Neurology

The first updated guidelines for specialized epilepsy centers in a decade reflect a shift toward addressing patients’ overall well-being, including recommendations for genetic testing and counseling, mental health screening, and greater attention to special-needs populations. 

The guidelines — the first from the National Association of Epilepsy Centers (NAEC) in a decade — describe the comprehensive services and resources specialized epilepsy centers should provide to improve quality of care for people living with epilepsy.

“In addition to advances in medicine, there has been a shift toward addressing overall well-being beyond seizure management,” Fred A. Lado, MD, PhD, NAEC president and guideline panel cochair, said in a news release. “This includes care for comorbid conditions like anxiety and depression, enhanced communication between the patient and care team, and addressing health disparities in the epilepsy community.

The guidance was developed by a panel of multidisciplinary experts, which is the first time that the NAEC has gone beyond the field of neurology to seek input from other medical specialists and allied health personnel, the panel noted. 

“Expanded guidelines are also sorely needed to help centers and hospitals obtain the resources to provide this level of comprehensive care,” said Dr. Lado, regional director of epilepsy and professor of neurology at Zucker School of Medicine at Hofstra/Northwell in Hempstead, New York. 

An executive summary of the guidelines was published online in Neurology. 
 

A Multidisciplinary Approach

Epilepsy is one of the most common chronic neurologic conditions worldwide, affecting an estimated 3.4 million people in the United States alone. Recurring seizures can be debilitating and, in some cases, life-threatening. 

To update epilepsy care guidelines, an expert panel of 41 stakeholders with diverse expertise evaluated the latest evidence and reached consensus on 52 recommendations spanning a range of services that make up high-quality epilepsy care. 

“This is exhibited in a greater emphasis on multidisciplinary care conferences, screening for comorbidities of epilepsy, and providing access to other specialty services in addition to the core epilepsy center components of outpatient care, diagnostic procedures, and epilepsy surgery,” they wrote. 

For the first time, the guidelines advise specialized epilepsy centers to offer genetic testing and counseling, provide more education and communication for patients, give greater attention to special-needs populations, employ a care coordinator to organize and facilitate multidisciplinary care, provide mental health screening, and address health disparities and inequities.

“All recommendations quickly reached consensus despite there being such a diverse panel of stakeholders, which emphasizes that the recommendations reflect the important elements of healthcare services that should be in place for an epilepsy center to provide the highest quality of care,” said Susan Arnold, MD, guideline panel co-chair and a pediatric epileptologist at Yale University School of Medicine, New Haven, Connecticut.

“But epilepsy centers will need the resources to provide this comprehensive level of care. We hope the guidelines will help increase health insurer and institutional support and recognition of these recommendations,” Dr. Arnold added. 

The guidelines were funded by NAEC. Dr. Lado has no relevant disclosures. Dr. Arnold holds stock in Pfizer. A complete list of disclosures for the guideline panel is available with the original article. 
 

A version of this article appeared on Medscape.com.

The first updated guidelines for specialized epilepsy centers in a decade reflect a shift toward addressing patients’ overall well-being, including recommendations for genetic testing and counseling, mental health screening, and greater attention to special-needs populations. 

The guidelines — the first from the National Association of Epilepsy Centers (NAEC) in a decade — describe the comprehensive services and resources specialized epilepsy centers should provide to improve quality of care for people living with epilepsy.

“In addition to advances in medicine, there has been a shift toward addressing overall well-being beyond seizure management,” Fred A. Lado, MD, PhD, NAEC president and guideline panel cochair, said in a news release. “This includes care for comorbid conditions like anxiety and depression, enhanced communication between the patient and care team, and addressing health disparities in the epilepsy community.

The guidance was developed by a panel of multidisciplinary experts, which is the first time that the NAEC has gone beyond the field of neurology to seek input from other medical specialists and allied health personnel, the panel noted. 

“Expanded guidelines are also sorely needed to help centers and hospitals obtain the resources to provide this level of comprehensive care,” said Dr. Lado, regional director of epilepsy and professor of neurology at Zucker School of Medicine at Hofstra/Northwell in Hempstead, New York. 

An executive summary of the guidelines was published online in Neurology. 
 

A Multidisciplinary Approach

Epilepsy is one of the most common chronic neurologic conditions worldwide, affecting an estimated 3.4 million people in the United States alone. Recurring seizures can be debilitating and, in some cases, life-threatening. 

To update epilepsy care guidelines, an expert panel of 41 stakeholders with diverse expertise evaluated the latest evidence and reached consensus on 52 recommendations spanning a range of services that make up high-quality epilepsy care. 

“This is exhibited in a greater emphasis on multidisciplinary care conferences, screening for comorbidities of epilepsy, and providing access to other specialty services in addition to the core epilepsy center components of outpatient care, diagnostic procedures, and epilepsy surgery,” they wrote. 

For the first time, the guidelines advise specialized epilepsy centers to offer genetic testing and counseling, provide more education and communication for patients, give greater attention to special-needs populations, employ a care coordinator to organize and facilitate multidisciplinary care, provide mental health screening, and address health disparities and inequities.

“All recommendations quickly reached consensus despite there being such a diverse panel of stakeholders, which emphasizes that the recommendations reflect the important elements of healthcare services that should be in place for an epilepsy center to provide the highest quality of care,” said Susan Arnold, MD, guideline panel co-chair and a pediatric epileptologist at Yale University School of Medicine, New Haven, Connecticut.

“But epilepsy centers will need the resources to provide this comprehensive level of care. We hope the guidelines will help increase health insurer and institutional support and recognition of these recommendations,” Dr. Arnold added. 

The guidelines were funded by NAEC. Dr. Lado has no relevant disclosures. Dr. Arnold holds stock in Pfizer. A complete list of disclosures for the guideline panel is available with the original article. 
 

A version of this article appeared on Medscape.com.

The first updated guidelines for specialized epilepsy centers in a decade reflect a shift toward addressing patients’ overall well-being, including recommendations for genetic testing and counseling, mental health screening, and greater attention to special-needs populations. 

The guidelines — the first from the National Association of Epilepsy Centers (NAEC) in a decade — describe the comprehensive services and resources specialized epilepsy centers should provide to improve quality of care for people living with epilepsy.

“In addition to advances in medicine, there has been a shift toward addressing overall well-being beyond seizure management,” Fred A. Lado, MD, PhD, NAEC president and guideline panel cochair, said in a news release. “This includes care for comorbid conditions like anxiety and depression, enhanced communication between the patient and care team, and addressing health disparities in the epilepsy community.

The guidance was developed by a panel of multidisciplinary experts, which is the first time that the NAEC has gone beyond the field of neurology to seek input from other medical specialists and allied health personnel, the panel noted. 

“Expanded guidelines are also sorely needed to help centers and hospitals obtain the resources to provide this level of comprehensive care,” said Dr. Lado, regional director of epilepsy and professor of neurology at Zucker School of Medicine at Hofstra/Northwell in Hempstead, New York. 

An executive summary of the guidelines was published online in Neurology. 
 

A Multidisciplinary Approach

Epilepsy is one of the most common chronic neurologic conditions worldwide, affecting an estimated 3.4 million people in the United States alone. Recurring seizures can be debilitating and, in some cases, life-threatening. 

To update epilepsy care guidelines, an expert panel of 41 stakeholders with diverse expertise evaluated the latest evidence and reached consensus on 52 recommendations spanning a range of services that make up high-quality epilepsy care. 

“This is exhibited in a greater emphasis on multidisciplinary care conferences, screening for comorbidities of epilepsy, and providing access to other specialty services in addition to the core epilepsy center components of outpatient care, diagnostic procedures, and epilepsy surgery,” they wrote. 

For the first time, the guidelines advise specialized epilepsy centers to offer genetic testing and counseling, provide more education and communication for patients, give greater attention to special-needs populations, employ a care coordinator to organize and facilitate multidisciplinary care, provide mental health screening, and address health disparities and inequities.

“All recommendations quickly reached consensus despite there being such a diverse panel of stakeholders, which emphasizes that the recommendations reflect the important elements of healthcare services that should be in place for an epilepsy center to provide the highest quality of care,” said Susan Arnold, MD, guideline panel co-chair and a pediatric epileptologist at Yale University School of Medicine, New Haven, Connecticut.

“But epilepsy centers will need the resources to provide this comprehensive level of care. We hope the guidelines will help increase health insurer and institutional support and recognition of these recommendations,” Dr. Arnold added. 

The guidelines were funded by NAEC. Dr. Lado has no relevant disclosures. Dr. Arnold holds stock in Pfizer. A complete list of disclosures for the guideline panel is available with the original article. 
 

A version of this article appeared on Medscape.com.

TOPLINE:

People with polycystic ovary syndrome (PCOS) may score lower on cognitive tests than people without the condition, a research showed. They also may have worse integrity of brain tissue as evident on an MRI.

METHODOLOGY:

• Researchers used data from the Coronary Artery Risk Development in Young Adults Women’s Study; individuals were 18-30 years old at the beginning of the study and were followed over 30 years.
• A little over 900 women were included in the study, of which 66 had PCOS, which was defined as having elevated androgen levels or self-reported hirsutism and irregular menstrual cycles more than 32 days apart.
• Study participants completed tests measuring verbal learning and memory, processing speed and executive function, attention and cognitive control, and semantics and attention.
• Researchers analyzed brain white matter integrity for 291 of the individuals, including 25 with PCOS, who underwent MRI.

TAKEAWAY:

• Individuals with PCOS had worse memory, attention, and verbal ability scores than those without the disorder.
• MRI scans showed that those with PCOS had lower white matter integrity, an indicator of cognitive deficits, including poorer decision-making abilities.
• Those in the PCOS group were more likely to be White and have diabetes than those in the control group.

IN PRACTICE:

“This report of midlife cognition in PCOS raises a new concern about another potential comorbidity for individuals with this common disorder; given that up to 10% of women may be affected by PCOS, these results have important implications for public health at large,” the authors concluded.

SOURCE:

Heather G. Huddleston, MD, director of the PCOS Clinic at the UCSF Health, San Francisco, California, is the lead author of the study published in Neurology.

LIMITATIONS:

PCOS was determined on the basis of serum androgen levels and self-reporting of hirsutism and oligomenorrhea, so some cases may have been misclassified without the official diagnosis of a clinician.

DISCLOSURES:

The authors did not report any relevant financial conflicts. The study was funded by a grant from the University of California, San Francisco, California.

A version of this article appeared on Medscape.com.

TOPLINE:

People with polycystic ovary syndrome (PCOS) may score lower on cognitive tests than people without the condition, a research showed. They also may have worse integrity of brain tissue as evident on an MRI.

METHODOLOGY:

• Researchers used data from the Coronary Artery Risk Development in Young Adults Women’s Study; individuals were 18-30 years old at the beginning of the study and were followed over 30 years.
• A little over 900 women were included in the study, of which 66 had PCOS, which was defined as having elevated androgen levels or self-reported hirsutism and irregular menstrual cycles more than 32 days apart.
• Study participants completed tests measuring verbal learning and memory, processing speed and executive function, attention and cognitive control, and semantics and attention.
• Researchers analyzed brain white matter integrity for 291 of the individuals, including 25 with PCOS, who underwent MRI.

TAKEAWAY:

• Individuals with PCOS had worse memory, attention, and verbal ability scores than those without the disorder.
• MRI scans showed that those with PCOS had lower white matter integrity, an indicator of cognitive deficits, including poorer decision-making abilities.
• Those in the PCOS group were more likely to be White and have diabetes than those in the control group.

IN PRACTICE:

“This report of midlife cognition in PCOS raises a new concern about another potential comorbidity for individuals with this common disorder; given that up to 10% of women may be affected by PCOS, these results have important implications for public health at large,” the authors concluded.

SOURCE:

Heather G. Huddleston, MD, director of the PCOS Clinic at the UCSF Health, San Francisco, California, is the lead author of the study published in Neurology.

LIMITATIONS:

PCOS was determined on the basis of serum androgen levels and self-reporting of hirsutism and oligomenorrhea, so some cases may have been misclassified without the official diagnosis of a clinician.

DISCLOSURES:

The authors did not report any relevant financial conflicts. The study was funded by a grant from the University of California, San Francisco, California.

A version of this article appeared on Medscape.com.

TOPLINE:

People with polycystic ovary syndrome (PCOS) may score lower on cognitive tests than people without the condition, a research showed. They also may have worse integrity of brain tissue as evident on an MRI.

METHODOLOGY:

• Researchers used data from the Coronary Artery Risk Development in Young Adults Women’s Study; individuals were 18-30 years old at the beginning of the study and were followed over 30 years.
• A little over 900 women were included in the study, of which 66 had PCOS, which was defined as having elevated androgen levels or self-reported hirsutism and irregular menstrual cycles more than 32 days apart.
• Study participants completed tests measuring verbal learning and memory, processing speed and executive function, attention and cognitive control, and semantics and attention.
• Researchers analyzed brain white matter integrity for 291 of the individuals, including 25 with PCOS, who underwent MRI.

TAKEAWAY:

• Individuals with PCOS had worse memory, attention, and verbal ability scores than those without the disorder.
• MRI scans showed that those with PCOS had lower white matter integrity, an indicator of cognitive deficits, including poorer decision-making abilities.
• Those in the PCOS group were more likely to be White and have diabetes than those in the control group.

IN PRACTICE:

“This report of midlife cognition in PCOS raises a new concern about another potential comorbidity for individuals with this common disorder; given that up to 10% of women may be affected by PCOS, these results have important implications for public health at large,” the authors concluded.

SOURCE:

Heather G. Huddleston, MD, director of the PCOS Clinic at the UCSF Health, San Francisco, California, is the lead author of the study published in Neurology.

LIMITATIONS:

PCOS was determined on the basis of serum androgen levels and self-reporting of hirsutism and oligomenorrhea, so some cases may have been misclassified without the official diagnosis of a clinician.

DISCLOSURES:

The authors did not report any relevant financial conflicts. The study was funded by a grant from the University of California, San Francisco, California.

A version of this article appeared on Medscape.com.

TOPLINE:

Social frailty, the lack of resources to meet basic social needs, is associated with an increased risk for motoric cognitive risk syndrome (MCR), a predementia syndrome characterized by cognitive complaints and slow gait, results of a large, population-based study suggested.

METHODOLOGY:

• The study used 2011 (Round 1) to 2018 (Round 8) data on a discovery sample of 4657 individuals without MCR or dementia at baseline from the National Health and Aging Trends Study (NHATS), a longitudinal survey of older adult Medicare beneficiaries.
• Researchers also collected data on 3075 newly recruited individuals in Round 5 and followed to Round 8 as an independent validation sample to create a pooled sample of 7732 older adults, mean age 76.06, without MCR at baseline.
• Social frailty, assessed at baseline, included five social items: Going out less, not feeling confident, rarely visiting friends/family, not talking with others, and without live-in partner/spouse (researchers divided participants into normal [zero to one items] and social frailty [two to five items] groups).
• Individuals were considered to have MCR if they had both subjective cognitive complaints and slow gait speed (greater than 1 standard deviation below age-specific level) without dementia or mobility disability.
• Covariates included demographic and lifestyle data, presence of depression and/or anxiety symptoms, and number of chronic diseases.

TAKEAWAY:

• During a median follow-up period of 4 years, 10.35% individuals were diagnosed with MCR.
• After the researchers controlled for confounding factors, those with social frailty had an increased risk for MCR compared with the normal group (pooled sample: hazard ratio [HR], 1.57; 95% CI, 1.34-1.84; P < .001).
• Each additional unfavorable social item was associated with an increased risk for MCR (pooled sample: HR, 1.32; 95% CI, 1.22-1.43; P < .001).
• Results of stratified analyses across subgroups suggested individuals with social frailty had a significantly higher risk for incident MCR than that of those without social frailty, regardless of socioeconomic status, lifestyle factors, chronic diseases, and mental health.

IN PRACTICE:

The findings suggest assessing social frailty using simple questions “is an efficient tool for detecting older individuals with a high risk of MCR,” the authors wrote. They noted that the addition of such a tool in clinical practice may facilitate “timely implementation of prevention strategies.”

SOURCE:

The research was led by Hui Zhang, Human Phenome Institute, Zhangjiang Fudan International Innovation Centre, Fudan University, Shanghai, China. It was published online on January 29, 2024, in Alzheimer’s & Dementia.

LIMITATIONS:

The study was observational, so the association between social frailty and MCR is merely correlational. Due to the lack of genetic information in NHATS data, researchers didn’t evaluate the effect of genetic factors such as apolipoprotein E on the association between social frailty and MCR. Social frailty was assessed at a single time point. In addition, the researchers were unable examine the time sequence between social frailty and MCR and so could not determine the cause of this association.

DISCLOSURES:

The study was supported by the National Natural Science Foundation of China-Youth Science Fund, Shanghai Rising-Star Program, Shanghai Municipal Health Commission and Key Discipline Construction Project of Pudong Health, and Family Planning Commission of Shanghai. The authors reported no relevant conflicts of interest.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Social frailty, the lack of resources to meet basic social needs, is associated with an increased risk for motoric cognitive risk syndrome (MCR), a predementia syndrome characterized by cognitive complaints and slow gait, results of a large, population-based study suggested.

METHODOLOGY:

• The study used 2011 (Round 1) to 2018 (Round 8) data on a discovery sample of 4657 individuals without MCR or dementia at baseline from the National Health and Aging Trends Study (NHATS), a longitudinal survey of older adult Medicare beneficiaries.
• Researchers also collected data on 3075 newly recruited individuals in Round 5 and followed to Round 8 as an independent validation sample to create a pooled sample of 7732 older adults, mean age 76.06, without MCR at baseline.
• Social frailty, assessed at baseline, included five social items: Going out less, not feeling confident, rarely visiting friends/family, not talking with others, and without live-in partner/spouse (researchers divided participants into normal [zero to one items] and social frailty [two to five items] groups).
• Individuals were considered to have MCR if they had both subjective cognitive complaints and slow gait speed (greater than 1 standard deviation below age-specific level) without dementia or mobility disability.
• Covariates included demographic and lifestyle data, presence of depression and/or anxiety symptoms, and number of chronic diseases.

TAKEAWAY:

• During a median follow-up period of 4 years, 10.35% individuals were diagnosed with MCR.
• After the researchers controlled for confounding factors, those with social frailty had an increased risk for MCR compared with the normal group (pooled sample: hazard ratio [HR], 1.57; 95% CI, 1.34-1.84; P < .001).
• Each additional unfavorable social item was associated with an increased risk for MCR (pooled sample: HR, 1.32; 95% CI, 1.22-1.43; P < .001).
• Results of stratified analyses across subgroups suggested individuals with social frailty had a significantly higher risk for incident MCR than that of those without social frailty, regardless of socioeconomic status, lifestyle factors, chronic diseases, and mental health.

IN PRACTICE:

The findings suggest assessing social frailty using simple questions “is an efficient tool for detecting older individuals with a high risk of MCR,” the authors wrote. They noted that the addition of such a tool in clinical practice may facilitate “timely implementation of prevention strategies.”

SOURCE:

The research was led by Hui Zhang, Human Phenome Institute, Zhangjiang Fudan International Innovation Centre, Fudan University, Shanghai, China. It was published online on January 29, 2024, in Alzheimer’s & Dementia.

LIMITATIONS:

The study was observational, so the association between social frailty and MCR is merely correlational. Due to the lack of genetic information in NHATS data, researchers didn’t evaluate the effect of genetic factors such as apolipoprotein E on the association between social frailty and MCR. Social frailty was assessed at a single time point. In addition, the researchers were unable examine the time sequence between social frailty and MCR and so could not determine the cause of this association.

DISCLOSURES:

The study was supported by the National Natural Science Foundation of China-Youth Science Fund, Shanghai Rising-Star Program, Shanghai Municipal Health Commission and Key Discipline Construction Project of Pudong Health, and Family Planning Commission of Shanghai. The authors reported no relevant conflicts of interest.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Social frailty, the lack of resources to meet basic social needs, is associated with an increased risk for motoric cognitive risk syndrome (MCR), a predementia syndrome characterized by cognitive complaints and slow gait, results of a large, population-based study suggested.

METHODOLOGY:

• The study used 2011 (Round 1) to 2018 (Round 8) data on a discovery sample of 4657 individuals without MCR or dementia at baseline from the National Health and Aging Trends Study (NHATS), a longitudinal survey of older adult Medicare beneficiaries.
• Researchers also collected data on 3075 newly recruited individuals in Round 5 and followed to Round 8 as an independent validation sample to create a pooled sample of 7732 older adults, mean age 76.06, without MCR at baseline.
• Social frailty, assessed at baseline, included five social items: Going out less, not feeling confident, rarely visiting friends/family, not talking with others, and without live-in partner/spouse (researchers divided participants into normal [zero to one items] and social frailty [two to five items] groups).
• Individuals were considered to have MCR if they had both subjective cognitive complaints and slow gait speed (greater than 1 standard deviation below age-specific level) without dementia or mobility disability.
• Covariates included demographic and lifestyle data, presence of depression and/or anxiety symptoms, and number of chronic diseases.

TAKEAWAY:

• During a median follow-up period of 4 years, 10.35% individuals were diagnosed with MCR.
• After the researchers controlled for confounding factors, those with social frailty had an increased risk for MCR compared with the normal group (pooled sample: hazard ratio [HR], 1.57; 95% CI, 1.34-1.84; P < .001).
• Each additional unfavorable social item was associated with an increased risk for MCR (pooled sample: HR, 1.32; 95% CI, 1.22-1.43; P < .001).
• Results of stratified analyses across subgroups suggested individuals with social frailty had a significantly higher risk for incident MCR than that of those without social frailty, regardless of socioeconomic status, lifestyle factors, chronic diseases, and mental health.

IN PRACTICE:

The findings suggest assessing social frailty using simple questions “is an efficient tool for detecting older individuals with a high risk of MCR,” the authors wrote. They noted that the addition of such a tool in clinical practice may facilitate “timely implementation of prevention strategies.”

SOURCE:

The research was led by Hui Zhang, Human Phenome Institute, Zhangjiang Fudan International Innovation Centre, Fudan University, Shanghai, China. It was published online on January 29, 2024, in Alzheimer’s & Dementia.

LIMITATIONS:

The study was observational, so the association between social frailty and MCR is merely correlational. Due to the lack of genetic information in NHATS data, researchers didn’t evaluate the effect of genetic factors such as apolipoprotein E on the association between social frailty and MCR. Social frailty was assessed at a single time point. In addition, the researchers were unable examine the time sequence between social frailty and MCR and so could not determine the cause of this association.

DISCLOSURES:

The study was supported by the National Natural Science Foundation of China-Youth Science Fund, Shanghai Rising-Star Program, Shanghai Municipal Health Commission and Key Discipline Construction Project of Pudong Health, and Family Planning Commission of Shanghai. The authors reported no relevant conflicts of interest.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Migraine is associated with a significantly increased risk of developing inflammatory bowel disease (IBD), including both Crohn’s disease (CD) and ulcerative colitis (UC), a new nationwide, population-based cohort study showed.

METHODOLOGY:

• Investigators analyzed data from South Korea’s National Health Insurance Service (NHIS) database, which houses data for the nationwide obligatory health system for South Korean citizens.
• Individuals aged ≥ 20 years who had at least one national health screening in 2009 were enrolled in the study and followed until December 2019.
• Investigators searched the data for International Classification of Diseases (10th Revision) codes corresponding to migraine and IBD. IBD diagnoses were also based on clinical manifestation, endoscopic findings, and pathologic findings.

TAKEAWAY:

• More than 10 million people were enrolled in the study (55% male; mean age, 47 years), and of these, 2.8% were diagnosed with migraine during the study period.
• During a median follow-up of 10 years, the incidence of IBD was significantly higher in patients with migraine (adjusted hazard ratio [aHR], 1.31; P < .001), CD (aHR, 1.58; P < .001) and UC (aHR, 1.26; P < .001) than in those without migraine.
• in men vs women (aHR, 1.43 vs 1.12; P = .042).
• Investigators could only speculate about the mechanisms underlying the association between migraine and IBD but suggest pathological processes underlying both migraine and IBD, including proinflammatory cytokines and tumor necrosis factor alpha, may be involved.

IN PRACTICE:

“Clinicians should be aware of the potential risk of IBD in patients diagnosed with migraine especially in men for the development of UC and in migraineurs with a long disease duration for a further risk of CD,” the authors wrote.

SOURCE:

Hyunjung Lee, MD, of Seoul National University College of Medicine, Seoul, South Korea, led the study, which was published online on January 12, 2024, in Scientific Reports.

LIMITATIONS:

Disease severity of migraine and IBD was not available. In addition, certain medications taken to relieve migraine, such as nonsteroidal anti-inflammatory drugs like ibuprofen, could cause intestinal inflammation, but there was no medication information available.

DISCLOSURES:

There was no information about study funding nor disclosures from study authors.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Migraine is associated with a significantly increased risk of developing inflammatory bowel disease (IBD), including both Crohn’s disease (CD) and ulcerative colitis (UC), a new nationwide, population-based cohort study showed.

METHODOLOGY:

• Investigators analyzed data from South Korea’s National Health Insurance Service (NHIS) database, which houses data for the nationwide obligatory health system for South Korean citizens.
• Individuals aged ≥ 20 years who had at least one national health screening in 2009 were enrolled in the study and followed until December 2019.
• Investigators searched the data for International Classification of Diseases (10th Revision) codes corresponding to migraine and IBD. IBD diagnoses were also based on clinical manifestation, endoscopic findings, and pathologic findings.

TAKEAWAY:

• More than 10 million people were enrolled in the study (55% male; mean age, 47 years), and of these, 2.8% were diagnosed with migraine during the study period.
• During a median follow-up of 10 years, the incidence of IBD was significantly higher in patients with migraine (adjusted hazard ratio [aHR], 1.31; P < .001), CD (aHR, 1.58; P < .001) and UC (aHR, 1.26; P < .001) than in those without migraine.
• in men vs women (aHR, 1.43 vs 1.12; P = .042).
• Investigators could only speculate about the mechanisms underlying the association between migraine and IBD but suggest pathological processes underlying both migraine and IBD, including proinflammatory cytokines and tumor necrosis factor alpha, may be involved.

IN PRACTICE:

“Clinicians should be aware of the potential risk of IBD in patients diagnosed with migraine especially in men for the development of UC and in migraineurs with a long disease duration for a further risk of CD,” the authors wrote.

SOURCE:

Hyunjung Lee, MD, of Seoul National University College of Medicine, Seoul, South Korea, led the study, which was published online on January 12, 2024, in Scientific Reports.

LIMITATIONS:

Disease severity of migraine and IBD was not available. In addition, certain medications taken to relieve migraine, such as nonsteroidal anti-inflammatory drugs like ibuprofen, could cause intestinal inflammation, but there was no medication information available.

DISCLOSURES:

There was no information about study funding nor disclosures from study authors.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Migraine is associated with a significantly increased risk of developing inflammatory bowel disease (IBD), including both Crohn’s disease (CD) and ulcerative colitis (UC), a new nationwide, population-based cohort study showed.

METHODOLOGY:

• Investigators analyzed data from South Korea’s National Health Insurance Service (NHIS) database, which houses data for the nationwide obligatory health system for South Korean citizens.
• Individuals aged ≥ 20 years who had at least one national health screening in 2009 were enrolled in the study and followed until December 2019.
• Investigators searched the data for International Classification of Diseases (10th Revision) codes corresponding to migraine and IBD. IBD diagnoses were also based on clinical manifestation, endoscopic findings, and pathologic findings.

TAKEAWAY:

• More than 10 million people were enrolled in the study (55% male; mean age, 47 years), and of these, 2.8% were diagnosed with migraine during the study period.
• During a median follow-up of 10 years, the incidence of IBD was significantly higher in patients with migraine (adjusted hazard ratio [aHR], 1.31; P < .001), CD (aHR, 1.58; P < .001) and UC (aHR, 1.26; P < .001) than in those without migraine.
• in men vs women (aHR, 1.43 vs 1.12; P = .042).
• Investigators could only speculate about the mechanisms underlying the association between migraine and IBD but suggest pathological processes underlying both migraine and IBD, including proinflammatory cytokines and tumor necrosis factor alpha, may be involved.

IN PRACTICE:

“Clinicians should be aware of the potential risk of IBD in patients diagnosed with migraine especially in men for the development of UC and in migraineurs with a long disease duration for a further risk of CD,” the authors wrote.

SOURCE:

Hyunjung Lee, MD, of Seoul National University College of Medicine, Seoul, South Korea, led the study, which was published online on January 12, 2024, in Scientific Reports.

LIMITATIONS:

Disease severity of migraine and IBD was not available. In addition, certain medications taken to relieve migraine, such as nonsteroidal anti-inflammatory drugs like ibuprofen, could cause intestinal inflammation, but there was no medication information available.

DISCLOSURES:

There was no information about study funding nor disclosures from study authors.
 

A version of this article appeared on Medscape.com.

Modern technology for recording deep-brain activity involves sharp metal electrodes that penetrate the tissue, causing damage that can compromise the signal and limiting how often they can be used. 

A rapidly growing area in materials science and engineering aims to fix the problem by designing electrodes that are softer, smaller, and flexible — safer for use inside the delicate tissues of the brain. On January 17, researchers from the University of California, San Diego, reported the development of a thin, flexible electrode that can be inserted deep within the brain and communicate with sensors on the surface. 

But what if you could record detailed deep-brain activity without piercing the brain? 

A team of researchers (as it happens, also from UC San Diego) have developed a thin, flexible implant that “resides on the brain’s surface” and “can infer neural activity from deeper layers,” said Duygu Kuzum, PhD, a professor of electrical and computer engineering, who led the research. 

By combining electrical and optical imaging methods, and artificial intelligence, the researchers used the device — a polymer strip packed with graphene electrodes — to predict deep calcium activity from surface signals, according to a proof-of-concept study published this month in Nature Nanotechnology. 

“Almost everything we know about how neurons behave in living brains comes from data collected with either electrophysiology or two-photon imaging,” said neuroscientist Joshua H. Siegle, PhD, of the Allen Institute for Neural Dynamics in Seattle , who not involved in the study. “ Until now, these two methods have rarely been used simultaneously.”

The technology, which has been tested in mice, could help advance our knowledge of how the brain works and may lead to new minimally invasive treatments for neurologic disorders. 
 

Multimodal Neurotech: The Power of 2-in-1

Electrical and optical methods for recording brain activity have been crucial in advancing neurophysiologic science, but each technique has its limits. Electrical recordings provide high “temporal resolution”; they reveal when activation is happening, but not really where. Optical imaging, on the other hand, offers high “spatial resolution,” showing which area of the brain is lighting up, but its measurements may not correspond with the activity’s timing. 

Research over the past decade has explored how to combine and harness the strengths of both methods. One potential solution is to use electrodes made of transparent materials such as graphene, allowing a clear field of view for a microscope during imaging. Recently, University of Pennsylvania scientists used graphene electrodes to illuminate the neural dynamics of seizures. 

But there are challenges. If graphene electrodes are very small — in this case, 20 µm in diameter — they become more resistant to the flow of electricity. Dr. Kuzum and colleagues addressed this by adding tiny platinum particles to improve electrical conductivity. Long graphene wires connect electrodes to the circuit board, but defects in graphene can interrupt the signal, so they made each wire with two layers; any defects in one wire could be hidden by the other.

By combining the two methods (microelectrode arrays and two-photon imaging), the researchers could see both when brain activity was happening and where, including in deeper layers. They discovered a correlation between electrical responses on the surface and cellular calcium activity deeper down. The team used these data to create a neural network (a type of artificial intelligence that learns to recognize patterns) that predicts deep calcium activity from surface-level readings.

The tech could help scientists study brain activity “in a way not possible with current single-function tools,” said Luyao Lu, PhD, professor of biomedical engineering at George Washington University in Washington, DC, who was not involved in the study. It could shed light on interactions between vascular and electrical activity, or explain how place cells (neurons in the hippocampus) are so efficient at creating spatial memory. 

It could also pave the way for minimally invasive neural prosthetics or targeted treatments for neurologic disorders, the researchers say. Implanting the device would be a “straightforward process” similar to placing electrocorticography grids in patients with epilepsy, said Dr. Kuzum. 

But first, the team plans to do more studies in animal models before testing the tech in clinical settings, Dr. Kuzum added.

A version of this article appeared on Medscape.com.

Modern technology for recording deep-brain activity involves sharp metal electrodes that penetrate the tissue, causing damage that can compromise the signal and limiting how often they can be used. 

A rapidly growing area in materials science and engineering aims to fix the problem by designing electrodes that are softer, smaller, and flexible — safer for use inside the delicate tissues of the brain. On January 17, researchers from the University of California, San Diego, reported the development of a thin, flexible electrode that can be inserted deep within the brain and communicate with sensors on the surface. 

But what if you could record detailed deep-brain activity without piercing the brain? 

A team of researchers (as it happens, also from UC San Diego) have developed a thin, flexible implant that “resides on the brain’s surface” and “can infer neural activity from deeper layers,” said Duygu Kuzum, PhD, a professor of electrical and computer engineering, who led the research. 

By combining electrical and optical imaging methods, and artificial intelligence, the researchers used the device — a polymer strip packed with graphene electrodes — to predict deep calcium activity from surface signals, according to a proof-of-concept study published this month in Nature Nanotechnology. 

“Almost everything we know about how neurons behave in living brains comes from data collected with either electrophysiology or two-photon imaging,” said neuroscientist Joshua H. Siegle, PhD, of the Allen Institute for Neural Dynamics in Seattle , who not involved in the study. “ Until now, these two methods have rarely been used simultaneously.”

The technology, which has been tested in mice, could help advance our knowledge of how the brain works and may lead to new minimally invasive treatments for neurologic disorders. 
 

Multimodal Neurotech: The Power of 2-in-1

Electrical and optical methods for recording brain activity have been crucial in advancing neurophysiologic science, but each technique has its limits. Electrical recordings provide high “temporal resolution”; they reveal when activation is happening, but not really where. Optical imaging, on the other hand, offers high “spatial resolution,” showing which area of the brain is lighting up, but its measurements may not correspond with the activity’s timing. 

Research over the past decade has explored how to combine and harness the strengths of both methods. One potential solution is to use electrodes made of transparent materials such as graphene, allowing a clear field of view for a microscope during imaging. Recently, University of Pennsylvania scientists used graphene electrodes to illuminate the neural dynamics of seizures. 

But there are challenges. If graphene electrodes are very small — in this case, 20 µm in diameter — they become more resistant to the flow of electricity. Dr. Kuzum and colleagues addressed this by adding tiny platinum particles to improve electrical conductivity. Long graphene wires connect electrodes to the circuit board, but defects in graphene can interrupt the signal, so they made each wire with two layers; any defects in one wire could be hidden by the other.

By combining the two methods (microelectrode arrays and two-photon imaging), the researchers could see both when brain activity was happening and where, including in deeper layers. They discovered a correlation between electrical responses on the surface and cellular calcium activity deeper down. The team used these data to create a neural network (a type of artificial intelligence that learns to recognize patterns) that predicts deep calcium activity from surface-level readings.

The tech could help scientists study brain activity “in a way not possible with current single-function tools,” said Luyao Lu, PhD, professor of biomedical engineering at George Washington University in Washington, DC, who was not involved in the study. It could shed light on interactions between vascular and electrical activity, or explain how place cells (neurons in the hippocampus) are so efficient at creating spatial memory. 

It could also pave the way for minimally invasive neural prosthetics or targeted treatments for neurologic disorders, the researchers say. Implanting the device would be a “straightforward process” similar to placing electrocorticography grids in patients with epilepsy, said Dr. Kuzum. 

But first, the team plans to do more studies in animal models before testing the tech in clinical settings, Dr. Kuzum added.

A version of this article appeared on Medscape.com.

Modern technology for recording deep-brain activity involves sharp metal electrodes that penetrate the tissue, causing damage that can compromise the signal and limiting how often they can be used. 

A rapidly growing area in materials science and engineering aims to fix the problem by designing electrodes that are softer, smaller, and flexible — safer for use inside the delicate tissues of the brain. On January 17, researchers from the University of California, San Diego, reported the development of a thin, flexible electrode that can be inserted deep within the brain and communicate with sensors on the surface. 

But what if you could record detailed deep-brain activity without piercing the brain? 

A team of researchers (as it happens, also from UC San Diego) have developed a thin, flexible implant that “resides on the brain’s surface” and “can infer neural activity from deeper layers,” said Duygu Kuzum, PhD, a professor of electrical and computer engineering, who led the research. 

By combining electrical and optical imaging methods, and artificial intelligence, the researchers used the device — a polymer strip packed with graphene electrodes — to predict deep calcium activity from surface signals, according to a proof-of-concept study published this month in Nature Nanotechnology. 

“Almost everything we know about how neurons behave in living brains comes from data collected with either electrophysiology or two-photon imaging,” said neuroscientist Joshua H. Siegle, PhD, of the Allen Institute for Neural Dynamics in Seattle , who not involved in the study. “ Until now, these two methods have rarely been used simultaneously.”

The technology, which has been tested in mice, could help advance our knowledge of how the brain works and may lead to new minimally invasive treatments for neurologic disorders. 
 

Multimodal Neurotech: The Power of 2-in-1

Electrical and optical methods for recording brain activity have been crucial in advancing neurophysiologic science, but each technique has its limits. Electrical recordings provide high “temporal resolution”; they reveal when activation is happening, but not really where. Optical imaging, on the other hand, offers high “spatial resolution,” showing which area of the brain is lighting up, but its measurements may not correspond with the activity’s timing. 

Research over the past decade has explored how to combine and harness the strengths of both methods. One potential solution is to use electrodes made of transparent materials such as graphene, allowing a clear field of view for a microscope during imaging. Recently, University of Pennsylvania scientists used graphene electrodes to illuminate the neural dynamics of seizures. 

But there are challenges. If graphene electrodes are very small — in this case, 20 µm in diameter — they become more resistant to the flow of electricity. Dr. Kuzum and colleagues addressed this by adding tiny platinum particles to improve electrical conductivity. Long graphene wires connect electrodes to the circuit board, but defects in graphene can interrupt the signal, so they made each wire with two layers; any defects in one wire could be hidden by the other.

By combining the two methods (microelectrode arrays and two-photon imaging), the researchers could see both when brain activity was happening and where, including in deeper layers. They discovered a correlation between electrical responses on the surface and cellular calcium activity deeper down. The team used these data to create a neural network (a type of artificial intelligence that learns to recognize patterns) that predicts deep calcium activity from surface-level readings.

The tech could help scientists study brain activity “in a way not possible with current single-function tools,” said Luyao Lu, PhD, professor of biomedical engineering at George Washington University in Washington, DC, who was not involved in the study. It could shed light on interactions between vascular and electrical activity, or explain how place cells (neurons in the hippocampus) are so efficient at creating spatial memory. 

It could also pave the way for minimally invasive neural prosthetics or targeted treatments for neurologic disorders, the researchers say. Implanting the device would be a “straightforward process” similar to placing electrocorticography grids in patients with epilepsy, said Dr. Kuzum. 

But first, the team plans to do more studies in animal models before testing the tech in clinical settings, Dr. Kuzum added.

A version of this article appeared on Medscape.com.

When pediatric patients with epilepsy shift to adult care, inherent challenges are complicated by a near-total lack of efforts to smooth the transition, according to a recent survey. Many respondents received little to no information regarding the process, and many adults were still receiving care from family physicians or pediatric neurologists. The study was published online in Epilepsy & Behavior.

Room for Improvement

“We are not doing as good a job with planning for transition as we should,” said Elaine C. Wirrell, MD, who was not involved with the study. “It is not just a simple issue of sending your patient to an adult neurologist. Transition is a process that happens over time, so we need to do a better job getting our families ready for moving on to an adult provider.” Dr. Wirrell is director of pediatric epilepsy and professor of neurology at the Mayo Clinic in Rochester, Minnesota.

Mayo Clinic

Clumsy Transitions

Investigators distributed a 25-question survey to patients and caregivers who attended the 2019 Epilepsy Awareness Day at Disneyland, and through online support groups in North America. Among 58 responses, 32 came from patients between ages 12 and 17 years or their caregivers.

Despite attempts to recruit a diverse cross-section of respondents, most patients had severe epilepsy and comorbidities: 43% had daily or weekly seizures; 45% were on three or more antiseizure medications; and 74% had intellectual disabilities.

Many children with early-life epilepsies suffer from developmental and epileptic encephalopathy, which has associated non-seizure symptoms including learning challenges, behavioral issues, and other medical concerns, Dr. Wirrell said. Therefore, she said, finding a neurologist who treats adults — and has the expertise and interest to care for such patients — can be difficult.

“We’re seeing many patients not making that transition, or maybe not making it appropriately, so they’re not necessarily getting to the providers who have the most expertise in managing their epilepsy.” Among adults surveyed, 27% were still being followed by pediatric neurologists, and 35% were visiting family doctors for epilepsy-related treatment.

Because the needs of children with complex epilepsy can extend well beyond neurology, Dr. Wirrell added, managing such cases often requires multidisciplinary pediatric teams. “Finding that team on the adult side is more challenging.” As a result, she said, patients may transfer their neurology care without getting additional support for comorbidities such as mood disorders and learning disabilities.

The foregoing challenges are complicated by the fact that pediatric neurologists often lack the time (and in the United States, reimbursement) to adequately address the transition process, said Dr. Wirrell. Providers in freestanding children’s hospitals may face additional challenges coordinating with adult-care providers outside their facilities, she said.

“There’s also potentially a reluctance of both families and physicians to transition the patient on, because there’s concern that maybe there isn’t anybody on the adult side who is able to do as good a job as what they have on the pediatric side.”
 

Well-Coordinated Transitions Should Have No Surprises

Transition should be a planned, independence-promoting process that results in smooth, well-coordinated movement of pediatric patients into adult care — one without surprises or disconnections, the authors wrote. However, 55% of respondents never heard the term “transition” from any provider, even though 69% of patients were being treated in academic specialty centers.

Among 12- to 17-year-olds, 72% had never discussed transition with their healthcare team. That figure includes no 17-year-olds. Approximately 90% of respondents said they received sufficient time during healthcare visits, but 54% reported feeling stressed when moving from pediatric to adult care.

Given resource constraints in many pediatric epilepsy programs, the study authors recommended patient-empowerment tools such as a transition toolkit to help patients and families navigate the transition process even in places without formal transition programs.

“Many of these children are coming over with boatloads of medical records,” Dr. Wirrell said. “It’s not fair to the adult provider, who then has to go through all those records.” Instead, she said, pediatric teams should provide succinct summaries of relevant test results, medication side effects, prior treatments tried, and the like. “Those summaries are critically important so that we can get information to the person who needs it.”

Although successful transition requires significant coordination, she added, much of the process can often be handled by nonphysicians. “There are some very good nurse-led transition programs. Often, we can have a nurse providing education to the family and even potentially having a joint visit with an adult epilepsy nurse for complex patients.”

Pediatric providers also must know when to begin the transition process, Dr. Wirrell said. As soon as patients are 13 or 14 years old, she suggested discussing the process with them and their families every 6 to 12 months, covering specifics ranging from how to order medications to why adult patients may need power of attorney designees.

On a broader scale, said Dr. Wirrell, a smooth handoff requires planning. Fortunately, she said, the topic is becoming a significant priority for a growing number of children’s hospitals specific not only to epilepsy, but also to other chronic illnesses.

Dr. Wirrell is co–editor-in-chief for epilepsy.com. She reports no relevant financial interests.

When pediatric patients with epilepsy shift to adult care, inherent challenges are complicated by a near-total lack of efforts to smooth the transition, according to a recent survey. Many respondents received little to no information regarding the process, and many adults were still receiving care from family physicians or pediatric neurologists. The study was published online in Epilepsy & Behavior.

Room for Improvement

“We are not doing as good a job with planning for transition as we should,” said Elaine C. Wirrell, MD, who was not involved with the study. “It is not just a simple issue of sending your patient to an adult neurologist. Transition is a process that happens over time, so we need to do a better job getting our families ready for moving on to an adult provider.” Dr. Wirrell is director of pediatric epilepsy and professor of neurology at the Mayo Clinic in Rochester, Minnesota.

Mayo Clinic

Clumsy Transitions

Investigators distributed a 25-question survey to patients and caregivers who attended the 2019 Epilepsy Awareness Day at Disneyland, and through online support groups in North America. Among 58 responses, 32 came from patients between ages 12 and 17 years or their caregivers.

Despite attempts to recruit a diverse cross-section of respondents, most patients had severe epilepsy and comorbidities: 43% had daily or weekly seizures; 45% were on three or more antiseizure medications; and 74% had intellectual disabilities.

Many children with early-life epilepsies suffer from developmental and epileptic encephalopathy, which has associated non-seizure symptoms including learning challenges, behavioral issues, and other medical concerns, Dr. Wirrell said. Therefore, she said, finding a neurologist who treats adults — and has the expertise and interest to care for such patients — can be difficult.

“We’re seeing many patients not making that transition, or maybe not making it appropriately, so they’re not necessarily getting to the providers who have the most expertise in managing their epilepsy.” Among adults surveyed, 27% were still being followed by pediatric neurologists, and 35% were visiting family doctors for epilepsy-related treatment.

Because the needs of children with complex epilepsy can extend well beyond neurology, Dr. Wirrell added, managing such cases often requires multidisciplinary pediatric teams. “Finding that team on the adult side is more challenging.” As a result, she said, patients may transfer their neurology care without getting additional support for comorbidities such as mood disorders and learning disabilities.

The foregoing challenges are complicated by the fact that pediatric neurologists often lack the time (and in the United States, reimbursement) to adequately address the transition process, said Dr. Wirrell. Providers in freestanding children’s hospitals may face additional challenges coordinating with adult-care providers outside their facilities, she said.

“There’s also potentially a reluctance of both families and physicians to transition the patient on, because there’s concern that maybe there isn’t anybody on the adult side who is able to do as good a job as what they have on the pediatric side.”
 

Well-Coordinated Transitions Should Have No Surprises

Transition should be a planned, independence-promoting process that results in smooth, well-coordinated movement of pediatric patients into adult care — one without surprises or disconnections, the authors wrote. However, 55% of respondents never heard the term “transition” from any provider, even though 69% of patients were being treated in academic specialty centers.

Among 12- to 17-year-olds, 72% had never discussed transition with their healthcare team. That figure includes no 17-year-olds. Approximately 90% of respondents said they received sufficient time during healthcare visits, but 54% reported feeling stressed when moving from pediatric to adult care.

Given resource constraints in many pediatric epilepsy programs, the study authors recommended patient-empowerment tools such as a transition toolkit to help patients and families navigate the transition process even in places without formal transition programs.

“Many of these children are coming over with boatloads of medical records,” Dr. Wirrell said. “It’s not fair to the adult provider, who then has to go through all those records.” Instead, she said, pediatric teams should provide succinct summaries of relevant test results, medication side effects, prior treatments tried, and the like. “Those summaries are critically important so that we can get information to the person who needs it.”

Although successful transition requires significant coordination, she added, much of the process can often be handled by nonphysicians. “There are some very good nurse-led transition programs. Often, we can have a nurse providing education to the family and even potentially having a joint visit with an adult epilepsy nurse for complex patients.”

Pediatric providers also must know when to begin the transition process, Dr. Wirrell said. As soon as patients are 13 or 14 years old, she suggested discussing the process with them and their families every 6 to 12 months, covering specifics ranging from how to order medications to why adult patients may need power of attorney designees.

On a broader scale, said Dr. Wirrell, a smooth handoff requires planning. Fortunately, she said, the topic is becoming a significant priority for a growing number of children’s hospitals specific not only to epilepsy, but also to other chronic illnesses.

Dr. Wirrell is co–editor-in-chief for epilepsy.com. She reports no relevant financial interests.

When pediatric patients with epilepsy shift to adult care, inherent challenges are complicated by a near-total lack of efforts to smooth the transition, according to a recent survey. Many respondents received little to no information regarding the process, and many adults were still receiving care from family physicians or pediatric neurologists. The study was published online in Epilepsy & Behavior.

Room for Improvement

“We are not doing as good a job with planning for transition as we should,” said Elaine C. Wirrell, MD, who was not involved with the study. “It is not just a simple issue of sending your patient to an adult neurologist. Transition is a process that happens over time, so we need to do a better job getting our families ready for moving on to an adult provider.” Dr. Wirrell is director of pediatric epilepsy and professor of neurology at the Mayo Clinic in Rochester, Minnesota.

Mayo Clinic

Clumsy Transitions

Investigators distributed a 25-question survey to patients and caregivers who attended the 2019 Epilepsy Awareness Day at Disneyland, and through online support groups in North America. Among 58 responses, 32 came from patients between ages 12 and 17 years or their caregivers.

Despite attempts to recruit a diverse cross-section of respondents, most patients had severe epilepsy and comorbidities: 43% had daily or weekly seizures; 45% were on three or more antiseizure medications; and 74% had intellectual disabilities.

Many children with early-life epilepsies suffer from developmental and epileptic encephalopathy, which has associated non-seizure symptoms including learning challenges, behavioral issues, and other medical concerns, Dr. Wirrell said. Therefore, she said, finding a neurologist who treats adults — and has the expertise and interest to care for such patients — can be difficult.

“We’re seeing many patients not making that transition, or maybe not making it appropriately, so they’re not necessarily getting to the providers who have the most expertise in managing their epilepsy.” Among adults surveyed, 27% were still being followed by pediatric neurologists, and 35% were visiting family doctors for epilepsy-related treatment.

Because the needs of children with complex epilepsy can extend well beyond neurology, Dr. Wirrell added, managing such cases often requires multidisciplinary pediatric teams. “Finding that team on the adult side is more challenging.” As a result, she said, patients may transfer their neurology care without getting additional support for comorbidities such as mood disorders and learning disabilities.

The foregoing challenges are complicated by the fact that pediatric neurologists often lack the time (and in the United States, reimbursement) to adequately address the transition process, said Dr. Wirrell. Providers in freestanding children’s hospitals may face additional challenges coordinating with adult-care providers outside their facilities, she said.

“There’s also potentially a reluctance of both families and physicians to transition the patient on, because there’s concern that maybe there isn’t anybody on the adult side who is able to do as good a job as what they have on the pediatric side.”
 

Well-Coordinated Transitions Should Have No Surprises

Transition should be a planned, independence-promoting process that results in smooth, well-coordinated movement of pediatric patients into adult care — one without surprises or disconnections, the authors wrote. However, 55% of respondents never heard the term “transition” from any provider, even though 69% of patients were being treated in academic specialty centers.

Among 12- to 17-year-olds, 72% had never discussed transition with their healthcare team. That figure includes no 17-year-olds. Approximately 90% of respondents said they received sufficient time during healthcare visits, but 54% reported feeling stressed when moving from pediatric to adult care.

Given resource constraints in many pediatric epilepsy programs, the study authors recommended patient-empowerment tools such as a transition toolkit to help patients and families navigate the transition process even in places without formal transition programs.

“Many of these children are coming over with boatloads of medical records,” Dr. Wirrell said. “It’s not fair to the adult provider, who then has to go through all those records.” Instead, she said, pediatric teams should provide succinct summaries of relevant test results, medication side effects, prior treatments tried, and the like. “Those summaries are critically important so that we can get information to the person who needs it.”

Although successful transition requires significant coordination, she added, much of the process can often be handled by nonphysicians. “There are some very good nurse-led transition programs. Often, we can have a nurse providing education to the family and even potentially having a joint visit with an adult epilepsy nurse for complex patients.”

Pediatric providers also must know when to begin the transition process, Dr. Wirrell said. As soon as patients are 13 or 14 years old, she suggested discussing the process with them and their families every 6 to 12 months, covering specifics ranging from how to order medications to why adult patients may need power of attorney designees.

On a broader scale, said Dr. Wirrell, a smooth handoff requires planning. Fortunately, she said, the topic is becoming a significant priority for a growing number of children’s hospitals specific not only to epilepsy, but also to other chronic illnesses.

Dr. Wirrell is co–editor-in-chief for epilepsy.com. She reports no relevant financial interests.

Five people in the United Kingdom have been diagnosed with Alzheimer’s disease resulting from a medical treatment they received decades earlier, new research shows. 

Investigators say they are the first known cases of medically acquired AD in living people, but outside experts say the findings should be interpreted cautiously.

The individuals received treatment as children with human growth hormone extracted from pituitary glands of cadavers (c-hGH). Between 1958-1985, an estimated 30,000 people worldwide, mostly children, were treated with c-hGH for genetic disorders and growth hormone deficiencies. 

The therapy was halted in 1985 after three patients in the US who received the treatment later died of Creutzfeldt-Jakob disease (CJD) transmitted through batches of c-hGH that were contaminated with disease-causing prions. 

The new study builds on the investigators’ earlier work that showed the batches of c-hGH also contained amyloid-beta protein and that the protein could be transmitted decades later. These five cases were referred to or reviewed by researchers and clinicians at a prion clinic led by one of the lead researchers.

There are no reports of amyloid-beta transmission through any other medical or surgical procedures, researchers stress, and there is no evidence that amyloid-beta can be passed on during routine patient care or in daily activities. 

“However, the recognition of transmission of amyloid-beta pathology in these rare situations should lead us to review measures to prevent accidental transmission via other medical or surgical procedures, in order to prevent such cases occurring in future,” lead author John Collinge, MD, director of the University of College London Institute of Prion Diseases, London, England, and leader of the UK’s National Prion Clinic, said in a press release. 

“Importantly, our findings also suggest that Alzheimer’s and some other neurological conditions share similar disease processes to CJD, and this may have important implications for understanding and treating Alzheimer’s disease in the future,” Dr. Collinge continued.

The findings were published online January 29 in Nature Medicine. 
 

Building on Earlier Work

The research builds on investigators’ previous 2015 work that found archived samples of c-hGH were also contaminated with amyloid-beta protein. In 2018, mouse studies showed that c-hGH samples stored for decades could still transmit amyloid-beta via injection. 

Researchers said the findings suggested that individuals exposed to contaminated c-hGH who did not die from CJD might eventually develop AD.

Patients in the new study developed neurological symptoms consistent with AD between the ages of 38 and 55 years. The individual cases were either referred to or reviewed by experts in the National Prion Clinic in the UK between 2017 and 2022. The clinic coordinates the National Prion Monitoring Cohort, a longitudinal study of individuals with confirmed prion diseases. 

Of the eight cases, three were diagnosed with AD before referral to the clinic; two others met criteria for an AD diagnosis; and three did not meet the criteria. Three of the patients — two of whom had AD — are now deceased. 

All patients in the study received c-hGH prepared using a method called Wilhelmi or Hartree-modified Wilhelmi preparation (HWP).

Biomarker analyses confirmed the AD diagnosis in two patients. Other cases showed either progressive brain volume loss on brain imaging or elevated cerebrospinal fluid total tau and phosphorylated tau, or evidence of amyloid-beta deposits on autopsy. 
 

‘Potentially Transmissible’

The cases offered diverse presentations. Some were not symptomatic and some failed to meet current diagnostic criteria for sporadic Alzheimer’s disease. Treatment duration and frequency differed among those in the study, as did their age at treatment onset and completion. That and other factors could contribute to the diverse phenotype recorded in individuals, investigators note. 

Investigators examined and ruled out other factors that might explain the individuals’ cognitive symptoms, including childhood intellectual disability, which has been linked to dementia risk, the underlying condition that prompted their treatment with c-hGH, growth hormone deficiency, and cranial radiotherapy, which four of the individuals had received. They also ruled out inherited disease in all five of the cases with samples available for testing. 

“Taken together, the only factor common to all of the patients whom we describe is treatment with the HWP subtype of c-hGH,” the authors write. “Given the strong experimental evidence for A-beta transmission from relevant archived HWP c-hGH batches, we conclude that this is the most plausible explanation for the findings observed.”

Investigators say the findings show that, like other prion diseases, AD has three etiologies: sporadic, inherited, and rare acquired forms, or iatrogenic AD. 

“The clinical syndrome developed by these individuals can, therefore, be termed iatrogenic Alzheimer’s disease, and Alzheimer’s disease should now be recognized as a potentially transmissible disorder,” the authors write. 

“Our cases suggest that, similarly to what is observed in human prion diseases, iatrogenic forms of Alzheimer’s disease differ phenotypically from sporadic and inherited forms, with some individuals remaining asymptomatic despite exposure to A-beta seeds due to protective factors that, at present, are unknown,” they continue
 

‘Measure of Skepticism’

In an accompanying editorial, Mathias Jucker, PhD, of the Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany, and Lary C. Walker, PhD, in the Department of Neurology at Emory University, Atlanta, write that the findings should be considered “with a measure of skepticism.”

“The cases presented are diverse and complicated; the individuals had undergone a variety of medical interventions for various disorders earlier in life, and it is difficult to exclude a contribution of these circumstances to the complex disease phenotypes that appeared many years later,” they write. 

However, they continue, “there is good reason to take the findings seriously.”

“From a practical standpoint, this report reinforces the potential of amyloid-beta seeds as targets for early prevention, and it underscores the importance of informed caution in the preparation of surgical instruments, handling of tissues, and implementation of therapeutic biologics, particularly those derived from human sources,” Dr. Jucker and Dr. Walker write. 

Commenting on the findings for this news organization, Christopher Weber, PhD, director of global science initiatives for the Alzheimer’s Association, says the idea that amyloid-beta is transmissible between individuals has been shown before. 

“We’ve known for a long time that it is possible to create abnormal amyloid buildup — similar to that seen in Alzheimer’s – in the brain of an animal by injecting it with amyloid-beta. We also transfer human Alzheimer’s genes into animals to initiate abnormal, Alzheimer’s-like processes in their brains,” he said. “Thus, the idea that amyloid is transferable between individuals is not so novel as implied in the new paper.”

However, the study does highlight the importance of safety measures to prevent the accidental transmission of amyloid-beta, Weber added. 

“It is a reasonable and actionable caution that the scientific and clinical communities must understand the possible risks and ensure that all methods of transmission are eliminated — for example, with complete and conscientious sterilization of surgical instruments,” he said. “Bottom line: We shouldn’t put amyloid-beta into people’s brains, either accidentally or on purpose, and appropriate measures should be in place to ensure that doesn’t happen.”

The study was supported by the Medical Research Council, the National Institute for Health and Care Research (NIHR), the NIHR University College of London Hospital Biomedical Research Centre, Alzheimer’s Research UK, and the Stroke Association. Dr. Collinge is a shareholder and director of D-Gen, Ltd., an academic spin-out company working in the field of prion disease diagnosis, decontamination and therapeutics. Dr. Jucker and Dr. Walker report no conflicts of interest. 

A version of this article appeared on Medscape.com.

Five people in the United Kingdom have been diagnosed with Alzheimer’s disease resulting from a medical treatment they received decades earlier, new research shows. 

Investigators say they are the first known cases of medically acquired AD in living people, but outside experts say the findings should be interpreted cautiously.

The individuals received treatment as children with human growth hormone extracted from pituitary glands of cadavers (c-hGH). Between 1958-1985, an estimated 30,000 people worldwide, mostly children, were treated with c-hGH for genetic disorders and growth hormone deficiencies. 

The therapy was halted in 1985 after three patients in the US who received the treatment later died of Creutzfeldt-Jakob disease (CJD) transmitted through batches of c-hGH that were contaminated with disease-causing prions. 

The new study builds on the investigators’ earlier work that showed the batches of c-hGH also contained amyloid-beta protein and that the protein could be transmitted decades later. These five cases were referred to or reviewed by researchers and clinicians at a prion clinic led by one of the lead researchers.

There are no reports of amyloid-beta transmission through any other medical or surgical procedures, researchers stress, and there is no evidence that amyloid-beta can be passed on during routine patient care or in daily activities. 

“However, the recognition of transmission of amyloid-beta pathology in these rare situations should lead us to review measures to prevent accidental transmission via other medical or surgical procedures, in order to prevent such cases occurring in future,” lead author John Collinge, MD, director of the University of College London Institute of Prion Diseases, London, England, and leader of the UK’s National Prion Clinic, said in a press release. 

“Importantly, our findings also suggest that Alzheimer’s and some other neurological conditions share similar disease processes to CJD, and this may have important implications for understanding and treating Alzheimer’s disease in the future,” Dr. Collinge continued.

The findings were published online January 29 in Nature Medicine. 
 

Building on Earlier Work

The research builds on investigators’ previous 2015 work that found archived samples of c-hGH were also contaminated with amyloid-beta protein. In 2018, mouse studies showed that c-hGH samples stored for decades could still transmit amyloid-beta via injection. 

Researchers said the findings suggested that individuals exposed to contaminated c-hGH who did not die from CJD might eventually develop AD.

Patients in the new study developed neurological symptoms consistent with AD between the ages of 38 and 55 years. The individual cases were either referred to or reviewed by experts in the National Prion Clinic in the UK between 2017 and 2022. The clinic coordinates the National Prion Monitoring Cohort, a longitudinal study of individuals with confirmed prion diseases. 

Of the eight cases, three were diagnosed with AD before referral to the clinic; two others met criteria for an AD diagnosis; and three did not meet the criteria. Three of the patients — two of whom had AD — are now deceased. 

All patients in the study received c-hGH prepared using a method called Wilhelmi or Hartree-modified Wilhelmi preparation (HWP).

Biomarker analyses confirmed the AD diagnosis in two patients. Other cases showed either progressive brain volume loss on brain imaging or elevated cerebrospinal fluid total tau and phosphorylated tau, or evidence of amyloid-beta deposits on autopsy. 
 

‘Potentially Transmissible’

The cases offered diverse presentations. Some were not symptomatic and some failed to meet current diagnostic criteria for sporadic Alzheimer’s disease. Treatment duration and frequency differed among those in the study, as did their age at treatment onset and completion. That and other factors could contribute to the diverse phenotype recorded in individuals, investigators note. 

Investigators examined and ruled out other factors that might explain the individuals’ cognitive symptoms, including childhood intellectual disability, which has been linked to dementia risk, the underlying condition that prompted their treatment with c-hGH, growth hormone deficiency, and cranial radiotherapy, which four of the individuals had received. They also ruled out inherited disease in all five of the cases with samples available for testing. 

“Taken together, the only factor common to all of the patients whom we describe is treatment with the HWP subtype of c-hGH,” the authors write. “Given the strong experimental evidence for A-beta transmission from relevant archived HWP c-hGH batches, we conclude that this is the most plausible explanation for the findings observed.”

Investigators say the findings show that, like other prion diseases, AD has three etiologies: sporadic, inherited, and rare acquired forms, or iatrogenic AD. 

“The clinical syndrome developed by these individuals can, therefore, be termed iatrogenic Alzheimer’s disease, and Alzheimer’s disease should now be recognized as a potentially transmissible disorder,” the authors write. 

“Our cases suggest that, similarly to what is observed in human prion diseases, iatrogenic forms of Alzheimer’s disease differ phenotypically from sporadic and inherited forms, with some individuals remaining asymptomatic despite exposure to A-beta seeds due to protective factors that, at present, are unknown,” they continue
 

‘Measure of Skepticism’

In an accompanying editorial, Mathias Jucker, PhD, of the Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany, and Lary C. Walker, PhD, in the Department of Neurology at Emory University, Atlanta, write that the findings should be considered “with a measure of skepticism.”

“The cases presented are diverse and complicated; the individuals had undergone a variety of medical interventions for various disorders earlier in life, and it is difficult to exclude a contribution of these circumstances to the complex disease phenotypes that appeared many years later,” they write. 

However, they continue, “there is good reason to take the findings seriously.”

“From a practical standpoint, this report reinforces the potential of amyloid-beta seeds as targets for early prevention, and it underscores the importance of informed caution in the preparation of surgical instruments, handling of tissues, and implementation of therapeutic biologics, particularly those derived from human sources,” Dr. Jucker and Dr. Walker write. 

Commenting on the findings for this news organization, Christopher Weber, PhD, director of global science initiatives for the Alzheimer’s Association, says the idea that amyloid-beta is transmissible between individuals has been shown before. 

“We’ve known for a long time that it is possible to create abnormal amyloid buildup — similar to that seen in Alzheimer’s – in the brain of an animal by injecting it with amyloid-beta. We also transfer human Alzheimer’s genes into animals to initiate abnormal, Alzheimer’s-like processes in their brains,” he said. “Thus, the idea that amyloid is transferable between individuals is not so novel as implied in the new paper.”

However, the study does highlight the importance of safety measures to prevent the accidental transmission of amyloid-beta, Weber added. 

“It is a reasonable and actionable caution that the scientific and clinical communities must understand the possible risks and ensure that all methods of transmission are eliminated — for example, with complete and conscientious sterilization of surgical instruments,” he said. “Bottom line: We shouldn’t put amyloid-beta into people’s brains, either accidentally or on purpose, and appropriate measures should be in place to ensure that doesn’t happen.”

The study was supported by the Medical Research Council, the National Institute for Health and Care Research (NIHR), the NIHR University College of London Hospital Biomedical Research Centre, Alzheimer’s Research UK, and the Stroke Association. Dr. Collinge is a shareholder and director of D-Gen, Ltd., an academic spin-out company working in the field of prion disease diagnosis, decontamination and therapeutics. Dr. Jucker and Dr. Walker report no conflicts of interest. 

A version of this article appeared on Medscape.com.

Five people in the United Kingdom have been diagnosed with Alzheimer’s disease resulting from a medical treatment they received decades earlier, new research shows. 

Investigators say they are the first known cases of medically acquired AD in living people, but outside experts say the findings should be interpreted cautiously.

The individuals received treatment as children with human growth hormone extracted from pituitary glands of cadavers (c-hGH). Between 1958-1985, an estimated 30,000 people worldwide, mostly children, were treated with c-hGH for genetic disorders and growth hormone deficiencies. 

The therapy was halted in 1985 after three patients in the US who received the treatment later died of Creutzfeldt-Jakob disease (CJD) transmitted through batches of c-hGH that were contaminated with disease-causing prions. 

The new study builds on the investigators’ earlier work that showed the batches of c-hGH also contained amyloid-beta protein and that the protein could be transmitted decades later. These five cases were referred to or reviewed by researchers and clinicians at a prion clinic led by one of the lead researchers.

There are no reports of amyloid-beta transmission through any other medical or surgical procedures, researchers stress, and there is no evidence that amyloid-beta can be passed on during routine patient care or in daily activities. 

“However, the recognition of transmission of amyloid-beta pathology in these rare situations should lead us to review measures to prevent accidental transmission via other medical or surgical procedures, in order to prevent such cases occurring in future,” lead author John Collinge, MD, director of the University of College London Institute of Prion Diseases, London, England, and leader of the UK’s National Prion Clinic, said in a press release. 

“Importantly, our findings also suggest that Alzheimer’s and some other neurological conditions share similar disease processes to CJD, and this may have important implications for understanding and treating Alzheimer’s disease in the future,” Dr. Collinge continued.

The findings were published online January 29 in Nature Medicine. 
 

Building on Earlier Work

The research builds on investigators’ previous 2015 work that found archived samples of c-hGH were also contaminated with amyloid-beta protein. In 2018, mouse studies showed that c-hGH samples stored for decades could still transmit amyloid-beta via injection. 

Researchers said the findings suggested that individuals exposed to contaminated c-hGH who did not die from CJD might eventually develop AD.

Patients in the new study developed neurological symptoms consistent with AD between the ages of 38 and 55 years. The individual cases were either referred to or reviewed by experts in the National Prion Clinic in the UK between 2017 and 2022. The clinic coordinates the National Prion Monitoring Cohort, a longitudinal study of individuals with confirmed prion diseases. 

Of the eight cases, three were diagnosed with AD before referral to the clinic; two others met criteria for an AD diagnosis; and three did not meet the criteria. Three of the patients — two of whom had AD — are now deceased. 

All patients in the study received c-hGH prepared using a method called Wilhelmi or Hartree-modified Wilhelmi preparation (HWP).

Biomarker analyses confirmed the AD diagnosis in two patients. Other cases showed either progressive brain volume loss on brain imaging or elevated cerebrospinal fluid total tau and phosphorylated tau, or evidence of amyloid-beta deposits on autopsy. 
 

‘Potentially Transmissible’

The cases offered diverse presentations. Some were not symptomatic and some failed to meet current diagnostic criteria for sporadic Alzheimer’s disease. Treatment duration and frequency differed among those in the study, as did their age at treatment onset and completion. That and other factors could contribute to the diverse phenotype recorded in individuals, investigators note. 

Investigators examined and ruled out other factors that might explain the individuals’ cognitive symptoms, including childhood intellectual disability, which has been linked to dementia risk, the underlying condition that prompted their treatment with c-hGH, growth hormone deficiency, and cranial radiotherapy, which four of the individuals had received. They also ruled out inherited disease in all five of the cases with samples available for testing. 

“Taken together, the only factor common to all of the patients whom we describe is treatment with the HWP subtype of c-hGH,” the authors write. “Given the strong experimental evidence for A-beta transmission from relevant archived HWP c-hGH batches, we conclude that this is the most plausible explanation for the findings observed.”

Investigators say the findings show that, like other prion diseases, AD has three etiologies: sporadic, inherited, and rare acquired forms, or iatrogenic AD. 

“The clinical syndrome developed by these individuals can, therefore, be termed iatrogenic Alzheimer’s disease, and Alzheimer’s disease should now be recognized as a potentially transmissible disorder,” the authors write. 

“Our cases suggest that, similarly to what is observed in human prion diseases, iatrogenic forms of Alzheimer’s disease differ phenotypically from sporadic and inherited forms, with some individuals remaining asymptomatic despite exposure to A-beta seeds due to protective factors that, at present, are unknown,” they continue
 

‘Measure of Skepticism’

In an accompanying editorial, Mathias Jucker, PhD, of the Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany, and Lary C. Walker, PhD, in the Department of Neurology at Emory University, Atlanta, write that the findings should be considered “with a measure of skepticism.”

“The cases presented are diverse and complicated; the individuals had undergone a variety of medical interventions for various disorders earlier in life, and it is difficult to exclude a contribution of these circumstances to the complex disease phenotypes that appeared many years later,” they write. 

However, they continue, “there is good reason to take the findings seriously.”

“From a practical standpoint, this report reinforces the potential of amyloid-beta seeds as targets for early prevention, and it underscores the importance of informed caution in the preparation of surgical instruments, handling of tissues, and implementation of therapeutic biologics, particularly those derived from human sources,” Dr. Jucker and Dr. Walker write. 

Commenting on the findings for this news organization, Christopher Weber, PhD, director of global science initiatives for the Alzheimer’s Association, says the idea that amyloid-beta is transmissible between individuals has been shown before. 

“We’ve known for a long time that it is possible to create abnormal amyloid buildup — similar to that seen in Alzheimer’s – in the brain of an animal by injecting it with amyloid-beta. We also transfer human Alzheimer’s genes into animals to initiate abnormal, Alzheimer’s-like processes in their brains,” he said. “Thus, the idea that amyloid is transferable between individuals is not so novel as implied in the new paper.”

However, the study does highlight the importance of safety measures to prevent the accidental transmission of amyloid-beta, Weber added. 

“It is a reasonable and actionable caution that the scientific and clinical communities must understand the possible risks and ensure that all methods of transmission are eliminated — for example, with complete and conscientious sterilization of surgical instruments,” he said. “Bottom line: We shouldn’t put amyloid-beta into people’s brains, either accidentally or on purpose, and appropriate measures should be in place to ensure that doesn’t happen.”

The study was supported by the Medical Research Council, the National Institute for Health and Care Research (NIHR), the NIHR University College of London Hospital Biomedical Research Centre, Alzheimer’s Research UK, and the Stroke Association. Dr. Collinge is a shareholder and director of D-Gen, Ltd., an academic spin-out company working in the field of prion disease diagnosis, decontamination and therapeutics. Dr. Jucker and Dr. Walker report no conflicts of interest. 

A version of this article appeared on Medscape.com.

A wearable, soft, robotic device could help patients with Parkinson’s disease (PD) walk without experiencing freezing of gait (FoG), early research suggested.

The robotic apparel, worn around the hips and thighs, gently pushes the hips as the leg swings, facilitating a longer stride and preventing FoG, a common disorder in PD that affects nearly all patients over the disease course.

The small, proof-of-concept study included one person with PD. But investigators noted the reduction in freezing and falls and improvement in walking distance and speed was dramatic. Incidence of FoG decreased from 63% to just 6% when the patient wore the robotic garment outdoors. Wearing the device indoors eliminated freezing altogether.

“We demonstrate proof-of-concept that FoG can be averted using a soft robotic device — a machine that aims to apply physical assistance to movement with minimal restriction, a fundamentally different approach to rigid exoskeletons,” lead investigators Conor Walsh, PhD, and Terry Ellis, PhD, PT, told this news organization.

Walsh is a professor at Harvard John A. Paulson School of Engineering and Applied Sciences in Boston, and Ellis is a professor and chair of the physical therapy department and director of the Center for Neurorehabilitation, Boston University, Boston, Massachusetts.

The study was published online on January 5, 2024, in Nature Medicine.

Disabling Disturbance

From a biomechanical perspective, FoG is manifested by an overt breakdown in spatial and temporal mechanics of walking. The impaired limb coordination occurs during the “swing phase” of the gait cycle.

There are currently no interventions that prevent FoG. Available treatment interventions include pharmacotherapy, such as dopamine replacement; deep brain stimulation (DBS) of the subthalamic nucleus; and behavioral interventions, such as cueing strategies. All have shown only modest effects in reducing FoG and, in some cases, might even worsen it, the investigators noted.

“This challenge led us to become interested in leveraging soft wearable robots to deliver mechanical cues to disrupt aberrant gait mechanics and prevent FOG in people with PD,” Dr. Walsh and Dr. Ellis said.

“Wearable robots” have been used to augment kinematics in neurologic conditions, such as stroke, cerebral palsy, and spinal cord injury. Harnessing this technology to address FoG required “a collaboration between engineers, rehabilitation scientists, physical therapists, biomechanists, and apparel designers,” the researchers said.

The wearable robotic device uses cable-driven actuators, which enable physical movement by converting electrical energy into mechanical force, and sensors worn around the waist and thighs. Using motion data collected by the sensors, algorithms estimate the phase of the walking cycle and generate assistive forces in concert with biological muscles.

Real-World Testing

The researchers tested the robotic garment on a 73-year-old man with idiopathic PD of 10-year duration. The man’s ongoing pharmacologic treatment included 1.5 tablets of 25- to 100-mg carbidopa/levodopa taken four times per day, one tablet of 100-mg amantadine twice per day, and one tablet of 200-mg entacapone taken four times per day.

He had also undergone DBS to the globus pallidus internus and utilized behavioral strategies. Despite these interventions, he continued to endure more than 10 episodes of FoG per day and numerous falls.

The patient tended to use walls to stabilize himself when walking. Freezing episodes were observed mostly when he walked in open hallways, turned, walked outdoors, and when he tried to walk and talk simultaneously.

The research was conducted over a 6-month period, with a total of five study sessions that consisted of walking trials. Four were administered in the laboratory. The fifth was conducted in a real-world outdoor community setting.

During the first visit, a biomechanical analysis of walking was performed under single-task conditions during the medication-on phase.

Testing was usually conducted during medication-on phase and under single-task conditions. But testing conditions also included attention-demanding dual tasks and single-task walking during the medication-off phase.

The researchers compared the effects of the assistance of the robotic apparel to no apparel and with the apparel turned off. They measured the percentage of time spent freezing and the total distance walked.

Robust Response

The participant demonstrated a “robust response” to the robotic apparel. With the garment’s assistance, FoG was eliminated when worn indoors, and walking distance increased by 55%. The participant walked faster and had a 25% reduction in gait variability.

These beneficial effects were repeated across multiple days as well as different types of provoking conditions and environmental contexts. When the device was tried outdoors, FoG decreased from 63% to 6% of the time. The patient was also able to simultaneously walk and talk without freezing.

“When the device assisted with hip flexion during the terminal stance phase of walking (when lifting the toe), FoG was instantaneously eliminated during inner walking, accompanied by clinically significant improvement in walking speeds and distance,” Dr. Walsh and Dr. Ellis reported.

The approach “suggests the potential benefits of a ‘bottom-up’ rather than a ‘top-down’ solution to treating gait freezing,” they commented. “We see that restoring almost-normal biomechanics alters the peripheral dynamics of gait and may influence the central processing of gait control.”

Bringing Hope

Rebecca Gilbert MD, PhD, chief mission officer, American Parkinson Disease Association, said this new approach is “exciting.”

Whether the benefits will be as robust in other people with PD “remains to be seen,” said Dr. Gilbert, who was not involved with the study.

“The paper states that multiple experimental variables utilizing the device could potentially be adjusted to serve different people with PD, and these will need to be tested in clinical trials as well,” Dr. Gilbert said.

Additionally, “the device itself is complex and may be challenging to get on and off without help, which may limit its usability in the community,” Dr. Gilbert noted.

Although more work is needed, the study “represents a remarkable proof of concept that brings hope to those with FoG,” she added.

These “promising findings prompt further investigation to validate the effects of the robotic apparel on a broader range of individuals with PD experiencing FoG and across various FoG phenotypes and environments and task contexts, complemented with FoG metrics that include quantification of the severity of the freezing episodes,” Walsh and Ellis added.

This study was based on work supported by the National Science Foundation, the National Institutes of Health, and the Massachusetts Technology Collaborative, Collaborative Research and Development Matching Grant. This work was also partially funded by the John A. Paulson School of Engineering and Applied Sciences at Harvard University as well as received financial support from the Samsung Scholarship.
 

A version of this article appeared on Medscape.com.

A wearable, soft, robotic device could help patients with Parkinson’s disease (PD) walk without experiencing freezing of gait (FoG), early research suggested.

The robotic apparel, worn around the hips and thighs, gently pushes the hips as the leg swings, facilitating a longer stride and preventing FoG, a common disorder in PD that affects nearly all patients over the disease course.

The small, proof-of-concept study included one person with PD. But investigators noted the reduction in freezing and falls and improvement in walking distance and speed was dramatic. Incidence of FoG decreased from 63% to just 6% when the patient wore the robotic garment outdoors. Wearing the device indoors eliminated freezing altogether.

“We demonstrate proof-of-concept that FoG can be averted using a soft robotic device — a machine that aims to apply physical assistance to movement with minimal restriction, a fundamentally different approach to rigid exoskeletons,” lead investigators Conor Walsh, PhD, and Terry Ellis, PhD, PT, told this news organization.

Walsh is a professor at Harvard John A. Paulson School of Engineering and Applied Sciences in Boston, and Ellis is a professor and chair of the physical therapy department and director of the Center for Neurorehabilitation, Boston University, Boston, Massachusetts.

The study was published online on January 5, 2024, in Nature Medicine.

Disabling Disturbance

From a biomechanical perspective, FoG is manifested by an overt breakdown in spatial and temporal mechanics of walking. The impaired limb coordination occurs during the “swing phase” of the gait cycle.

There are currently no interventions that prevent FoG. Available treatment interventions include pharmacotherapy, such as dopamine replacement; deep brain stimulation (DBS) of the subthalamic nucleus; and behavioral interventions, such as cueing strategies. All have shown only modest effects in reducing FoG and, in some cases, might even worsen it, the investigators noted.

“This challenge led us to become interested in leveraging soft wearable robots to deliver mechanical cues to disrupt aberrant gait mechanics and prevent FOG in people with PD,” Dr. Walsh and Dr. Ellis said.

“Wearable robots” have been used to augment kinematics in neurologic conditions, such as stroke, cerebral palsy, and spinal cord injury. Harnessing this technology to address FoG required “a collaboration between engineers, rehabilitation scientists, physical therapists, biomechanists, and apparel designers,” the researchers said.

The wearable robotic device uses cable-driven actuators, which enable physical movement by converting electrical energy into mechanical force, and sensors worn around the waist and thighs. Using motion data collected by the sensors, algorithms estimate the phase of the walking cycle and generate assistive forces in concert with biological muscles.

Real-World Testing

The researchers tested the robotic garment on a 73-year-old man with idiopathic PD of 10-year duration. The man’s ongoing pharmacologic treatment included 1.5 tablets of 25- to 100-mg carbidopa/levodopa taken four times per day, one tablet of 100-mg amantadine twice per day, and one tablet of 200-mg entacapone taken four times per day.

He had also undergone DBS to the globus pallidus internus and utilized behavioral strategies. Despite these interventions, he continued to endure more than 10 episodes of FoG per day and numerous falls.

The patient tended to use walls to stabilize himself when walking. Freezing episodes were observed mostly when he walked in open hallways, turned, walked outdoors, and when he tried to walk and talk simultaneously.

The research was conducted over a 6-month period, with a total of five study sessions that consisted of walking trials. Four were administered in the laboratory. The fifth was conducted in a real-world outdoor community setting.

During the first visit, a biomechanical analysis of walking was performed under single-task conditions during the medication-on phase.

Testing was usually conducted during medication-on phase and under single-task conditions. But testing conditions also included attention-demanding dual tasks and single-task walking during the medication-off phase.

The researchers compared the effects of the assistance of the robotic apparel to no apparel and with the apparel turned off. They measured the percentage of time spent freezing and the total distance walked.

Robust Response

The participant demonstrated a “robust response” to the robotic apparel. With the garment’s assistance, FoG was eliminated when worn indoors, and walking distance increased by 55%. The participant walked faster and had a 25% reduction in gait variability.

These beneficial effects were repeated across multiple days as well as different types of provoking conditions and environmental contexts. When the device was tried outdoors, FoG decreased from 63% to 6% of the time. The patient was also able to simultaneously walk and talk without freezing.

“When the device assisted with hip flexion during the terminal stance phase of walking (when lifting the toe), FoG was instantaneously eliminated during inner walking, accompanied by clinically significant improvement in walking speeds and distance,” Dr. Walsh and Dr. Ellis reported.

The approach “suggests the potential benefits of a ‘bottom-up’ rather than a ‘top-down’ solution to treating gait freezing,” they commented. “We see that restoring almost-normal biomechanics alters the peripheral dynamics of gait and may influence the central processing of gait control.”

Bringing Hope

Rebecca Gilbert MD, PhD, chief mission officer, American Parkinson Disease Association, said this new approach is “exciting.”

Whether the benefits will be as robust in other people with PD “remains to be seen,” said Dr. Gilbert, who was not involved with the study.

“The paper states that multiple experimental variables utilizing the device could potentially be adjusted to serve different people with PD, and these will need to be tested in clinical trials as well,” Dr. Gilbert said.

Additionally, “the device itself is complex and may be challenging to get on and off without help, which may limit its usability in the community,” Dr. Gilbert noted.

Although more work is needed, the study “represents a remarkable proof of concept that brings hope to those with FoG,” she added.

These “promising findings prompt further investigation to validate the effects of the robotic apparel on a broader range of individuals with PD experiencing FoG and across various FoG phenotypes and environments and task contexts, complemented with FoG metrics that include quantification of the severity of the freezing episodes,” Walsh and Ellis added.

This study was based on work supported by the National Science Foundation, the National Institutes of Health, and the Massachusetts Technology Collaborative, Collaborative Research and Development Matching Grant. This work was also partially funded by the John A. Paulson School of Engineering and Applied Sciences at Harvard University as well as received financial support from the Samsung Scholarship.
 

A version of this article appeared on Medscape.com.

A wearable, soft, robotic device could help patients with Parkinson’s disease (PD) walk without experiencing freezing of gait (FoG), early research suggested.

The robotic apparel, worn around the hips and thighs, gently pushes the hips as the leg swings, facilitating a longer stride and preventing FoG, a common disorder in PD that affects nearly all patients over the disease course.

The small, proof-of-concept study included one person with PD. But investigators noted the reduction in freezing and falls and improvement in walking distance and speed was dramatic. Incidence of FoG decreased from 63% to just 6% when the patient wore the robotic garment outdoors. Wearing the device indoors eliminated freezing altogether.

“We demonstrate proof-of-concept that FoG can be averted using a soft robotic device — a machine that aims to apply physical assistance to movement with minimal restriction, a fundamentally different approach to rigid exoskeletons,” lead investigators Conor Walsh, PhD, and Terry Ellis, PhD, PT, told this news organization.

Walsh is a professor at Harvard John A. Paulson School of Engineering and Applied Sciences in Boston, and Ellis is a professor and chair of the physical therapy department and director of the Center for Neurorehabilitation, Boston University, Boston, Massachusetts.

The study was published online on January 5, 2024, in Nature Medicine.

Disabling Disturbance

From a biomechanical perspective, FoG is manifested by an overt breakdown in spatial and temporal mechanics of walking. The impaired limb coordination occurs during the “swing phase” of the gait cycle.

There are currently no interventions that prevent FoG. Available treatment interventions include pharmacotherapy, such as dopamine replacement; deep brain stimulation (DBS) of the subthalamic nucleus; and behavioral interventions, such as cueing strategies. All have shown only modest effects in reducing FoG and, in some cases, might even worsen it, the investigators noted.

“This challenge led us to become interested in leveraging soft wearable robots to deliver mechanical cues to disrupt aberrant gait mechanics and prevent FOG in people with PD,” Dr. Walsh and Dr. Ellis said.

“Wearable robots” have been used to augment kinematics in neurologic conditions, such as stroke, cerebral palsy, and spinal cord injury. Harnessing this technology to address FoG required “a collaboration between engineers, rehabilitation scientists, physical therapists, biomechanists, and apparel designers,” the researchers said.

The wearable robotic device uses cable-driven actuators, which enable physical movement by converting electrical energy into mechanical force, and sensors worn around the waist and thighs. Using motion data collected by the sensors, algorithms estimate the phase of the walking cycle and generate assistive forces in concert with biological muscles.

Real-World Testing

The researchers tested the robotic garment on a 73-year-old man with idiopathic PD of 10-year duration. The man’s ongoing pharmacologic treatment included 1.5 tablets of 25- to 100-mg carbidopa/levodopa taken four times per day, one tablet of 100-mg amantadine twice per day, and one tablet of 200-mg entacapone taken four times per day.

He had also undergone DBS to the globus pallidus internus and utilized behavioral strategies. Despite these interventions, he continued to endure more than 10 episodes of FoG per day and numerous falls.

The patient tended to use walls to stabilize himself when walking. Freezing episodes were observed mostly when he walked in open hallways, turned, walked outdoors, and when he tried to walk and talk simultaneously.

The research was conducted over a 6-month period, with a total of five study sessions that consisted of walking trials. Four were administered in the laboratory. The fifth was conducted in a real-world outdoor community setting.

During the first visit, a biomechanical analysis of walking was performed under single-task conditions during the medication-on phase.

Testing was usually conducted during medication-on phase and under single-task conditions. But testing conditions also included attention-demanding dual tasks and single-task walking during the medication-off phase.

The researchers compared the effects of the assistance of the robotic apparel to no apparel and with the apparel turned off. They measured the percentage of time spent freezing and the total distance walked.

Robust Response

The participant demonstrated a “robust response” to the robotic apparel. With the garment’s assistance, FoG was eliminated when worn indoors, and walking distance increased by 55%. The participant walked faster and had a 25% reduction in gait variability.

These beneficial effects were repeated across multiple days as well as different types of provoking conditions and environmental contexts. When the device was tried outdoors, FoG decreased from 63% to 6% of the time. The patient was also able to simultaneously walk and talk without freezing.

“When the device assisted with hip flexion during the terminal stance phase of walking (when lifting the toe), FoG was instantaneously eliminated during inner walking, accompanied by clinically significant improvement in walking speeds and distance,” Dr. Walsh and Dr. Ellis reported.

The approach “suggests the potential benefits of a ‘bottom-up’ rather than a ‘top-down’ solution to treating gait freezing,” they commented. “We see that restoring almost-normal biomechanics alters the peripheral dynamics of gait and may influence the central processing of gait control.”

Bringing Hope

Rebecca Gilbert MD, PhD, chief mission officer, American Parkinson Disease Association, said this new approach is “exciting.”

Whether the benefits will be as robust in other people with PD “remains to be seen,” said Dr. Gilbert, who was not involved with the study.

“The paper states that multiple experimental variables utilizing the device could potentially be adjusted to serve different people with PD, and these will need to be tested in clinical trials as well,” Dr. Gilbert said.

Additionally, “the device itself is complex and may be challenging to get on and off without help, which may limit its usability in the community,” Dr. Gilbert noted.

Although more work is needed, the study “represents a remarkable proof of concept that brings hope to those with FoG,” she added.

These “promising findings prompt further investigation to validate the effects of the robotic apparel on a broader range of individuals with PD experiencing FoG and across various FoG phenotypes and environments and task contexts, complemented with FoG metrics that include quantification of the severity of the freezing episodes,” Walsh and Ellis added.

This study was based on work supported by the National Science Foundation, the National Institutes of Health, and the Massachusetts Technology Collaborative, Collaborative Research and Development Matching Grant. This work was also partially funded by the John A. Paulson School of Engineering and Applied Sciences at Harvard University as well as received financial support from the Samsung Scholarship.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Cognitive function in children aged 18 months to 10 years is associated with the enrichment or depletion of specific species of gut microbes, new research reveals.

METHODOLOGY: 

• Researchers analyzed the relationship between the microbiome, neuroanatomy, and cognition (ie, the microbiome-gut-brain axis) in stool samples from 381 neurotypically developing children aged 40 days to 10 years (mean age, 2 years and 2 months).
• Stool samples were taken within a week of age-appropriate cognitive and behavioral assessments.
• Shotgun metagenomic sequencing was used to analyze the DNA of the organisms present in each sample.
• MRI data were obtained, with machine models then used to predict whether participants’ brain region volume was influenced by microbial profiles.

TAKEAWAY: 

• Researchers found increasing variation in microbial species and microbial gene functions in children older than 18 months, and the overall variation was significantly associated with variation in cognitive function scores.
• Several microbial species were significantly enriched in children with higher cognitive function scores (eg, Alistipes obesi, Asaccharobacter celatus, Eubacterium eligens, and Faecalibacterium prausnitzii), with Sutterella wadsworthensis being the only species significantly negatively associated with these scores.
• Machine models indicated that taxa key in predicting cognitive function were similarly important for predicting individual brain regions and subscales of cognitive function.

IN PRACTICE:

“Understanding the gut-brain-microbiome axis in early life is particularly important since differences or interventions in early life can have outsized and longer-term consequences than those at later ages,” the authors wrote.

SOURCE:

The study, led by Kevin S. Bonham, PhD, Wellesley College, Wellesley, Massachusetts, was published online on December 22, 2023, in Science Advances.

LIMITATIONS:

Use of multiple age-appropriate cognitive assessments enabled analysis across multiple developmental periods, but test-retest reliability and differences between test administrators may have introduced noise into these observations, particularly in the youngest children. The study period overlapped with the beginning of the pandemic, and score reductions due to the lockdowns were more pronounced in some age groups than during the recruitment period. 

DISCLOSURES:

The study was funded by the US National Institutes of Health and Wellcome: LEAP 1kD. The authors declared no competing interests.

A version of this article appeared on Medscape.com.

TOPLINE:

Cognitive function in children aged 18 months to 10 years is associated with the enrichment or depletion of specific species of gut microbes, new research reveals.

METHODOLOGY: 

• Researchers analyzed the relationship between the microbiome, neuroanatomy, and cognition (ie, the microbiome-gut-brain axis) in stool samples from 381 neurotypically developing children aged 40 days to 10 years (mean age, 2 years and 2 months).
• Stool samples were taken within a week of age-appropriate cognitive and behavioral assessments.
• Shotgun metagenomic sequencing was used to analyze the DNA of the organisms present in each sample.
• MRI data were obtained, with machine models then used to predict whether participants’ brain region volume was influenced by microbial profiles.

TAKEAWAY: 

• Researchers found increasing variation in microbial species and microbial gene functions in children older than 18 months, and the overall variation was significantly associated with variation in cognitive function scores.
• Several microbial species were significantly enriched in children with higher cognitive function scores (eg, Alistipes obesi, Asaccharobacter celatus, Eubacterium eligens, and Faecalibacterium prausnitzii), with Sutterella wadsworthensis being the only species significantly negatively associated with these scores.
• Machine models indicated that taxa key in predicting cognitive function were similarly important for predicting individual brain regions and subscales of cognitive function.

IN PRACTICE:

“Understanding the gut-brain-microbiome axis in early life is particularly important since differences or interventions in early life can have outsized and longer-term consequences than those at later ages,” the authors wrote.

SOURCE:

The study, led by Kevin S. Bonham, PhD, Wellesley College, Wellesley, Massachusetts, was published online on December 22, 2023, in Science Advances.

LIMITATIONS:

Use of multiple age-appropriate cognitive assessments enabled analysis across multiple developmental periods, but test-retest reliability and differences between test administrators may have introduced noise into these observations, particularly in the youngest children. The study period overlapped with the beginning of the pandemic, and score reductions due to the lockdowns were more pronounced in some age groups than during the recruitment period. 

DISCLOSURES:

The study was funded by the US National Institutes of Health and Wellcome: LEAP 1kD. The authors declared no competing interests.

A version of this article appeared on Medscape.com.

TOPLINE:

Cognitive function in children aged 18 months to 10 years is associated with the enrichment or depletion of specific species of gut microbes, new research reveals.

METHODOLOGY: 

• Researchers analyzed the relationship between the microbiome, neuroanatomy, and cognition (ie, the microbiome-gut-brain axis) in stool samples from 381 neurotypically developing children aged 40 days to 10 years (mean age, 2 years and 2 months).
• Stool samples were taken within a week of age-appropriate cognitive and behavioral assessments.
• Shotgun metagenomic sequencing was used to analyze the DNA of the organisms present in each sample.
• MRI data were obtained, with machine models then used to predict whether participants’ brain region volume was influenced by microbial profiles.

TAKEAWAY: 

• Researchers found increasing variation in microbial species and microbial gene functions in children older than 18 months, and the overall variation was significantly associated with variation in cognitive function scores.
• Several microbial species were significantly enriched in children with higher cognitive function scores (eg, Alistipes obesi, Asaccharobacter celatus, Eubacterium eligens, and Faecalibacterium prausnitzii), with Sutterella wadsworthensis being the only species significantly negatively associated with these scores.
• Machine models indicated that taxa key in predicting cognitive function were similarly important for predicting individual brain regions and subscales of cognitive function.

IN PRACTICE:

“Understanding the gut-brain-microbiome axis in early life is particularly important since differences or interventions in early life can have outsized and longer-term consequences than those at later ages,” the authors wrote.

SOURCE:

The study, led by Kevin S. Bonham, PhD, Wellesley College, Wellesley, Massachusetts, was published online on December 22, 2023, in Science Advances.

LIMITATIONS:

Use of multiple age-appropriate cognitive assessments enabled analysis across multiple developmental periods, but test-retest reliability and differences between test administrators may have introduced noise into these observations, particularly in the youngest children. The study period overlapped with the beginning of the pandemic, and score reductions due to the lockdowns were more pronounced in some age groups than during the recruitment period. 

DISCLOSURES:

The study was funded by the US National Institutes of Health and Wellcome: LEAP 1kD. The authors declared no competing interests.

A version of this article appeared on Medscape.com.

The long-term impact of traumatic brain injury (TBI) on neurologic and psychiatric function is well-established, but a growing body of research is pointing to unexpected medical sequalae, including cardiovascular disease (CVD).

A recent review looked at the investigation to date into this surprising connection, not only summarizing study findings but also suggesting potential mechanisms that might account for the association.

“This work offers further evidence that individuals with TBI are at an elevated risk of unfavorable cardiovascular outcomes for an extended period following the initial incident; consequently, they should undergo regular monitoring,” senior author Ross Zafonte, DO, president of Spaulding Rehabilitation Network, Boston, and lead author Saef Izzy, MD, MBChB, a neurologist at the Stroke and Cerebrovascular Center of Brigham and Women’s Hospital, Boston, Massachusetts, told this news organization.

“This holds significant importance for healthcare practitioners, as there exist several strategies to mitigate cardiovascular disease risk — including weight management, adopting a healthy diet, engaging in regular physical activity, and quitting smoking,” they stated.

Leslie Croll, MD, American Heart Association volunteer and assistant professor of clinical neurology at the Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, told this news organization that it’s “extremely important to learn more about the interplay between TBI, neurologic disease, psychiatric complications, and the cardiovascular system.”

Hopefully, she added, “future research will help us understand what kind of cardiovascular disease monitoring and prevention measures stand to give TBI patients the most benefit.”
 

Chronic Condition

TBI is “a major cause of long-term disability and premature death,” and is “highly prevalent among contact sports players, military personnel (eg, due to injuries sustained during conflict), and the general population (eg, due to falls and road traffic incidents),” the authors wrote.

Most studies pertaining to TBI have “primarily focused on establishing connections between single TBI, repetitive TBI, and their acute and chronic neurological and psychiatric consequences, such as Parkinson’s disease, Alzheimer’s disease, and chronic traumatic encephalopathy (CTE),” Drs. Zafonte and Izzy noted. By contrast, there has been a “notable lack of research attention given to non-neurological conditions associated with TBI.”

They pointed out that recent insights into TBI — particularly the acknowledgment of TBI as an “emerging chronic condition rather than merely an acute aftermath of brain injury” — have come to light through epidemiologic and pathologic investigations involving military veterans, professional American-style football players, and the civilian population. “This recognition opens up an opportunity to broaden our perspective and delve into the medical aspects of health that may be influenced by TBI.”

To broaden the investigation, the researchers reviewed literature published between January 1, 2001, and June 18, 2023. Of 26,335 articles, they narrowed their review down to 15 studies that investigated CVD, CVD risk factors, and cerebrovascular disease in the chronic phase of TBI, including community, military, or sport-related brain trauma, regardless of the timing of disease occurrence with respect to brain injury via TBI or repetitive head impact.
 

New Cardiovascular Risk

Studies that used national or local registries tended to be retrospective and predominantly conducted in people with preexisting cardiovascular conditions. In these studies, TBI was found to be an independent risk factor for myocardial dysfunction. However, although these studies do provide evidence of elevated cardiovascular risk subsequent to a single TBI, including individuals with preexisting medical comorbidities “makes it difficult to determine the timing of incident cardiovascular disease and cardiovascular risk factors subsequent to brain injury,” they wrote.

However, some studies showed that even individuals with TBI but without preexisting myocardial dysfunction at baseline had a significantly higher risk for CVD than those without a history of TBI.

In fact, several studies included populations without preexisting medical and cardiovascular comorbidities to “better refine the order and timing of CVD and other risk factors in individuals with TBI.”

For example, one study of concussion survivors without preexisting diagnoses showed that cardiovascular, endocrinological, and neuropsychiatric comorbidities occurred at a “significantly higher incidence within 5 years after concussive TBI compared with healthy individuals who were matched in terms of age, race, and sex and didn’t have a TBI exposure.” Other studies yielded similar findings.

Because cardiovascular risk factors and events become more common with age, it’s important to account for age in evaluating the effects of TBI. Although many studies of TBI and subsequent CVD didn’t stratify individuals by age, one 10-year study of people without any known cardiovascular or neuropsychiatric conditions who sustained TBI found that people as young as 18-40 years were more likely to develop hypertension, hyperlipidemia, obesity, and diabetes within 3-5 years following brain injury than matched individuals in the control group.

“Individuals who have encountered TBI, surprisingly even those who are young and in good health with no prior comorbid conditions, face an increased risk of adverse cardiovascular outcomes for an extended duration after the initial event,” Drs. Zafonte and Izzy summarized. “Therefore, it’s imperative that they receive regular and long-term screenings for CVD and associated risk factors.”
 

Bidirectional Relationship

Brain injury has been associated with acute cardiovascular dysfunction, including autonomic heart-brain axis dysregulation, imbalances between the sympathetic and parasympathetic nervous systems, and excessive catecholamine release, the authors noted.

Drs. Zafonte and Izzy suggested several plausible links between TBI and cardiovascular dysfunction, noting that they are “likely multifaceted, potentially encompassing risk factors that span the pre-injury, injury, and post-injury phases of the condition.”

TBI may induce alterations in neurobiological processes, which have been reported to be associated with an increased risk for CVD (eg, chronic dysfunction of the autonomic system, systemic inflammation, and modifications in the brain-gut connection).

Patients with TBI might develop additional risk factors following the injury, including conditions like posttraumatic stress disorder, depression, and other psychiatric illnesses, which are “known to augment the risk of CVD.”

TBI can lead to subsequent behavioral and lifestyle changes that place patients at an elevated risk for both cardiovascular and cognitive dysfunction when compared to the general population of TBI survivors.

There may be additional as yet undefined risks.

They believe there’s a bidirectional relationship between TBI and CVD. “On one hand, TBI has been associated with an elevated risk of CVD,” they said. “Conversely, cardiovascular risk factors such as diabetes, hypertension, hyperlipidemia, and sleep disturbances that have been demonstrated to negatively influence cognitive function and heighten the risk of dementia. Consequently, this interplay can further compound the long-term consequences of the injury.”

Their work aims to try and disentangle this “complex series of relationships.”

They recommend screening to identify diseases in their earliest and “most manageable phases” because TBI has been “unveiled as an underappreciated risk factor for CVD within contact sports, military, and community setting.”

An effective screening program “should rely on quantifiable and dependable biomarkers such as blood pressure, BMI, waist circumference, blood lipid levels, and glucose. Additionally, it should take into account other factors like smoking habits, physical activity, and dietary choices,” they recommended.
 

Heart-Brain Connection

Dr. Croll noted that TBI is “associated with many poorly understood physiologic changes and complications, so it’s exciting to see research aimed at clarifying this chronic disease process.”

In recent years, “we have seen a greater appreciation and understanding of the heart-brain connection,” she said. “Moving forward, more research, including TBI research, will target that connection.”

She added that there are probably “multiple mechanisms” at play underlying the connection between TBI and CVD.

Most importantly, “we are increasingly learning that TBI is not only a discrete event that requires immediate treatment but also a chronic disease process,” and when we “think about the substantial long-term morbidity associated with TBI, we should keep increased risk for CVD on top of mind,” said Dr. Croll.

The review received no funding. Izzy reported receiving grants from the US National Institutes of Health (NIH) and 2023 Stepping Strong Innovator Award. Dr. Zafonte reported receiving grants from the NIH and royalties from Springer and Demos publishing for serving as a coeditor of Brain Injury Medicine. Dr. Zafonte has also served as an adviser to Myomo, Oncare.ai, Nanodiagnostics, and Kisbee. He reported evaluating patients in the Massachusetts General Hospital Brain and Body–TRUST Program, which is funded by the NFL Players Association. The other authors’ disclosures are listed on the original paper. Dr. Croll declared no relevant financial relationships.

A version of this article appeared on Medscape.com.

The long-term impact of traumatic brain injury (TBI) on neurologic and psychiatric function is well-established, but a growing body of research is pointing to unexpected medical sequalae, including cardiovascular disease (CVD).

A recent review looked at the investigation to date into this surprising connection, not only summarizing study findings but also suggesting potential mechanisms that might account for the association.

“This work offers further evidence that individuals with TBI are at an elevated risk of unfavorable cardiovascular outcomes for an extended period following the initial incident; consequently, they should undergo regular monitoring,” senior author Ross Zafonte, DO, president of Spaulding Rehabilitation Network, Boston, and lead author Saef Izzy, MD, MBChB, a neurologist at the Stroke and Cerebrovascular Center of Brigham and Women’s Hospital, Boston, Massachusetts, told this news organization.

“This holds significant importance for healthcare practitioners, as there exist several strategies to mitigate cardiovascular disease risk — including weight management, adopting a healthy diet, engaging in regular physical activity, and quitting smoking,” they stated.

Leslie Croll, MD, American Heart Association volunteer and assistant professor of clinical neurology at the Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, told this news organization that it’s “extremely important to learn more about the interplay between TBI, neurologic disease, psychiatric complications, and the cardiovascular system.”

Hopefully, she added, “future research will help us understand what kind of cardiovascular disease monitoring and prevention measures stand to give TBI patients the most benefit.”
 

Chronic Condition

TBI is “a major cause of long-term disability and premature death,” and is “highly prevalent among contact sports players, military personnel (eg, due to injuries sustained during conflict), and the general population (eg, due to falls and road traffic incidents),” the authors wrote.

Most studies pertaining to TBI have “primarily focused on establishing connections between single TBI, repetitive TBI, and their acute and chronic neurological and psychiatric consequences, such as Parkinson’s disease, Alzheimer’s disease, and chronic traumatic encephalopathy (CTE),” Drs. Zafonte and Izzy noted. By contrast, there has been a “notable lack of research attention given to non-neurological conditions associated with TBI.”

They pointed out that recent insights into TBI — particularly the acknowledgment of TBI as an “emerging chronic condition rather than merely an acute aftermath of brain injury” — have come to light through epidemiologic and pathologic investigations involving military veterans, professional American-style football players, and the civilian population. “This recognition opens up an opportunity to broaden our perspective and delve into the medical aspects of health that may be influenced by TBI.”

To broaden the investigation, the researchers reviewed literature published between January 1, 2001, and June 18, 2023. Of 26,335 articles, they narrowed their review down to 15 studies that investigated CVD, CVD risk factors, and cerebrovascular disease in the chronic phase of TBI, including community, military, or sport-related brain trauma, regardless of the timing of disease occurrence with respect to brain injury via TBI or repetitive head impact.
 

New Cardiovascular Risk

Studies that used national or local registries tended to be retrospective and predominantly conducted in people with preexisting cardiovascular conditions. In these studies, TBI was found to be an independent risk factor for myocardial dysfunction. However, although these studies do provide evidence of elevated cardiovascular risk subsequent to a single TBI, including individuals with preexisting medical comorbidities “makes it difficult to determine the timing of incident cardiovascular disease and cardiovascular risk factors subsequent to brain injury,” they wrote.

However, some studies showed that even individuals with TBI but without preexisting myocardial dysfunction at baseline had a significantly higher risk for CVD than those without a history of TBI.

In fact, several studies included populations without preexisting medical and cardiovascular comorbidities to “better refine the order and timing of CVD and other risk factors in individuals with TBI.”

For example, one study of concussion survivors without preexisting diagnoses showed that cardiovascular, endocrinological, and neuropsychiatric comorbidities occurred at a “significantly higher incidence within 5 years after concussive TBI compared with healthy individuals who were matched in terms of age, race, and sex and didn’t have a TBI exposure.” Other studies yielded similar findings.

Because cardiovascular risk factors and events become more common with age, it’s important to account for age in evaluating the effects of TBI. Although many studies of TBI and subsequent CVD didn’t stratify individuals by age, one 10-year study of people without any known cardiovascular or neuropsychiatric conditions who sustained TBI found that people as young as 18-40 years were more likely to develop hypertension, hyperlipidemia, obesity, and diabetes within 3-5 years following brain injury than matched individuals in the control group.

“Individuals who have encountered TBI, surprisingly even those who are young and in good health with no prior comorbid conditions, face an increased risk of adverse cardiovascular outcomes for an extended duration after the initial event,” Drs. Zafonte and Izzy summarized. “Therefore, it’s imperative that they receive regular and long-term screenings for CVD and associated risk factors.”
 

Bidirectional Relationship

Brain injury has been associated with acute cardiovascular dysfunction, including autonomic heart-brain axis dysregulation, imbalances between the sympathetic and parasympathetic nervous systems, and excessive catecholamine release, the authors noted.

Drs. Zafonte and Izzy suggested several plausible links between TBI and cardiovascular dysfunction, noting that they are “likely multifaceted, potentially encompassing risk factors that span the pre-injury, injury, and post-injury phases of the condition.”

TBI may induce alterations in neurobiological processes, which have been reported to be associated with an increased risk for CVD (eg, chronic dysfunction of the autonomic system, systemic inflammation, and modifications in the brain-gut connection).

Patients with TBI might develop additional risk factors following the injury, including conditions like posttraumatic stress disorder, depression, and other psychiatric illnesses, which are “known to augment the risk of CVD.”

TBI can lead to subsequent behavioral and lifestyle changes that place patients at an elevated risk for both cardiovascular and cognitive dysfunction when compared to the general population of TBI survivors.

There may be additional as yet undefined risks.

They believe there’s a bidirectional relationship between TBI and CVD. “On one hand, TBI has been associated with an elevated risk of CVD,” they said. “Conversely, cardiovascular risk factors such as diabetes, hypertension, hyperlipidemia, and sleep disturbances that have been demonstrated to negatively influence cognitive function and heighten the risk of dementia. Consequently, this interplay can further compound the long-term consequences of the injury.”

Their work aims to try and disentangle this “complex series of relationships.”

They recommend screening to identify diseases in their earliest and “most manageable phases” because TBI has been “unveiled as an underappreciated risk factor for CVD within contact sports, military, and community setting.”

An effective screening program “should rely on quantifiable and dependable biomarkers such as blood pressure, BMI, waist circumference, blood lipid levels, and glucose. Additionally, it should take into account other factors like smoking habits, physical activity, and dietary choices,” they recommended.
 

Heart-Brain Connection

Dr. Croll noted that TBI is “associated with many poorly understood physiologic changes and complications, so it’s exciting to see research aimed at clarifying this chronic disease process.”

In recent years, “we have seen a greater appreciation and understanding of the heart-brain connection,” she said. “Moving forward, more research, including TBI research, will target that connection.”

She added that there are probably “multiple mechanisms” at play underlying the connection between TBI and CVD.

Most importantly, “we are increasingly learning that TBI is not only a discrete event that requires immediate treatment but also a chronic disease process,” and when we “think about the substantial long-term morbidity associated with TBI, we should keep increased risk for CVD on top of mind,” said Dr. Croll.

The review received no funding. Izzy reported receiving grants from the US National Institutes of Health (NIH) and 2023 Stepping Strong Innovator Award. Dr. Zafonte reported receiving grants from the NIH and royalties from Springer and Demos publishing for serving as a coeditor of Brain Injury Medicine. Dr. Zafonte has also served as an adviser to Myomo, Oncare.ai, Nanodiagnostics, and Kisbee. He reported evaluating patients in the Massachusetts General Hospital Brain and Body–TRUST Program, which is funded by the NFL Players Association. The other authors’ disclosures are listed on the original paper. Dr. Croll declared no relevant financial relationships.

A version of this article appeared on Medscape.com.

The long-term impact of traumatic brain injury (TBI) on neurologic and psychiatric function is well-established, but a growing body of research is pointing to unexpected medical sequalae, including cardiovascular disease (CVD).

A recent review looked at the investigation to date into this surprising connection, not only summarizing study findings but also suggesting potential mechanisms that might account for the association.

“This work offers further evidence that individuals with TBI are at an elevated risk of unfavorable cardiovascular outcomes for an extended period following the initial incident; consequently, they should undergo regular monitoring,” senior author Ross Zafonte, DO, president of Spaulding Rehabilitation Network, Boston, and lead author Saef Izzy, MD, MBChB, a neurologist at the Stroke and Cerebrovascular Center of Brigham and Women’s Hospital, Boston, Massachusetts, told this news organization.

“This holds significant importance for healthcare practitioners, as there exist several strategies to mitigate cardiovascular disease risk — including weight management, adopting a healthy diet, engaging in regular physical activity, and quitting smoking,” they stated.

Leslie Croll, MD, American Heart Association volunteer and assistant professor of clinical neurology at the Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, told this news organization that it’s “extremely important to learn more about the interplay between TBI, neurologic disease, psychiatric complications, and the cardiovascular system.”

Hopefully, she added, “future research will help us understand what kind of cardiovascular disease monitoring and prevention measures stand to give TBI patients the most benefit.”
 

Chronic Condition

TBI is “a major cause of long-term disability and premature death,” and is “highly prevalent among contact sports players, military personnel (eg, due to injuries sustained during conflict), and the general population (eg, due to falls and road traffic incidents),” the authors wrote.

Most studies pertaining to TBI have “primarily focused on establishing connections between single TBI, repetitive TBI, and their acute and chronic neurological and psychiatric consequences, such as Parkinson’s disease, Alzheimer’s disease, and chronic traumatic encephalopathy (CTE),” Drs. Zafonte and Izzy noted. By contrast, there has been a “notable lack of research attention given to non-neurological conditions associated with TBI.”

They pointed out that recent insights into TBI — particularly the acknowledgment of TBI as an “emerging chronic condition rather than merely an acute aftermath of brain injury” — have come to light through epidemiologic and pathologic investigations involving military veterans, professional American-style football players, and the civilian population. “This recognition opens up an opportunity to broaden our perspective and delve into the medical aspects of health that may be influenced by TBI.”

To broaden the investigation, the researchers reviewed literature published between January 1, 2001, and June 18, 2023. Of 26,335 articles, they narrowed their review down to 15 studies that investigated CVD, CVD risk factors, and cerebrovascular disease in the chronic phase of TBI, including community, military, or sport-related brain trauma, regardless of the timing of disease occurrence with respect to brain injury via TBI or repetitive head impact.
 

New Cardiovascular Risk

Studies that used national or local registries tended to be retrospective and predominantly conducted in people with preexisting cardiovascular conditions. In these studies, TBI was found to be an independent risk factor for myocardial dysfunction. However, although these studies do provide evidence of elevated cardiovascular risk subsequent to a single TBI, including individuals with preexisting medical comorbidities “makes it difficult to determine the timing of incident cardiovascular disease and cardiovascular risk factors subsequent to brain injury,” they wrote.

However, some studies showed that even individuals with TBI but without preexisting myocardial dysfunction at baseline had a significantly higher risk for CVD than those without a history of TBI.

In fact, several studies included populations without preexisting medical and cardiovascular comorbidities to “better refine the order and timing of CVD and other risk factors in individuals with TBI.”

For example, one study of concussion survivors without preexisting diagnoses showed that cardiovascular, endocrinological, and neuropsychiatric comorbidities occurred at a “significantly higher incidence within 5 years after concussive TBI compared with healthy individuals who were matched in terms of age, race, and sex and didn’t have a TBI exposure.” Other studies yielded similar findings.

Because cardiovascular risk factors and events become more common with age, it’s important to account for age in evaluating the effects of TBI. Although many studies of TBI and subsequent CVD didn’t stratify individuals by age, one 10-year study of people without any known cardiovascular or neuropsychiatric conditions who sustained TBI found that people as young as 18-40 years were more likely to develop hypertension, hyperlipidemia, obesity, and diabetes within 3-5 years following brain injury than matched individuals in the control group.

“Individuals who have encountered TBI, surprisingly even those who are young and in good health with no prior comorbid conditions, face an increased risk of adverse cardiovascular outcomes for an extended duration after the initial event,” Drs. Zafonte and Izzy summarized. “Therefore, it’s imperative that they receive regular and long-term screenings for CVD and associated risk factors.”
 

Bidirectional Relationship

Brain injury has been associated with acute cardiovascular dysfunction, including autonomic heart-brain axis dysregulation, imbalances between the sympathetic and parasympathetic nervous systems, and excessive catecholamine release, the authors noted.

Drs. Zafonte and Izzy suggested several plausible links between TBI and cardiovascular dysfunction, noting that they are “likely multifaceted, potentially encompassing risk factors that span the pre-injury, injury, and post-injury phases of the condition.”

TBI may induce alterations in neurobiological processes, which have been reported to be associated with an increased risk for CVD (eg, chronic dysfunction of the autonomic system, systemic inflammation, and modifications in the brain-gut connection).

Patients with TBI might develop additional risk factors following the injury, including conditions like posttraumatic stress disorder, depression, and other psychiatric illnesses, which are “known to augment the risk of CVD.”

TBI can lead to subsequent behavioral and lifestyle changes that place patients at an elevated risk for both cardiovascular and cognitive dysfunction when compared to the general population of TBI survivors.

There may be additional as yet undefined risks.

They believe there’s a bidirectional relationship between TBI and CVD. “On one hand, TBI has been associated with an elevated risk of CVD,” they said. “Conversely, cardiovascular risk factors such as diabetes, hypertension, hyperlipidemia, and sleep disturbances that have been demonstrated to negatively influence cognitive function and heighten the risk of dementia. Consequently, this interplay can further compound the long-term consequences of the injury.”

Their work aims to try and disentangle this “complex series of relationships.”

They recommend screening to identify diseases in their earliest and “most manageable phases” because TBI has been “unveiled as an underappreciated risk factor for CVD within contact sports, military, and community setting.”

An effective screening program “should rely on quantifiable and dependable biomarkers such as blood pressure, BMI, waist circumference, blood lipid levels, and glucose. Additionally, it should take into account other factors like smoking habits, physical activity, and dietary choices,” they recommended.
 

Heart-Brain Connection

Dr. Croll noted that TBI is “associated with many poorly understood physiologic changes and complications, so it’s exciting to see research aimed at clarifying this chronic disease process.”

In recent years, “we have seen a greater appreciation and understanding of the heart-brain connection,” she said. “Moving forward, more research, including TBI research, will target that connection.”

She added that there are probably “multiple mechanisms” at play underlying the connection between TBI and CVD.

Most importantly, “we are increasingly learning that TBI is not only a discrete event that requires immediate treatment but also a chronic disease process,” and when we “think about the substantial long-term morbidity associated with TBI, we should keep increased risk for CVD on top of mind,” said Dr. Croll.

The review received no funding. Izzy reported receiving grants from the US National Institutes of Health (NIH) and 2023 Stepping Strong Innovator Award. Dr. Zafonte reported receiving grants from the NIH and royalties from Springer and Demos publishing for serving as a coeditor of Brain Injury Medicine. Dr. Zafonte has also served as an adviser to Myomo, Oncare.ai, Nanodiagnostics, and Kisbee. He reported evaluating patients in the Massachusetts General Hospital Brain and Body–TRUST Program, which is funded by the NFL Players Association. The other authors’ disclosures are listed on the original paper. Dr. Croll declared no relevant financial relationships.

A version of this article appeared on Medscape.com.