Neurology

A simple skin biopsy test is able to detect an abnormal form of alpha-synuclein with high accuracy in individuals with neurodegenerative disorders such as Parkinson’s disease (PD).

Researchers are hopeful that the test — which identified phosphorylated alpha-synuclein (P-SYN) with 95.5% accuracy in the blinded, multicenter trial — will accelerate not just early identification of synucleinopathies but also drug development.

Synucleinopathies include PD, dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and pure autonomic failure (PAF).

“Each year, there are nearly 200,000 people in the U.S. who face a diagnosis of Parkinson’s disease, dementia with Lewy bodies, and related disorders,” study investigator Christopher H. Gibbons, MD, professor of neurology at Harvard Medical School in Boston, said in a press release.

He explained that patients often experience delays in diagnosis or are misdiagnosed due to the complexity of synucleinopathies.

“With a simple, minimally invasive skin biopsy test, this blinded, multicenter study demonstrated how we can more objectively identify the underlying pathology of synucleinopathies and offer better diagnostic answers and care for patients.”

The findings were published online on March 20 in JAMA.
 

An Urgent Priority

Affecting an estimated 2.5 million people in the United States, synucleinopathies are progressive neurodegenerative diseases with varying prognoses, so identifying a reliable diagnostic biomarker is an “urgent unmet priority,” the researchers noted.

The disorders share some symptoms such as tremors and cognitive changes, and all are characterized by P-SYN, an abnormal protein found in the cutaneous nerve fibers.

The study included 428 adults aged 40-99 years (mean age, 70 years) recruited from 30 academic and community-based neurology practices across the United States, with 277 diagnosed with PD, DLB, MSA, or PAF. It also included a control group of 120 participants with no symptoms suggestive of synucleinopathy.

Investigators used the commercially available Syn-One Test, developed in 2019 by CND Life Sciences, to analyze levels of P-SYN via 3-mm punch skin biopsies from each participant.

The test detected P-SYN in 95.5% of study participants overall, including 89 of 96 (92.7%) with PD, 54 of 55 (98.2%) with MSA, 48 of 50 (96%) with DLB, 22 of 22 (100%) with PAF, and 4 of 120 (3.3%) of the controls with no synucleinopathy.

The investigators said it is possible that some of the controls who tested positive had a subclinical form of synucleinopathy, which would explain the false positives.

Study limitations include clinical consensus diagnostic criteria without video or autopsy confirmation, a lack of genetic testing on participants (some genetic forms of PD do not have alpha-synuclein deposition), and the fact that controls were younger than those in disease groups.

“Further research is needed in unselected clinical populations to externally validate the findings and fully characterize the potential role of skin biopsy detection of P-SYN in clinical care,” the authors wrote.

Syn-One is not approved by the US Food and Drug Administration as a diagnostic test for PD but is available as a pathologic assay that determines whether a tissue sample contains phosphorylated alpha-synuclein and can be billed through Medicare.

The study was funded by the National Institutes of Health. Dr. Gibbons reported having stock options in CND Life Sciences outside the submitted work. Other disclosures are noted in the original article.

A version of this article appeared on Medscape.com.

A simple skin biopsy test is able to detect an abnormal form of alpha-synuclein with high accuracy in individuals with neurodegenerative disorders such as Parkinson’s disease (PD).

Researchers are hopeful that the test — which identified phosphorylated alpha-synuclein (P-SYN) with 95.5% accuracy in the blinded, multicenter trial — will accelerate not just early identification of synucleinopathies but also drug development.

Synucleinopathies include PD, dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and pure autonomic failure (PAF).

“Each year, there are nearly 200,000 people in the U.S. who face a diagnosis of Parkinson’s disease, dementia with Lewy bodies, and related disorders,” study investigator Christopher H. Gibbons, MD, professor of neurology at Harvard Medical School in Boston, said in a press release.

He explained that patients often experience delays in diagnosis or are misdiagnosed due to the complexity of synucleinopathies.

“With a simple, minimally invasive skin biopsy test, this blinded, multicenter study demonstrated how we can more objectively identify the underlying pathology of synucleinopathies and offer better diagnostic answers and care for patients.”

The findings were published online on March 20 in JAMA.
 

An Urgent Priority

Affecting an estimated 2.5 million people in the United States, synucleinopathies are progressive neurodegenerative diseases with varying prognoses, so identifying a reliable diagnostic biomarker is an “urgent unmet priority,” the researchers noted.

The disorders share some symptoms such as tremors and cognitive changes, and all are characterized by P-SYN, an abnormal protein found in the cutaneous nerve fibers.

The study included 428 adults aged 40-99 years (mean age, 70 years) recruited from 30 academic and community-based neurology practices across the United States, with 277 diagnosed with PD, DLB, MSA, or PAF. It also included a control group of 120 participants with no symptoms suggestive of synucleinopathy.

Investigators used the commercially available Syn-One Test, developed in 2019 by CND Life Sciences, to analyze levels of P-SYN via 3-mm punch skin biopsies from each participant.

The test detected P-SYN in 95.5% of study participants overall, including 89 of 96 (92.7%) with PD, 54 of 55 (98.2%) with MSA, 48 of 50 (96%) with DLB, 22 of 22 (100%) with PAF, and 4 of 120 (3.3%) of the controls with no synucleinopathy.

The investigators said it is possible that some of the controls who tested positive had a subclinical form of synucleinopathy, which would explain the false positives.

Study limitations include clinical consensus diagnostic criteria without video or autopsy confirmation, a lack of genetic testing on participants (some genetic forms of PD do not have alpha-synuclein deposition), and the fact that controls were younger than those in disease groups.

“Further research is needed in unselected clinical populations to externally validate the findings and fully characterize the potential role of skin biopsy detection of P-SYN in clinical care,” the authors wrote.

Syn-One is not approved by the US Food and Drug Administration as a diagnostic test for PD but is available as a pathologic assay that determines whether a tissue sample contains phosphorylated alpha-synuclein and can be billed through Medicare.

The study was funded by the National Institutes of Health. Dr. Gibbons reported having stock options in CND Life Sciences outside the submitted work. Other disclosures are noted in the original article.

A version of this article appeared on Medscape.com.

A simple skin biopsy test is able to detect an abnormal form of alpha-synuclein with high accuracy in individuals with neurodegenerative disorders such as Parkinson’s disease (PD).

Researchers are hopeful that the test — which identified phosphorylated alpha-synuclein (P-SYN) with 95.5% accuracy in the blinded, multicenter trial — will accelerate not just early identification of synucleinopathies but also drug development.

Synucleinopathies include PD, dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and pure autonomic failure (PAF).

“Each year, there are nearly 200,000 people in the U.S. who face a diagnosis of Parkinson’s disease, dementia with Lewy bodies, and related disorders,” study investigator Christopher H. Gibbons, MD, professor of neurology at Harvard Medical School in Boston, said in a press release.

He explained that patients often experience delays in diagnosis or are misdiagnosed due to the complexity of synucleinopathies.

“With a simple, minimally invasive skin biopsy test, this blinded, multicenter study demonstrated how we can more objectively identify the underlying pathology of synucleinopathies and offer better diagnostic answers and care for patients.”

The findings were published online on March 20 in JAMA.
 

An Urgent Priority

Affecting an estimated 2.5 million people in the United States, synucleinopathies are progressive neurodegenerative diseases with varying prognoses, so identifying a reliable diagnostic biomarker is an “urgent unmet priority,” the researchers noted.

The disorders share some symptoms such as tremors and cognitive changes, and all are characterized by P-SYN, an abnormal protein found in the cutaneous nerve fibers.

The study included 428 adults aged 40-99 years (mean age, 70 years) recruited from 30 academic and community-based neurology practices across the United States, with 277 diagnosed with PD, DLB, MSA, or PAF. It also included a control group of 120 participants with no symptoms suggestive of synucleinopathy.

Investigators used the commercially available Syn-One Test, developed in 2019 by CND Life Sciences, to analyze levels of P-SYN via 3-mm punch skin biopsies from each participant.

The test detected P-SYN in 95.5% of study participants overall, including 89 of 96 (92.7%) with PD, 54 of 55 (98.2%) with MSA, 48 of 50 (96%) with DLB, 22 of 22 (100%) with PAF, and 4 of 120 (3.3%) of the controls with no synucleinopathy.

The investigators said it is possible that some of the controls who tested positive had a subclinical form of synucleinopathy, which would explain the false positives.

Study limitations include clinical consensus diagnostic criteria without video or autopsy confirmation, a lack of genetic testing on participants (some genetic forms of PD do not have alpha-synuclein deposition), and the fact that controls were younger than those in disease groups.

“Further research is needed in unselected clinical populations to externally validate the findings and fully characterize the potential role of skin biopsy detection of P-SYN in clinical care,” the authors wrote.

Syn-One is not approved by the US Food and Drug Administration as a diagnostic test for PD but is available as a pathologic assay that determines whether a tissue sample contains phosphorylated alpha-synuclein and can be billed through Medicare.

The study was funded by the National Institutes of Health. Dr. Gibbons reported having stock options in CND Life Sciences outside the submitted work. Other disclosures are noted in the original article.

A version of this article appeared on Medscape.com.

TOPLINE:

Hospitalization for influenza is linked to a greater risk for subsequent neurologic disorders including migraine, stroke, or epilepsy than is hospitalization for COVID-19, results of a large study show.

METHODOLOGY:

• Researchers used healthcare claims data to compare 77,300 people hospitalized with COVID-19 with 77,300 hospitalized with influenza. The study did not include individuals with long COVID.
• In the final sample of 154,500 participants, the mean age was 51 years, and more than half (58%) were female.
• Investigators followed participants from both cohorts for a year to find out how many of them had medical care for six of the most common neurologic disorders: migraine, epilepsy, stroke, neuropathy, movement disorders, and dementia.
• If participants had one of these neurologic disorders prior to the original hospitalization, the primary outcome involved subsequent healthcare encounters for the neurologic diagnosis.

TAKEAWAY:

• Participants hospitalized with COVID-19 versus influenza were significantly less likely to require care in the following year for migraine (2% vs 3.2%), epilepsy (1.6% vs 2.1%), neuropathy (1.9% vs 3.6%), movement disorders (1.5% vs 2.5%), stroke (2% vs 2.4%), and dementia (2% vs 2.3%) (all P < .001).
• After adjusting for age, sex, and other health conditions, researchers found that people hospitalized with COVID-19 had a 35% lower risk of receiving care for migraine, a 22% lower risk of receiving care for epilepsy, and a 44% lower risk of receiving care for neuropathy than those with influenza. They also had a 36% lower risk of receiving care for movement disorders, a 10% lower risk for stroke (all P < .001), as well as a 7% lower risk for dementia (P = .0007).
• In participants who did not have a preexisting neurologic condition at the time of hospitalization for either COVID-19 or influenza, 2.8% hospitalized with COVID-19 developed one in the next year compared with 5% of those hospitalized with influenza.

IN PRACTICE:

“While the results were not what we expected to find, they are reassuring in that we found being hospitalized with COVID did not lead to more care for common neurologic conditions when compared to being hospitalized with influenza,” study investigator Brian C. Callaghan, MD, of University of Michigan, Ann Arbor, said in a press release.

SOURCE:

Adam de Havenon, MD, of Yale University in New Haven, Connecticut, led the study, which was published online on March 20 in Neurology.

LIMITATIONS:

The study relied on ICD codes in health claims databases, which could introduce misclassification bias. Also, by selecting only individuals who had associated hospital-based care, there may have been a selection bias based on disease severity.

DISCLOSURES:

The study was funded by the American Academy of Neurology. Dr. De Havenon reported receiving consultant fees from Integra and Novo Nordisk and royalty fees from UpToDate and has equity in Titin KM and Certus. Dr. Callaghan has consulted for DynaMed and the Vaccine Injury Compensation Program. Other disclosures were noted in the original article.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Hospitalization for influenza is linked to a greater risk for subsequent neurologic disorders including migraine, stroke, or epilepsy than is hospitalization for COVID-19, results of a large study show.

METHODOLOGY:

• Researchers used healthcare claims data to compare 77,300 people hospitalized with COVID-19 with 77,300 hospitalized with influenza. The study did not include individuals with long COVID.
• In the final sample of 154,500 participants, the mean age was 51 years, and more than half (58%) were female.
• Investigators followed participants from both cohorts for a year to find out how many of them had medical care for six of the most common neurologic disorders: migraine, epilepsy, stroke, neuropathy, movement disorders, and dementia.
• If participants had one of these neurologic disorders prior to the original hospitalization, the primary outcome involved subsequent healthcare encounters for the neurologic diagnosis.

TAKEAWAY:

• Participants hospitalized with COVID-19 versus influenza were significantly less likely to require care in the following year for migraine (2% vs 3.2%), epilepsy (1.6% vs 2.1%), neuropathy (1.9% vs 3.6%), movement disorders (1.5% vs 2.5%), stroke (2% vs 2.4%), and dementia (2% vs 2.3%) (all P < .001).
• After adjusting for age, sex, and other health conditions, researchers found that people hospitalized with COVID-19 had a 35% lower risk of receiving care for migraine, a 22% lower risk of receiving care for epilepsy, and a 44% lower risk of receiving care for neuropathy than those with influenza. They also had a 36% lower risk of receiving care for movement disorders, a 10% lower risk for stroke (all P < .001), as well as a 7% lower risk for dementia (P = .0007).
• In participants who did not have a preexisting neurologic condition at the time of hospitalization for either COVID-19 or influenza, 2.8% hospitalized with COVID-19 developed one in the next year compared with 5% of those hospitalized with influenza.

IN PRACTICE:

“While the results were not what we expected to find, they are reassuring in that we found being hospitalized with COVID did not lead to more care for common neurologic conditions when compared to being hospitalized with influenza,” study investigator Brian C. Callaghan, MD, of University of Michigan, Ann Arbor, said in a press release.

SOURCE:

Adam de Havenon, MD, of Yale University in New Haven, Connecticut, led the study, which was published online on March 20 in Neurology.

LIMITATIONS:

The study relied on ICD codes in health claims databases, which could introduce misclassification bias. Also, by selecting only individuals who had associated hospital-based care, there may have been a selection bias based on disease severity.

DISCLOSURES:

The study was funded by the American Academy of Neurology. Dr. De Havenon reported receiving consultant fees from Integra and Novo Nordisk and royalty fees from UpToDate and has equity in Titin KM and Certus. Dr. Callaghan has consulted for DynaMed and the Vaccine Injury Compensation Program. Other disclosures were noted in the original article.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Hospitalization for influenza is linked to a greater risk for subsequent neurologic disorders including migraine, stroke, or epilepsy than is hospitalization for COVID-19, results of a large study show.

METHODOLOGY:

• Researchers used healthcare claims data to compare 77,300 people hospitalized with COVID-19 with 77,300 hospitalized with influenza. The study did not include individuals with long COVID.
• In the final sample of 154,500 participants, the mean age was 51 years, and more than half (58%) were female.
• Investigators followed participants from both cohorts for a year to find out how many of them had medical care for six of the most common neurologic disorders: migraine, epilepsy, stroke, neuropathy, movement disorders, and dementia.
• If participants had one of these neurologic disorders prior to the original hospitalization, the primary outcome involved subsequent healthcare encounters for the neurologic diagnosis.

TAKEAWAY:

• Participants hospitalized with COVID-19 versus influenza were significantly less likely to require care in the following year for migraine (2% vs 3.2%), epilepsy (1.6% vs 2.1%), neuropathy (1.9% vs 3.6%), movement disorders (1.5% vs 2.5%), stroke (2% vs 2.4%), and dementia (2% vs 2.3%) (all P < .001).
• After adjusting for age, sex, and other health conditions, researchers found that people hospitalized with COVID-19 had a 35% lower risk of receiving care for migraine, a 22% lower risk of receiving care for epilepsy, and a 44% lower risk of receiving care for neuropathy than those with influenza. They also had a 36% lower risk of receiving care for movement disorders, a 10% lower risk for stroke (all P < .001), as well as a 7% lower risk for dementia (P = .0007).
• In participants who did not have a preexisting neurologic condition at the time of hospitalization for either COVID-19 or influenza, 2.8% hospitalized with COVID-19 developed one in the next year compared with 5% of those hospitalized with influenza.

IN PRACTICE:

“While the results were not what we expected to find, they are reassuring in that we found being hospitalized with COVID did not lead to more care for common neurologic conditions when compared to being hospitalized with influenza,” study investigator Brian C. Callaghan, MD, of University of Michigan, Ann Arbor, said in a press release.

SOURCE:

Adam de Havenon, MD, of Yale University in New Haven, Connecticut, led the study, which was published online on March 20 in Neurology.

LIMITATIONS:

The study relied on ICD codes in health claims databases, which could introduce misclassification bias. Also, by selecting only individuals who had associated hospital-based care, there may have been a selection bias based on disease severity.

DISCLOSURES:

The study was funded by the American Academy of Neurology. Dr. De Havenon reported receiving consultant fees from Integra and Novo Nordisk and royalty fees from UpToDate and has equity in Titin KM and Certus. Dr. Callaghan has consulted for DynaMed and the Vaccine Injury Compensation Program. Other disclosures were noted in the original article.
 

A version of this article appeared on Medscape.com.

Symptoms of sleep apnea, including snorting, gasping, or paused breathing during sleep, are associated with a significantly greater risk for problems with cognitive and memory problems, results from a large study showed.

Data from a representative sample of US adults show that those who reported sleep apnea symptoms were about 50% more likely to also report cognitive issues versus their counterparts without such symptoms.

“For clinicians, these findings suggest a potential benefit of considering sleep apnea as a possible contributing or exacerbating factor in individuals experiencing memory or cognitive problems. This could prompt further evaluation for sleep apnea, particularly in at-risk individuals,” said study investigator Dominique Low, MD, MPH, Department of Neurology, Boston Medical Center.

The findings were released ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology.
 

Need to Raise Awareness

The findings are based on 4257 adults who participated in the 2017-2018 National Health and Nutrition Examination Survey and completed questionnaires covering sleep, memory, cognition, and decision-making abilities.

Those who reported snorting, gasping, or breathing pauses during sleep were categorized as experiencing sleep apnea symptoms. Those who reported memory trouble, periods of confusion, difficulty concentrating, or decision-making problems were classified as having memory or cognitive symptoms.

Overall, 1079 participants reported symptoms of sleep apnea. Compared with people without sleep apnea, those with symptoms were more likely to have cognitive problems (33% vs 20%) and have greater odds of having memory or cognitive symptoms, even after adjusting for age, gender, race, and education (adjusted odds ratio, 2.02; P < .001).

“While the study did not establish a cause-and-effect relationship, the findings suggest the importance of raising awareness about the potential link between sleep and cognitive function. Early identification and treatment may improve overall health and potentially lead to a better quality of life,” Dr. Low said.

Limitations of the study include self-reported data on sleep apnea symptoms and cognitive issues sourced from one survey.
 

Consistent Data

Reached for comment, Matthew Pase, PhD, with the Turner Institute for Brain and Mental Health, Monash University, Melbourne, Australia, said the results are similar to earlier work that found a link between obstructive sleep apnea and cognition.

For example, in a recent study, the presence of mild to severe OSA, identified using overnight polysomnography in five community-based cohorts with more than 5900 adults, was associated with poorer cognitive test performance, Dr. Pase said.

“These and other results underscore the importance of healthy sleep for optimal brain health. Future research is needed to test if treating OSA and other sleep disorders can reduce the risk of cognitive impairment,” Dr. Pase said.

Yet, in its latest statement on the topic, the US Preventive Services Task Force concluded there remains insufficient evidence to weigh the balance of benefits and harms of screening for OSA among asymptomatic adults and those with unrecognized symptoms.

The study had no specific funding. Dr. Low and Dr. Pase had no relevant disclosures.
 

A version of this article appeared on Medscape.com.

Symptoms of sleep apnea, including snorting, gasping, or paused breathing during sleep, are associated with a significantly greater risk for problems with cognitive and memory problems, results from a large study showed.

Data from a representative sample of US adults show that those who reported sleep apnea symptoms were about 50% more likely to also report cognitive issues versus their counterparts without such symptoms.

“For clinicians, these findings suggest a potential benefit of considering sleep apnea as a possible contributing or exacerbating factor in individuals experiencing memory or cognitive problems. This could prompt further evaluation for sleep apnea, particularly in at-risk individuals,” said study investigator Dominique Low, MD, MPH, Department of Neurology, Boston Medical Center.

The findings were released ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology.
 

Need to Raise Awareness

The findings are based on 4257 adults who participated in the 2017-2018 National Health and Nutrition Examination Survey and completed questionnaires covering sleep, memory, cognition, and decision-making abilities.

Those who reported snorting, gasping, or breathing pauses during sleep were categorized as experiencing sleep apnea symptoms. Those who reported memory trouble, periods of confusion, difficulty concentrating, or decision-making problems were classified as having memory or cognitive symptoms.

Overall, 1079 participants reported symptoms of sleep apnea. Compared with people without sleep apnea, those with symptoms were more likely to have cognitive problems (33% vs 20%) and have greater odds of having memory or cognitive symptoms, even after adjusting for age, gender, race, and education (adjusted odds ratio, 2.02; P < .001).

“While the study did not establish a cause-and-effect relationship, the findings suggest the importance of raising awareness about the potential link between sleep and cognitive function. Early identification and treatment may improve overall health and potentially lead to a better quality of life,” Dr. Low said.

Limitations of the study include self-reported data on sleep apnea symptoms and cognitive issues sourced from one survey.
 

Consistent Data

Reached for comment, Matthew Pase, PhD, with the Turner Institute for Brain and Mental Health, Monash University, Melbourne, Australia, said the results are similar to earlier work that found a link between obstructive sleep apnea and cognition.

For example, in a recent study, the presence of mild to severe OSA, identified using overnight polysomnography in five community-based cohorts with more than 5900 adults, was associated with poorer cognitive test performance, Dr. Pase said.

“These and other results underscore the importance of healthy sleep for optimal brain health. Future research is needed to test if treating OSA and other sleep disorders can reduce the risk of cognitive impairment,” Dr. Pase said.

Yet, in its latest statement on the topic, the US Preventive Services Task Force concluded there remains insufficient evidence to weigh the balance of benefits and harms of screening for OSA among asymptomatic adults and those with unrecognized symptoms.

The study had no specific funding. Dr. Low and Dr. Pase had no relevant disclosures.
 

A version of this article appeared on Medscape.com.

Symptoms of sleep apnea, including snorting, gasping, or paused breathing during sleep, are associated with a significantly greater risk for problems with cognitive and memory problems, results from a large study showed.

Data from a representative sample of US adults show that those who reported sleep apnea symptoms were about 50% more likely to also report cognitive issues versus their counterparts without such symptoms.

“For clinicians, these findings suggest a potential benefit of considering sleep apnea as a possible contributing or exacerbating factor in individuals experiencing memory or cognitive problems. This could prompt further evaluation for sleep apnea, particularly in at-risk individuals,” said study investigator Dominique Low, MD, MPH, Department of Neurology, Boston Medical Center.

The findings were released ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology.
 

Need to Raise Awareness

The findings are based on 4257 adults who participated in the 2017-2018 National Health and Nutrition Examination Survey and completed questionnaires covering sleep, memory, cognition, and decision-making abilities.

Those who reported snorting, gasping, or breathing pauses during sleep were categorized as experiencing sleep apnea symptoms. Those who reported memory trouble, periods of confusion, difficulty concentrating, or decision-making problems were classified as having memory or cognitive symptoms.

Overall, 1079 participants reported symptoms of sleep apnea. Compared with people without sleep apnea, those with symptoms were more likely to have cognitive problems (33% vs 20%) and have greater odds of having memory or cognitive symptoms, even after adjusting for age, gender, race, and education (adjusted odds ratio, 2.02; P < .001).

“While the study did not establish a cause-and-effect relationship, the findings suggest the importance of raising awareness about the potential link between sleep and cognitive function. Early identification and treatment may improve overall health and potentially lead to a better quality of life,” Dr. Low said.

Limitations of the study include self-reported data on sleep apnea symptoms and cognitive issues sourced from one survey.
 

Consistent Data

Reached for comment, Matthew Pase, PhD, with the Turner Institute for Brain and Mental Health, Monash University, Melbourne, Australia, said the results are similar to earlier work that found a link between obstructive sleep apnea and cognition.

For example, in a recent study, the presence of mild to severe OSA, identified using overnight polysomnography in five community-based cohorts with more than 5900 adults, was associated with poorer cognitive test performance, Dr. Pase said.

“These and other results underscore the importance of healthy sleep for optimal brain health. Future research is needed to test if treating OSA and other sleep disorders can reduce the risk of cognitive impairment,” Dr. Pase said.

Yet, in its latest statement on the topic, the US Preventive Services Task Force concluded there remains insufficient evidence to weigh the balance of benefits and harms of screening for OSA among asymptomatic adults and those with unrecognized symptoms.

The study had no specific funding. Dr. Low and Dr. Pase had no relevant disclosures.
 

A version of this article appeared on Medscape.com.

Living in a disadvantaged neighborhood is associated with accelerated brain aging and a higher risk for early dementia, regardless of income level or education, new research suggested.

Analysis of two datasets revealed that people living in the most disadvantaged neighborhoods had a more than 20% higher risk for dementia than those in other areas and measurably poorer brain health as early as age 45, regardless of their own personal income and education.

“If you want to prevent dementia and you’re not asking someone about their neighborhood, you’re missing information that’s important to know,” lead author Aaron Reuben, PhD, postdoctoral scholar in neuropsychology and environmental health at Duke University, Durham, North Carolina, said in a news release.

The study was published online in Alzheimer’s & Dementia.

Higher Risk in Men

Few interventions exist to halt or delay the progression of Alzheimer’s disease and related dementias (ADRD), which has increasingly led to a focus on primary prevention.

Although previous research pointed to a link between socioeconomically disadvantaged neighborhoods and a greater risk for cognitive deficits, mild cognitive impairment, dementia, and poor brain health, the timeline for the emergence of that risk is unknown.

To fill in the gaps, investigators studied data on all 1.4 million New Zealand residents, dividing neighborhoods into quintiles based on level of disadvantage (assessed by the New Zealand Index of Deprivation) to see whether dementia diagnoses followed neighborhood socioeconomic gradients.

After adjusting for covariates, they found that overall, those living in disadvantaged areas were slightly more likely to develop dementia across the 20-year study period (adjusted hazard ratio [HR], 1.09; 95% CI, 1.08-1.10).

The more disadvantaged the neighborhood, the higher the dementia risk, with a 43% higher risk for ADRD among those in the highest quintile than among those in the lowest quintile (HR, 1.43; 95% CI, 1.36-1.49).

The effect was larger in men than in women and in younger vs older individuals, with the youngest age group showing 21% greater risk in women and 26% greater risk in men vs the oldest age group.

Dementia Prevention Starts Early

Researchers then turned to the Dunedin Study, a cohort of 938 New Zealanders (50% female) followed from birth to age 45 to track their psychological, social, and physiological health with brain scans, memory tests, and cognitive self-assessments.

The analysis suggested that by age 45, those living in more disadvantaged neighborhoods across adulthood had accumulated a significantly greater number of midlife risk factors for later ADRD.

They also had worse structural brain integrity, with each standard deviation increase in neighborhood disadvantage resulting in a thinner cortex, greater white matter hyperintensities volume, and older brain age.

Those living in poorer areas had lower cognitive test scores, reported more issues with everyday cognitive function, and showed a greater reduction in IQ from childhood to midlife. Analysis of brain scans also revealed mean brain ages 2.98 years older than those living in the least disadvantaged areas (P = .001).

Limitations included the study’s observational design, which could not establish causation, and the fact that the researchers did not have access to individual-level socioeconomic information for the entire population. Additionally, brain-integrity measures in the Dunedin Study were largely cross-sectional.

“If you want to truly prevent dementia, you’ve got to start early because 20 years before anyone will get a diagnosis, we’re seeing dementia’s emergence,” Dr. Reuben said. “And it could be even earlier.”

Funding for the study was provided by the National Institutes for Health; UK Medical Research Council; Health Research Council of New Zealand; Brain Research New Zealand; New Zealand Ministry of Business, Innovation, & Employment; and the Duke University and the University of North Carolina Alzheimer’s Disease Research Center. The authors declared no relevant financial relationships.

A version of this article appeared on Medscape.com.

Living in a disadvantaged neighborhood is associated with accelerated brain aging and a higher risk for early dementia, regardless of income level or education, new research suggested.

Analysis of two datasets revealed that people living in the most disadvantaged neighborhoods had a more than 20% higher risk for dementia than those in other areas and measurably poorer brain health as early as age 45, regardless of their own personal income and education.

“If you want to prevent dementia and you’re not asking someone about their neighborhood, you’re missing information that’s important to know,” lead author Aaron Reuben, PhD, postdoctoral scholar in neuropsychology and environmental health at Duke University, Durham, North Carolina, said in a news release.

The study was published online in Alzheimer’s & Dementia.

Higher Risk in Men

Few interventions exist to halt or delay the progression of Alzheimer’s disease and related dementias (ADRD), which has increasingly led to a focus on primary prevention.

Although previous research pointed to a link between socioeconomically disadvantaged neighborhoods and a greater risk for cognitive deficits, mild cognitive impairment, dementia, and poor brain health, the timeline for the emergence of that risk is unknown.

To fill in the gaps, investigators studied data on all 1.4 million New Zealand residents, dividing neighborhoods into quintiles based on level of disadvantage (assessed by the New Zealand Index of Deprivation) to see whether dementia diagnoses followed neighborhood socioeconomic gradients.

After adjusting for covariates, they found that overall, those living in disadvantaged areas were slightly more likely to develop dementia across the 20-year study period (adjusted hazard ratio [HR], 1.09; 95% CI, 1.08-1.10).

The more disadvantaged the neighborhood, the higher the dementia risk, with a 43% higher risk for ADRD among those in the highest quintile than among those in the lowest quintile (HR, 1.43; 95% CI, 1.36-1.49).

The effect was larger in men than in women and in younger vs older individuals, with the youngest age group showing 21% greater risk in women and 26% greater risk in men vs the oldest age group.

Dementia Prevention Starts Early

Researchers then turned to the Dunedin Study, a cohort of 938 New Zealanders (50% female) followed from birth to age 45 to track their psychological, social, and physiological health with brain scans, memory tests, and cognitive self-assessments.

The analysis suggested that by age 45, those living in more disadvantaged neighborhoods across adulthood had accumulated a significantly greater number of midlife risk factors for later ADRD.

They also had worse structural brain integrity, with each standard deviation increase in neighborhood disadvantage resulting in a thinner cortex, greater white matter hyperintensities volume, and older brain age.

Those living in poorer areas had lower cognitive test scores, reported more issues with everyday cognitive function, and showed a greater reduction in IQ from childhood to midlife. Analysis of brain scans also revealed mean brain ages 2.98 years older than those living in the least disadvantaged areas (P = .001).

Limitations included the study’s observational design, which could not establish causation, and the fact that the researchers did not have access to individual-level socioeconomic information for the entire population. Additionally, brain-integrity measures in the Dunedin Study were largely cross-sectional.

“If you want to truly prevent dementia, you’ve got to start early because 20 years before anyone will get a diagnosis, we’re seeing dementia’s emergence,” Dr. Reuben said. “And it could be even earlier.”

Funding for the study was provided by the National Institutes for Health; UK Medical Research Council; Health Research Council of New Zealand; Brain Research New Zealand; New Zealand Ministry of Business, Innovation, & Employment; and the Duke University and the University of North Carolina Alzheimer’s Disease Research Center. The authors declared no relevant financial relationships.

A version of this article appeared on Medscape.com.

Living in a disadvantaged neighborhood is associated with accelerated brain aging and a higher risk for early dementia, regardless of income level or education, new research suggested.

Analysis of two datasets revealed that people living in the most disadvantaged neighborhoods had a more than 20% higher risk for dementia than those in other areas and measurably poorer brain health as early as age 45, regardless of their own personal income and education.

“If you want to prevent dementia and you’re not asking someone about their neighborhood, you’re missing information that’s important to know,” lead author Aaron Reuben, PhD, postdoctoral scholar in neuropsychology and environmental health at Duke University, Durham, North Carolina, said in a news release.

The study was published online in Alzheimer’s & Dementia.

Higher Risk in Men

Few interventions exist to halt or delay the progression of Alzheimer’s disease and related dementias (ADRD), which has increasingly led to a focus on primary prevention.

Although previous research pointed to a link between socioeconomically disadvantaged neighborhoods and a greater risk for cognitive deficits, mild cognitive impairment, dementia, and poor brain health, the timeline for the emergence of that risk is unknown.

To fill in the gaps, investigators studied data on all 1.4 million New Zealand residents, dividing neighborhoods into quintiles based on level of disadvantage (assessed by the New Zealand Index of Deprivation) to see whether dementia diagnoses followed neighborhood socioeconomic gradients.

After adjusting for covariates, they found that overall, those living in disadvantaged areas were slightly more likely to develop dementia across the 20-year study period (adjusted hazard ratio [HR], 1.09; 95% CI, 1.08-1.10).

The more disadvantaged the neighborhood, the higher the dementia risk, with a 43% higher risk for ADRD among those in the highest quintile than among those in the lowest quintile (HR, 1.43; 95% CI, 1.36-1.49).

The effect was larger in men than in women and in younger vs older individuals, with the youngest age group showing 21% greater risk in women and 26% greater risk in men vs the oldest age group.

Dementia Prevention Starts Early

Researchers then turned to the Dunedin Study, a cohort of 938 New Zealanders (50% female) followed from birth to age 45 to track their psychological, social, and physiological health with brain scans, memory tests, and cognitive self-assessments.

The analysis suggested that by age 45, those living in more disadvantaged neighborhoods across adulthood had accumulated a significantly greater number of midlife risk factors for later ADRD.

They also had worse structural brain integrity, with each standard deviation increase in neighborhood disadvantage resulting in a thinner cortex, greater white matter hyperintensities volume, and older brain age.

Those living in poorer areas had lower cognitive test scores, reported more issues with everyday cognitive function, and showed a greater reduction in IQ from childhood to midlife. Analysis of brain scans also revealed mean brain ages 2.98 years older than those living in the least disadvantaged areas (P = .001).

Limitations included the study’s observational design, which could not establish causation, and the fact that the researchers did not have access to individual-level socioeconomic information for the entire population. Additionally, brain-integrity measures in the Dunedin Study were largely cross-sectional.

“If you want to truly prevent dementia, you’ve got to start early because 20 years before anyone will get a diagnosis, we’re seeing dementia’s emergence,” Dr. Reuben said. “And it could be even earlier.”

Funding for the study was provided by the National Institutes for Health; UK Medical Research Council; Health Research Council of New Zealand; Brain Research New Zealand; New Zealand Ministry of Business, Innovation, & Employment; and the Duke University and the University of North Carolina Alzheimer’s Disease Research Center. The authors declared no relevant financial relationships.

A version of this article appeared on Medscape.com.

TOPLINE:

Vitamin D deficiency is independently linked to the risk for diabetic peripheral neuropathy (DPN) by potentially affecting large nerve fibers in older patients with type 2 diabetes (T2D).

METHODOLOGY:

• Although previous research has shown that vitamin D deficiency is common in patients with diabetes and may increase the risk for peripheral neuropathy, its effects on large and small nerve fiber lesions have not been well explored yet.
• Researchers conducted a cross-sectional study to understand the association between vitamin D deficiency and DPN development in 230 older patients (mean age, 67 years) with T2D for about 15 years who were recruited from Beijing Hospital between 2020 and 2023.
• All patients were evaluated for DPN based on poor blood sugar control or symptoms such as pain and sensory abnormalities, of which 175 patients diagnosed with DPN were propensity-matched with 55 patients without DPN.
• Vitamin D deficiency, defined as serum 25-hydroxyvitamin D circulating levels below 20 ng/mL, was reported in 169 patients.
• Large nerve fiber lesions were evaluated using electromyography, and small nerve fiber lesions were assessed by measuring skin conductance.

TAKEAWAY:

• Vitamin D deficiency was more likely to affect large fiber lesions, suggested by longer median sensory nerve latency, minimum latency of the F-wave, and median nerve motor evoked potential latency than those in the vitamin D–sufficient group.
• Furthermore, vitamin D deficiency was linked to large fiber neuropathy with increased odds of prolongation of motor nerve latency (odds ratio, 1.362; P = .038).
• The electrochemical skin conductance, which indicates damage to small nerve fibers, was comparable between patients with and without vitamin D deficiency.

IN PRACTICE:

This study is too preliminary to have practice application.

SOURCE:

This study was led by Sijia Fei, Department of Endocrinology, Beijing Hospital, Beijing, People’s Republic of China, and was published online in Diabetes Research and Clinical Practice.

LIMITATIONS:

Skin biopsy, the “gold-standard” for quantifying intraepidermal nerve fiber density, was not used to assess small nerve fiber lesions. Additionally, a causal link between vitamin D deficiency and diabetic nerve damage was not established owing to the cross-sectional nature of the study. Some patients with T2D may have been receiving insulin therapy, which may have affected vitamin D levels.

DISCLOSURES:

The study was supported by grants from the National Natural Science Foundation of China and China National Key R&D Program. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

Vitamin D deficiency is independently linked to the risk for diabetic peripheral neuropathy (DPN) by potentially affecting large nerve fibers in older patients with type 2 diabetes (T2D).

METHODOLOGY:

• Although previous research has shown that vitamin D deficiency is common in patients with diabetes and may increase the risk for peripheral neuropathy, its effects on large and small nerve fiber lesions have not been well explored yet.
• Researchers conducted a cross-sectional study to understand the association between vitamin D deficiency and DPN development in 230 older patients (mean age, 67 years) with T2D for about 15 years who were recruited from Beijing Hospital between 2020 and 2023.
• All patients were evaluated for DPN based on poor blood sugar control or symptoms such as pain and sensory abnormalities, of which 175 patients diagnosed with DPN were propensity-matched with 55 patients without DPN.
• Vitamin D deficiency, defined as serum 25-hydroxyvitamin D circulating levels below 20 ng/mL, was reported in 169 patients.
• Large nerve fiber lesions were evaluated using electromyography, and small nerve fiber lesions were assessed by measuring skin conductance.

TAKEAWAY:

• Vitamin D deficiency was more likely to affect large fiber lesions, suggested by longer median sensory nerve latency, minimum latency of the F-wave, and median nerve motor evoked potential latency than those in the vitamin D–sufficient group.
• Furthermore, vitamin D deficiency was linked to large fiber neuropathy with increased odds of prolongation of motor nerve latency (odds ratio, 1.362; P = .038).
• The electrochemical skin conductance, which indicates damage to small nerve fibers, was comparable between patients with and without vitamin D deficiency.

IN PRACTICE:

This study is too preliminary to have practice application.

SOURCE:

This study was led by Sijia Fei, Department of Endocrinology, Beijing Hospital, Beijing, People’s Republic of China, and was published online in Diabetes Research and Clinical Practice.

LIMITATIONS:

Skin biopsy, the “gold-standard” for quantifying intraepidermal nerve fiber density, was not used to assess small nerve fiber lesions. Additionally, a causal link between vitamin D deficiency and diabetic nerve damage was not established owing to the cross-sectional nature of the study. Some patients with T2D may have been receiving insulin therapy, which may have affected vitamin D levels.

DISCLOSURES:

The study was supported by grants from the National Natural Science Foundation of China and China National Key R&D Program. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

Vitamin D deficiency is independently linked to the risk for diabetic peripheral neuropathy (DPN) by potentially affecting large nerve fibers in older patients with type 2 diabetes (T2D).

METHODOLOGY:

• Although previous research has shown that vitamin D deficiency is common in patients with diabetes and may increase the risk for peripheral neuropathy, its effects on large and small nerve fiber lesions have not been well explored yet.
• Researchers conducted a cross-sectional study to understand the association between vitamin D deficiency and DPN development in 230 older patients (mean age, 67 years) with T2D for about 15 years who were recruited from Beijing Hospital between 2020 and 2023.
• All patients were evaluated for DPN based on poor blood sugar control or symptoms such as pain and sensory abnormalities, of which 175 patients diagnosed with DPN were propensity-matched with 55 patients without DPN.
• Vitamin D deficiency, defined as serum 25-hydroxyvitamin D circulating levels below 20 ng/mL, was reported in 169 patients.
• Large nerve fiber lesions were evaluated using electromyography, and small nerve fiber lesions were assessed by measuring skin conductance.

TAKEAWAY:

• Vitamin D deficiency was more likely to affect large fiber lesions, suggested by longer median sensory nerve latency, minimum latency of the F-wave, and median nerve motor evoked potential latency than those in the vitamin D–sufficient group.
• Furthermore, vitamin D deficiency was linked to large fiber neuropathy with increased odds of prolongation of motor nerve latency (odds ratio, 1.362; P = .038).
• The electrochemical skin conductance, which indicates damage to small nerve fibers, was comparable between patients with and without vitamin D deficiency.

IN PRACTICE:

This study is too preliminary to have practice application.

SOURCE:

This study was led by Sijia Fei, Department of Endocrinology, Beijing Hospital, Beijing, People’s Republic of China, and was published online in Diabetes Research and Clinical Practice.

LIMITATIONS:

Skin biopsy, the “gold-standard” for quantifying intraepidermal nerve fiber density, was not used to assess small nerve fiber lesions. Additionally, a causal link between vitamin D deficiency and diabetic nerve damage was not established owing to the cross-sectional nature of the study. Some patients with T2D may have been receiving insulin therapy, which may have affected vitamin D levels.

DISCLOSURES:

The study was supported by grants from the National Natural Science Foundation of China and China National Key R&D Program. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

In middle-aged men at high risk for Alzheimer’s disease (AD), higher pancreatic fat is linked to lower cognition and brain volumes.

METHODOLOGY:

• Obesity is a well-known risk factor for poorer cognition and dementia, but the distribution of body fat may influence the risk and underlying mechanisms in the fat-brain-cognition pathway.
• The study examined associations of several abdominal fat depots with cognitive functioning and AD-related brain volumes.
• The study sample included 204 men and women from the Israel Registry for Alzheimer’s Prevention (mean age, 59 years; 60% women) who had a high AD risk due to parental family history.
• Abdominal MRI scans assessed fat stored as subcutaneous adipose tissue (SAT) beneath the skin, visceral adipose tissue (VAT) around abdominal organs, and ectopic, a harmful condition in which lipids accumulate in lean tissues such as the liver and pancreas.
• A structural volumetric brain MRI scan was undertaken by 142 participants to assess specific regions implicated in chosen previous research.

TAKEAWAY:

• High body mass index was associated with high pancreatic fat percentage in both men and women (P < .001) and with high SAT percentage in women (P = .01) but not with VAT percentage in either sex.
• After adjustment for cardiovascular risk factors, a higher pancreatic fat percentage was linked to lower global cognition (beta, −0.33; P = .02) and executive function (beta, −0.32; P = .02) in men, and with lower hippocampal volume in women (beta, −0.25; P = .03).
• In men only, a higher SAT percentage was associated with a lower middle frontal gyrus volume (beta, −0.27; P = .03), while a higher VAT percentage was linked to higher middle frontal gyrus (beta, 0.29; P = .03) and superior frontal gyrus volumes (beta, 0.31; P = .02).
• Hepatic fat was not associated with brain volumes or cognition in either men or women.

IN PRACTICE:

“These results suggest that already in midlife, abdominal fat accumulation may have deleterious effects on brain health, especially in men,” the authors wrote.

SOURCE:

This study was led by Sapir G. Shekhtman, Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel, and published online in Obesity (Silver Spring).

LIMITATIONS:

No causal inferences could be drawn from this study due to its cross-sectional nature. It did not represent the population of middle-aged adults as a whole, but rather those at high risk of developing AD. Factors contributing to fat accumulation, such as menopausal status or treatment, inflammation, insulin resistance, daily exercise, and dietary factors, were not included in this study.

DISCLOSURES:

This work was supported by grants from the National Institutes of Health. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

In middle-aged men at high risk for Alzheimer’s disease (AD), higher pancreatic fat is linked to lower cognition and brain volumes.

METHODOLOGY:

• Obesity is a well-known risk factor for poorer cognition and dementia, but the distribution of body fat may influence the risk and underlying mechanisms in the fat-brain-cognition pathway.
• The study examined associations of several abdominal fat depots with cognitive functioning and AD-related brain volumes.
• The study sample included 204 men and women from the Israel Registry for Alzheimer’s Prevention (mean age, 59 years; 60% women) who had a high AD risk due to parental family history.
• Abdominal MRI scans assessed fat stored as subcutaneous adipose tissue (SAT) beneath the skin, visceral adipose tissue (VAT) around abdominal organs, and ectopic, a harmful condition in which lipids accumulate in lean tissues such as the liver and pancreas.
• A structural volumetric brain MRI scan was undertaken by 142 participants to assess specific regions implicated in chosen previous research.

TAKEAWAY:

• High body mass index was associated with high pancreatic fat percentage in both men and women (P < .001) and with high SAT percentage in women (P = .01) but not with VAT percentage in either sex.
• After adjustment for cardiovascular risk factors, a higher pancreatic fat percentage was linked to lower global cognition (beta, −0.33; P = .02) and executive function (beta, −0.32; P = .02) in men, and with lower hippocampal volume in women (beta, −0.25; P = .03).
• In men only, a higher SAT percentage was associated with a lower middle frontal gyrus volume (beta, −0.27; P = .03), while a higher VAT percentage was linked to higher middle frontal gyrus (beta, 0.29; P = .03) and superior frontal gyrus volumes (beta, 0.31; P = .02).
• Hepatic fat was not associated with brain volumes or cognition in either men or women.

IN PRACTICE:

“These results suggest that already in midlife, abdominal fat accumulation may have deleterious effects on brain health, especially in men,” the authors wrote.

SOURCE:

This study was led by Sapir G. Shekhtman, Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel, and published online in Obesity (Silver Spring).

LIMITATIONS:

No causal inferences could be drawn from this study due to its cross-sectional nature. It did not represent the population of middle-aged adults as a whole, but rather those at high risk of developing AD. Factors contributing to fat accumulation, such as menopausal status or treatment, inflammation, insulin resistance, daily exercise, and dietary factors, were not included in this study.

DISCLOSURES:

This work was supported by grants from the National Institutes of Health. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

In middle-aged men at high risk for Alzheimer’s disease (AD), higher pancreatic fat is linked to lower cognition and brain volumes.

METHODOLOGY:

• Obesity is a well-known risk factor for poorer cognition and dementia, but the distribution of body fat may influence the risk and underlying mechanisms in the fat-brain-cognition pathway.
• The study examined associations of several abdominal fat depots with cognitive functioning and AD-related brain volumes.
• The study sample included 204 men and women from the Israel Registry for Alzheimer’s Prevention (mean age, 59 years; 60% women) who had a high AD risk due to parental family history.
• Abdominal MRI scans assessed fat stored as subcutaneous adipose tissue (SAT) beneath the skin, visceral adipose tissue (VAT) around abdominal organs, and ectopic, a harmful condition in which lipids accumulate in lean tissues such as the liver and pancreas.
• A structural volumetric brain MRI scan was undertaken by 142 participants to assess specific regions implicated in chosen previous research.

TAKEAWAY:

• High body mass index was associated with high pancreatic fat percentage in both men and women (P < .001) and with high SAT percentage in women (P = .01) but not with VAT percentage in either sex.
• After adjustment for cardiovascular risk factors, a higher pancreatic fat percentage was linked to lower global cognition (beta, −0.33; P = .02) and executive function (beta, −0.32; P = .02) in men, and with lower hippocampal volume in women (beta, −0.25; P = .03).
• In men only, a higher SAT percentage was associated with a lower middle frontal gyrus volume (beta, −0.27; P = .03), while a higher VAT percentage was linked to higher middle frontal gyrus (beta, 0.29; P = .03) and superior frontal gyrus volumes (beta, 0.31; P = .02).
• Hepatic fat was not associated with brain volumes or cognition in either men or women.

IN PRACTICE:

“These results suggest that already in midlife, abdominal fat accumulation may have deleterious effects on brain health, especially in men,” the authors wrote.

SOURCE:

This study was led by Sapir G. Shekhtman, Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel, and published online in Obesity (Silver Spring).

LIMITATIONS:

No causal inferences could be drawn from this study due to its cross-sectional nature. It did not represent the population of middle-aged adults as a whole, but rather those at high risk of developing AD. Factors contributing to fat accumulation, such as menopausal status or treatment, inflammation, insulin resistance, daily exercise, and dietary factors, were not included in this study.

DISCLOSURES:

This work was supported by grants from the National Institutes of Health. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

Cervical manipulations have been associated with vascular complications. While the incidence of carotid dissections does not seem to have increased, the question remains open for vertebral artery injuries. We must remain vigilant!

Resorting to joint manipulation for neck pain is not unusual. Currently, cervical manipulation remains a popular first-line treatment for cervicodynia or headaches. Although evidence exists showing that specific joint mobilization can improve this type of symptomatology, there is a possibility that it may risk damaging the cervical arteries and causing ischemic stroke through arterial dissection.

Epidemiologically, internal carotid artery dissection is a relatively rare event with an estimated annual incidence of 1.72 per 100,000 individuals (those most likely to be diagnosed being obviously those leading to hospitalization for stroke) but represents one of the most common causes of stroke in young and middle-aged adults. Faced with case reports that may raise concerns and hypotheses about an associated risk, two studies have sought to delve into the issue.
 

No Increased Carotid Risk Identified

The first study, of a case-cross design, identified all incident cases of ischemic stroke in the territory of the internal carotid artery admitted to the hospital over a 9-year period using administrative healthcare data, the cases being used as their own control by sampling control periods before the date of the index stroke. Thus, 15,523 cases were compared with 62,092 control periods using exposure windows of 1, 3, 7, and 14 days before the stroke. The study also compared post-medical consultation and post-chiropractic consultation outcomes, knowing that as a first-line for complaints of neck pain or headache, patients often turn to one of these two types of primary care clinicians.

However, data analysis shows, among subjects aged under 45 years, positive associations for both different consultations in cases of subsequent carotid stroke (but no association for those aged over 45 years). These associations tended to increase when analyses were limited to visits for diagnoses of neck pain and headaches. Nevertheless, there was no significant difference between risk estimates after chiropractic or general medical consultation.

A notable limitation of this work is that it did not focus on strokes due to vertebral artery dissections that run through the transverse foramina of the cervical vertebrae.
 

A Screening Test Lacking Precision

More recently, the International Federation of Orthopedic Manual Physical Therapists has looked into the subject to refine the assessment of the risk for vascular complications in patients seeking physiotherapy/osteopathy care for neck pain and/or headaches. Through a cross-sectional study involving 150 patients, it tested a vascular complication risk index (from high to low grade, based on history taking and clinical examination), developed to estimate the risk for the presence of vascular rather than musculoskeletal pathology, to determine whether or not there is a contraindication to cervical manipulation.

However, the developed index had only low sensitivity (0.50; 95% CI, 0.39-0.61) and moderate specificity (0.63; 95% CI, 0.51-0.75), knowing that the reference test was a consensus medical decision made by a vascular neurologist, an interventional neurologist, and a neuroradiologist (based on clinical data and cervical MRI). Similarly, positive and negative likelihood ratios were low at 1.36 (95% CI, 0.93-1.99) and 0.79 (95% CI, 0.60-1.05), respectively.

In conclusion, the data from the case-cross study did not seem to demonstrate an excess risk for stroke in the territory of the internal carotid artery after cervical joint manipulations. Associations between cervical manipulation sessions or medical consultations and carotid strokes appear similar and could have been due to the fact that patients with early symptoms related to arterial dissection seek care before developing their stroke.

However, it is regrettable that the study did not focus on vertebral artery dissections, which are anatomically more exposed to cervical chiropractic sessions. Nevertheless, because indices defined from joint tests and medical history are insufficient to identify patients “at risk or in the process of arterial dissection,” and because stroke can result in severe disability, practitioners managing patients with neck pain cannot take this type of complication lightly.

This story was translated from JIM using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Cervical manipulations have been associated with vascular complications. While the incidence of carotid dissections does not seem to have increased, the question remains open for vertebral artery injuries. We must remain vigilant!

Resorting to joint manipulation for neck pain is not unusual. Currently, cervical manipulation remains a popular first-line treatment for cervicodynia or headaches. Although evidence exists showing that specific joint mobilization can improve this type of symptomatology, there is a possibility that it may risk damaging the cervical arteries and causing ischemic stroke through arterial dissection.

Epidemiologically, internal carotid artery dissection is a relatively rare event with an estimated annual incidence of 1.72 per 100,000 individuals (those most likely to be diagnosed being obviously those leading to hospitalization for stroke) but represents one of the most common causes of stroke in young and middle-aged adults. Faced with case reports that may raise concerns and hypotheses about an associated risk, two studies have sought to delve into the issue.
 

No Increased Carotid Risk Identified

The first study, of a case-cross design, identified all incident cases of ischemic stroke in the territory of the internal carotid artery admitted to the hospital over a 9-year period using administrative healthcare data, the cases being used as their own control by sampling control periods before the date of the index stroke. Thus, 15,523 cases were compared with 62,092 control periods using exposure windows of 1, 3, 7, and 14 days before the stroke. The study also compared post-medical consultation and post-chiropractic consultation outcomes, knowing that as a first-line for complaints of neck pain or headache, patients often turn to one of these two types of primary care clinicians.

However, data analysis shows, among subjects aged under 45 years, positive associations for both different consultations in cases of subsequent carotid stroke (but no association for those aged over 45 years). These associations tended to increase when analyses were limited to visits for diagnoses of neck pain and headaches. Nevertheless, there was no significant difference between risk estimates after chiropractic or general medical consultation.

A notable limitation of this work is that it did not focus on strokes due to vertebral artery dissections that run through the transverse foramina of the cervical vertebrae.
 

A Screening Test Lacking Precision

More recently, the International Federation of Orthopedic Manual Physical Therapists has looked into the subject to refine the assessment of the risk for vascular complications in patients seeking physiotherapy/osteopathy care for neck pain and/or headaches. Through a cross-sectional study involving 150 patients, it tested a vascular complication risk index (from high to low grade, based on history taking and clinical examination), developed to estimate the risk for the presence of vascular rather than musculoskeletal pathology, to determine whether or not there is a contraindication to cervical manipulation.

However, the developed index had only low sensitivity (0.50; 95% CI, 0.39-0.61) and moderate specificity (0.63; 95% CI, 0.51-0.75), knowing that the reference test was a consensus medical decision made by a vascular neurologist, an interventional neurologist, and a neuroradiologist (based on clinical data and cervical MRI). Similarly, positive and negative likelihood ratios were low at 1.36 (95% CI, 0.93-1.99) and 0.79 (95% CI, 0.60-1.05), respectively.

In conclusion, the data from the case-cross study did not seem to demonstrate an excess risk for stroke in the territory of the internal carotid artery after cervical joint manipulations. Associations between cervical manipulation sessions or medical consultations and carotid strokes appear similar and could have been due to the fact that patients with early symptoms related to arterial dissection seek care before developing their stroke.

However, it is regrettable that the study did not focus on vertebral artery dissections, which are anatomically more exposed to cervical chiropractic sessions. Nevertheless, because indices defined from joint tests and medical history are insufficient to identify patients “at risk or in the process of arterial dissection,” and because stroke can result in severe disability, practitioners managing patients with neck pain cannot take this type of complication lightly.

This story was translated from JIM using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Cervical manipulations have been associated with vascular complications. While the incidence of carotid dissections does not seem to have increased, the question remains open for vertebral artery injuries. We must remain vigilant!

Resorting to joint manipulation for neck pain is not unusual. Currently, cervical manipulation remains a popular first-line treatment for cervicodynia or headaches. Although evidence exists showing that specific joint mobilization can improve this type of symptomatology, there is a possibility that it may risk damaging the cervical arteries and causing ischemic stroke through arterial dissection.

Epidemiologically, internal carotid artery dissection is a relatively rare event with an estimated annual incidence of 1.72 per 100,000 individuals (those most likely to be diagnosed being obviously those leading to hospitalization for stroke) but represents one of the most common causes of stroke in young and middle-aged adults. Faced with case reports that may raise concerns and hypotheses about an associated risk, two studies have sought to delve into the issue.
 

No Increased Carotid Risk Identified

The first study, of a case-cross design, identified all incident cases of ischemic stroke in the territory of the internal carotid artery admitted to the hospital over a 9-year period using administrative healthcare data, the cases being used as their own control by sampling control periods before the date of the index stroke. Thus, 15,523 cases were compared with 62,092 control periods using exposure windows of 1, 3, 7, and 14 days before the stroke. The study also compared post-medical consultation and post-chiropractic consultation outcomes, knowing that as a first-line for complaints of neck pain or headache, patients often turn to one of these two types of primary care clinicians.

However, data analysis shows, among subjects aged under 45 years, positive associations for both different consultations in cases of subsequent carotid stroke (but no association for those aged over 45 years). These associations tended to increase when analyses were limited to visits for diagnoses of neck pain and headaches. Nevertheless, there was no significant difference between risk estimates after chiropractic or general medical consultation.

A notable limitation of this work is that it did not focus on strokes due to vertebral artery dissections that run through the transverse foramina of the cervical vertebrae.
 

A Screening Test Lacking Precision

More recently, the International Federation of Orthopedic Manual Physical Therapists has looked into the subject to refine the assessment of the risk for vascular complications in patients seeking physiotherapy/osteopathy care for neck pain and/or headaches. Through a cross-sectional study involving 150 patients, it tested a vascular complication risk index (from high to low grade, based on history taking and clinical examination), developed to estimate the risk for the presence of vascular rather than musculoskeletal pathology, to determine whether or not there is a contraindication to cervical manipulation.

However, the developed index had only low sensitivity (0.50; 95% CI, 0.39-0.61) and moderate specificity (0.63; 95% CI, 0.51-0.75), knowing that the reference test was a consensus medical decision made by a vascular neurologist, an interventional neurologist, and a neuroradiologist (based on clinical data and cervical MRI). Similarly, positive and negative likelihood ratios were low at 1.36 (95% CI, 0.93-1.99) and 0.79 (95% CI, 0.60-1.05), respectively.

In conclusion, the data from the case-cross study did not seem to demonstrate an excess risk for stroke in the territory of the internal carotid artery after cervical joint manipulations. Associations between cervical manipulation sessions or medical consultations and carotid strokes appear similar and could have been due to the fact that patients with early symptoms related to arterial dissection seek care before developing their stroke.

However, it is regrettable that the study did not focus on vertebral artery dissections, which are anatomically more exposed to cervical chiropractic sessions. Nevertheless, because indices defined from joint tests and medical history are insufficient to identify patients “at risk or in the process of arterial dissection,” and because stroke can result in severe disability, practitioners managing patients with neck pain cannot take this type of complication lightly.

This story was translated from JIM using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

New research shows increased screen time in children aged 12-36 months is associated with reduced verbal interactions between toddlers and their parents, which in turn could affect language development. 

METHODOLOGY:

• The study included data from 220 families in Australia.
• Researchers used advanced speech recognition technology to capture children’s screen time and language environment at home during a 16-hour window every 6 months.
• They adjusted for variables such as the sex of the child, the education level of the mother, and psychological distress in the primary caregiver.

TAKEAWAY: 

• Increases in screen time were associated with decreases in words spoken near children by adults, vocalizations by children, and back-and-forth interactions between adults and children. This correlation was especially notable at age 36 months.
• At age 36 months, each additional minute of screen time was linked to children hearing 6.6 fewer adult words, making 4.9 fewer vocalizations, and participating in 1.1 fewer conversational interactions.
• Based on the average daily screen time at that age seen in the study — 172 minutes (2.87 hours) — “children could be missing out on 1139 adult words, 843 vocalizations, and 194 conversational turns per day,” the researchers estimated.

IN PRACTICE:

“Identifying different ways that screen time could facilitate parent-child interactions, such as through interactive co-viewing, may be important strategies to support families given the current ubiquitous nature of screen time in families’ lives,” the authors of the study wrote.

What children watch and listen to may be an important consideration, according to a developmental scientist who was not involved with the study.

“It could be that less communicative contact with the caregiver is not as detrimental if the screen time is of high quality and developmentally appropriate, educational content,” Marina Bazhydai, PhD, with Lancaster University in Lancaster, United Kingdom, said in her comments on the research. 

SOURCE:

Mary E. Brushe, PhD, with Telethon Kids Institute and the University of Western Australia in Adelaide, was the corresponding author of the study. The research was published online in JAMA Pediatrics.

LIMITATIONS:

The study’s reliance on speech recognition technology did not capture all nuances of screen exposure.

DISCLOSURES:

This study was supported by grants from the Australian National Health and Medical Research Council.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

New research shows increased screen time in children aged 12-36 months is associated with reduced verbal interactions between toddlers and their parents, which in turn could affect language development. 

METHODOLOGY:

• The study included data from 220 families in Australia.
• Researchers used advanced speech recognition technology to capture children’s screen time and language environment at home during a 16-hour window every 6 months.
• They adjusted for variables such as the sex of the child, the education level of the mother, and psychological distress in the primary caregiver.

TAKEAWAY: 

• Increases in screen time were associated with decreases in words spoken near children by adults, vocalizations by children, and back-and-forth interactions between adults and children. This correlation was especially notable at age 36 months.
• At age 36 months, each additional minute of screen time was linked to children hearing 6.6 fewer adult words, making 4.9 fewer vocalizations, and participating in 1.1 fewer conversational interactions.
• Based on the average daily screen time at that age seen in the study — 172 minutes (2.87 hours) — “children could be missing out on 1139 adult words, 843 vocalizations, and 194 conversational turns per day,” the researchers estimated.

IN PRACTICE:

“Identifying different ways that screen time could facilitate parent-child interactions, such as through interactive co-viewing, may be important strategies to support families given the current ubiquitous nature of screen time in families’ lives,” the authors of the study wrote.

What children watch and listen to may be an important consideration, according to a developmental scientist who was not involved with the study.

“It could be that less communicative contact with the caregiver is not as detrimental if the screen time is of high quality and developmentally appropriate, educational content,” Marina Bazhydai, PhD, with Lancaster University in Lancaster, United Kingdom, said in her comments on the research. 

SOURCE:

Mary E. Brushe, PhD, with Telethon Kids Institute and the University of Western Australia in Adelaide, was the corresponding author of the study. The research was published online in JAMA Pediatrics.

LIMITATIONS:

The study’s reliance on speech recognition technology did not capture all nuances of screen exposure.

DISCLOSURES:

This study was supported by grants from the Australian National Health and Medical Research Council.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

New research shows increased screen time in children aged 12-36 months is associated with reduced verbal interactions between toddlers and their parents, which in turn could affect language development. 

METHODOLOGY:

• The study included data from 220 families in Australia.
• Researchers used advanced speech recognition technology to capture children’s screen time and language environment at home during a 16-hour window every 6 months.
• They adjusted for variables such as the sex of the child, the education level of the mother, and psychological distress in the primary caregiver.

TAKEAWAY: 

• Increases in screen time were associated with decreases in words spoken near children by adults, vocalizations by children, and back-and-forth interactions between adults and children. This correlation was especially notable at age 36 months.
• At age 36 months, each additional minute of screen time was linked to children hearing 6.6 fewer adult words, making 4.9 fewer vocalizations, and participating in 1.1 fewer conversational interactions.
• Based on the average daily screen time at that age seen in the study — 172 minutes (2.87 hours) — “children could be missing out on 1139 adult words, 843 vocalizations, and 194 conversational turns per day,” the researchers estimated.

IN PRACTICE:

“Identifying different ways that screen time could facilitate parent-child interactions, such as through interactive co-viewing, may be important strategies to support families given the current ubiquitous nature of screen time in families’ lives,” the authors of the study wrote.

What children watch and listen to may be an important consideration, according to a developmental scientist who was not involved with the study.

“It could be that less communicative contact with the caregiver is not as detrimental if the screen time is of high quality and developmentally appropriate, educational content,” Marina Bazhydai, PhD, with Lancaster University in Lancaster, United Kingdom, said in her comments on the research. 

SOURCE:

Mary E. Brushe, PhD, with Telethon Kids Institute and the University of Western Australia in Adelaide, was the corresponding author of the study. The research was published online in JAMA Pediatrics.

LIMITATIONS:

The study’s reliance on speech recognition technology did not capture all nuances of screen exposure.

DISCLOSURES:

This study was supported by grants from the Australian National Health and Medical Research Council.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Skipping meals, mood and anxiety disorders, as well as vaping and substance use, all raise the risk for frequent recurrent headaches in children and adolescents, new data from a population-based study showed.

Children and teens with anxiety or mood disorders had twice the risk for frequent headaches, defined as occurring once or more per week, and those who regularly ate breakfast and dinners with their family had an 8% lower risk for frequent headaches than those who did not eat regular meals.

“It is not uncommon for children and teens to have headaches, and while medications are used to stop and sometimes prevent headaches, lifestyle changes also may offer an effective route to relief by preventing headaches from happening and improving quality of life,” study investigator Serena L. Orr, MD, MSc, University of Calgary in Alberta, Canada, said in a press release.

The findings were published online in Neurology.
 

Negative Consequences

Previous research shows frequent recurrent headaches occur in up to 30% of children and adolescents and can lead to lower academic achievement and lower quality of life.

Treatment recommendations often focus on adjusting lifestyle behaviors, such as sleep and meal timing or smoking.

To further investigate these links, researchers used data from the 2019 Canadian Health Survey on Children and Youth and included about 5 million children and teens aged 5-17 years. In most cases, a parent or guardian answered the survey questions.

In addition to assessing participants for headache frequency in the past week, the survey included questions about how often they had breakfast, were physically active, or spent playing video games or with a mobile device, for instance. Parents/guardians were also asked whether the youth had ever been diagnosed with a mood or anxiety disorder.

For participants aged between 12 and 17 years, there were also questions about smoking, alcohol consumption, and substance use.

The mean age of participants was 11 years, and 48% were female. About 6% of the participants had frequent recurrent headaches.

Investigators found that meal regularity was inversely associated with frequent headaches (P < .001). In an adjusted model, youth who often ate breakfast and dinner with their families had an 8% lower risk for frequent headaches than those who didn’t dine with their families regularly.

“It is possible regular family meals may lead to greater connectedness and communication within the family and better mental health outcomes, which in turn may impact headache frequency,” Dr. Orr noted.

Youth who spent more than 21 hours per week in front of computer screens or with video games had higher odds for frequent headaches (P < .001), but this association did not survive statistical adjustment for demographics or lifestyle factors.

Both mood and anxiety disorders were associated with twice the risk for frequent headaches, and this risk survived adjustment for age, sex, household income, and other lifestyle factors.

In adolescents aged 12-17 years, there was an association between drinking alcohol and frequent headache, with higher alcohol consumption increasing the likelihood of frequent headache. For instance, those who drank once or more per week had three times the risk for frequent headache (P < .001), and those who indulged in binge drinking at least five times per month had five times the risk for frequent headache (P < .001).

Smoking cannabis was also associated with frequent headache in a dose-dependent manner. Daily users had a threefold increased risk for frequent headache vs those who didn’t use cannabis (P < .001).

Similarly, those who smoked or used e-cigarettes daily also had a threefold increased risk for frequent headaches versus nonusers.

One of the study’s limitations was that it didn’t include participants living in foster homes, institutions or on First Nation reserves. Investigators also were not able to determine headache type and did not assess hydration, which can be an important lifestyle factor in headache etiology.
 

Prioritize Questions About Lifestyle?

In an accompanying editorial, Irene Patniyot, MD, of Baylor College of Medicine in Houston, Texas, noted that lifestyle advice is an important part of managing headache disorders in children and youth and questioned whether neurologists should prioritize discussions about lifestyle habits in this patient population. However, she noted, given the heavy demands on neurologists’ time, this may be “idealistic.”

One potential solution may lie in automating electronic questionnaires for inclusion in patients’ medical records. “Data extraction from electronic questionnaires has already led to new data on symptoms associated with headache in youth and can potentially lead to earlier identification and treatment of mental health disorders and lifestyle habits that negatively affect headache burden and overall well-being,” Dr. Patniyot wrote.

The study was funded by the Social Sciences and Humanities Research Council of Canada, the Canadian Institutes of Health Research, the Canada Foundation for Innovation, and Statistics Canada. Dr. Orr reported receiving royalties from Cambridge University Press; serving on the editorial boards of Headache, Neurology, and the American Migraine Foundation; and receiving research funding from the Canadian Institutes of Health Research and the Alberta Children’s Hospital Research Institute. Other disclosures were noted in the original article.

A version of this article appeared on Medscape.com.

Skipping meals, mood and anxiety disorders, as well as vaping and substance use, all raise the risk for frequent recurrent headaches in children and adolescents, new data from a population-based study showed.

Children and teens with anxiety or mood disorders had twice the risk for frequent headaches, defined as occurring once or more per week, and those who regularly ate breakfast and dinners with their family had an 8% lower risk for frequent headaches than those who did not eat regular meals.

“It is not uncommon for children and teens to have headaches, and while medications are used to stop and sometimes prevent headaches, lifestyle changes also may offer an effective route to relief by preventing headaches from happening and improving quality of life,” study investigator Serena L. Orr, MD, MSc, University of Calgary in Alberta, Canada, said in a press release.

The findings were published online in Neurology.
 

Negative Consequences

Previous research shows frequent recurrent headaches occur in up to 30% of children and adolescents and can lead to lower academic achievement and lower quality of life.

Treatment recommendations often focus on adjusting lifestyle behaviors, such as sleep and meal timing or smoking.

To further investigate these links, researchers used data from the 2019 Canadian Health Survey on Children and Youth and included about 5 million children and teens aged 5-17 years. In most cases, a parent or guardian answered the survey questions.

In addition to assessing participants for headache frequency in the past week, the survey included questions about how often they had breakfast, were physically active, or spent playing video games or with a mobile device, for instance. Parents/guardians were also asked whether the youth had ever been diagnosed with a mood or anxiety disorder.

For participants aged between 12 and 17 years, there were also questions about smoking, alcohol consumption, and substance use.

The mean age of participants was 11 years, and 48% were female. About 6% of the participants had frequent recurrent headaches.

Investigators found that meal regularity was inversely associated with frequent headaches (P < .001). In an adjusted model, youth who often ate breakfast and dinner with their families had an 8% lower risk for frequent headaches than those who didn’t dine with their families regularly.

“It is possible regular family meals may lead to greater connectedness and communication within the family and better mental health outcomes, which in turn may impact headache frequency,” Dr. Orr noted.

Youth who spent more than 21 hours per week in front of computer screens or with video games had higher odds for frequent headaches (P < .001), but this association did not survive statistical adjustment for demographics or lifestyle factors.

Both mood and anxiety disorders were associated with twice the risk for frequent headaches, and this risk survived adjustment for age, sex, household income, and other lifestyle factors.

In adolescents aged 12-17 years, there was an association between drinking alcohol and frequent headache, with higher alcohol consumption increasing the likelihood of frequent headache. For instance, those who drank once or more per week had three times the risk for frequent headache (P < .001), and those who indulged in binge drinking at least five times per month had five times the risk for frequent headache (P < .001).

Smoking cannabis was also associated with frequent headache in a dose-dependent manner. Daily users had a threefold increased risk for frequent headache vs those who didn’t use cannabis (P < .001).

Similarly, those who smoked or used e-cigarettes daily also had a threefold increased risk for frequent headaches versus nonusers.

One of the study’s limitations was that it didn’t include participants living in foster homes, institutions or on First Nation reserves. Investigators also were not able to determine headache type and did not assess hydration, which can be an important lifestyle factor in headache etiology.
 

Prioritize Questions About Lifestyle?

In an accompanying editorial, Irene Patniyot, MD, of Baylor College of Medicine in Houston, Texas, noted that lifestyle advice is an important part of managing headache disorders in children and youth and questioned whether neurologists should prioritize discussions about lifestyle habits in this patient population. However, she noted, given the heavy demands on neurologists’ time, this may be “idealistic.”

One potential solution may lie in automating electronic questionnaires for inclusion in patients’ medical records. “Data extraction from electronic questionnaires has already led to new data on symptoms associated with headache in youth and can potentially lead to earlier identification and treatment of mental health disorders and lifestyle habits that negatively affect headache burden and overall well-being,” Dr. Patniyot wrote.

The study was funded by the Social Sciences and Humanities Research Council of Canada, the Canadian Institutes of Health Research, the Canada Foundation for Innovation, and Statistics Canada. Dr. Orr reported receiving royalties from Cambridge University Press; serving on the editorial boards of Headache, Neurology, and the American Migraine Foundation; and receiving research funding from the Canadian Institutes of Health Research and the Alberta Children’s Hospital Research Institute. Other disclosures were noted in the original article.

A version of this article appeared on Medscape.com.

Skipping meals, mood and anxiety disorders, as well as vaping and substance use, all raise the risk for frequent recurrent headaches in children and adolescents, new data from a population-based study showed.

Children and teens with anxiety or mood disorders had twice the risk for frequent headaches, defined as occurring once or more per week, and those who regularly ate breakfast and dinners with their family had an 8% lower risk for frequent headaches than those who did not eat regular meals.

“It is not uncommon for children and teens to have headaches, and while medications are used to stop and sometimes prevent headaches, lifestyle changes also may offer an effective route to relief by preventing headaches from happening and improving quality of life,” study investigator Serena L. Orr, MD, MSc, University of Calgary in Alberta, Canada, said in a press release.

The findings were published online in Neurology.
 

Negative Consequences

Previous research shows frequent recurrent headaches occur in up to 30% of children and adolescents and can lead to lower academic achievement and lower quality of life.

Treatment recommendations often focus on adjusting lifestyle behaviors, such as sleep and meal timing or smoking.

To further investigate these links, researchers used data from the 2019 Canadian Health Survey on Children and Youth and included about 5 million children and teens aged 5-17 years. In most cases, a parent or guardian answered the survey questions.

In addition to assessing participants for headache frequency in the past week, the survey included questions about how often they had breakfast, were physically active, or spent playing video games or with a mobile device, for instance. Parents/guardians were also asked whether the youth had ever been diagnosed with a mood or anxiety disorder.

For participants aged between 12 and 17 years, there were also questions about smoking, alcohol consumption, and substance use.

The mean age of participants was 11 years, and 48% were female. About 6% of the participants had frequent recurrent headaches.

Investigators found that meal regularity was inversely associated with frequent headaches (P < .001). In an adjusted model, youth who often ate breakfast and dinner with their families had an 8% lower risk for frequent headaches than those who didn’t dine with their families regularly.

“It is possible regular family meals may lead to greater connectedness and communication within the family and better mental health outcomes, which in turn may impact headache frequency,” Dr. Orr noted.

Youth who spent more than 21 hours per week in front of computer screens or with video games had higher odds for frequent headaches (P < .001), but this association did not survive statistical adjustment for demographics or lifestyle factors.

Both mood and anxiety disorders were associated with twice the risk for frequent headaches, and this risk survived adjustment for age, sex, household income, and other lifestyle factors.

In adolescents aged 12-17 years, there was an association between drinking alcohol and frequent headache, with higher alcohol consumption increasing the likelihood of frequent headache. For instance, those who drank once or more per week had three times the risk for frequent headache (P < .001), and those who indulged in binge drinking at least five times per month had five times the risk for frequent headache (P < .001).

Smoking cannabis was also associated with frequent headache in a dose-dependent manner. Daily users had a threefold increased risk for frequent headache vs those who didn’t use cannabis (P < .001).

Similarly, those who smoked or used e-cigarettes daily also had a threefold increased risk for frequent headaches versus nonusers.

One of the study’s limitations was that it didn’t include participants living in foster homes, institutions or on First Nation reserves. Investigators also were not able to determine headache type and did not assess hydration, which can be an important lifestyle factor in headache etiology.
 

Prioritize Questions About Lifestyle?

In an accompanying editorial, Irene Patniyot, MD, of Baylor College of Medicine in Houston, Texas, noted that lifestyle advice is an important part of managing headache disorders in children and youth and questioned whether neurologists should prioritize discussions about lifestyle habits in this patient population. However, she noted, given the heavy demands on neurologists’ time, this may be “idealistic.”

One potential solution may lie in automating electronic questionnaires for inclusion in patients’ medical records. “Data extraction from electronic questionnaires has already led to new data on symptoms associated with headache in youth and can potentially lead to earlier identification and treatment of mental health disorders and lifestyle habits that negatively affect headache burden and overall well-being,” Dr. Patniyot wrote.

The study was funded by the Social Sciences and Humanities Research Council of Canada, the Canadian Institutes of Health Research, the Canada Foundation for Innovation, and Statistics Canada. Dr. Orr reported receiving royalties from Cambridge University Press; serving on the editorial boards of Headache, Neurology, and the American Migraine Foundation; and receiving research funding from the Canadian Institutes of Health Research and the Alberta Children’s Hospital Research Institute. Other disclosures were noted in the original article.

A version of this article appeared on Medscape.com.

Epilepsy was linked to a significantly increased the risk for hospitalization and death from COVID-19 early in the pandemic, while healthcare utilization rates in this patient population declined, data from two linked studies showed. 

Results showed that individuals with epilepsy had a 60% higher risk for hospitalization and a 33% higher risk of dying from COVID-19 than those without the disorder. However, during the pandemic, the number of hospitalizations and ER visits by people with epilepsy dropped by as much as 30%. 

“The neurotropic effects of Sars-CoV-2 might explain some of this increased risk for people with epilepsy, or epilepsy might be associated with alterations in the immune system, predisposing to more severe COVID-19,” wrote the investigators, led by Owen Pickrell, MBBChirm, PhD, Swansea University, United Kingdom.

The findings were published online March 5 in Epilepsia. 
 

Skill Shifting 

Epilepsy is one of the most common neurological conditions and affects approximately 50 million people worldwide, with significant comorbidity and an increased risk for early death.

During the pandemic, clinicians treating people with epilepsy and other conditions shifted their skills to treat an ever-increasing number of patients with COVID-19, which may have hindered epilepsy-specific services for a time.

To further explore how the COVID-19 pandemic may have affected the health of this patient population, researchers analyzed health records from a large database with information about hospital admissions, primary care visits, COVID-19 vaccination status, and demographics of 90% of Welsh residents.

Those living with epilepsy before or during the study period (March 1, 2020, to June 31, 2021) were identified and compared with controls without epilepsy. 

The analysis included approximately 27,280 people with epilepsy and 136,400 matched controls. Among those with epilepsy, there were 158 deaths (0.58%) and 933 hospitalizations (3.4%). In comparison, there were 370 deaths (0.27%) and 1871 hospitalizations (1.4%) in the control group.

Unadjusted analyses showed the risk of dying from COVID-19 for those with epilepsy vs controls was more than twofold higher (hazard ratio [HR], 2.15; 95% CI; 1.78-2.59) and the increase in the risk for hospitalization was similar (HR, 2.15; 95% CI; 1.94-2.37). 

After adjusting for 40 comorbidities, including serious mental illness, asthma, and diabetes, those with epilepsy had a 60% increased risk for hospitalization (adjusted HR [aHR], 1.60) and a 33% increased risk for death (aHR, 1.33) than those without epilepsy (all P < .0001). 

The findings “may have implications for prioritizing future COVID-19 treatments and vaccinations for people with epilepsy,” the investigators wrote.

Study limitations included the inability to account for the effect of vaccinations or prior infections with SARS-CoV-2. Moreover, the study did not account for geographical or temporal variations in prevalence and COVID-19 variants. 
 

Consultations Canceled 

In the related study, researchers analyzed healthcare utilization by people with epilepsy before and after the pandemic using the same database. Results showed hospital admissions, ER visits, and outpatient visits significantly decreased during the pandemic. 

In the year before the pandemic, people with epilepsy had double the rate of ER visits (rate ratio [RR], 2.36), hospital admissions (RR, 2.08), and outpatient appointments (RR, 1.92) compared with matched controls. 

However, during the pandemic there was a greater reduction in hospital admissions (RR, 0.70; 95% CI, 0.69-0.72) and ER visits (RR, 0.78; 95% CI, 0.77-0.70) in those with epilepsy versus matched controls (RR, 0.82; 95% CI, 0.81-0.83) as well as hospital visits and ER visits (RR, 0.87; 95% CI, 0.86-0.88; all P < .0001). New epilepsy diagnoses also decreased during the pandemic (RR, 0.73; P < .0001)

The redeployment of epileptologists during the pandemic also meant that epilepsy consultations and investigations were canceled, making it harder for people with epilepsy to access specialty care, the researchers noted. 

“Our research also showed that there were fewer new diagnoses of epilepsy and fewer contacts with health services by people with epilepsy, during the period we examined,” Huw Strafford, lead data analyst for the studies, said in a release.

Both studies were funded by Health and Care Research Wales. Dr. Pickrell reported receiving speaker fees from UCB Pharma and Angelini Pharma, travel grants from Angelini Pharma, and an unrestricted grant from UCB Pharma.

A version of this article appeared on Medscape.com .

Epilepsy was linked to a significantly increased the risk for hospitalization and death from COVID-19 early in the pandemic, while healthcare utilization rates in this patient population declined, data from two linked studies showed. 

Results showed that individuals with epilepsy had a 60% higher risk for hospitalization and a 33% higher risk of dying from COVID-19 than those without the disorder. However, during the pandemic, the number of hospitalizations and ER visits by people with epilepsy dropped by as much as 30%. 

“The neurotropic effects of Sars-CoV-2 might explain some of this increased risk for people with epilepsy, or epilepsy might be associated with alterations in the immune system, predisposing to more severe COVID-19,” wrote the investigators, led by Owen Pickrell, MBBChirm, PhD, Swansea University, United Kingdom.

The findings were published online March 5 in Epilepsia. 
 

Skill Shifting 

Epilepsy is one of the most common neurological conditions and affects approximately 50 million people worldwide, with significant comorbidity and an increased risk for early death.

During the pandemic, clinicians treating people with epilepsy and other conditions shifted their skills to treat an ever-increasing number of patients with COVID-19, which may have hindered epilepsy-specific services for a time.

To further explore how the COVID-19 pandemic may have affected the health of this patient population, researchers analyzed health records from a large database with information about hospital admissions, primary care visits, COVID-19 vaccination status, and demographics of 90% of Welsh residents.

Those living with epilepsy before or during the study period (March 1, 2020, to June 31, 2021) were identified and compared with controls without epilepsy. 

The analysis included approximately 27,280 people with epilepsy and 136,400 matched controls. Among those with epilepsy, there were 158 deaths (0.58%) and 933 hospitalizations (3.4%). In comparison, there were 370 deaths (0.27%) and 1871 hospitalizations (1.4%) in the control group.

Unadjusted analyses showed the risk of dying from COVID-19 for those with epilepsy vs controls was more than twofold higher (hazard ratio [HR], 2.15; 95% CI; 1.78-2.59) and the increase in the risk for hospitalization was similar (HR, 2.15; 95% CI; 1.94-2.37). 

After adjusting for 40 comorbidities, including serious mental illness, asthma, and diabetes, those with epilepsy had a 60% increased risk for hospitalization (adjusted HR [aHR], 1.60) and a 33% increased risk for death (aHR, 1.33) than those without epilepsy (all P < .0001). 

The findings “may have implications for prioritizing future COVID-19 treatments and vaccinations for people with epilepsy,” the investigators wrote.

Study limitations included the inability to account for the effect of vaccinations or prior infections with SARS-CoV-2. Moreover, the study did not account for geographical or temporal variations in prevalence and COVID-19 variants. 
 

Consultations Canceled 

In the related study, researchers analyzed healthcare utilization by people with epilepsy before and after the pandemic using the same database. Results showed hospital admissions, ER visits, and outpatient visits significantly decreased during the pandemic. 

In the year before the pandemic, people with epilepsy had double the rate of ER visits (rate ratio [RR], 2.36), hospital admissions (RR, 2.08), and outpatient appointments (RR, 1.92) compared with matched controls. 

However, during the pandemic there was a greater reduction in hospital admissions (RR, 0.70; 95% CI, 0.69-0.72) and ER visits (RR, 0.78; 95% CI, 0.77-0.70) in those with epilepsy versus matched controls (RR, 0.82; 95% CI, 0.81-0.83) as well as hospital visits and ER visits (RR, 0.87; 95% CI, 0.86-0.88; all P < .0001). New epilepsy diagnoses also decreased during the pandemic (RR, 0.73; P < .0001)

The redeployment of epileptologists during the pandemic also meant that epilepsy consultations and investigations were canceled, making it harder for people with epilepsy to access specialty care, the researchers noted. 

“Our research also showed that there were fewer new diagnoses of epilepsy and fewer contacts with health services by people with epilepsy, during the period we examined,” Huw Strafford, lead data analyst for the studies, said in a release.

Both studies were funded by Health and Care Research Wales. Dr. Pickrell reported receiving speaker fees from UCB Pharma and Angelini Pharma, travel grants from Angelini Pharma, and an unrestricted grant from UCB Pharma.

A version of this article appeared on Medscape.com .

Epilepsy was linked to a significantly increased the risk for hospitalization and death from COVID-19 early in the pandemic, while healthcare utilization rates in this patient population declined, data from two linked studies showed. 

Results showed that individuals with epilepsy had a 60% higher risk for hospitalization and a 33% higher risk of dying from COVID-19 than those without the disorder. However, during the pandemic, the number of hospitalizations and ER visits by people with epilepsy dropped by as much as 30%. 

“The neurotropic effects of Sars-CoV-2 might explain some of this increased risk for people with epilepsy, or epilepsy might be associated with alterations in the immune system, predisposing to more severe COVID-19,” wrote the investigators, led by Owen Pickrell, MBBChirm, PhD, Swansea University, United Kingdom.

The findings were published online March 5 in Epilepsia. 
 

Skill Shifting 

Epilepsy is one of the most common neurological conditions and affects approximately 50 million people worldwide, with significant comorbidity and an increased risk for early death.

During the pandemic, clinicians treating people with epilepsy and other conditions shifted their skills to treat an ever-increasing number of patients with COVID-19, which may have hindered epilepsy-specific services for a time.

To further explore how the COVID-19 pandemic may have affected the health of this patient population, researchers analyzed health records from a large database with information about hospital admissions, primary care visits, COVID-19 vaccination status, and demographics of 90% of Welsh residents.

Those living with epilepsy before or during the study period (March 1, 2020, to June 31, 2021) were identified and compared with controls without epilepsy. 

The analysis included approximately 27,280 people with epilepsy and 136,400 matched controls. Among those with epilepsy, there were 158 deaths (0.58%) and 933 hospitalizations (3.4%). In comparison, there were 370 deaths (0.27%) and 1871 hospitalizations (1.4%) in the control group.

Unadjusted analyses showed the risk of dying from COVID-19 for those with epilepsy vs controls was more than twofold higher (hazard ratio [HR], 2.15; 95% CI; 1.78-2.59) and the increase in the risk for hospitalization was similar (HR, 2.15; 95% CI; 1.94-2.37). 

After adjusting for 40 comorbidities, including serious mental illness, asthma, and diabetes, those with epilepsy had a 60% increased risk for hospitalization (adjusted HR [aHR], 1.60) and a 33% increased risk for death (aHR, 1.33) than those without epilepsy (all P < .0001). 

The findings “may have implications for prioritizing future COVID-19 treatments and vaccinations for people with epilepsy,” the investigators wrote.

Study limitations included the inability to account for the effect of vaccinations or prior infections with SARS-CoV-2. Moreover, the study did not account for geographical or temporal variations in prevalence and COVID-19 variants. 
 

Consultations Canceled 

In the related study, researchers analyzed healthcare utilization by people with epilepsy before and after the pandemic using the same database. Results showed hospital admissions, ER visits, and outpatient visits significantly decreased during the pandemic. 

In the year before the pandemic, people with epilepsy had double the rate of ER visits (rate ratio [RR], 2.36), hospital admissions (RR, 2.08), and outpatient appointments (RR, 1.92) compared with matched controls. 

However, during the pandemic there was a greater reduction in hospital admissions (RR, 0.70; 95% CI, 0.69-0.72) and ER visits (RR, 0.78; 95% CI, 0.77-0.70) in those with epilepsy versus matched controls (RR, 0.82; 95% CI, 0.81-0.83) as well as hospital visits and ER visits (RR, 0.87; 95% CI, 0.86-0.88; all P < .0001). New epilepsy diagnoses also decreased during the pandemic (RR, 0.73; P < .0001)

The redeployment of epileptologists during the pandemic also meant that epilepsy consultations and investigations were canceled, making it harder for people with epilepsy to access specialty care, the researchers noted. 

“Our research also showed that there were fewer new diagnoses of epilepsy and fewer contacts with health services by people with epilepsy, during the period we examined,” Huw Strafford, lead data analyst for the studies, said in a release.

Both studies were funded by Health and Care Research Wales. Dr. Pickrell reported receiving speaker fees from UCB Pharma and Angelini Pharma, travel grants from Angelini Pharma, and an unrestricted grant from UCB Pharma.

A version of this article appeared on Medscape.com .