies should focus on racism experienced by Black Americans to further understand their risk for dementia.

“This research can help inform policies and interventions to reduce racial disparities and reduce dementia risk,” she said.

Study limitations include the absence of amyloid biomarkers. Investigators noted that participants had non-detectable levels of amyloid, likely due to the use of serum vs cerebrospinal fluid.

The study was funded by the National Institute on Aging and the National Heart, Lung, and Blood Institute. Mielke reported serving on scientific advisory boards and/or having consulted for Acadia, Biogen, Eisai, LabCorp, Lilly, Merck, PeerView Institute, Roche, Siemens Healthineers, and Sunbird Bio.

A version of this article appeared on Medscape.com.

Clinicians interested in treating patients with symptoms of mild cognitive impairment or mild dementia should carefully analyze the potential benefits and harms of monoclonal amyloid beta therapy, including likelihood of side effects and overall burden on the patient, according to researchers at the annual meeting of the American Geriatrics Society (AGS). 

Lecanemab (Leqembi) may help some patients by lowering the level of beta-amyloid protein in the brain. Results from a phase 3 trial presented at the conference showed participants with Alzheimer’s disease had a 27% slower progression of the disease compared with placebo.

But clinicians must weigh that advantage against risks and contraindications, according to Esther Oh, MD, PhD, an associate professor in the Division of Geriatric Medicine and Gerontology and co-director of the Johns Hopkins Memory and Alzheimer’s Treatment Center, Johns Hopkins University, Baltimore, Maryland, who spoke during a plenary session. Lecanemab gained accelerated approval by the US Food and Drug Administration in January 2023 and full approval in July 2023.

The results from CLARITY, an 18-month, multicenter, double-blind trial involving 1795 participants aged 50-90 years, showed that the variation between treatment and placebo did not meet the criteria for a minimum clinically important difference for mild cognitive impairment or mild Alzheimer’s disease.

Even more concerning to Dr. Oh was the rate of amyloid-related abnormalities on brain imaging, which can cause brain edema and hemorrhage (12.6% and 17.3%, respectively). Almost 85% of cases were asymptomatic. 

The risk for abnormalities indicates that thrombolytics are contraindicated for patients taking the drug, according to Dr. Oh. 

“Appropriate use recommendations exclude vitamin K antagonists such as warfarin, direct oral anticoagulants and heparin, although aspirin and other antiplatelet agents are allowed,” Dr. Oh said during the presentation.

Blood biomarkers, PET imaging, and levels of amyloid-beta proteins in cerebrospinal fluid are used to determine eligibility for lecanemab. However, tau biomarkers may indicate signs of cognitive impairment decades prior to symptoms. Some evidence indicates that the drug may be more effective in individuals with low tau levels that are evident in earlier stages of disease. Tau can also be determined from cerebrospinal fluid, however, “we do not factor in tau protein as a biomarker for treatment eligibility, but this may become an important biomarker in the future,” Dr. Oh said.

Lecanemab is cost-prohibitive for many patients, with an annual price tag of $26,000. Treatment also requires monthly infusions, a PET, intravenous administration, lab work, multiple MRIs, and potentially an APOE4 serum test.

Medicare covers the majority of services, but patients are responsible for deductibles and copays, an estimated $7000 annually, according to Shari Ling, MD, deputy chief medical officer with the US Centers for Medicare & Medicaid Services, who also spoke during the session. Supplemental or other insurance such as Medicaid are also not included in this estimate.

The Medicare population is growing more complex over time, Dr. Ling said. In 2021, 54% of beneficiaries had five or more comorbidities, which can affect eligibility for lecanemab. 

“Across the healthcare system, we are learning what is necessary for coordination of delivery, for evaluation of people who receive these treatments, and for the care that is not anticipated,” Dr. Ling noted.

Neither speaker reported any financial conflicts of interest.

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

Clinicians interested in treating patients with symptoms of mild cognitive impairment or mild dementia should carefully analyze the potential benefits and harms of monoclonal amyloid beta therapy, including likelihood of side effects and overall burden on the patient, according to researchers at the annual meeting of the American Geriatrics Society (AGS). 

Lecanemab (Leqembi) may help some patients by lowering the level of beta-amyloid protein in the brain. Results from a phase 3 trial presented at the conference showed participants with Alzheimer’s disease had a 27% slower progression of the disease compared with placebo.

But clinicians must weigh that advantage against risks and contraindications, according to Esther Oh, MD, PhD, an associate professor in the Division of Geriatric Medicine and Gerontology and co-director of the Johns Hopkins Memory and Alzheimer’s Treatment Center, Johns Hopkins University, Baltimore, Maryland, who spoke during a plenary session. Lecanemab gained accelerated approval by the US Food and Drug Administration in January 2023 and full approval in July 2023.

The results from CLARITY, an 18-month, multicenter, double-blind trial involving 1795 participants aged 50-90 years, showed that the variation between treatment and placebo did not meet the criteria for a minimum clinically important difference for mild cognitive impairment or mild Alzheimer’s disease.

Even more concerning to Dr. Oh was the rate of amyloid-related abnormalities on brain imaging, which can cause brain edema and hemorrhage (12.6% and 17.3%, respectively). Almost 85% of cases were asymptomatic. 

The risk for abnormalities indicates that thrombolytics are contraindicated for patients taking the drug, according to Dr. Oh. 

“Appropriate use recommendations exclude vitamin K antagonists such as warfarin, direct oral anticoagulants and heparin, although aspirin and other antiplatelet agents are allowed,” Dr. Oh said during the presentation.

Blood biomarkers, PET imaging, and levels of amyloid-beta proteins in cerebrospinal fluid are used to determine eligibility for lecanemab. However, tau biomarkers may indicate signs of cognitive impairment decades prior to symptoms. Some evidence indicates that the drug may be more effective in individuals with low tau levels that are evident in earlier stages of disease. Tau can also be determined from cerebrospinal fluid, however, “we do not factor in tau protein as a biomarker for treatment eligibility, but this may become an important biomarker in the future,” Dr. Oh said.

Lecanemab is cost-prohibitive for many patients, with an annual price tag of $26,000. Treatment also requires monthly infusions, a PET, intravenous administration, lab work, multiple MRIs, and potentially an APOE4 serum test.

Medicare covers the majority of services, but patients are responsible for deductibles and copays, an estimated $7000 annually, according to Shari Ling, MD, deputy chief medical officer with the US Centers for Medicare & Medicaid Services, who also spoke during the session. Supplemental or other insurance such as Medicaid are also not included in this estimate.

The Medicare population is growing more complex over time, Dr. Ling said. In 2021, 54% of beneficiaries had five or more comorbidities, which can affect eligibility for lecanemab. 

“Across the healthcare system, we are learning what is necessary for coordination of delivery, for evaluation of people who receive these treatments, and for the care that is not anticipated,” Dr. Ling noted.

Neither speaker reported any financial conflicts of interest.

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

Clinicians interested in treating patients with symptoms of mild cognitive impairment or mild dementia should carefully analyze the potential benefits and harms of monoclonal amyloid beta therapy, including likelihood of side effects and overall burden on the patient, according to researchers at the annual meeting of the American Geriatrics Society (AGS). 

Lecanemab (Leqembi) may help some patients by lowering the level of beta-amyloid protein in the brain. Results from a phase 3 trial presented at the conference showed participants with Alzheimer’s disease had a 27% slower progression of the disease compared with placebo.

But clinicians must weigh that advantage against risks and contraindications, according to Esther Oh, MD, PhD, an associate professor in the Division of Geriatric Medicine and Gerontology and co-director of the Johns Hopkins Memory and Alzheimer’s Treatment Center, Johns Hopkins University, Baltimore, Maryland, who spoke during a plenary session. Lecanemab gained accelerated approval by the US Food and Drug Administration in January 2023 and full approval in July 2023.

The results from CLARITY, an 18-month, multicenter, double-blind trial involving 1795 participants aged 50-90 years, showed that the variation between treatment and placebo did not meet the criteria for a minimum clinically important difference for mild cognitive impairment or mild Alzheimer’s disease.

Even more concerning to Dr. Oh was the rate of amyloid-related abnormalities on brain imaging, which can cause brain edema and hemorrhage (12.6% and 17.3%, respectively). Almost 85% of cases were asymptomatic. 

The risk for abnormalities indicates that thrombolytics are contraindicated for patients taking the drug, according to Dr. Oh. 

“Appropriate use recommendations exclude vitamin K antagonists such as warfarin, direct oral anticoagulants and heparin, although aspirin and other antiplatelet agents are allowed,” Dr. Oh said during the presentation.

Blood biomarkers, PET imaging, and levels of amyloid-beta proteins in cerebrospinal fluid are used to determine eligibility for lecanemab. However, tau biomarkers may indicate signs of cognitive impairment decades prior to symptoms. Some evidence indicates that the drug may be more effective in individuals with low tau levels that are evident in earlier stages of disease. Tau can also be determined from cerebrospinal fluid, however, “we do not factor in tau protein as a biomarker for treatment eligibility, but this may become an important biomarker in the future,” Dr. Oh said.

Lecanemab is cost-prohibitive for many patients, with an annual price tag of $26,000. Treatment also requires monthly infusions, a PET, intravenous administration, lab work, multiple MRIs, and potentially an APOE4 serum test.

Medicare covers the majority of services, but patients are responsible for deductibles and copays, an estimated $7000 annually, according to Shari Ling, MD, deputy chief medical officer with the US Centers for Medicare & Medicaid Services, who also spoke during the session. Supplemental or other insurance such as Medicaid are also not included in this estimate.

The Medicare population is growing more complex over time, Dr. Ling said. In 2021, 54% of beneficiaries had five or more comorbidities, which can affect eligibility for lecanemab. 

“Across the healthcare system, we are learning what is necessary for coordination of delivery, for evaluation of people who receive these treatments, and for the care that is not anticipated,” Dr. Ling noted.

Neither speaker reported any financial conflicts of interest.

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

In a recent article in the American Journal of Obstetrics & Gynecology, Rebecca C. Thurston, PhD, and Pauline Maki, PhD, leading scientists in the area of menopause’s impact on brain function, presented data from their assessment of 248 late perimenopausal and postmenopausal women who reported hot flashes, also known as vasomotor symptoms (VMS).

Hot flashes are known to be associated with changes in brain white matter, carotid atherosclerosis, brain function, and memory. Dr. Thurston and colleagues objectively measured VMS over 24 hours, using skin conductance monitoring. Plasma concentrations of Alzheimer’s disease biomarkers, including the amyloid beta 42–to–amyloid beta 40 ratio, were assessed. The mean age of study participants was 59 years, and they experienced a mean of five objective VMS daily.

A key finding was that VMS, particularly those occurring during sleep, were associated with a significantly lower amyloid beta 42–to–beta 40 ratio. This finding suggests that nighttime VMS may be a marker of risk for Alzheimer’s disease.

Previous research has found that menopausal hormone therapy is associated with favorable changes in Alzheimer’s disease biomarkers. Likewise, large observational studies have shown a lower incidence of Alzheimer’s disease among women who initiate hormone therapy in their late perimenopausal or early postmenopausal years and continue such therapy long term.

The findings of this important study by Thurston and colleagues provide further evidence to support the tantalizing possibility that agents that reduce nighttime hot flashes (including hormone therapy) may lower the subsequent incidence of Alzheimer’s disease in high-risk women.
 

Dr. Kaunitz is a tenured professor and associate chair in the department of obstetrics and gynecology at the University of Florida College of Medicine–Jacksonville, and medical director and director of menopause and gynecologic ultrasound services at the University of Florida Southside Women’s Health, Jacksonville. He disclosed ties to Sumitomo Pharma America, Mithra, Viatris, Bayer, Merck, Mylan (Viatris), and UpToDate.

A version of this article appeared on Medscape.com.

In a recent article in the American Journal of Obstetrics & Gynecology, Rebecca C. Thurston, PhD, and Pauline Maki, PhD, leading scientists in the area of menopause’s impact on brain function, presented data from their assessment of 248 late perimenopausal and postmenopausal women who reported hot flashes, also known as vasomotor symptoms (VMS).

Hot flashes are known to be associated with changes in brain white matter, carotid atherosclerosis, brain function, and memory. Dr. Thurston and colleagues objectively measured VMS over 24 hours, using skin conductance monitoring. Plasma concentrations of Alzheimer’s disease biomarkers, including the amyloid beta 42–to–amyloid beta 40 ratio, were assessed. The mean age of study participants was 59 years, and they experienced a mean of five objective VMS daily.

A key finding was that VMS, particularly those occurring during sleep, were associated with a significantly lower amyloid beta 42–to–beta 40 ratio. This finding suggests that nighttime VMS may be a marker of risk for Alzheimer’s disease.

Previous research has found that menopausal hormone therapy is associated with favorable changes in Alzheimer’s disease biomarkers. Likewise, large observational studies have shown a lower incidence of Alzheimer’s disease among women who initiate hormone therapy in their late perimenopausal or early postmenopausal years and continue such therapy long term.

The findings of this important study by Thurston and colleagues provide further evidence to support the tantalizing possibility that agents that reduce nighttime hot flashes (including hormone therapy) may lower the subsequent incidence of Alzheimer’s disease in high-risk women.
 

Dr. Kaunitz is a tenured professor and associate chair in the department of obstetrics and gynecology at the University of Florida College of Medicine–Jacksonville, and medical director and director of menopause and gynecologic ultrasound services at the University of Florida Southside Women’s Health, Jacksonville. He disclosed ties to Sumitomo Pharma America, Mithra, Viatris, Bayer, Merck, Mylan (Viatris), and UpToDate.

A version of this article appeared on Medscape.com.

In a recent article in the American Journal of Obstetrics & Gynecology, Rebecca C. Thurston, PhD, and Pauline Maki, PhD, leading scientists in the area of menopause’s impact on brain function, presented data from their assessment of 248 late perimenopausal and postmenopausal women who reported hot flashes, also known as vasomotor symptoms (VMS).

Hot flashes are known to be associated with changes in brain white matter, carotid atherosclerosis, brain function, and memory. Dr. Thurston and colleagues objectively measured VMS over 24 hours, using skin conductance monitoring. Plasma concentrations of Alzheimer’s disease biomarkers, including the amyloid beta 42–to–amyloid beta 40 ratio, were assessed. The mean age of study participants was 59 years, and they experienced a mean of five objective VMS daily.

A key finding was that VMS, particularly those occurring during sleep, were associated with a significantly lower amyloid beta 42–to–beta 40 ratio. This finding suggests that nighttime VMS may be a marker of risk for Alzheimer’s disease.

Previous research has found that menopausal hormone therapy is associated with favorable changes in Alzheimer’s disease biomarkers. Likewise, large observational studies have shown a lower incidence of Alzheimer’s disease among women who initiate hormone therapy in their late perimenopausal or early postmenopausal years and continue such therapy long term.

The findings of this important study by Thurston and colleagues provide further evidence to support the tantalizing possibility that agents that reduce nighttime hot flashes (including hormone therapy) may lower the subsequent incidence of Alzheimer’s disease in high-risk women.
 

Dr. Kaunitz is a tenured professor and associate chair in the department of obstetrics and gynecology at the University of Florida College of Medicine–Jacksonville, and medical director and director of menopause and gynecologic ultrasound services at the University of Florida Southside Women’s Health, Jacksonville. He disclosed ties to Sumitomo Pharma America, Mithra, Viatris, Bayer, Merck, Mylan (Viatris), and UpToDate.

A version of this article appeared on Medscape.com.

Lower urinary tract symptoms were significantly associated with lower scores on measures of cognitive impairment in older adults, based on data from approximately 10,000 individuals.

“We know that lower urinary tract symptoms are very common in aging men and women;” however, older adults often underreport symptoms and avoid seeking treatment, Belinda Williams, MD, of the University of Alabama, Birmingham, said in a presentation at the annual meeting of the American Geriatrics Society.

“Evidence also shows us that the incidence of lower urinary tract symptoms (LUTS) is higher in patients with dementia,” she said. However, the association between cognitive impairment and LUTS has not been well studied, she said.

To address this knowledge gap, Dr. Williams and colleagues reviewed data from older adults with and without LUTS who were enrolled in the REasons for Geographic and Racial Differences in Stroke (REGARDS) study, a cohort study including 30,239 Black or White adults aged 45 years and older who completed telephone or in-home assessments in 2003-2007 and in 2013-2017.

The study population included 6062 women and 4438 men who responded to questionnaires about LUTS and completed several cognitive tests via telephone in 2019-2010. The tests evaluated verbal fluency, executive function, and memory, and included the Six-Item Screener, Animal Naming, Letter F naming, and word list learning; lower scores indicated poorer cognitive performance.

Participants who met the criteria for LUTS were categorized as having mild, moderate, or severe symptoms.

The researchers controlled for age, race, education, income, and urban/rural setting in a multivariate analysis. The mean ages of the women and men were 69 years and 63 years, respectively; 41% and 32% were Black, 59% and 68% were White.

Overall, 70% of women and 62% of men reported LUTS; 6.2% and 8.2%, respectively, met criteria for cognitive impairment. The association between cognitive impairment and LUTS was statistically significant for all specific tests (P < .01), but not for the global cognitive domain tests.

Black men were more likely to report LUTS than White men, but LUTS reports were similar between Black and White women.

Moderate LUTS was the most common degree of severity for men and women (54% and 64%, respectively).

The most common symptom overall was pre-toilet leakage (urge urinary incontinence), reported by 94% of women and 91% of men. The next most common symptoms for men and women were nocturia and urgency.

“We found that, across the board, in all the cognitive tests, LUTS were associated with lower cognitive test scores,” Dr. Williams said in her presentation. Little differences were seen on the Six-Item Screener, she noted, but when they further analyzed the data using scores lower than 4 to indicate cognitive impairment, they found significant association with LUTS, she said.

The results showing that the presence of LUTS was consistently associated with lower cognitive test scores of verbal fluency, executive function, and memory, are applicable in clinical practice, Dr. Williams said in her presentation.

“Recognizing the subtle changes in cognition among older adults with LUTS may impact treatment decisions,” she said. “For example, we can encourage and advise our patients to be physically and cognitively active and to avoid anticholinergic medications.”

Next steps for research include analyzing longitudinal changes in cognition among participants with and without LUTS, said Dr. Williams.

During a question-and-answer session, Dr. Williams agreed with a comment that incorporating cognitive screening strategies in to LUTS clinical pathways might be helpful, such as conducting a baseline Montreal Cognitive Assessment Test (MoCA) in patients with LUTS. “Periodic repeat MoCAs thereafter can help assess decline in cognition,” she said.

The study was supported by the National Institutes of Neurological Disorders and Stroke and the National Institute on Aging. The researchers had no financial conflicts to disclose.

Lower urinary tract symptoms were significantly associated with lower scores on measures of cognitive impairment in older adults, based on data from approximately 10,000 individuals.

“We know that lower urinary tract symptoms are very common in aging men and women;” however, older adults often underreport symptoms and avoid seeking treatment, Belinda Williams, MD, of the University of Alabama, Birmingham, said in a presentation at the annual meeting of the American Geriatrics Society.

“Evidence also shows us that the incidence of lower urinary tract symptoms (LUTS) is higher in patients with dementia,” she said. However, the association between cognitive impairment and LUTS has not been well studied, she said.

To address this knowledge gap, Dr. Williams and colleagues reviewed data from older adults with and without LUTS who were enrolled in the REasons for Geographic and Racial Differences in Stroke (REGARDS) study, a cohort study including 30,239 Black or White adults aged 45 years and older who completed telephone or in-home assessments in 2003-2007 and in 2013-2017.

The study population included 6062 women and 4438 men who responded to questionnaires about LUTS and completed several cognitive tests via telephone in 2019-2010. The tests evaluated verbal fluency, executive function, and memory, and included the Six-Item Screener, Animal Naming, Letter F naming, and word list learning; lower scores indicated poorer cognitive performance.

Participants who met the criteria for LUTS were categorized as having mild, moderate, or severe symptoms.

The researchers controlled for age, race, education, income, and urban/rural setting in a multivariate analysis. The mean ages of the women and men were 69 years and 63 years, respectively; 41% and 32% were Black, 59% and 68% were White.

Overall, 70% of women and 62% of men reported LUTS; 6.2% and 8.2%, respectively, met criteria for cognitive impairment. The association between cognitive impairment and LUTS was statistically significant for all specific tests (P < .01), but not for the global cognitive domain tests.

Black men were more likely to report LUTS than White men, but LUTS reports were similar between Black and White women.

Moderate LUTS was the most common degree of severity for men and women (54% and 64%, respectively).

The most common symptom overall was pre-toilet leakage (urge urinary incontinence), reported by 94% of women and 91% of men. The next most common symptoms for men and women were nocturia and urgency.

“We found that, across the board, in all the cognitive tests, LUTS were associated with lower cognitive test scores,” Dr. Williams said in her presentation. Little differences were seen on the Six-Item Screener, she noted, but when they further analyzed the data using scores lower than 4 to indicate cognitive impairment, they found significant association with LUTS, she said.

The results showing that the presence of LUTS was consistently associated with lower cognitive test scores of verbal fluency, executive function, and memory, are applicable in clinical practice, Dr. Williams said in her presentation.

“Recognizing the subtle changes in cognition among older adults with LUTS may impact treatment decisions,” she said. “For example, we can encourage and advise our patients to be physically and cognitively active and to avoid anticholinergic medications.”

Next steps for research include analyzing longitudinal changes in cognition among participants with and without LUTS, said Dr. Williams.

During a question-and-answer session, Dr. Williams agreed with a comment that incorporating cognitive screening strategies in to LUTS clinical pathways might be helpful, such as conducting a baseline Montreal Cognitive Assessment Test (MoCA) in patients with LUTS. “Periodic repeat MoCAs thereafter can help assess decline in cognition,” she said.

The study was supported by the National Institutes of Neurological Disorders and Stroke and the National Institute on Aging. The researchers had no financial conflicts to disclose.

Lower urinary tract symptoms were significantly associated with lower scores on measures of cognitive impairment in older adults, based on data from approximately 10,000 individuals.

“We know that lower urinary tract symptoms are very common in aging men and women;” however, older adults often underreport symptoms and avoid seeking treatment, Belinda Williams, MD, of the University of Alabama, Birmingham, said in a presentation at the annual meeting of the American Geriatrics Society.

“Evidence also shows us that the incidence of lower urinary tract symptoms (LUTS) is higher in patients with dementia,” she said. However, the association between cognitive impairment and LUTS has not been well studied, she said.

To address this knowledge gap, Dr. Williams and colleagues reviewed data from older adults with and without LUTS who were enrolled in the REasons for Geographic and Racial Differences in Stroke (REGARDS) study, a cohort study including 30,239 Black or White adults aged 45 years and older who completed telephone or in-home assessments in 2003-2007 and in 2013-2017.

The study population included 6062 women and 4438 men who responded to questionnaires about LUTS and completed several cognitive tests via telephone in 2019-2010. The tests evaluated verbal fluency, executive function, and memory, and included the Six-Item Screener, Animal Naming, Letter F naming, and word list learning; lower scores indicated poorer cognitive performance.

Participants who met the criteria for LUTS were categorized as having mild, moderate, or severe symptoms.

The researchers controlled for age, race, education, income, and urban/rural setting in a multivariate analysis. The mean ages of the women and men were 69 years and 63 years, respectively; 41% and 32% were Black, 59% and 68% were White.

Overall, 70% of women and 62% of men reported LUTS; 6.2% and 8.2%, respectively, met criteria for cognitive impairment. The association between cognitive impairment and LUTS was statistically significant for all specific tests (P < .01), but not for the global cognitive domain tests.

Black men were more likely to report LUTS than White men, but LUTS reports were similar between Black and White women.

Moderate LUTS was the most common degree of severity for men and women (54% and 64%, respectively).

The most common symptom overall was pre-toilet leakage (urge urinary incontinence), reported by 94% of women and 91% of men. The next most common symptoms for men and women were nocturia and urgency.

“We found that, across the board, in all the cognitive tests, LUTS were associated with lower cognitive test scores,” Dr. Williams said in her presentation. Little differences were seen on the Six-Item Screener, she noted, but when they further analyzed the data using scores lower than 4 to indicate cognitive impairment, they found significant association with LUTS, she said.

The results showing that the presence of LUTS was consistently associated with lower cognitive test scores of verbal fluency, executive function, and memory, are applicable in clinical practice, Dr. Williams said in her presentation.

“Recognizing the subtle changes in cognition among older adults with LUTS may impact treatment decisions,” she said. “For example, we can encourage and advise our patients to be physically and cognitively active and to avoid anticholinergic medications.”

Next steps for research include analyzing longitudinal changes in cognition among participants with and without LUTS, said Dr. Williams.

During a question-and-answer session, Dr. Williams agreed with a comment that incorporating cognitive screening strategies in to LUTS clinical pathways might be helpful, such as conducting a baseline Montreal Cognitive Assessment Test (MoCA) in patients with LUTS. “Periodic repeat MoCAs thereafter can help assess decline in cognition,” she said.

The study was supported by the National Institutes of Neurological Disorders and Stroke and the National Institute on Aging. The researchers had no financial conflicts to disclose.

It’s becoming clear that the adolescent brain is particularly vulnerable to cannabis, especially today’s higher-potency products, which put teens at risk for impaired brain development; mental health issues, including psychosis; and cannabis-use disorder (CUD). 

That was the message delivered by Yasmin Hurd, PhD, director of the Addiction Institute at Mount Sinai in New York, during a press briefing at the American Psychiatric Association (APA) 2024 annual meeting. 

“We’re actually in historic times in that we now have highly concentrated, highly potent cannabis products that are administered in various routes,” Dr. Hurd told reporters. 

Tetrahydrocannabinol (THC) concentrations in cannabis products have increased over the years, from around 2%-4% to 15%-24% now, Dr. Hurd noted.

The impact of high-potency cannabis products and increased risk for CUD and mental health problems, particularly in adolescents, “must be taken seriously, especially in light of the current mental health crisis,” Dr. Hurd and colleagues wrote in a commentary on the developmental trajectory of CUD published simultaneously in the American Journal of Psychiatry. 
 

Dramatic Increase in Teen Cannabis Use

A recent study from Oregon Health & Science University showed that adolescent cannabis abuse in the United States has increased dramatically, by about 245%, since 2000. 

“Drug abuse is often driven by what is in front of you,” Nora Volkow, MD, director of the National Institute on Drug Abuse, noted in an interview. 

“Right now, cannabis is widely available. So, guess what? Cannabis becomes the drug that people take. Nicotine is much harder to get. It is regulated to a much greater extent than cannabis, so fewer teenagers are consuming nicotine than are consuming cannabis,” Dr. Volkow said. 

Cannabis exposure during neurodevelopment has the potential to alter the endocannabinoid system, which in turn, can affect the development of neural pathways that mediate reward; emotional regulation; and multiple cognitive domains including executive functioning and decision-making, learning, abstraction, and attention — all processes central to substance use disorder and other psychiatric disorders, Dr. Hurd said at the briefing.

Dr. Volkow said that cannabis use in adolescence and young adulthood is “very concerning because that’s also the age of risk for psychosis, particularly schizophrenia, with one study showing that use of cannabis in high doses can trigger psychotic episodes, particularly among young males.”

Dr. Hurd noted that not all young people who use cannabis develop CUD, “but a significant number do,” and large-scale studies have consistently reported two main factors associated with CUD risk.

The first is age, both for the onset and frequency of use at younger age. Those who start using cannabis before age 16 years are at the highest risk for CUD. The risk for CUD also increases significantly among youth who use cannabis at least weekly, with the highest prevalence among youth who use cannabis daily. One large study linked increased frequency of use with up to a 17-fold increased risk for CUD.

The second factor consistently associated with the risk for CUD is biologic sex, with CUD rates typically higher in male individuals.
 

Treatment Challenges

For young people who develop CUD, access to and uptake of treatment can be challenging.

“Given that the increased potency of cannabis and cannabinoid products is expected to increase CUD risk, it is disturbing that less than 10% of youth who meet the criteria for a substance use disorder, including CUD, receive treatment,” Dr. Hurd and colleagues point out in their commentary. 

Another challenge is that treatment strategies for CUD are currently limited and consist mainly of motivational enhancement and cognitive-behavioral therapies. 

“Clearly new treatment strategies are needed to address the mounting challenge of CUD risk in teens and young adults,” Dr. Hurd and colleagues wrote. 

Summing up, Dr. Hurd told reporters, “We now know that most psychiatric disorders have a developmental origin, and the adolescent time period is a critical window for cannabis use disorder risk.”

Yet, on a positive note, the “plasticity of the developing brain that makes it vulnerable to cannabis use disorder and psychiatric comorbidities also provides an opportunity for prevention and early intervention to change that trajectory,” Dr. Hurd said. 

The changing legal landscape of cannabis — the US Drug Enforcement Agency is moving forward with plans to move marijuana from a Schedule I to a Schedule III controlled substance under the Controlled Substance Act — makes addressing these risks all the timelier. 

“As states vie to leverage tax dollars from the growing cannabis industry, a significant portion of such funds must be used for early intervention/prevention strategies to reduce the impact of cannabis on the developing brain,” Dr. Hurd and colleagues wrote. 

This research was supported in part by the National Institute on Drug Abuse and the National Institutes of Health. Dr. Hurd and Dr. Volkow have no relevant disclosures. 

A version of this article appeared on Medscape.com.

It’s becoming clear that the adolescent brain is particularly vulnerable to cannabis, especially today’s higher-potency products, which put teens at risk for impaired brain development; mental health issues, including psychosis; and cannabis-use disorder (CUD). 

That was the message delivered by Yasmin Hurd, PhD, director of the Addiction Institute at Mount Sinai in New York, during a press briefing at the American Psychiatric Association (APA) 2024 annual meeting. 

“We’re actually in historic times in that we now have highly concentrated, highly potent cannabis products that are administered in various routes,” Dr. Hurd told reporters. 

Tetrahydrocannabinol (THC) concentrations in cannabis products have increased over the years, from around 2%-4% to 15%-24% now, Dr. Hurd noted.

The impact of high-potency cannabis products and increased risk for CUD and mental health problems, particularly in adolescents, “must be taken seriously, especially in light of the current mental health crisis,” Dr. Hurd and colleagues wrote in a commentary on the developmental trajectory of CUD published simultaneously in the American Journal of Psychiatry. 
 

Dramatic Increase in Teen Cannabis Use

A recent study from Oregon Health & Science University showed that adolescent cannabis abuse in the United States has increased dramatically, by about 245%, since 2000. 

“Drug abuse is often driven by what is in front of you,” Nora Volkow, MD, director of the National Institute on Drug Abuse, noted in an interview. 

“Right now, cannabis is widely available. So, guess what? Cannabis becomes the drug that people take. Nicotine is much harder to get. It is regulated to a much greater extent than cannabis, so fewer teenagers are consuming nicotine than are consuming cannabis,” Dr. Volkow said. 

Cannabis exposure during neurodevelopment has the potential to alter the endocannabinoid system, which in turn, can affect the development of neural pathways that mediate reward; emotional regulation; and multiple cognitive domains including executive functioning and decision-making, learning, abstraction, and attention — all processes central to substance use disorder and other psychiatric disorders, Dr. Hurd said at the briefing.

Dr. Volkow said that cannabis use in adolescence and young adulthood is “very concerning because that’s also the age of risk for psychosis, particularly schizophrenia, with one study showing that use of cannabis in high doses can trigger psychotic episodes, particularly among young males.”

Dr. Hurd noted that not all young people who use cannabis develop CUD, “but a significant number do,” and large-scale studies have consistently reported two main factors associated with CUD risk.

The first is age, both for the onset and frequency of use at younger age. Those who start using cannabis before age 16 years are at the highest risk for CUD. The risk for CUD also increases significantly among youth who use cannabis at least weekly, with the highest prevalence among youth who use cannabis daily. One large study linked increased frequency of use with up to a 17-fold increased risk for CUD.

The second factor consistently associated with the risk for CUD is biologic sex, with CUD rates typically higher in male individuals.
 

Treatment Challenges

For young people who develop CUD, access to and uptake of treatment can be challenging.

“Given that the increased potency of cannabis and cannabinoid products is expected to increase CUD risk, it is disturbing that less than 10% of youth who meet the criteria for a substance use disorder, including CUD, receive treatment,” Dr. Hurd and colleagues point out in their commentary. 

Another challenge is that treatment strategies for CUD are currently limited and consist mainly of motivational enhancement and cognitive-behavioral therapies. 

“Clearly new treatment strategies are needed to address the mounting challenge of CUD risk in teens and young adults,” Dr. Hurd and colleagues wrote. 

Summing up, Dr. Hurd told reporters, “We now know that most psychiatric disorders have a developmental origin, and the adolescent time period is a critical window for cannabis use disorder risk.”

Yet, on a positive note, the “plasticity of the developing brain that makes it vulnerable to cannabis use disorder and psychiatric comorbidities also provides an opportunity for prevention and early intervention to change that trajectory,” Dr. Hurd said. 

The changing legal landscape of cannabis — the US Drug Enforcement Agency is moving forward with plans to move marijuana from a Schedule I to a Schedule III controlled substance under the Controlled Substance Act — makes addressing these risks all the timelier. 

“As states vie to leverage tax dollars from the growing cannabis industry, a significant portion of such funds must be used for early intervention/prevention strategies to reduce the impact of cannabis on the developing brain,” Dr. Hurd and colleagues wrote. 

This research was supported in part by the National Institute on Drug Abuse and the National Institutes of Health. Dr. Hurd and Dr. Volkow have no relevant disclosures. 

A version of this article appeared on Medscape.com.

It’s becoming clear that the adolescent brain is particularly vulnerable to cannabis, especially today’s higher-potency products, which put teens at risk for impaired brain development; mental health issues, including psychosis; and cannabis-use disorder (CUD). 

That was the message delivered by Yasmin Hurd, PhD, director of the Addiction Institute at Mount Sinai in New York, during a press briefing at the American Psychiatric Association (APA) 2024 annual meeting. 

“We’re actually in historic times in that we now have highly concentrated, highly potent cannabis products that are administered in various routes,” Dr. Hurd told reporters. 

Tetrahydrocannabinol (THC) concentrations in cannabis products have increased over the years, from around 2%-4% to 15%-24% now, Dr. Hurd noted.

The impact of high-potency cannabis products and increased risk for CUD and mental health problems, particularly in adolescents, “must be taken seriously, especially in light of the current mental health crisis,” Dr. Hurd and colleagues wrote in a commentary on the developmental trajectory of CUD published simultaneously in the American Journal of Psychiatry. 
 

Dramatic Increase in Teen Cannabis Use

A recent study from Oregon Health & Science University showed that adolescent cannabis abuse in the United States has increased dramatically, by about 245%, since 2000. 

“Drug abuse is often driven by what is in front of you,” Nora Volkow, MD, director of the National Institute on Drug Abuse, noted in an interview. 

“Right now, cannabis is widely available. So, guess what? Cannabis becomes the drug that people take. Nicotine is much harder to get. It is regulated to a much greater extent than cannabis, so fewer teenagers are consuming nicotine than are consuming cannabis,” Dr. Volkow said. 

Cannabis exposure during neurodevelopment has the potential to alter the endocannabinoid system, which in turn, can affect the development of neural pathways that mediate reward; emotional regulation; and multiple cognitive domains including executive functioning and decision-making, learning, abstraction, and attention — all processes central to substance use disorder and other psychiatric disorders, Dr. Hurd said at the briefing.

Dr. Volkow said that cannabis use in adolescence and young adulthood is “very concerning because that’s also the age of risk for psychosis, particularly schizophrenia, with one study showing that use of cannabis in high doses can trigger psychotic episodes, particularly among young males.”

Dr. Hurd noted that not all young people who use cannabis develop CUD, “but a significant number do,” and large-scale studies have consistently reported two main factors associated with CUD risk.

The first is age, both for the onset and frequency of use at younger age. Those who start using cannabis before age 16 years are at the highest risk for CUD. The risk for CUD also increases significantly among youth who use cannabis at least weekly, with the highest prevalence among youth who use cannabis daily. One large study linked increased frequency of use with up to a 17-fold increased risk for CUD.

The second factor consistently associated with the risk for CUD is biologic sex, with CUD rates typically higher in male individuals.
 

Treatment Challenges

For young people who develop CUD, access to and uptake of treatment can be challenging.

“Given that the increased potency of cannabis and cannabinoid products is expected to increase CUD risk, it is disturbing that less than 10% of youth who meet the criteria for a substance use disorder, including CUD, receive treatment,” Dr. Hurd and colleagues point out in their commentary. 

Another challenge is that treatment strategies for CUD are currently limited and consist mainly of motivational enhancement and cognitive-behavioral therapies. 

“Clearly new treatment strategies are needed to address the mounting challenge of CUD risk in teens and young adults,” Dr. Hurd and colleagues wrote. 

Summing up, Dr. Hurd told reporters, “We now know that most psychiatric disorders have a developmental origin, and the adolescent time period is a critical window for cannabis use disorder risk.”

Yet, on a positive note, the “plasticity of the developing brain that makes it vulnerable to cannabis use disorder and psychiatric comorbidities also provides an opportunity for prevention and early intervention to change that trajectory,” Dr. Hurd said. 

The changing legal landscape of cannabis — the US Drug Enforcement Agency is moving forward with plans to move marijuana from a Schedule I to a Schedule III controlled substance under the Controlled Substance Act — makes addressing these risks all the timelier. 

“As states vie to leverage tax dollars from the growing cannabis industry, a significant portion of such funds must be used for early intervention/prevention strategies to reduce the impact of cannabis on the developing brain,” Dr. Hurd and colleagues wrote. 

This research was supported in part by the National Institute on Drug Abuse and the National Institutes of Health. Dr. Hurd and Dr. Volkow have no relevant disclosures. 

A version of this article appeared on Medscape.com.