Neurology Reviews

Obstructive sleep apnea (OSA) was associated with both impaired functional performance during exercise and overall worse outcomes in patients with chronic obstructive pulmonary disease (COPD), based on data from 34 adults.

Individuals with COPD are at increased risk for hospital readmissions and disease exacerbations, Patricia Faria Camargo, PhD, of Federal University of São Carlos (Brazil), and colleagues wrote. These patients often have concomitant obstructive sleep apnea, which itself can promote adverse cardiovascular events, but the impact of the overlap of these two conditions on clinical outcomes has not been explored.

In a study published in Heart & Lung, the researchers recruited 17 adults with COPD only and 17 with OSA and COPD. At baseline, patients underwent pulmonary function tests, echocardiography, and polysomnography to confirm their OSA and COPD diagnoses.

The primary endpoint was the impact of OSA on functional performance and cardiac autonomic control in COPD patients, based on measures of heart rate variability and the 6-minute walk test (6MWT). Participants were followed for 1 year, with telephone contacts every 3 months. A secondary endpoint was the number of exacerbations, hospitalizations, and deaths. At baseline, OSA-COPD patients had worse polysomnographic function, compared with COPD patients; they also tended to be older and have higher body mass index, but other demographics were similar between the groups.

Overall, patients in the OSA-COPD group had significantly greater functional impairment, compared with the COPD group (P = .003), as measured by the 6MWT. The OSA-COPD patients also showed significantly worse autonomic response during exercise, compared with the COPD group.

A lower work load during exercise and the interaction between group and time factors suggests that OSA impacts the exercise capacity of COPD patients, the researchers said. Notably, however, neither age nor body mass index was associated with functional performance in the OSA-COPD group.

Patients in the OSA-COPD group also were significantly more likely to experience exacerbations during the study period, compared with the COPD-only group (67.4% vs. 23.5; P = .03). However, the severity of COPD was similar between the groups, which further illustrates that OSA can impair functional performance in COPD patients, the researchers said.

The findings were limited by several factors including the small sample size and restricted collection of follow-up data during the pandemic, the researchers noted. However, the results support previous studies, and suggest that overlapping OSA and COPD produces worse outcomes.

“Future studies can confirm our findings, providing new clinical evidences to the assessment of sleep quality in COPD patients and its implications for the general health status of these individuals, in addition to contributing to more assertive clinical and therapeutic alternative support the need for more research into the mechanisms behind this overlap in larger samples to develop treatment alternatives,” they concluded.

The study was supported by the Federal University of Sao Carlos. The researchers had no financial conflicts to disclose.
 

Obstructive sleep apnea (OSA) was associated with both impaired functional performance during exercise and overall worse outcomes in patients with chronic obstructive pulmonary disease (COPD), based on data from 34 adults.

Individuals with COPD are at increased risk for hospital readmissions and disease exacerbations, Patricia Faria Camargo, PhD, of Federal University of São Carlos (Brazil), and colleagues wrote. These patients often have concomitant obstructive sleep apnea, which itself can promote adverse cardiovascular events, but the impact of the overlap of these two conditions on clinical outcomes has not been explored.

In a study published in Heart & Lung, the researchers recruited 17 adults with COPD only and 17 with OSA and COPD. At baseline, patients underwent pulmonary function tests, echocardiography, and polysomnography to confirm their OSA and COPD diagnoses.

The primary endpoint was the impact of OSA on functional performance and cardiac autonomic control in COPD patients, based on measures of heart rate variability and the 6-minute walk test (6MWT). Participants were followed for 1 year, with telephone contacts every 3 months. A secondary endpoint was the number of exacerbations, hospitalizations, and deaths. At baseline, OSA-COPD patients had worse polysomnographic function, compared with COPD patients; they also tended to be older and have higher body mass index, but other demographics were similar between the groups.

Overall, patients in the OSA-COPD group had significantly greater functional impairment, compared with the COPD group (P = .003), as measured by the 6MWT. The OSA-COPD patients also showed significantly worse autonomic response during exercise, compared with the COPD group.

A lower work load during exercise and the interaction between group and time factors suggests that OSA impacts the exercise capacity of COPD patients, the researchers said. Notably, however, neither age nor body mass index was associated with functional performance in the OSA-COPD group.

Patients in the OSA-COPD group also were significantly more likely to experience exacerbations during the study period, compared with the COPD-only group (67.4% vs. 23.5; P = .03). However, the severity of COPD was similar between the groups, which further illustrates that OSA can impair functional performance in COPD patients, the researchers said.

The findings were limited by several factors including the small sample size and restricted collection of follow-up data during the pandemic, the researchers noted. However, the results support previous studies, and suggest that overlapping OSA and COPD produces worse outcomes.

“Future studies can confirm our findings, providing new clinical evidences to the assessment of sleep quality in COPD patients and its implications for the general health status of these individuals, in addition to contributing to more assertive clinical and therapeutic alternative support the need for more research into the mechanisms behind this overlap in larger samples to develop treatment alternatives,” they concluded.

The study was supported by the Federal University of Sao Carlos. The researchers had no financial conflicts to disclose.
 

Obstructive sleep apnea (OSA) was associated with both impaired functional performance during exercise and overall worse outcomes in patients with chronic obstructive pulmonary disease (COPD), based on data from 34 adults.

Individuals with COPD are at increased risk for hospital readmissions and disease exacerbations, Patricia Faria Camargo, PhD, of Federal University of São Carlos (Brazil), and colleagues wrote. These patients often have concomitant obstructive sleep apnea, which itself can promote adverse cardiovascular events, but the impact of the overlap of these two conditions on clinical outcomes has not been explored.

In a study published in Heart & Lung, the researchers recruited 17 adults with COPD only and 17 with OSA and COPD. At baseline, patients underwent pulmonary function tests, echocardiography, and polysomnography to confirm their OSA and COPD diagnoses.

The primary endpoint was the impact of OSA on functional performance and cardiac autonomic control in COPD patients, based on measures of heart rate variability and the 6-minute walk test (6MWT). Participants were followed for 1 year, with telephone contacts every 3 months. A secondary endpoint was the number of exacerbations, hospitalizations, and deaths. At baseline, OSA-COPD patients had worse polysomnographic function, compared with COPD patients; they also tended to be older and have higher body mass index, but other demographics were similar between the groups.

Overall, patients in the OSA-COPD group had significantly greater functional impairment, compared with the COPD group (P = .003), as measured by the 6MWT. The OSA-COPD patients also showed significantly worse autonomic response during exercise, compared with the COPD group.

A lower work load during exercise and the interaction between group and time factors suggests that OSA impacts the exercise capacity of COPD patients, the researchers said. Notably, however, neither age nor body mass index was associated with functional performance in the OSA-COPD group.

Patients in the OSA-COPD group also were significantly more likely to experience exacerbations during the study period, compared with the COPD-only group (67.4% vs. 23.5; P = .03). However, the severity of COPD was similar between the groups, which further illustrates that OSA can impair functional performance in COPD patients, the researchers said.

The findings were limited by several factors including the small sample size and restricted collection of follow-up data during the pandemic, the researchers noted. However, the results support previous studies, and suggest that overlapping OSA and COPD produces worse outcomes.

“Future studies can confirm our findings, providing new clinical evidences to the assessment of sleep quality in COPD patients and its implications for the general health status of these individuals, in addition to contributing to more assertive clinical and therapeutic alternative support the need for more research into the mechanisms behind this overlap in larger samples to develop treatment alternatives,” they concluded.

The study was supported by the Federal University of Sao Carlos. The researchers had no financial conflicts to disclose.
 

While having proper indoor ventilation is recognized as a way to reduce the spread of COVID-19, a new study from MIT says maintaining the proper relative humidity in indoor spaces like your residence might help keep you healthy.

The “sweet spot” associated with reduced COVID-19 cases and deaths is 40%-60% indoor relative humidity, an MIT news release said. People who maintained indoor relative humidity outside those parameters had higher rates of catching COVID-19. 

Most people are comfortable with 30%-50% relative humidity, researchers said. An airplane cabin has about 20% relative humidity.

Relative humidity is the amount of moisture in the air, compared with the total moisture the air can hold at a given temperature before saturating and forming condensation.

The study was published in The Journal of the Royal Society Interface. Researchers examined COVID-19 data and meteorological measurements from 121 countries from January 2020 through August 2020, before vaccines became available to the public. 

“When outdoor temperatures were below the typical human comfort range, they assumed indoor spaces were heated to reach that comfort range. Based on the added heating, they calculated the associated drop in indoor relative humidity,” the MIT news release said.

The research teams found that when a region reported a rise in COVID-19 cases and deaths, the region’s estimated indoor relative humidity was either lower than 40% or higher than 60%, the release said. 

“There’s potentially a protective effect of this intermediate indoor relative humidity,” said Connor Verheyen, the lead author and a PhD student in medical engineering and medical physics in the Harvard-MIT Program in Health Sciences and Technology.

Widespread use of the 40%-60% indoor humidity range could reduce the need for lockdowns and other widespread restrictions, the study concluded.

“Unlike measures that depend on individual compliance (for example, masking or hand-washing), indoor RH optimization would achieve high compliance because all occupants of a common indoor space would be exposed to similar ambient conditions,” the study said. “Compared to the long timelines and high costs of vaccine production and distribution, humidity control systems could potentially be implemented more quickly and cheaply in certain indoor settings.”

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

While having proper indoor ventilation is recognized as a way to reduce the spread of COVID-19, a new study from MIT says maintaining the proper relative humidity in indoor spaces like your residence might help keep you healthy.

The “sweet spot” associated with reduced COVID-19 cases and deaths is 40%-60% indoor relative humidity, an MIT news release said. People who maintained indoor relative humidity outside those parameters had higher rates of catching COVID-19. 

Most people are comfortable with 30%-50% relative humidity, researchers said. An airplane cabin has about 20% relative humidity.

Relative humidity is the amount of moisture in the air, compared with the total moisture the air can hold at a given temperature before saturating and forming condensation.

The study was published in The Journal of the Royal Society Interface. Researchers examined COVID-19 data and meteorological measurements from 121 countries from January 2020 through August 2020, before vaccines became available to the public. 

“When outdoor temperatures were below the typical human comfort range, they assumed indoor spaces were heated to reach that comfort range. Based on the added heating, they calculated the associated drop in indoor relative humidity,” the MIT news release said.

The research teams found that when a region reported a rise in COVID-19 cases and deaths, the region’s estimated indoor relative humidity was either lower than 40% or higher than 60%, the release said. 

“There’s potentially a protective effect of this intermediate indoor relative humidity,” said Connor Verheyen, the lead author and a PhD student in medical engineering and medical physics in the Harvard-MIT Program in Health Sciences and Technology.

Widespread use of the 40%-60% indoor humidity range could reduce the need for lockdowns and other widespread restrictions, the study concluded.

“Unlike measures that depend on individual compliance (for example, masking or hand-washing), indoor RH optimization would achieve high compliance because all occupants of a common indoor space would be exposed to similar ambient conditions,” the study said. “Compared to the long timelines and high costs of vaccine production and distribution, humidity control systems could potentially be implemented more quickly and cheaply in certain indoor settings.”

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

While having proper indoor ventilation is recognized as a way to reduce the spread of COVID-19, a new study from MIT says maintaining the proper relative humidity in indoor spaces like your residence might help keep you healthy.

The “sweet spot” associated with reduced COVID-19 cases and deaths is 40%-60% indoor relative humidity, an MIT news release said. People who maintained indoor relative humidity outside those parameters had higher rates of catching COVID-19. 

Most people are comfortable with 30%-50% relative humidity, researchers said. An airplane cabin has about 20% relative humidity.

Relative humidity is the amount of moisture in the air, compared with the total moisture the air can hold at a given temperature before saturating and forming condensation.

The study was published in The Journal of the Royal Society Interface. Researchers examined COVID-19 data and meteorological measurements from 121 countries from January 2020 through August 2020, before vaccines became available to the public. 

“When outdoor temperatures were below the typical human comfort range, they assumed indoor spaces were heated to reach that comfort range. Based on the added heating, they calculated the associated drop in indoor relative humidity,” the MIT news release said.

The research teams found that when a region reported a rise in COVID-19 cases and deaths, the region’s estimated indoor relative humidity was either lower than 40% or higher than 60%, the release said. 

“There’s potentially a protective effect of this intermediate indoor relative humidity,” said Connor Verheyen, the lead author and a PhD student in medical engineering and medical physics in the Harvard-MIT Program in Health Sciences and Technology.

Widespread use of the 40%-60% indoor humidity range could reduce the need for lockdowns and other widespread restrictions, the study concluded.

“Unlike measures that depend on individual compliance (for example, masking or hand-washing), indoor RH optimization would achieve high compliance because all occupants of a common indoor space would be exposed to similar ambient conditions,” the study said. “Compared to the long timelines and high costs of vaccine production and distribution, humidity control systems could potentially be implemented more quickly and cheaply in certain indoor settings.”

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

A California nurse practitioner was fined nearly $20,000 for false advertising and fraud after referring to herself as “Dr. Sarah” and failing to file necessary business paperwork, according to a settlement announced on Nov. 14.  

Last month, the San Luis Obispo County, California, District Attorney Dan Dow filed a complaint against Sarah Erny, RN, NP, citing unfair business practices and unprofessional conduct.

According to court documents, California’s Medical Practice Act does not permit individuals to refer to themselves as “doctor, physician, or any other terms or letters indicating or implying that he or she is a physician and surgeon ... without having ... a certificate as a physician and surgeon.”

Individuals who misrepresent themselves are subject to misdemeanor charges and civil penalties. 

In addition to the fine, Ms. Erny agreed to refrain from referring to herself as a doctor in her practice and on social media. She has already deleted her Twitter account.

The case underscores tensions between physicians fighting to preserve their scope of practice and the allied professionals that U.S. lawmakers increasingly see as a less expensive way to improve access to health care.

The American Medical Association and specialty groups strongly oppose a new bill, the Improving Care and Access to Nurses Act, that would expand the scope of practice for nurse practitioners and physician assistants.

Court records show that Ms. Erny earned a doctor of nursing practice (DNP) degree from Vanderbilt University, Nashville, Tenn., and that she met the state requirements to obtain licensure as a registered nurse and nurse practitioner. In 2018, she opened a practice in Arroyo Grande, California, called Holistic Women’s Healing, where she provided medical services and drug supplements to patients.

She also entered a collaborative agreement with ob.gyn. Anika Moore, MD, for approximately 3 years. Dr. Moore’s medical practice was in another county and state, and the physician returned every 2 to 3 months to review a portion of Ms. Erny’s patient files.

Ms. Erny and Dr. Moore terminated the collaborative agreement in March, according to court documents.

However, Mr. Dow alleged that Ms. Erny regularly referred to herself as “Dr. Sarah” or “Dr. Sarah Erny” in her online advertising and social media accounts. Her patients “were so proud of her” that they called her doctor, and her supervising physician instructed staff to do the same.

Mr. Dow said Ms. Erny did not clearly advise the public that she was not a medical doctor and failed to identify her supervising physician. “Simply put, there is a great need for health care providers to state their level of training and licensing clearly and honestly in all of their advertising and marketing materials,” he said in a press release.

In California, nurse practitioners who have been certified by the Board of Registered Nursing may use the following titles: Advanced Practice Registered Nurse; Certified Nurse Practitioner; APRN-CNP; RN and NP; or a combination of other letters or words to identify specialization, such as adult nurse practitioner, pediatric nurse practitioner, obstetrical-gynecological nurse practitioner, and family nurse practitioner.

As educational requirements shift for advanced practice clinicians, similar cases will likely emerge, said Grant Martsolf, PhD, MPH, RN, FAAN, professor at the University of Pittsburgh School of Nursing.

“Scope of practice is governed by states, [so they] will have to figure [it] out as more professional disciplines move to clinical doctorates as the entry to practice. Pharma, [physical therapy], and [occupational therapy] have already done this, and advanced practice nursing is on its way. [Certified registered nurse anesthetists] are already required to get a DNP to sit for certification,” he said.

More guidance is needed, especially when considering other professions like dentists, clinical psychologists, and individuals with clinical or research doctorates who often call themselves doctors, Dr. Martsolf said.

“It seems that the honorific of ‘Dr.’ emerges from the degree, not from being a physician or surgeon,” he said.

Beyond the false advertising, Mr. Dow alleged that Ms. Erny did not file a fictitious business name statement for 2020 and 2021 – a requirement under the California Business and Professions Code to identify who is operating the business.

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

A California nurse practitioner was fined nearly $20,000 for false advertising and fraud after referring to herself as “Dr. Sarah” and failing to file necessary business paperwork, according to a settlement announced on Nov. 14.  

Last month, the San Luis Obispo County, California, District Attorney Dan Dow filed a complaint against Sarah Erny, RN, NP, citing unfair business practices and unprofessional conduct.

According to court documents, California’s Medical Practice Act does not permit individuals to refer to themselves as “doctor, physician, or any other terms or letters indicating or implying that he or she is a physician and surgeon ... without having ... a certificate as a physician and surgeon.”

Individuals who misrepresent themselves are subject to misdemeanor charges and civil penalties. 

In addition to the fine, Ms. Erny agreed to refrain from referring to herself as a doctor in her practice and on social media. She has already deleted her Twitter account.

The case underscores tensions between physicians fighting to preserve their scope of practice and the allied professionals that U.S. lawmakers increasingly see as a less expensive way to improve access to health care.

The American Medical Association and specialty groups strongly oppose a new bill, the Improving Care and Access to Nurses Act, that would expand the scope of practice for nurse practitioners and physician assistants.

Court records show that Ms. Erny earned a doctor of nursing practice (DNP) degree from Vanderbilt University, Nashville, Tenn., and that she met the state requirements to obtain licensure as a registered nurse and nurse practitioner. In 2018, she opened a practice in Arroyo Grande, California, called Holistic Women’s Healing, where she provided medical services and drug supplements to patients.

She also entered a collaborative agreement with ob.gyn. Anika Moore, MD, for approximately 3 years. Dr. Moore’s medical practice was in another county and state, and the physician returned every 2 to 3 months to review a portion of Ms. Erny’s patient files.

Ms. Erny and Dr. Moore terminated the collaborative agreement in March, according to court documents.

However, Mr. Dow alleged that Ms. Erny regularly referred to herself as “Dr. Sarah” or “Dr. Sarah Erny” in her online advertising and social media accounts. Her patients “were so proud of her” that they called her doctor, and her supervising physician instructed staff to do the same.

Mr. Dow said Ms. Erny did not clearly advise the public that she was not a medical doctor and failed to identify her supervising physician. “Simply put, there is a great need for health care providers to state their level of training and licensing clearly and honestly in all of their advertising and marketing materials,” he said in a press release.

In California, nurse practitioners who have been certified by the Board of Registered Nursing may use the following titles: Advanced Practice Registered Nurse; Certified Nurse Practitioner; APRN-CNP; RN and NP; or a combination of other letters or words to identify specialization, such as adult nurse practitioner, pediatric nurse practitioner, obstetrical-gynecological nurse practitioner, and family nurse practitioner.

As educational requirements shift for advanced practice clinicians, similar cases will likely emerge, said Grant Martsolf, PhD, MPH, RN, FAAN, professor at the University of Pittsburgh School of Nursing.

“Scope of practice is governed by states, [so they] will have to figure [it] out as more professional disciplines move to clinical doctorates as the entry to practice. Pharma, [physical therapy], and [occupational therapy] have already done this, and advanced practice nursing is on its way. [Certified registered nurse anesthetists] are already required to get a DNP to sit for certification,” he said.

More guidance is needed, especially when considering other professions like dentists, clinical psychologists, and individuals with clinical or research doctorates who often call themselves doctors, Dr. Martsolf said.

“It seems that the honorific of ‘Dr.’ emerges from the degree, not from being a physician or surgeon,” he said.

Beyond the false advertising, Mr. Dow alleged that Ms. Erny did not file a fictitious business name statement for 2020 and 2021 – a requirement under the California Business and Professions Code to identify who is operating the business.

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

A California nurse practitioner was fined nearly $20,000 for false advertising and fraud after referring to herself as “Dr. Sarah” and failing to file necessary business paperwork, according to a settlement announced on Nov. 14.  

Last month, the San Luis Obispo County, California, District Attorney Dan Dow filed a complaint against Sarah Erny, RN, NP, citing unfair business practices and unprofessional conduct.

According to court documents, California’s Medical Practice Act does not permit individuals to refer to themselves as “doctor, physician, or any other terms or letters indicating or implying that he or she is a physician and surgeon ... without having ... a certificate as a physician and surgeon.”

Individuals who misrepresent themselves are subject to misdemeanor charges and civil penalties. 

In addition to the fine, Ms. Erny agreed to refrain from referring to herself as a doctor in her practice and on social media. She has already deleted her Twitter account.

The case underscores tensions between physicians fighting to preserve their scope of practice and the allied professionals that U.S. lawmakers increasingly see as a less expensive way to improve access to health care.

The American Medical Association and specialty groups strongly oppose a new bill, the Improving Care and Access to Nurses Act, that would expand the scope of practice for nurse practitioners and physician assistants.

Court records show that Ms. Erny earned a doctor of nursing practice (DNP) degree from Vanderbilt University, Nashville, Tenn., and that she met the state requirements to obtain licensure as a registered nurse and nurse practitioner. In 2018, she opened a practice in Arroyo Grande, California, called Holistic Women’s Healing, where she provided medical services and drug supplements to patients.

She also entered a collaborative agreement with ob.gyn. Anika Moore, MD, for approximately 3 years. Dr. Moore’s medical practice was in another county and state, and the physician returned every 2 to 3 months to review a portion of Ms. Erny’s patient files.

Ms. Erny and Dr. Moore terminated the collaborative agreement in March, according to court documents.

However, Mr. Dow alleged that Ms. Erny regularly referred to herself as “Dr. Sarah” or “Dr. Sarah Erny” in her online advertising and social media accounts. Her patients “were so proud of her” that they called her doctor, and her supervising physician instructed staff to do the same.

Mr. Dow said Ms. Erny did not clearly advise the public that she was not a medical doctor and failed to identify her supervising physician. “Simply put, there is a great need for health care providers to state their level of training and licensing clearly and honestly in all of their advertising and marketing materials,” he said in a press release.

In California, nurse practitioners who have been certified by the Board of Registered Nursing may use the following titles: Advanced Practice Registered Nurse; Certified Nurse Practitioner; APRN-CNP; RN and NP; or a combination of other letters or words to identify specialization, such as adult nurse practitioner, pediatric nurse practitioner, obstetrical-gynecological nurse practitioner, and family nurse practitioner.

As educational requirements shift for advanced practice clinicians, similar cases will likely emerge, said Grant Martsolf, PhD, MPH, RN, FAAN, professor at the University of Pittsburgh School of Nursing.

“Scope of practice is governed by states, [so they] will have to figure [it] out as more professional disciplines move to clinical doctorates as the entry to practice. Pharma, [physical therapy], and [occupational therapy] have already done this, and advanced practice nursing is on its way. [Certified registered nurse anesthetists] are already required to get a DNP to sit for certification,” he said.

More guidance is needed, especially when considering other professions like dentists, clinical psychologists, and individuals with clinical or research doctorates who often call themselves doctors, Dr. Martsolf said.

“It seems that the honorific of ‘Dr.’ emerges from the degree, not from being a physician or surgeon,” he said.

Beyond the false advertising, Mr. Dow alleged that Ms. Erny did not file a fictitious business name statement for 2020 and 2021 – a requirement under the California Business and Professions Code to identify who is operating the business.

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

In the October 2022 issue of JAMA Neurology was a research article and accompanying editorial on the ATN (amyloid/tau/neurodegeneration) framework for diagnosing and treating Alzheimer’s disease.

There are valid concerns with any system centered on early dementia diagnosis. If the new generation of Alzheimer’s treatments can reverse pathology before the symptoms are apparent, it certainly makes sense to treat people as early as possible. In a terrible disease with only partially effective treatments now, this is encouraging news.

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

In the October 2022 issue of JAMA Neurology was a research article and accompanying editorial on the ATN (amyloid/tau/neurodegeneration) framework for diagnosing and treating Alzheimer’s disease.

There are valid concerns with any system centered on early dementia diagnosis. If the new generation of Alzheimer’s treatments can reverse pathology before the symptoms are apparent, it certainly makes sense to treat people as early as possible. In a terrible disease with only partially effective treatments now, this is encouraging news.

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

In the October 2022 issue of JAMA Neurology was a research article and accompanying editorial on the ATN (amyloid/tau/neurodegeneration) framework for diagnosing and treating Alzheimer’s disease.

There are valid concerns with any system centered on early dementia diagnosis. If the new generation of Alzheimer’s treatments can reverse pathology before the symptoms are apparent, it certainly makes sense to treat people as early as possible. In a terrible disease with only partially effective treatments now, this is encouraging news.

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

Of the more than 6 million patients with Alzheimer’s disease in the United States aged 65 or older, nearly two-thirds are women. A new study published online in Cell may help explain the gender gap – and offer clues to new treatments for helping patients of both sexes fight back.

Researchers zeroed in on a gene named USP11, found on the X chromosome. People assigned female at birth have two X chromosomes, while people assigned male at birth have one X and one Y. So while all males have one copy of USP11, females have two.
 

The body’s trash collection system

In the normal course of events, the brain creates waste that must be removed lest it becomes toxic. One waste product is the protein tau. Too little tau can damage nerve cells, explained researchers David Kang, PhD, and Jung-A “Alexa” Woo, PhD, who led the study. But too much becomes toxic and can lead to neurodegenerative diseases such as Alzheimer’s disease. In fact, new research suggests that testing for changes in tau may someday help doctors diagnose Alzheimer’s disease earlier.

To manage tau, the brain uses a regulatory protein called ubiquitin to “tag” or signal the body that extra tau should be removed.

USP11’s job is to give instructions to make an enzyme that removes the ubiquitin tag to maintain balance. But if too much of the enzyme is present, too much tau gets untagged – and not enough of it gets cleared.

“Our study showed USP11 is higher in females than males in both humans and in mice,” Dr. Kang said. “That’s already true before the onset of dementia. But once someone has Alzheimer’s disease, USP11 is much higher – regardless of sex.”

The study adds to a growing body of evidence that shows that women may be more vulnerable than men to higher levels of tau, possibly explaining why women are affected by the disease more often than men.

But what if there was a way to “turn off” or deactivate the USP11 gene? Might that help prevent Alzheimer’s disease? And could it be done safely?
 

What happened when the gene was eliminated?

To examine these questions, researchers used a method of gene manipulation to completely delete the USP11 gene in mice. They then examined the mice for changes. The result? The mice seemed fine.

“The mice bred well. Their brains looked fine,” Dr. Woo said.

It would not be possible – or ethical – to remove a gene from humans. But when a medical condition makes a certain gene unhelpful, that gene can be partially blocked or expression of the gene can be reduced with medication. In fact, medications targeting enzymes are common. Examples include statins for cardiovascular disease or HIV treatments that inhibit protease enzymes.

“If we are able to identify some type of medicine that would inhibit USP11, our study suggests it would be well tolerated and benefit women,” Dr. Woo said.

Dr. Kang also cautions that the process for creating such a therapy takes at least 10-15 years. The researchers said they’d like to shorten the timeline and plan to study currently approved FDA medications to see if any might work to target USP11 gene activity – and hopefully bring forth a new treatment for Alzheimer’s disease sooner.

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

Of the more than 6 million patients with Alzheimer’s disease in the United States aged 65 or older, nearly two-thirds are women. A new study published online in Cell may help explain the gender gap – and offer clues to new treatments for helping patients of both sexes fight back.

Researchers zeroed in on a gene named USP11, found on the X chromosome. People assigned female at birth have two X chromosomes, while people assigned male at birth have one X and one Y. So while all males have one copy of USP11, females have two.
 

The body’s trash collection system

In the normal course of events, the brain creates waste that must be removed lest it becomes toxic. One waste product is the protein tau. Too little tau can damage nerve cells, explained researchers David Kang, PhD, and Jung-A “Alexa” Woo, PhD, who led the study. But too much becomes toxic and can lead to neurodegenerative diseases such as Alzheimer’s disease. In fact, new research suggests that testing for changes in tau may someday help doctors diagnose Alzheimer’s disease earlier.

To manage tau, the brain uses a regulatory protein called ubiquitin to “tag” or signal the body that extra tau should be removed.

USP11’s job is to give instructions to make an enzyme that removes the ubiquitin tag to maintain balance. But if too much of the enzyme is present, too much tau gets untagged – and not enough of it gets cleared.

“Our study showed USP11 is higher in females than males in both humans and in mice,” Dr. Kang said. “That’s already true before the onset of dementia. But once someone has Alzheimer’s disease, USP11 is much higher – regardless of sex.”

The study adds to a growing body of evidence that shows that women may be more vulnerable than men to higher levels of tau, possibly explaining why women are affected by the disease more often than men.

But what if there was a way to “turn off” or deactivate the USP11 gene? Might that help prevent Alzheimer’s disease? And could it be done safely?
 

What happened when the gene was eliminated?

To examine these questions, researchers used a method of gene manipulation to completely delete the USP11 gene in mice. They then examined the mice for changes. The result? The mice seemed fine.

“The mice bred well. Their brains looked fine,” Dr. Woo said.

It would not be possible – or ethical – to remove a gene from humans. But when a medical condition makes a certain gene unhelpful, that gene can be partially blocked or expression of the gene can be reduced with medication. In fact, medications targeting enzymes are common. Examples include statins for cardiovascular disease or HIV treatments that inhibit protease enzymes.

“If we are able to identify some type of medicine that would inhibit USP11, our study suggests it would be well tolerated and benefit women,” Dr. Woo said.

Dr. Kang also cautions that the process for creating such a therapy takes at least 10-15 years. The researchers said they’d like to shorten the timeline and plan to study currently approved FDA medications to see if any might work to target USP11 gene activity – and hopefully bring forth a new treatment for Alzheimer’s disease sooner.

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

Of the more than 6 million patients with Alzheimer’s disease in the United States aged 65 or older, nearly two-thirds are women. A new study published online in Cell may help explain the gender gap – and offer clues to new treatments for helping patients of both sexes fight back.

Researchers zeroed in on a gene named USP11, found on the X chromosome. People assigned female at birth have two X chromosomes, while people assigned male at birth have one X and one Y. So while all males have one copy of USP11, females have two.
 

The body’s trash collection system

In the normal course of events, the brain creates waste that must be removed lest it becomes toxic. One waste product is the protein tau. Too little tau can damage nerve cells, explained researchers David Kang, PhD, and Jung-A “Alexa” Woo, PhD, who led the study. But too much becomes toxic and can lead to neurodegenerative diseases such as Alzheimer’s disease. In fact, new research suggests that testing for changes in tau may someday help doctors diagnose Alzheimer’s disease earlier.

To manage tau, the brain uses a regulatory protein called ubiquitin to “tag” or signal the body that extra tau should be removed.

USP11’s job is to give instructions to make an enzyme that removes the ubiquitin tag to maintain balance. But if too much of the enzyme is present, too much tau gets untagged – and not enough of it gets cleared.

“Our study showed USP11 is higher in females than males in both humans and in mice,” Dr. Kang said. “That’s already true before the onset of dementia. But once someone has Alzheimer’s disease, USP11 is much higher – regardless of sex.”

The study adds to a growing body of evidence that shows that women may be more vulnerable than men to higher levels of tau, possibly explaining why women are affected by the disease more often than men.

But what if there was a way to “turn off” or deactivate the USP11 gene? Might that help prevent Alzheimer’s disease? And could it be done safely?
 

What happened when the gene was eliminated?

To examine these questions, researchers used a method of gene manipulation to completely delete the USP11 gene in mice. They then examined the mice for changes. The result? The mice seemed fine.

“The mice bred well. Their brains looked fine,” Dr. Woo said.

It would not be possible – or ethical – to remove a gene from humans. But when a medical condition makes a certain gene unhelpful, that gene can be partially blocked or expression of the gene can be reduced with medication. In fact, medications targeting enzymes are common. Examples include statins for cardiovascular disease or HIV treatments that inhibit protease enzymes.

“If we are able to identify some type of medicine that would inhibit USP11, our study suggests it would be well tolerated and benefit women,” Dr. Woo said.

Dr. Kang also cautions that the process for creating such a therapy takes at least 10-15 years. The researchers said they’d like to shorten the timeline and plan to study currently approved FDA medications to see if any might work to target USP11 gene activity – and hopefully bring forth a new treatment for Alzheimer’s disease sooner.

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

Brain indicators of motor impairment were distinct among children with autism spectrum disorder (ASD), those with developmental coordination disorder (DCD), and controls, in a new study.

Previous research suggests that individuals with ASD overlap in motor impairment with those with DCD. But these two conditions may differ significantly in some areas, as children with ASD tend to show weaker skills in social motor tasks such as imitation, wrote Emil Kilroy, PhD, of the University of Southern California, Los Angeles, and colleagues.

The neurobiological basis of autism remains unknown, despite many research efforts, in part because of the heterogeneity of the disease, said corresponding author Lisa Aziz-Zadeh, PhD, also of the University of Southern California, in an interview.

Comorbidity with other disorders is a strong contributing factor to heterogeneity, and approximately 80% of autistic individuals have motor impairments and meet criteria for a diagnosis of DCD, said Dr. Aziz-Zadeh. “Controlling for other comorbidities, such as developmental coordination disorder, when trying to understand the neural basis of autism is important, so that we can understand which neural circuits are related to [core symptoms of autism] and which ones are related to motor impairments that are comorbid with autism, but not necessarily part of the core symptomology,” she explained. “We focused on white matter pathways here because many researchers now think the underlying basis of autism, besides genetics, is brain connectivity differences.”

In their study published in Scientific Reports, the researchers reviewed data from whole-brain correlational tractography for 22 individuals with autism spectrum disorder, 16 with developmental coordination disorder, and 21 normally developing individuals, who served as the control group. The mean age of the participants was approximately 11 years; the age range was 8-17 years.

Overall, patterns of brain diffusion (movement of fluid, mainly water molecules, in the brain) were significantly different in ASD children, compared with typically developing children.

The ASD group showed significantly reduced diffusivity in the bilateral fronto-parietal cingulum and the left parolfactory cingulum. This finding reflects previous studies suggesting an association between brain patterns in the cingulum area and ASD. But the current study is “the first to identify the fronto-parietal and the parolfactory portions of the cingulum as well as the anterior caudal u-fibers as specific to core ASD symptomatology and not related to motor-related comorbidity,” the researchers wrote.

Differences in brain diffusivity were associated with worse performance on motor skills and behavioral measures for children with ASD and children with DCD, compared with controls.

Motor development was assessed using the Total Movement Assessment Battery for Children-2 (MABC-2) and the Florida Apraxia Battery modified for children (FAB-M). The MABC-2 is among the most common tools for measuring motor skills and identifying clinically relevant motor deficits in children and teens aged 3-16 years. The test includes three subtest scores (manual dexterity, gross-motor aiming and catching, and balance) and a total score. Scores are based on a child’s best performance on each component, and higher scores indicate better functioning. In the new study, The MABC-2 total scores averaged 10.57 for controls, compared with 5.76 in the ASD group, and 4.31 in the DCD group.

Children with ASD differed from the other groups in social measures. Social skills were measured using several tools, including the Social Responsivity Scale (SRS Total), which is a parent-completed survey that includes a total score designed to reflect the severity of social deficits in ASD. It is divided into five subscales for parents to assess a child’s social skill impairment: social awareness, social cognition, social communication, social motivation, and mannerisms. Scores for the SRS are calculated in T-scores, in which a score of 50 represents the mean. T-scores of 59 and below are generally not associated with ASD, and patients with these scores are considered to have low to no symptomatology. Scores on the SRS Total in the new study were 45.95, 77.45, and 55.81 for the controls, ASD group, and DCD group, respectively.
 

Results should raise awareness

“The results were largely predicted in our hypotheses – that we would find specific white matter pathways in autism that would differ from [what we saw in typically developing patients and those with DCD], and that diffusivity in ASD would be related to socioemotional differences,” Dr. Aziz-Zadeh said, in an interview.

“What was surprising was that some pathways that had previously been thought to be different in autism were also compromised in DCD, indicating that they were common to motor deficits which both groups shared, not to core autism symptomology,” she noted.

A message for clinicians from the study is that a dual diagnosis of DCD is often missing in ASD practice, said Dr. Aziz-Zadeh. “Given that approximately 80% of children with ASD have DCD, testing for DCD and addressing potential motor issues should be more common practice,” she said.

Dr. Aziz-Zadeh and colleagues are now investigating relationships between the brain, behavior, and the gut microbiome. “We think that understanding autism from a full-body perspective, examining interactions between the brain and the body, will be an important step in this field,” she emphasized.

The study was limited by several factors, including the small sample size, the use of only right-handed participants, and the use of self-reports by children and parents, the researchers noted. Additionally, they noted that white matter develops at different rates in different age groups, and future studies might consider age as a factor, as well as further behavioral assessments, they said.
 

Small sample size limits conclusions

“Understanding the neuroanatomic differences that may contribute to the core symptoms of ASD is a very important goal for the field, particularly how they relate to other comorbid symptoms and neurodevelopmental disorders,” said Michael Gandal, MD, of the department of psychiatry at the University of Pennsylvania, Philadelphia, and a member of the Lifespan Brain Institute at the Children’s Hospital of Philadelphia, in an interview.

“While this study provides some clues into how structural connectivity may relate to motor coordination in ASD, it will be important to replicate these findings in a much larger sample before we can really appreciate how robust these findings are and how well they generalize to the broader ASD population,” Dr. Gandal emphasized.

The study was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development. The researchers had no financial conflicts to disclose. Dr. Gandal had no financial conflicts to disclose.

Brain indicators of motor impairment were distinct among children with autism spectrum disorder (ASD), those with developmental coordination disorder (DCD), and controls, in a new study.

Previous research suggests that individuals with ASD overlap in motor impairment with those with DCD. But these two conditions may differ significantly in some areas, as children with ASD tend to show weaker skills in social motor tasks such as imitation, wrote Emil Kilroy, PhD, of the University of Southern California, Los Angeles, and colleagues.

The neurobiological basis of autism remains unknown, despite many research efforts, in part because of the heterogeneity of the disease, said corresponding author Lisa Aziz-Zadeh, PhD, also of the University of Southern California, in an interview.

Comorbidity with other disorders is a strong contributing factor to heterogeneity, and approximately 80% of autistic individuals have motor impairments and meet criteria for a diagnosis of DCD, said Dr. Aziz-Zadeh. “Controlling for other comorbidities, such as developmental coordination disorder, when trying to understand the neural basis of autism is important, so that we can understand which neural circuits are related to [core symptoms of autism] and which ones are related to motor impairments that are comorbid with autism, but not necessarily part of the core symptomology,” she explained. “We focused on white matter pathways here because many researchers now think the underlying basis of autism, besides genetics, is brain connectivity differences.”

In their study published in Scientific Reports, the researchers reviewed data from whole-brain correlational tractography for 22 individuals with autism spectrum disorder, 16 with developmental coordination disorder, and 21 normally developing individuals, who served as the control group. The mean age of the participants was approximately 11 years; the age range was 8-17 years.

Overall, patterns of brain diffusion (movement of fluid, mainly water molecules, in the brain) were significantly different in ASD children, compared with typically developing children.

The ASD group showed significantly reduced diffusivity in the bilateral fronto-parietal cingulum and the left parolfactory cingulum. This finding reflects previous studies suggesting an association between brain patterns in the cingulum area and ASD. But the current study is “the first to identify the fronto-parietal and the parolfactory portions of the cingulum as well as the anterior caudal u-fibers as specific to core ASD symptomatology and not related to motor-related comorbidity,” the researchers wrote.

Differences in brain diffusivity were associated with worse performance on motor skills and behavioral measures for children with ASD and children with DCD, compared with controls.

Motor development was assessed using the Total Movement Assessment Battery for Children-2 (MABC-2) and the Florida Apraxia Battery modified for children (FAB-M). The MABC-2 is among the most common tools for measuring motor skills and identifying clinically relevant motor deficits in children and teens aged 3-16 years. The test includes three subtest scores (manual dexterity, gross-motor aiming and catching, and balance) and a total score. Scores are based on a child’s best performance on each component, and higher scores indicate better functioning. In the new study, The MABC-2 total scores averaged 10.57 for controls, compared with 5.76 in the ASD group, and 4.31 in the DCD group.

Children with ASD differed from the other groups in social measures. Social skills were measured using several tools, including the Social Responsivity Scale (SRS Total), which is a parent-completed survey that includes a total score designed to reflect the severity of social deficits in ASD. It is divided into five subscales for parents to assess a child’s social skill impairment: social awareness, social cognition, social communication, social motivation, and mannerisms. Scores for the SRS are calculated in T-scores, in which a score of 50 represents the mean. T-scores of 59 and below are generally not associated with ASD, and patients with these scores are considered to have low to no symptomatology. Scores on the SRS Total in the new study were 45.95, 77.45, and 55.81 for the controls, ASD group, and DCD group, respectively.
 

Results should raise awareness

“The results were largely predicted in our hypotheses – that we would find specific white matter pathways in autism that would differ from [what we saw in typically developing patients and those with DCD], and that diffusivity in ASD would be related to socioemotional differences,” Dr. Aziz-Zadeh said, in an interview.

“What was surprising was that some pathways that had previously been thought to be different in autism were also compromised in DCD, indicating that they were common to motor deficits which both groups shared, not to core autism symptomology,” she noted.

A message for clinicians from the study is that a dual diagnosis of DCD is often missing in ASD practice, said Dr. Aziz-Zadeh. “Given that approximately 80% of children with ASD have DCD, testing for DCD and addressing potential motor issues should be more common practice,” she said.

Dr. Aziz-Zadeh and colleagues are now investigating relationships between the brain, behavior, and the gut microbiome. “We think that understanding autism from a full-body perspective, examining interactions between the brain and the body, will be an important step in this field,” she emphasized.

The study was limited by several factors, including the small sample size, the use of only right-handed participants, and the use of self-reports by children and parents, the researchers noted. Additionally, they noted that white matter develops at different rates in different age groups, and future studies might consider age as a factor, as well as further behavioral assessments, they said.
 

Small sample size limits conclusions

“Understanding the neuroanatomic differences that may contribute to the core symptoms of ASD is a very important goal for the field, particularly how they relate to other comorbid symptoms and neurodevelopmental disorders,” said Michael Gandal, MD, of the department of psychiatry at the University of Pennsylvania, Philadelphia, and a member of the Lifespan Brain Institute at the Children’s Hospital of Philadelphia, in an interview.

“While this study provides some clues into how structural connectivity may relate to motor coordination in ASD, it will be important to replicate these findings in a much larger sample before we can really appreciate how robust these findings are and how well they generalize to the broader ASD population,” Dr. Gandal emphasized.

The study was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development. The researchers had no financial conflicts to disclose. Dr. Gandal had no financial conflicts to disclose.

Brain indicators of motor impairment were distinct among children with autism spectrum disorder (ASD), those with developmental coordination disorder (DCD), and controls, in a new study.

Previous research suggests that individuals with ASD overlap in motor impairment with those with DCD. But these two conditions may differ significantly in some areas, as children with ASD tend to show weaker skills in social motor tasks such as imitation, wrote Emil Kilroy, PhD, of the University of Southern California, Los Angeles, and colleagues.

The neurobiological basis of autism remains unknown, despite many research efforts, in part because of the heterogeneity of the disease, said corresponding author Lisa Aziz-Zadeh, PhD, also of the University of Southern California, in an interview.

Comorbidity with other disorders is a strong contributing factor to heterogeneity, and approximately 80% of autistic individuals have motor impairments and meet criteria for a diagnosis of DCD, said Dr. Aziz-Zadeh. “Controlling for other comorbidities, such as developmental coordination disorder, when trying to understand the neural basis of autism is important, so that we can understand which neural circuits are related to [core symptoms of autism] and which ones are related to motor impairments that are comorbid with autism, but not necessarily part of the core symptomology,” she explained. “We focused on white matter pathways here because many researchers now think the underlying basis of autism, besides genetics, is brain connectivity differences.”

In their study published in Scientific Reports, the researchers reviewed data from whole-brain correlational tractography for 22 individuals with autism spectrum disorder, 16 with developmental coordination disorder, and 21 normally developing individuals, who served as the control group. The mean age of the participants was approximately 11 years; the age range was 8-17 years.

Overall, patterns of brain diffusion (movement of fluid, mainly water molecules, in the brain) were significantly different in ASD children, compared with typically developing children.

The ASD group showed significantly reduced diffusivity in the bilateral fronto-parietal cingulum and the left parolfactory cingulum. This finding reflects previous studies suggesting an association between brain patterns in the cingulum area and ASD. But the current study is “the first to identify the fronto-parietal and the parolfactory portions of the cingulum as well as the anterior caudal u-fibers as specific to core ASD symptomatology and not related to motor-related comorbidity,” the researchers wrote.

Differences in brain diffusivity were associated with worse performance on motor skills and behavioral measures for children with ASD and children with DCD, compared with controls.

Motor development was assessed using the Total Movement Assessment Battery for Children-2 (MABC-2) and the Florida Apraxia Battery modified for children (FAB-M). The MABC-2 is among the most common tools for measuring motor skills and identifying clinically relevant motor deficits in children and teens aged 3-16 years. The test includes three subtest scores (manual dexterity, gross-motor aiming and catching, and balance) and a total score. Scores are based on a child’s best performance on each component, and higher scores indicate better functioning. In the new study, The MABC-2 total scores averaged 10.57 for controls, compared with 5.76 in the ASD group, and 4.31 in the DCD group.

Children with ASD differed from the other groups in social measures. Social skills were measured using several tools, including the Social Responsivity Scale (SRS Total), which is a parent-completed survey that includes a total score designed to reflect the severity of social deficits in ASD. It is divided into five subscales for parents to assess a child’s social skill impairment: social awareness, social cognition, social communication, social motivation, and mannerisms. Scores for the SRS are calculated in T-scores, in which a score of 50 represents the mean. T-scores of 59 and below are generally not associated with ASD, and patients with these scores are considered to have low to no symptomatology. Scores on the SRS Total in the new study were 45.95, 77.45, and 55.81 for the controls, ASD group, and DCD group, respectively.
 

Results should raise awareness

“The results were largely predicted in our hypotheses – that we would find specific white matter pathways in autism that would differ from [what we saw in typically developing patients and those with DCD], and that diffusivity in ASD would be related to socioemotional differences,” Dr. Aziz-Zadeh said, in an interview.

“What was surprising was that some pathways that had previously been thought to be different in autism were also compromised in DCD, indicating that they were common to motor deficits which both groups shared, not to core autism symptomology,” she noted.

A message for clinicians from the study is that a dual diagnosis of DCD is often missing in ASD practice, said Dr. Aziz-Zadeh. “Given that approximately 80% of children with ASD have DCD, testing for DCD and addressing potential motor issues should be more common practice,” she said.

Dr. Aziz-Zadeh and colleagues are now investigating relationships between the brain, behavior, and the gut microbiome. “We think that understanding autism from a full-body perspective, examining interactions between the brain and the body, will be an important step in this field,” she emphasized.

The study was limited by several factors, including the small sample size, the use of only right-handed participants, and the use of self-reports by children and parents, the researchers noted. Additionally, they noted that white matter develops at different rates in different age groups, and future studies might consider age as a factor, as well as further behavioral assessments, they said.
 

Small sample size limits conclusions

“Understanding the neuroanatomic differences that may contribute to the core symptoms of ASD is a very important goal for the field, particularly how they relate to other comorbid symptoms and neurodevelopmental disorders,” said Michael Gandal, MD, of the department of psychiatry at the University of Pennsylvania, Philadelphia, and a member of the Lifespan Brain Institute at the Children’s Hospital of Philadelphia, in an interview.

“While this study provides some clues into how structural connectivity may relate to motor coordination in ASD, it will be important to replicate these findings in a much larger sample before we can really appreciate how robust these findings are and how well they generalize to the broader ASD population,” Dr. Gandal emphasized.

The study was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development. The researchers had no financial conflicts to disclose. Dr. Gandal had no financial conflicts to disclose.

For people with clinically diagnosed “nightmare disorder,” learning to redirect disturbing dreams to more positive ones is usually the return ticket to sleep. 

But for nearly one-third of people, that method – called imagery rehearsal therapy – isn’t effective.

A new study shows that listening to positive sounds while sleeping reduces the frequency of nightmares.

“This is a promising development. It does appear that adding a well-timed sound during REM sleep augments the effect of image rehearsal therapy ... which is a standard and perhaps one of the most effective nonpharmacologic therapies at this time,” said Timothy Morgenthaler, MD, in an interview with CNN. 

Dr. Morgenthaler, who was not involved in this latest study, is lead author of the American Academy of Sleep Medicine’s current guidelines on nightmares.

For the new research, nightmares were defined as “the experience of strong negative emotions occurring usually during REM sleep. They involve images and thoughts of aggression, interpersonal conflict, and failure, and emotions like fear, anger, and sadness.” Nightmare disorder is characterized as having such dreams so frequently that they cause “significant distress or impairment in social, occupational, or other important areas of functioning.” 

Left untreated, nightmare disorder can persist for decades, the authors said.

The study, conducted in Switzerland, enrolled 36 participants with nightmare disorder. All 36 participated in a daytime lesson of imagery rehearsal therapy that taught them to redirect their nightmares to positive dreams. Participants were taught to recall a nightmare, change the negative story line toward a more positive one, and then rehearse the so-called “rewritten dream” during the day.

Half of the participants also had a special sound played while they practiced reimagining their new positive dreams. At night for the following 2 weeks while they slept, the sound was played during their REM cycles.

Those who heard the sound reported significantly fewer nightmares.

“This difference displayed a medium to large effect size and was sustainable at the 3-month follow-up,” the authors reported.

They did note that both groups showed improvement, likely because the lesson to reimagine nightmares into positive dreams is known to be effective. However, the authors allowed that other factors may have contributed in ways their study design could not control.

“The result should be replicated,” Dr. Morgenthaler said. “But I was a bit excited at this new possibility.”

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

For people with clinically diagnosed “nightmare disorder,” learning to redirect disturbing dreams to more positive ones is usually the return ticket to sleep. 

But for nearly one-third of people, that method – called imagery rehearsal therapy – isn’t effective.

A new study shows that listening to positive sounds while sleeping reduces the frequency of nightmares.

“This is a promising development. It does appear that adding a well-timed sound during REM sleep augments the effect of image rehearsal therapy ... which is a standard and perhaps one of the most effective nonpharmacologic therapies at this time,” said Timothy Morgenthaler, MD, in an interview with CNN. 

Dr. Morgenthaler, who was not involved in this latest study, is lead author of the American Academy of Sleep Medicine’s current guidelines on nightmares.

For the new research, nightmares were defined as “the experience of strong negative emotions occurring usually during REM sleep. They involve images and thoughts of aggression, interpersonal conflict, and failure, and emotions like fear, anger, and sadness.” Nightmare disorder is characterized as having such dreams so frequently that they cause “significant distress or impairment in social, occupational, or other important areas of functioning.” 

Left untreated, nightmare disorder can persist for decades, the authors said.

The study, conducted in Switzerland, enrolled 36 participants with nightmare disorder. All 36 participated in a daytime lesson of imagery rehearsal therapy that taught them to redirect their nightmares to positive dreams. Participants were taught to recall a nightmare, change the negative story line toward a more positive one, and then rehearse the so-called “rewritten dream” during the day.

Half of the participants also had a special sound played while they practiced reimagining their new positive dreams. At night for the following 2 weeks while they slept, the sound was played during their REM cycles.

Those who heard the sound reported significantly fewer nightmares.

“This difference displayed a medium to large effect size and was sustainable at the 3-month follow-up,” the authors reported.

They did note that both groups showed improvement, likely because the lesson to reimagine nightmares into positive dreams is known to be effective. However, the authors allowed that other factors may have contributed in ways their study design could not control.

“The result should be replicated,” Dr. Morgenthaler said. “But I was a bit excited at this new possibility.”

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

For people with clinically diagnosed “nightmare disorder,” learning to redirect disturbing dreams to more positive ones is usually the return ticket to sleep. 

But for nearly one-third of people, that method – called imagery rehearsal therapy – isn’t effective.

A new study shows that listening to positive sounds while sleeping reduces the frequency of nightmares.

“This is a promising development. It does appear that adding a well-timed sound during REM sleep augments the effect of image rehearsal therapy ... which is a standard and perhaps one of the most effective nonpharmacologic therapies at this time,” said Timothy Morgenthaler, MD, in an interview with CNN. 

Dr. Morgenthaler, who was not involved in this latest study, is lead author of the American Academy of Sleep Medicine’s current guidelines on nightmares.

For the new research, nightmares were defined as “the experience of strong negative emotions occurring usually during REM sleep. They involve images and thoughts of aggression, interpersonal conflict, and failure, and emotions like fear, anger, and sadness.” Nightmare disorder is characterized as having such dreams so frequently that they cause “significant distress or impairment in social, occupational, or other important areas of functioning.” 

Left untreated, nightmare disorder can persist for decades, the authors said.

The study, conducted in Switzerland, enrolled 36 participants with nightmare disorder. All 36 participated in a daytime lesson of imagery rehearsal therapy that taught them to redirect their nightmares to positive dreams. Participants were taught to recall a nightmare, change the negative story line toward a more positive one, and then rehearse the so-called “rewritten dream” during the day.

Half of the participants also had a special sound played while they practiced reimagining their new positive dreams. At night for the following 2 weeks while they slept, the sound was played during their REM cycles.

Those who heard the sound reported significantly fewer nightmares.

“This difference displayed a medium to large effect size and was sustainable at the 3-month follow-up,” the authors reported.

They did note that both groups showed improvement, likely because the lesson to reimagine nightmares into positive dreams is known to be effective. However, the authors allowed that other factors may have contributed in ways their study design could not control.

“The result should be replicated,” Dr. Morgenthaler said. “But I was a bit excited at this new possibility.”

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

The study covered in this summary was published on ResearchSquare.com as a preprint and has not yet been peer-reviewed.

Key takeaway

• Acute atrial fibrillation (AF) is an independent predictor of severity of neurological deficits from early acute ischemic stroke and a high-probability predictor of death within 30 days after such strokes.

Why this matters

• A comprehensive understanding of the relationship between acute AF and risk for acute ischemic stroke and prognosis will help improve management and treatment of patients with acute ischemic stroke.

Study design

• The retrospective study included patients with acute ischemic stroke within the prior 24 hours; 12-lead electrocardiogram in the emergency department; and hospitalization and treatment at the hospital stroke center.
• The cohort of 706 patients admitted to a single center in Shanghai, China, from December 2019 to December 2021, included 142 with episodes of acute AF and 564 without such episodes.
• Patients with acute ischemic stroke and acute AF – including AF of new onset, paroxysmal, persistent, or permanent with symptoms such as palpitations or dizziness attributed to rapid ventricular rates – were identified.
• Neurological deficits were assessed using the 7-day National Institutes of Health Stroke Scale/Score (NIHSS). Patients with a 7-day NIHSS score of at least 16 were considered to have moderate to severe stroke.
• Associations between acute AF onset and the severity of early neurological deficits were assessed and related to all-cause mortality within 30 days of the stroke.

Key results

• Patients with acute AF were older than those without acute AF (80.3 years vs. 71.0 years; P < .001).
• Baseline NIHSS scores averaged 16.09 for the stroke patients with acute AF and 8.65 for those without acute AF (P < .001).
• Significantly more patients with acute AF than without acute AF had a 7-day NIHSS score of at least 16 (45.1% vs. 14.4%; P < .001).
• More patients with than without acute AF underwent transcatheter thrombectomy (44.4% vs. 24.5%; P < .001) or received thrombolytic therapy (31.6% vs. 19.7%; P = .005).
• Patients aged 73 years or older showed baseline NIHSS score and acute AF as independent risk factors for early neurological deficits in stroke patients admitted to the emergency department.
• Mortality at 30 days was significantly higher in patients with acute AF than in those without acute AF (30.3% vs. 10.1%; P < .001).
• Baseline NIHSS had an adjusted odds ratio for 30-day mortality of 1.18 (95% confidence interval, 1.15-1.22; P < .001).  
• Other independent predictors included acute AF (1.87 [95% CI, 1.09-3.19; P = .022]) and age 73 or older (2.00 [95% CI, 1.18-3.37; P = .01]).

Limitations

• The study was retrospective and didn’t have access to some potentially relevant data, such as duration of AF.
• The single-center study with limited generalizability does not necessarily represent the broad population of stroke patients in China or elsewhere.

Disclosures

• This study was supported by the Cardiovascular Multidisciplinary Integrated Research Fund and Construction of Shanghai Municipal Health Commission.
• The authors report no relevant financial relationships.

This is a summary of a preprint research study, “Acute Atrial Fibrillation During Onset of Stroke Indicates Higher Probability of Post-Stroke Death Outcomes,” written by Yongxia Li, from the Shanghai Sixth People’s Hospital, and colleagues, on ResearchSquare.com. This study has not yet been peer reviewed. The full text of the study can be found on ResearchSquare.com.A version of this article first appeared on Medscape.com.

The study covered in this summary was published on ResearchSquare.com as a preprint and has not yet been peer-reviewed.

Key takeaway

• Acute atrial fibrillation (AF) is an independent predictor of severity of neurological deficits from early acute ischemic stroke and a high-probability predictor of death within 30 days after such strokes.

Why this matters

• A comprehensive understanding of the relationship between acute AF and risk for acute ischemic stroke and prognosis will help improve management and treatment of patients with acute ischemic stroke.

Study design

• The retrospective study included patients with acute ischemic stroke within the prior 24 hours; 12-lead electrocardiogram in the emergency department; and hospitalization and treatment at the hospital stroke center.
• The cohort of 706 patients admitted to a single center in Shanghai, China, from December 2019 to December 2021, included 142 with episodes of acute AF and 564 without such episodes.
• Patients with acute ischemic stroke and acute AF – including AF of new onset, paroxysmal, persistent, or permanent with symptoms such as palpitations or dizziness attributed to rapid ventricular rates – were identified.
• Neurological deficits were assessed using the 7-day National Institutes of Health Stroke Scale/Score (NIHSS). Patients with a 7-day NIHSS score of at least 16 were considered to have moderate to severe stroke.
• Associations between acute AF onset and the severity of early neurological deficits were assessed and related to all-cause mortality within 30 days of the stroke.

Key results

• Patients with acute AF were older than those without acute AF (80.3 years vs. 71.0 years; P < .001).
• Baseline NIHSS scores averaged 16.09 for the stroke patients with acute AF and 8.65 for those without acute AF (P < .001).
• Significantly more patients with acute AF than without acute AF had a 7-day NIHSS score of at least 16 (45.1% vs. 14.4%; P < .001).
• More patients with than without acute AF underwent transcatheter thrombectomy (44.4% vs. 24.5%; P < .001) or received thrombolytic therapy (31.6% vs. 19.7%; P = .005).
• Patients aged 73 years or older showed baseline NIHSS score and acute AF as independent risk factors for early neurological deficits in stroke patients admitted to the emergency department.
• Mortality at 30 days was significantly higher in patients with acute AF than in those without acute AF (30.3% vs. 10.1%; P < .001).
• Baseline NIHSS had an adjusted odds ratio for 30-day mortality of 1.18 (95% confidence interval, 1.15-1.22; P < .001).  
• Other independent predictors included acute AF (1.87 [95% CI, 1.09-3.19; P = .022]) and age 73 or older (2.00 [95% CI, 1.18-3.37; P = .01]).

Limitations

• The study was retrospective and didn’t have access to some potentially relevant data, such as duration of AF.
• The single-center study with limited generalizability does not necessarily represent the broad population of stroke patients in China or elsewhere.

Disclosures

• This study was supported by the Cardiovascular Multidisciplinary Integrated Research Fund and Construction of Shanghai Municipal Health Commission.
• The authors report no relevant financial relationships.

This is a summary of a preprint research study, “Acute Atrial Fibrillation During Onset of Stroke Indicates Higher Probability of Post-Stroke Death Outcomes,” written by Yongxia Li, from the Shanghai Sixth People’s Hospital, and colleagues, on ResearchSquare.com. This study has not yet been peer reviewed. The full text of the study can be found on ResearchSquare.com.A version of this article first appeared on Medscape.com.

The study covered in this summary was published on ResearchSquare.com as a preprint and has not yet been peer-reviewed.

Key takeaway

• Acute atrial fibrillation (AF) is an independent predictor of severity of neurological deficits from early acute ischemic stroke and a high-probability predictor of death within 30 days after such strokes.

Why this matters

• A comprehensive understanding of the relationship between acute AF and risk for acute ischemic stroke and prognosis will help improve management and treatment of patients with acute ischemic stroke.

Study design

• The retrospective study included patients with acute ischemic stroke within the prior 24 hours; 12-lead electrocardiogram in the emergency department; and hospitalization and treatment at the hospital stroke center.
• The cohort of 706 patients admitted to a single center in Shanghai, China, from December 2019 to December 2021, included 142 with episodes of acute AF and 564 without such episodes.
• Patients with acute ischemic stroke and acute AF – including AF of new onset, paroxysmal, persistent, or permanent with symptoms such as palpitations or dizziness attributed to rapid ventricular rates – were identified.
• Neurological deficits were assessed using the 7-day National Institutes of Health Stroke Scale/Score (NIHSS). Patients with a 7-day NIHSS score of at least 16 were considered to have moderate to severe stroke.
• Associations between acute AF onset and the severity of early neurological deficits were assessed and related to all-cause mortality within 30 days of the stroke.

Key results

• Patients with acute AF were older than those without acute AF (80.3 years vs. 71.0 years; P < .001).
• Baseline NIHSS scores averaged 16.09 for the stroke patients with acute AF and 8.65 for those without acute AF (P < .001).
• Significantly more patients with acute AF than without acute AF had a 7-day NIHSS score of at least 16 (45.1% vs. 14.4%; P < .001).
• More patients with than without acute AF underwent transcatheter thrombectomy (44.4% vs. 24.5%; P < .001) or received thrombolytic therapy (31.6% vs. 19.7%; P = .005).
• Patients aged 73 years or older showed baseline NIHSS score and acute AF as independent risk factors for early neurological deficits in stroke patients admitted to the emergency department.
• Mortality at 30 days was significantly higher in patients with acute AF than in those without acute AF (30.3% vs. 10.1%; P < .001).
• Baseline NIHSS had an adjusted odds ratio for 30-day mortality of 1.18 (95% confidence interval, 1.15-1.22; P < .001).  
• Other independent predictors included acute AF (1.87 [95% CI, 1.09-3.19; P = .022]) and age 73 or older (2.00 [95% CI, 1.18-3.37; P = .01]).

Limitations

• The study was retrospective and didn’t have access to some potentially relevant data, such as duration of AF.
• The single-center study with limited generalizability does not necessarily represent the broad population of stroke patients in China or elsewhere.

Disclosures

• This study was supported by the Cardiovascular Multidisciplinary Integrated Research Fund and Construction of Shanghai Municipal Health Commission.
• The authors report no relevant financial relationships.

This is a summary of a preprint research study, “Acute Atrial Fibrillation During Onset of Stroke Indicates Higher Probability of Post-Stroke Death Outcomes,” written by Yongxia Li, from the Shanghai Sixth People’s Hospital, and colleagues, on ResearchSquare.com. This study has not yet been peer reviewed. The full text of the study can be found on ResearchSquare.com.A version of this article first appeared on Medscape.com.

Texas-based researchers have developed a vaccine that blocks the euphoric effects of fentanyl, a potent synthetic opioid that is increasingly involved in opioid overdose deaths in the United States.

In studies in male and female mice, the vaccine generated significant and long-lasting levels of anti-fentanyl antibodies that were highly effective at reducing the antinociceptive, behavioral, and physiological effects of the drug.

The vaccine prevents fentanyl from entering the brain. “Thus, the individual will not feel the euphoric effects and can ‘get back on the wagon’ to sobriety,” lead investigator Colin Haile, MD, PhD, with University of Houston and founding member of the UH Drug Discovery Institute, said in a news release. The study was published online in the journal Pharmaceutics.

“The anti-fentanyl antibodies were specific to fentanyl and a fentanyl derivative and did not cross-react with other opioids, such as morphine. That means a vaccinated person would still be able to be treated for pain relief with other opioids,” said Dr. Haile.

The vaccine did not cause any adverse effects in the immunized mice. The research team plans to start manufacturing clinical-grade vaccine in the coming months with clinical trials in humans planned soon.

If proven safe and effective in clinical testing, the vaccine could have major implications for the nation’s opioid epidemic by becoming a relapse prevention agent for people trying to quit using opioids, the researchers note.

The United States in 2021 recorded more than 107,000 drug overdose deaths – a record high, according to federal health officials – and fentanyl was involved in most of these deaths. 

Senior author Therese Kosten, PhD, director of the UH Developmental, Cognitive & Behavioral Neuroscience program, calls the new fentanyl vaccine a potential “game changer.”

“Fentanyl use and overdose is a particular treatment challenge that is not adequately addressed with current medications because of its pharmacodynamics, and managing acute overdose with the short-acting naloxone [Narcan] is not appropriately effective as multiple doses of naloxone are often needed to reverse fentanyl’s fatal effects,” said Dr. Kosten.

Funding for the study was provided by the Department of Defense through the Alcohol and Substance Abuse Disorders Program managed by RTI International’s Pharmacotherapies for Alcohol and Substance Use Disorders Alliance, which has funded Dr. Haile’s lab for several years to develop the anti-fentanyl vaccine. The authors have no relevant conflicts of interest. A provisional patent has been submitted by the University of Houston on behalf of four of the investigators containing technology related to the fentanyl vaccine.

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

Texas-based researchers have developed a vaccine that blocks the euphoric effects of fentanyl, a potent synthetic opioid that is increasingly involved in opioid overdose deaths in the United States.

In studies in male and female mice, the vaccine generated significant and long-lasting levels of anti-fentanyl antibodies that were highly effective at reducing the antinociceptive, behavioral, and physiological effects of the drug.

The vaccine prevents fentanyl from entering the brain. “Thus, the individual will not feel the euphoric effects and can ‘get back on the wagon’ to sobriety,” lead investigator Colin Haile, MD, PhD, with University of Houston and founding member of the UH Drug Discovery Institute, said in a news release. The study was published online in the journal Pharmaceutics.

“The anti-fentanyl antibodies were specific to fentanyl and a fentanyl derivative and did not cross-react with other opioids, such as morphine. That means a vaccinated person would still be able to be treated for pain relief with other opioids,” said Dr. Haile.

The vaccine did not cause any adverse effects in the immunized mice. The research team plans to start manufacturing clinical-grade vaccine in the coming months with clinical trials in humans planned soon.

If proven safe and effective in clinical testing, the vaccine could have major implications for the nation’s opioid epidemic by becoming a relapse prevention agent for people trying to quit using opioids, the researchers note.

The United States in 2021 recorded more than 107,000 drug overdose deaths – a record high, according to federal health officials – and fentanyl was involved in most of these deaths. 

Senior author Therese Kosten, PhD, director of the UH Developmental, Cognitive & Behavioral Neuroscience program, calls the new fentanyl vaccine a potential “game changer.”

“Fentanyl use and overdose is a particular treatment challenge that is not adequately addressed with current medications because of its pharmacodynamics, and managing acute overdose with the short-acting naloxone [Narcan] is not appropriately effective as multiple doses of naloxone are often needed to reverse fentanyl’s fatal effects,” said Dr. Kosten.

Funding for the study was provided by the Department of Defense through the Alcohol and Substance Abuse Disorders Program managed by RTI International’s Pharmacotherapies for Alcohol and Substance Use Disorders Alliance, which has funded Dr. Haile’s lab for several years to develop the anti-fentanyl vaccine. The authors have no relevant conflicts of interest. A provisional patent has been submitted by the University of Houston on behalf of four of the investigators containing technology related to the fentanyl vaccine.

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

Texas-based researchers have developed a vaccine that blocks the euphoric effects of fentanyl, a potent synthetic opioid that is increasingly involved in opioid overdose deaths in the United States.

In studies in male and female mice, the vaccine generated significant and long-lasting levels of anti-fentanyl antibodies that were highly effective at reducing the antinociceptive, behavioral, and physiological effects of the drug.

The vaccine prevents fentanyl from entering the brain. “Thus, the individual will not feel the euphoric effects and can ‘get back on the wagon’ to sobriety,” lead investigator Colin Haile, MD, PhD, with University of Houston and founding member of the UH Drug Discovery Institute, said in a news release. The study was published online in the journal Pharmaceutics.

“The anti-fentanyl antibodies were specific to fentanyl and a fentanyl derivative and did not cross-react with other opioids, such as morphine. That means a vaccinated person would still be able to be treated for pain relief with other opioids,” said Dr. Haile.

The vaccine did not cause any adverse effects in the immunized mice. The research team plans to start manufacturing clinical-grade vaccine in the coming months with clinical trials in humans planned soon.

If proven safe and effective in clinical testing, the vaccine could have major implications for the nation’s opioid epidemic by becoming a relapse prevention agent for people trying to quit using opioids, the researchers note.

The United States in 2021 recorded more than 107,000 drug overdose deaths – a record high, according to federal health officials – and fentanyl was involved in most of these deaths. 

Senior author Therese Kosten, PhD, director of the UH Developmental, Cognitive & Behavioral Neuroscience program, calls the new fentanyl vaccine a potential “game changer.”

“Fentanyl use and overdose is a particular treatment challenge that is not adequately addressed with current medications because of its pharmacodynamics, and managing acute overdose with the short-acting naloxone [Narcan] is not appropriately effective as multiple doses of naloxone are often needed to reverse fentanyl’s fatal effects,” said Dr. Kosten.

Funding for the study was provided by the Department of Defense through the Alcohol and Substance Abuse Disorders Program managed by RTI International’s Pharmacotherapies for Alcohol and Substance Use Disorders Alliance, which has funded Dr. Haile’s lab for several years to develop the anti-fentanyl vaccine. The authors have no relevant conflicts of interest. A provisional patent has been submitted by the University of Houston on behalf of four of the investigators containing technology related to the fentanyl vaccine.

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

After recovery from acute infection with SARS-CoV-2, major stressful life events such as the death of a loved one or financial insecurity can have a significant impact on the development of long COVID symptoms, new research suggests.

Major life stressors in the year after hospital discharge for COVID-19 are “strongly predictive of a lot of the important outcomes that people may face after COVID,” lead investigator Jennifer A. Frontera, MD, a professor in the department of neurology at New York University Langone Health, said in an interview.

These outcomes include depression, brain fog, fatigue, trouble sleeping, and other long COVID symptoms.

The findings were published online in the Journal of the Neurological Sciences.
 

Major stressful events common

Dr. Frontera and the NYU Neurology COVID-19 study team evaluated 451 adults who survived a COVID hospital stay. Of these, 383 completed a 6-month follow-up, 242 completed a 12-month follow-up, and 174 completed follow-up at both time points. 

Within 1 year of discharge, 77 (17%) patients died and 51% suffered a major stressful life event.

In multivariable analyses, major life stressors – including financial insecurity, food insecurity, death of a close contact, and new disability – were strong independent predictors of disability, trouble with activities of daily living, depression, fatigue, sleep problems, and prolonged post-acute COVID symptoms. The adjusted odds ratios for these outcomes ranged from 2.5 to 20.8. 

The research also confirmed the contribution of traditional risk factors for long COVID symptoms, as shown in past studies. These include older age, poor pre-COVID functional status, and more severe initial COVID-19 infection.

Long-term sequelae of COVID are increasingly recognized as major public health issues. 

It has been estimated that roughly 16 million U.S. adults aged 18-65 years ave long COVID, with the often debilitating symptoms keeping up to 4 million out of work. 
 

Holistic approach

Dr. Frontera said it’s important to realize that “sleep, fatigue, anxiety, depression, even cognition are so interwoven with each other that anything that impacts any one of them could have repercussions on the other.”

She added that it “certainly makes sense that there is an interplay or even a bidirectional relationship between the stressors that people face and how well they can recover after COVID.”

Therapies that lessen the trauma of the most stress-inducing life events need to be a central part of treatment for long COVID, with more research needed to validate the best approaches, Dr. Frontera said.

She also noted that social services or case management resources may be able to help address at least some of the stressors that individuals are under – and it is important to refer them to these resources. Referral to mental health services is also important.

“I think it’s really important to take a holistic approach and try to deal with whatever the problem may be,” said Dr. Frontera.

“I’m a neurologist, but as part of my evaluation, I really need to address if there are life stressors or mental health issues that may be impacting this person’s function,” she added.

The study had no commercial funding. The investigators reported no relevant financial relationships.

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

After recovery from acute infection with SARS-CoV-2, major stressful life events such as the death of a loved one or financial insecurity can have a significant impact on the development of long COVID symptoms, new research suggests.

Major life stressors in the year after hospital discharge for COVID-19 are “strongly predictive of a lot of the important outcomes that people may face after COVID,” lead investigator Jennifer A. Frontera, MD, a professor in the department of neurology at New York University Langone Health, said in an interview.

These outcomes include depression, brain fog, fatigue, trouble sleeping, and other long COVID symptoms.

The findings were published online in the Journal of the Neurological Sciences.
 

Major stressful events common

Dr. Frontera and the NYU Neurology COVID-19 study team evaluated 451 adults who survived a COVID hospital stay. Of these, 383 completed a 6-month follow-up, 242 completed a 12-month follow-up, and 174 completed follow-up at both time points. 

Within 1 year of discharge, 77 (17%) patients died and 51% suffered a major stressful life event.

In multivariable analyses, major life stressors – including financial insecurity, food insecurity, death of a close contact, and new disability – were strong independent predictors of disability, trouble with activities of daily living, depression, fatigue, sleep problems, and prolonged post-acute COVID symptoms. The adjusted odds ratios for these outcomes ranged from 2.5 to 20.8. 

The research also confirmed the contribution of traditional risk factors for long COVID symptoms, as shown in past studies. These include older age, poor pre-COVID functional status, and more severe initial COVID-19 infection.

Long-term sequelae of COVID are increasingly recognized as major public health issues. 

It has been estimated that roughly 16 million U.S. adults aged 18-65 years ave long COVID, with the often debilitating symptoms keeping up to 4 million out of work. 
 

Holistic approach

Dr. Frontera said it’s important to realize that “sleep, fatigue, anxiety, depression, even cognition are so interwoven with each other that anything that impacts any one of them could have repercussions on the other.”

She added that it “certainly makes sense that there is an interplay or even a bidirectional relationship between the stressors that people face and how well they can recover after COVID.”

Therapies that lessen the trauma of the most stress-inducing life events need to be a central part of treatment for long COVID, with more research needed to validate the best approaches, Dr. Frontera said.

She also noted that social services or case management resources may be able to help address at least some of the stressors that individuals are under – and it is important to refer them to these resources. Referral to mental health services is also important.

“I think it’s really important to take a holistic approach and try to deal with whatever the problem may be,” said Dr. Frontera.

“I’m a neurologist, but as part of my evaluation, I really need to address if there are life stressors or mental health issues that may be impacting this person’s function,” she added.

The study had no commercial funding. The investigators reported no relevant financial relationships.

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

After recovery from acute infection with SARS-CoV-2, major stressful life events such as the death of a loved one or financial insecurity can have a significant impact on the development of long COVID symptoms, new research suggests.

Major life stressors in the year after hospital discharge for COVID-19 are “strongly predictive of a lot of the important outcomes that people may face after COVID,” lead investigator Jennifer A. Frontera, MD, a professor in the department of neurology at New York University Langone Health, said in an interview.

These outcomes include depression, brain fog, fatigue, trouble sleeping, and other long COVID symptoms.

The findings were published online in the Journal of the Neurological Sciences.
 

Major stressful events common

Dr. Frontera and the NYU Neurology COVID-19 study team evaluated 451 adults who survived a COVID hospital stay. Of these, 383 completed a 6-month follow-up, 242 completed a 12-month follow-up, and 174 completed follow-up at both time points. 

Within 1 year of discharge, 77 (17%) patients died and 51% suffered a major stressful life event.

In multivariable analyses, major life stressors – including financial insecurity, food insecurity, death of a close contact, and new disability – were strong independent predictors of disability, trouble with activities of daily living, depression, fatigue, sleep problems, and prolonged post-acute COVID symptoms. The adjusted odds ratios for these outcomes ranged from 2.5 to 20.8. 

The research also confirmed the contribution of traditional risk factors for long COVID symptoms, as shown in past studies. These include older age, poor pre-COVID functional status, and more severe initial COVID-19 infection.

Long-term sequelae of COVID are increasingly recognized as major public health issues. 

It has been estimated that roughly 16 million U.S. adults aged 18-65 years ave long COVID, with the often debilitating symptoms keeping up to 4 million out of work. 
 

Holistic approach

Dr. Frontera said it’s important to realize that “sleep, fatigue, anxiety, depression, even cognition are so interwoven with each other that anything that impacts any one of them could have repercussions on the other.”

She added that it “certainly makes sense that there is an interplay or even a bidirectional relationship between the stressors that people face and how well they can recover after COVID.”

Therapies that lessen the trauma of the most stress-inducing life events need to be a central part of treatment for long COVID, with more research needed to validate the best approaches, Dr. Frontera said.

She also noted that social services or case management resources may be able to help address at least some of the stressors that individuals are under – and it is important to refer them to these resources. Referral to mental health services is also important.

“I think it’s really important to take a holistic approach and try to deal with whatever the problem may be,” said Dr. Frontera.

“I’m a neurologist, but as part of my evaluation, I really need to address if there are life stressors or mental health issues that may be impacting this person’s function,” she added.

The study had no commercial funding. The investigators reported no relevant financial relationships.

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