Neurology Reviews

Rates of premature return to play (RTP) among student athletes following a sport-related concussion (SRC) have dropped substantially since 2011, according to a recent chart review. Rates of premature return to learn (RTL) are essentially unchanged, however.

“Delay in recovery is the major reason why it’s important not to RTL or RTP prematurely,” said James Carson, MD, associate professor of family and community medicine, University of Toronto.

“That delay in recovery only sets students further back in terms of the stress they get from being delayed with their schoolwork – they could lose their year in school, lose all their social contacts. So, there are a number of psychosocial issues that come into play if recovery is delayed, and that is what premature RTL and premature RTP will do – they delay the student’s recovery,” he emphasized.

The study was published in Canadian Family Physician.
 

Differences by sex

The study involved 241 students who had 258 distinct cases of SRC. The researchers defined premature RTP and RTL as chart records documenting the relapse, recurrence, or worsening of concussion symptoms that accompanied the patient’s RTP or RTL. Between 2011 and 2016, 26.7% of students had evidence of premature RTP, while 42.6% of them had evidence of premature RTL, the authors noted.

Compared with findings from an earlier survey of data from 2006 to 2011, the incidence of premature RTP dropped by 38.6% (P = .0003). In contrast, symptoms associated with premature RTL dropped by only 4.7% from the previous survey. This change was not statistically significant.

There was also a significant difference between males and females in the proportion of SRC cases with relapse of symptoms. Relapse occurred in 43.4% of female athletes with SRC versus 29.7% of male athletes with SRC (P = .023).

Female athletes also had significantly longer times before being cleared for RTP. The mean time was 74.5 days for females, compared with a mean of 42.3 days for male athletes (P < .001). “The median time to RTP clearance was nearly double [for female athletes] at 49 days versus 25 days [for male athletes],” wrote the authors.

The rate of premature RTL was also higher among secondary school students (48.8%), compared with 28% among elementary students and 42% among postsecondary students.
 

More concussions coming?

Before the first consensus conference, organized by the Concussion in Sport Group in 2001, management of concussion was based on rating and grading scales that had no medical evidence to support them, said Dr. Carson. After the consensus conference, it was recommended that physicians manage each concussion individually and, when it came to RTP, recommendations were based upon symptom resolution.

In contrast, there was nothing in the literature regarding how student athletes who sustain a concussion should RTL. Some schools made generous accommodations, and others none. This situation changed around 2011, when experts started publishing data about how better to accommodate student athletes who have a temporary disability for which schools need to introduce temporary accommodations to help them recover.

“Recommendations for RTP essentially had a 12-year head-start,” Dr. Carson emphasized, “and RTL had a much slower start.” Unfortunately, Dr. Carson foresees more athletes sustaining concussions as pandemic restrictions ease over the next few months. “As athletes RTP after the pandemic, they just will not be in game shape,” he said.

“In other words, athletes may not have the neuromuscular control to avoid these injuries as easily,” he added. Worse, athletes may not realize they are not quite ready to return to the expected level of participation so quickly. “I believe this scenario will lead to more concussions that will be difficult to manage in the context of an already strained health care system,” said Dr. Carson.

A limitation of the study was that it was difficult to assess whether all patients followed medical advice consistently.
 

“Very positive shifts”

Commenting on the findings, Nick Reed, PhD, Canada research chair in pediatric concussion and associate professor of occupational science and occupational therapy, University of Toronto, said that sports medicine physicians are seeing “very positive shifts” in concussion awareness and related behaviors such as providing education, support, and accommodations to students within the school environment. “More and more teachers are seeking education to learn what a concussion is and what to do to best support their students with concussion,” he said. Dr. Reed was not involved in the current study.

Indeed, this increasing awareness led to the development of a concussion education tool for teachers – SCHOOLFirst – although Dr. Reed did acknowledge that not all teachers have either the knowledge or the resources they need to optimally support their students with concussion. In the meantime, to reduce the risk of injury, Dr. Reed stressed that it is important for students to wear equipment appropriate for the game being played and to play by the rules.

“It is key to play sports in a way that is fair and respectful and not [engage] in behaviors with the intent of injuring an opponent,” he stressed. It is also important for athletes themselves to know the signs and symptoms of concussion and, if they think they have a concussion, to immediately stop playing, report how they are feeling to a coach, teacher, or parent, and to seek medical assessment to determine if they have a concussion or not.

“The key here is to focus on what the athlete can do after a concussion rather than what they can’t do,” Dr. Reed said. After even a few days of complete rest, students with a concussion can gradually introduce low levels of physical and cognitive activity that won’t make their symptoms worse. This activity can include going back to school with temporary accommodations in place, such as shorter school days and increased rest breaks. “When returning to school and to sport after a concussion, it is important to follow a stepwise and gradual return to activities so that you aren’t doing too much too fast,” Dr. Reed emphasized.

The study was conducted without external funding. Dr. Carson and Dr. Reed reported no conflicts of interest. 

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

Rates of premature return to play (RTP) among student athletes following a sport-related concussion (SRC) have dropped substantially since 2011, according to a recent chart review. Rates of premature return to learn (RTL) are essentially unchanged, however.

“Delay in recovery is the major reason why it’s important not to RTL or RTP prematurely,” said James Carson, MD, associate professor of family and community medicine, University of Toronto.

“That delay in recovery only sets students further back in terms of the stress they get from being delayed with their schoolwork – they could lose their year in school, lose all their social contacts. So, there are a number of psychosocial issues that come into play if recovery is delayed, and that is what premature RTL and premature RTP will do – they delay the student’s recovery,” he emphasized.

The study was published in Canadian Family Physician.
 

Differences by sex

The study involved 241 students who had 258 distinct cases of SRC. The researchers defined premature RTP and RTL as chart records documenting the relapse, recurrence, or worsening of concussion symptoms that accompanied the patient’s RTP or RTL. Between 2011 and 2016, 26.7% of students had evidence of premature RTP, while 42.6% of them had evidence of premature RTL, the authors noted.

Compared with findings from an earlier survey of data from 2006 to 2011, the incidence of premature RTP dropped by 38.6% (P = .0003). In contrast, symptoms associated with premature RTL dropped by only 4.7% from the previous survey. This change was not statistically significant.

There was also a significant difference between males and females in the proportion of SRC cases with relapse of symptoms. Relapse occurred in 43.4% of female athletes with SRC versus 29.7% of male athletes with SRC (P = .023).

Female athletes also had significantly longer times before being cleared for RTP. The mean time was 74.5 days for females, compared with a mean of 42.3 days for male athletes (P < .001). “The median time to RTP clearance was nearly double [for female athletes] at 49 days versus 25 days [for male athletes],” wrote the authors.

The rate of premature RTL was also higher among secondary school students (48.8%), compared with 28% among elementary students and 42% among postsecondary students.
 

More concussions coming?

Before the first consensus conference, organized by the Concussion in Sport Group in 2001, management of concussion was based on rating and grading scales that had no medical evidence to support them, said Dr. Carson. After the consensus conference, it was recommended that physicians manage each concussion individually and, when it came to RTP, recommendations were based upon symptom resolution.

In contrast, there was nothing in the literature regarding how student athletes who sustain a concussion should RTL. Some schools made generous accommodations, and others none. This situation changed around 2011, when experts started publishing data about how better to accommodate student athletes who have a temporary disability for which schools need to introduce temporary accommodations to help them recover.

“Recommendations for RTP essentially had a 12-year head-start,” Dr. Carson emphasized, “and RTL had a much slower start.” Unfortunately, Dr. Carson foresees more athletes sustaining concussions as pandemic restrictions ease over the next few months. “As athletes RTP after the pandemic, they just will not be in game shape,” he said.

“In other words, athletes may not have the neuromuscular control to avoid these injuries as easily,” he added. Worse, athletes may not realize they are not quite ready to return to the expected level of participation so quickly. “I believe this scenario will lead to more concussions that will be difficult to manage in the context of an already strained health care system,” said Dr. Carson.

A limitation of the study was that it was difficult to assess whether all patients followed medical advice consistently.
 

“Very positive shifts”

Commenting on the findings, Nick Reed, PhD, Canada research chair in pediatric concussion and associate professor of occupational science and occupational therapy, University of Toronto, said that sports medicine physicians are seeing “very positive shifts” in concussion awareness and related behaviors such as providing education, support, and accommodations to students within the school environment. “More and more teachers are seeking education to learn what a concussion is and what to do to best support their students with concussion,” he said. Dr. Reed was not involved in the current study.

Indeed, this increasing awareness led to the development of a concussion education tool for teachers – SCHOOLFirst – although Dr. Reed did acknowledge that not all teachers have either the knowledge or the resources they need to optimally support their students with concussion. In the meantime, to reduce the risk of injury, Dr. Reed stressed that it is important for students to wear equipment appropriate for the game being played and to play by the rules.

“It is key to play sports in a way that is fair and respectful and not [engage] in behaviors with the intent of injuring an opponent,” he stressed. It is also important for athletes themselves to know the signs and symptoms of concussion and, if they think they have a concussion, to immediately stop playing, report how they are feeling to a coach, teacher, or parent, and to seek medical assessment to determine if they have a concussion or not.

“The key here is to focus on what the athlete can do after a concussion rather than what they can’t do,” Dr. Reed said. After even a few days of complete rest, students with a concussion can gradually introduce low levels of physical and cognitive activity that won’t make their symptoms worse. This activity can include going back to school with temporary accommodations in place, such as shorter school days and increased rest breaks. “When returning to school and to sport after a concussion, it is important to follow a stepwise and gradual return to activities so that you aren’t doing too much too fast,” Dr. Reed emphasized.

The study was conducted without external funding. Dr. Carson and Dr. Reed reported no conflicts of interest. 

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

Rates of premature return to play (RTP) among student athletes following a sport-related concussion (SRC) have dropped substantially since 2011, according to a recent chart review. Rates of premature return to learn (RTL) are essentially unchanged, however.

“Delay in recovery is the major reason why it’s important not to RTL or RTP prematurely,” said James Carson, MD, associate professor of family and community medicine, University of Toronto.

“That delay in recovery only sets students further back in terms of the stress they get from being delayed with their schoolwork – they could lose their year in school, lose all their social contacts. So, there are a number of psychosocial issues that come into play if recovery is delayed, and that is what premature RTL and premature RTP will do – they delay the student’s recovery,” he emphasized.

The study was published in Canadian Family Physician.
 

Differences by sex

The study involved 241 students who had 258 distinct cases of SRC. The researchers defined premature RTP and RTL as chart records documenting the relapse, recurrence, or worsening of concussion symptoms that accompanied the patient’s RTP or RTL. Between 2011 and 2016, 26.7% of students had evidence of premature RTP, while 42.6% of them had evidence of premature RTL, the authors noted.

Compared with findings from an earlier survey of data from 2006 to 2011, the incidence of premature RTP dropped by 38.6% (P = .0003). In contrast, symptoms associated with premature RTL dropped by only 4.7% from the previous survey. This change was not statistically significant.

There was also a significant difference between males and females in the proportion of SRC cases with relapse of symptoms. Relapse occurred in 43.4% of female athletes with SRC versus 29.7% of male athletes with SRC (P = .023).

Female athletes also had significantly longer times before being cleared for RTP. The mean time was 74.5 days for females, compared with a mean of 42.3 days for male athletes (P < .001). “The median time to RTP clearance was nearly double [for female athletes] at 49 days versus 25 days [for male athletes],” wrote the authors.

The rate of premature RTL was also higher among secondary school students (48.8%), compared with 28% among elementary students and 42% among postsecondary students.
 

More concussions coming?

Before the first consensus conference, organized by the Concussion in Sport Group in 2001, management of concussion was based on rating and grading scales that had no medical evidence to support them, said Dr. Carson. After the consensus conference, it was recommended that physicians manage each concussion individually and, when it came to RTP, recommendations were based upon symptom resolution.

In contrast, there was nothing in the literature regarding how student athletes who sustain a concussion should RTL. Some schools made generous accommodations, and others none. This situation changed around 2011, when experts started publishing data about how better to accommodate student athletes who have a temporary disability for which schools need to introduce temporary accommodations to help them recover.

“Recommendations for RTP essentially had a 12-year head-start,” Dr. Carson emphasized, “and RTL had a much slower start.” Unfortunately, Dr. Carson foresees more athletes sustaining concussions as pandemic restrictions ease over the next few months. “As athletes RTP after the pandemic, they just will not be in game shape,” he said.

“In other words, athletes may not have the neuromuscular control to avoid these injuries as easily,” he added. Worse, athletes may not realize they are not quite ready to return to the expected level of participation so quickly. “I believe this scenario will lead to more concussions that will be difficult to manage in the context of an already strained health care system,” said Dr. Carson.

A limitation of the study was that it was difficult to assess whether all patients followed medical advice consistently.
 

“Very positive shifts”

Commenting on the findings, Nick Reed, PhD, Canada research chair in pediatric concussion and associate professor of occupational science and occupational therapy, University of Toronto, said that sports medicine physicians are seeing “very positive shifts” in concussion awareness and related behaviors such as providing education, support, and accommodations to students within the school environment. “More and more teachers are seeking education to learn what a concussion is and what to do to best support their students with concussion,” he said. Dr. Reed was not involved in the current study.

Indeed, this increasing awareness led to the development of a concussion education tool for teachers – SCHOOLFirst – although Dr. Reed did acknowledge that not all teachers have either the knowledge or the resources they need to optimally support their students with concussion. In the meantime, to reduce the risk of injury, Dr. Reed stressed that it is important for students to wear equipment appropriate for the game being played and to play by the rules.

“It is key to play sports in a way that is fair and respectful and not [engage] in behaviors with the intent of injuring an opponent,” he stressed. It is also important for athletes themselves to know the signs and symptoms of concussion and, if they think they have a concussion, to immediately stop playing, report how they are feeling to a coach, teacher, or parent, and to seek medical assessment to determine if they have a concussion or not.

“The key here is to focus on what the athlete can do after a concussion rather than what they can’t do,” Dr. Reed said. After even a few days of complete rest, students with a concussion can gradually introduce low levels of physical and cognitive activity that won’t make their symptoms worse. This activity can include going back to school with temporary accommodations in place, such as shorter school days and increased rest breaks. “When returning to school and to sport after a concussion, it is important to follow a stepwise and gradual return to activities so that you aren’t doing too much too fast,” Dr. Reed emphasized.

The study was conducted without external funding. Dr. Carson and Dr. Reed reported no conflicts of interest. 

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

The risk for dementia goes up in patients with atrial fibrillation (AFib), but some evidence suggests that risk can be blunted with therapies that restore sinus rhythm. But a new cohort study suggests that the treatment effect’s magnitude might depend on the rhythm control strategy. It hinted that AFib catheter ablation might be more effective than pharmacologic rhythm control alone at cutting the risk for dementia.

The case-matched study of more than 38,000 adults with AFib saw a 41% reduction (P < .0001) in risk for dementia among those who underwent catheter ablation after attempted rhythm control with antiarrhythmic drugs (AAD), compared with those managed with pharmacologic rhythm control therapy alone.

The observational study comprising 20 years of data comes with big limitations and can’t say for sure whether catheter ablation is better than AAD alone at cutting the dementia risk in AFib. But it and other evidence support the idea, which has yet to be explored in a randomized fashion.

In a secondary finding, the analysis showed a similar reduction in dementia risk from catheter ablation, compared with AAD, in women and in men by 40% and 45%, respectively (P < .0001 for both). The findings are particularly relevant “given the higher life-long risk of dementia among women and the lower likelihood that women will be offered ablation, which has been demonstrated repeatedly,” Emily P. Zeitler, MD, MHS, Dartmouth-Hitchcock Medical Center, Lebanon, N.H., said in an interview. “I think this is another reason to try to be more generous in offering ablation to women.”

Management of AFib certainly evolved in important ways from 2000 to 2021, the period covered by the study. But a sensitivity analysis based on data from 2010 to 2021 showed “no meaningful differences” in the results, said Dr. Zeitler, who is slated to present the findings at the annual scientific sessions of the Heart Rhythm Society.

Dr. Zeitler acknowledged that the observational study, even with its propensity-matched ablation and AAD cohorts, can only hint at a preference for ablation over AAD for lowering risk for AFib-associated dementia. “We know there’s unmeasured and unfixable confounding between those two groups, so we see this really as hypothesis-generating.”

It was “a well-done analysis,” and the conclusion that the dementia risk was lower with catheter ablation is “absolutely correct,” but only as far as the study and its limitations allow, agreed David Conen, MD, MPH, McMaster University, Hamilton, Ont., who is not a coauthor.

“Even with propensity matching, you can get rid of some sorts of confounding, but you can never get rid of all selection bias issues.” That, he said when interviewed, takes randomized trials.

Dr. Conen, who is studying cognitive decline in AFib as a SWISS-AF trial principal investigator, pointed to a secondary finding of the analysis as evidence for such confounding. He said the ablation group’s nearly 50% drop (P < .0001) in competing risk for death, compared with patients managed with AAD, isn’t plausible.

The finding “strongly suggests these people were healthier and that there’s some sort of selection bias. They were at lower risk of death, they were at lower risk of dementia, and they were probably also at lower risk of stroke, myocardial infarction, thrombosis, and cancer because they were just probably a little healthier than the others,” Dr. Conen said. The ablation and AAD groups “were two very different populations from the get-go.”

The analysis was based on U.S. insurance and Medicare claims data from AFib patients who either underwent catheter ablation after at least one AAD trial or filled prescriptions for at least two different antiarrhythmic agents in the year after AFib diagnosis. Patients with history of dementia, catheter or surgical AFib ablation, or a valve procedure were excluded.

The ablation and AAD-only groups each consisted of 19,066 patients after propensity matching, and the groups were balanced with respect to age, sex, type of insurance, CHA2DS2-VASc scores, and use of renin-angiotensin system inhibitors, oral anticoagulants, and antiplatelets.

The overall risk for dementia was 1.9% for the ablation group and 3.3% for AAD-only patients (hazard ratio, 0.59; 95% confidence interval, 0.52-0.67). Corresponding HRs by sex were 0.55 (95% CI, 0.46-0.66) for men and 0.60 (95% CI, 0.50-0.72) for women.

The competing risk for death was also significantly decreased in the ablation group (HR, 0.51; 95% CI, 0.46-0.55).

Dr. Zeitler pointed to a randomized trial now in the early stages called Neurocognition and Greater Maintenance of Sinus Rhythm in Atrial Fibrillation, or NOGGIN-AF, which will explore relationships between rhythm control therapy and dementia in patients with AFib, whether catheter ablation or AAD can mitigate that risk, and whether either strategy works better than the other, among other goals.

“I’m optimistic,” she said, “and I think it’s going to add to the growing motivations to get patients ablated more quickly and more broadly.”

The analysis was funded by Biosense-Webster. Dr. Zeitler disclosed consulting for Biosense-Webster and Arena Pharmaceuticals (now Pfizer); fees for speaking from Medtronic; and receiving research support from Boston Scientific, Sanofi, and Biosense-Webster. Dr. Conen has previously reported receiving speaker fees from Servier Canada.

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

The risk for dementia goes up in patients with atrial fibrillation (AFib), but some evidence suggests that risk can be blunted with therapies that restore sinus rhythm. But a new cohort study suggests that the treatment effect’s magnitude might depend on the rhythm control strategy. It hinted that AFib catheter ablation might be more effective than pharmacologic rhythm control alone at cutting the risk for dementia.

The case-matched study of more than 38,000 adults with AFib saw a 41% reduction (P < .0001) in risk for dementia among those who underwent catheter ablation after attempted rhythm control with antiarrhythmic drugs (AAD), compared with those managed with pharmacologic rhythm control therapy alone.

The observational study comprising 20 years of data comes with big limitations and can’t say for sure whether catheter ablation is better than AAD alone at cutting the dementia risk in AFib. But it and other evidence support the idea, which has yet to be explored in a randomized fashion.

In a secondary finding, the analysis showed a similar reduction in dementia risk from catheter ablation, compared with AAD, in women and in men by 40% and 45%, respectively (P < .0001 for both). The findings are particularly relevant “given the higher life-long risk of dementia among women and the lower likelihood that women will be offered ablation, which has been demonstrated repeatedly,” Emily P. Zeitler, MD, MHS, Dartmouth-Hitchcock Medical Center, Lebanon, N.H., said in an interview. “I think this is another reason to try to be more generous in offering ablation to women.”

Management of AFib certainly evolved in important ways from 2000 to 2021, the period covered by the study. But a sensitivity analysis based on data from 2010 to 2021 showed “no meaningful differences” in the results, said Dr. Zeitler, who is slated to present the findings at the annual scientific sessions of the Heart Rhythm Society.

Dr. Zeitler acknowledged that the observational study, even with its propensity-matched ablation and AAD cohorts, can only hint at a preference for ablation over AAD for lowering risk for AFib-associated dementia. “We know there’s unmeasured and unfixable confounding between those two groups, so we see this really as hypothesis-generating.”

It was “a well-done analysis,” and the conclusion that the dementia risk was lower with catheter ablation is “absolutely correct,” but only as far as the study and its limitations allow, agreed David Conen, MD, MPH, McMaster University, Hamilton, Ont., who is not a coauthor.

“Even with propensity matching, you can get rid of some sorts of confounding, but you can never get rid of all selection bias issues.” That, he said when interviewed, takes randomized trials.

Dr. Conen, who is studying cognitive decline in AFib as a SWISS-AF trial principal investigator, pointed to a secondary finding of the analysis as evidence for such confounding. He said the ablation group’s nearly 50% drop (P < .0001) in competing risk for death, compared with patients managed with AAD, isn’t plausible.

The finding “strongly suggests these people were healthier and that there’s some sort of selection bias. They were at lower risk of death, they were at lower risk of dementia, and they were probably also at lower risk of stroke, myocardial infarction, thrombosis, and cancer because they were just probably a little healthier than the others,” Dr. Conen said. The ablation and AAD groups “were two very different populations from the get-go.”

The analysis was based on U.S. insurance and Medicare claims data from AFib patients who either underwent catheter ablation after at least one AAD trial or filled prescriptions for at least two different antiarrhythmic agents in the year after AFib diagnosis. Patients with history of dementia, catheter or surgical AFib ablation, or a valve procedure were excluded.

The ablation and AAD-only groups each consisted of 19,066 patients after propensity matching, and the groups were balanced with respect to age, sex, type of insurance, CHA2DS2-VASc scores, and use of renin-angiotensin system inhibitors, oral anticoagulants, and antiplatelets.

The overall risk for dementia was 1.9% for the ablation group and 3.3% for AAD-only patients (hazard ratio, 0.59; 95% confidence interval, 0.52-0.67). Corresponding HRs by sex were 0.55 (95% CI, 0.46-0.66) for men and 0.60 (95% CI, 0.50-0.72) for women.

The competing risk for death was also significantly decreased in the ablation group (HR, 0.51; 95% CI, 0.46-0.55).

Dr. Zeitler pointed to a randomized trial now in the early stages called Neurocognition and Greater Maintenance of Sinus Rhythm in Atrial Fibrillation, or NOGGIN-AF, which will explore relationships between rhythm control therapy and dementia in patients with AFib, whether catheter ablation or AAD can mitigate that risk, and whether either strategy works better than the other, among other goals.

“I’m optimistic,” she said, “and I think it’s going to add to the growing motivations to get patients ablated more quickly and more broadly.”

The analysis was funded by Biosense-Webster. Dr. Zeitler disclosed consulting for Biosense-Webster and Arena Pharmaceuticals (now Pfizer); fees for speaking from Medtronic; and receiving research support from Boston Scientific, Sanofi, and Biosense-Webster. Dr. Conen has previously reported receiving speaker fees from Servier Canada.

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

The risk for dementia goes up in patients with atrial fibrillation (AFib), but some evidence suggests that risk can be blunted with therapies that restore sinus rhythm. But a new cohort study suggests that the treatment effect’s magnitude might depend on the rhythm control strategy. It hinted that AFib catheter ablation might be more effective than pharmacologic rhythm control alone at cutting the risk for dementia.

The case-matched study of more than 38,000 adults with AFib saw a 41% reduction (P < .0001) in risk for dementia among those who underwent catheter ablation after attempted rhythm control with antiarrhythmic drugs (AAD), compared with those managed with pharmacologic rhythm control therapy alone.

The observational study comprising 20 years of data comes with big limitations and can’t say for sure whether catheter ablation is better than AAD alone at cutting the dementia risk in AFib. But it and other evidence support the idea, which has yet to be explored in a randomized fashion.

In a secondary finding, the analysis showed a similar reduction in dementia risk from catheter ablation, compared with AAD, in women and in men by 40% and 45%, respectively (P < .0001 for both). The findings are particularly relevant “given the higher life-long risk of dementia among women and the lower likelihood that women will be offered ablation, which has been demonstrated repeatedly,” Emily P. Zeitler, MD, MHS, Dartmouth-Hitchcock Medical Center, Lebanon, N.H., said in an interview. “I think this is another reason to try to be more generous in offering ablation to women.”

Management of AFib certainly evolved in important ways from 2000 to 2021, the period covered by the study. But a sensitivity analysis based on data from 2010 to 2021 showed “no meaningful differences” in the results, said Dr. Zeitler, who is slated to present the findings at the annual scientific sessions of the Heart Rhythm Society.

Dr. Zeitler acknowledged that the observational study, even with its propensity-matched ablation and AAD cohorts, can only hint at a preference for ablation over AAD for lowering risk for AFib-associated dementia. “We know there’s unmeasured and unfixable confounding between those two groups, so we see this really as hypothesis-generating.”

It was “a well-done analysis,” and the conclusion that the dementia risk was lower with catheter ablation is “absolutely correct,” but only as far as the study and its limitations allow, agreed David Conen, MD, MPH, McMaster University, Hamilton, Ont., who is not a coauthor.

“Even with propensity matching, you can get rid of some sorts of confounding, but you can never get rid of all selection bias issues.” That, he said when interviewed, takes randomized trials.

Dr. Conen, who is studying cognitive decline in AFib as a SWISS-AF trial principal investigator, pointed to a secondary finding of the analysis as evidence for such confounding. He said the ablation group’s nearly 50% drop (P < .0001) in competing risk for death, compared with patients managed with AAD, isn’t plausible.

The finding “strongly suggests these people were healthier and that there’s some sort of selection bias. They were at lower risk of death, they were at lower risk of dementia, and they were probably also at lower risk of stroke, myocardial infarction, thrombosis, and cancer because they were just probably a little healthier than the others,” Dr. Conen said. The ablation and AAD groups “were two very different populations from the get-go.”

The analysis was based on U.S. insurance and Medicare claims data from AFib patients who either underwent catheter ablation after at least one AAD trial or filled prescriptions for at least two different antiarrhythmic agents in the year after AFib diagnosis. Patients with history of dementia, catheter or surgical AFib ablation, or a valve procedure were excluded.

The ablation and AAD-only groups each consisted of 19,066 patients after propensity matching, and the groups were balanced with respect to age, sex, type of insurance, CHA2DS2-VASc scores, and use of renin-angiotensin system inhibitors, oral anticoagulants, and antiplatelets.

The overall risk for dementia was 1.9% for the ablation group and 3.3% for AAD-only patients (hazard ratio, 0.59; 95% confidence interval, 0.52-0.67). Corresponding HRs by sex were 0.55 (95% CI, 0.46-0.66) for men and 0.60 (95% CI, 0.50-0.72) for women.

The competing risk for death was also significantly decreased in the ablation group (HR, 0.51; 95% CI, 0.46-0.55).

Dr. Zeitler pointed to a randomized trial now in the early stages called Neurocognition and Greater Maintenance of Sinus Rhythm in Atrial Fibrillation, or NOGGIN-AF, which will explore relationships between rhythm control therapy and dementia in patients with AFib, whether catheter ablation or AAD can mitigate that risk, and whether either strategy works better than the other, among other goals.

“I’m optimistic,” she said, “and I think it’s going to add to the growing motivations to get patients ablated more quickly and more broadly.”

The analysis was funded by Biosense-Webster. Dr. Zeitler disclosed consulting for Biosense-Webster and Arena Pharmaceuticals (now Pfizer); fees for speaking from Medtronic; and receiving research support from Boston Scientific, Sanofi, and Biosense-Webster. Dr. Conen has previously reported receiving speaker fees from Servier Canada.

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

Mild traumatic brain injury (TBI) is linked to a significantly increased risk for a host of subsequent cardiovascular, endocrine, neurologic, and psychiatric disorders, new research shows.

Incidence of hypertension, coronary heart disease, diabetes, stroke, depression, and dementia all began to increase soon after the brain injury and persisted over a decade in both mild and moderate to severe TBI.

Researchers found the multisystem comorbidities in all age groups, including in patients as young as 18. They also found that patients who developed multiple postinjury problems had higher mortality during the decade-long follow-up.

The findings suggest patients with TBI may require longer follow-up and proactive screening for multisystem disease, regardless of age or injury severity.

“The fact that both patients with mild and moderate to severe injuries both had long-term ongoing associations with comorbidities that continued over time and that they are cardiovascular, endocrine, neurologic, and behavioral health oriented was pretty striking,” study author Ross Zafonte, DO, PhD, president of Spaulding Rehab Hospital and professor and chair of physical medicine and rehab at Harvard Medical School, both in Boston, told this news organization.

The study was published online in JAMA Network Open.
 

Injury severity not a factor

An estimated 2.8 million individuals in the United States experience TBI every year. Worldwide, the figure may be as high as 74 million.

Studies have long suggested a link between brain injury and subsequent neurologic disorders, but research suggesting a possible link to cardiovascular and endocrine problems has recently gained attention.

Building on a 2021 study that showed increased incidence of cardiovascular issues following a concussion, the researchers examined medical records of previously healthy patients treated for TBI between 2000 and 2015 who also had at least 1 follow-up visit between 6 months and 10 years after the initial injury.

Researchers analyzed data from 13,053 individuals – 4,351 with mild injury (mTBI), 4351 with moderate to severe injury (msTBI), and 4351 with no TBI. The most common cause of injury was a fall. Patients with sports-related injuries were excluded.

Incidence of hypertension was significantly higher among patients with mTBI (hazard ratio, 2.5; 95% confidence interval, 2.1-2.9) and msTBI (HR, 2.4; 95% CI, 2.0-2.9), compared with the unaffected group. Risk for other cardiovascular problems, including hyperlipidemia, obesity, and coronary artery disease, were also higher in the affected groups.

TBI patients also reported higher incidence of endocrine diseases, including diabetes (mTBI: HR, 1.9; 95% CI, 1.4-2.7; msTBI: HR, 1.9; 95% CI, 1.4-2.6). Elevated risk for ischemic stroke or transient ischemic attack was also increased (mTBI: HR, 2.2; 95% CI, 1.4-3.3; msTBI: HR, 3.6; 95% CI, 2.4-5.3).

Regardless of injury severity, patients with TBI had a higher risk for neurologic and psychiatric diseases, particularly depression, dementia, and psychotic disorders. “This tells us that mild TBI is not clean of events,” Dr. Zafonte said.

Surprising rate of comorbidity in youth

Investigators found increased risk for posttrauma comorbidities in all age groups, but researchers were struck by the high rates in younger patients, aged 18-40. Compared with age-matched individuals with no TBI history, hypertension risk was nearly six times higher in those with mTBI (HR, 5.9; 95% CI, 3.9-9.1) and nearly four times higher in patients with msTBI (HR, 3.9; 95% CI, 2.5-6.1).

Rates of hyperlipidemia and diabetes were also higher in younger patients in the mTBI group and posttraumatic seizures and psychiatric disorders were elevated regardless of TBI severity.

Overall, patients with msTBI, but not those with mTBI, were at higher risk for mortality, compared with the unexposed group (432 deaths [9.9%] vs. 250 deaths [5.7%]; P < .001).

“It’s clear that what we may be dealing with is that it holds up even for the younger people,” Dr. Zafonte said. “We used to think brain injury risk is worse in the severe cases, which it is, and it’s worse later on among those who are older, which it is. But our younger folks don’t get away either.”

While the study offers associations between TBI and multisystem health problems, Dr. Zafonte said it’s impossible to say at this point whether the brain injury caused the increased risk for cardiovascular or endocrine problems. Other organ injuries sustained in the trauma may be a contributing factor.

“Further data is needed to elucidate the mechanism and the causative relationships, which we do not have here,” he said.

Many of the postinjury comorbidities emerged a median of 3.5 years after TBI, regardless of severity. But some of the cardiovascular and psychiatric conditions emerged far sooner than that.

That’s important because research suggests less than half of patients with TBI receive follow-up care.

“It does make sense for folks who are interacting with people who’ve had a TBI to be suspicious of medical comorbidities relatively early on, within the first couple of years,” Dr. Zafonte said.

In an invited commentary, Vijay Krishnamoorthy, MD, MPH, PhD, Duke University, Durham, N.C., and Monica S. Vavilala, MD, University of Washington, Seattle, highlight some of the study’s limitations, including a lack of information on comorbidity severity and the lack of a matched group of patients who experienced non-head trauma.

Despite those limitations, the study offers important information on how TBI may affect organs beyond the brain, they noted.

“These observations, if replicated in future studies, raise intriguing implications in the future care of patients with TBI, including heightened chronic disease-screening measures and possibly enhanced guidelines for chronic extracranial organ system care for patients who experience TBI,” Dr. Krishnamoorthy and Dr. Vavilala wrote.

The study received no specific funding. Dr. Zafonte reported having received personal fees from Springer/Demos, serving on scientific advisory boards for Myomo and OnCare and has received funding from the Football Players Health Study at Harvard, funded in part by the National Football League Players Association. Dr. Krishnamoorthy and Dr. Vavilala disclosed no relevant financial relationships.

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

Mild traumatic brain injury (TBI) is linked to a significantly increased risk for a host of subsequent cardiovascular, endocrine, neurologic, and psychiatric disorders, new research shows.

Incidence of hypertension, coronary heart disease, diabetes, stroke, depression, and dementia all began to increase soon after the brain injury and persisted over a decade in both mild and moderate to severe TBI.

Researchers found the multisystem comorbidities in all age groups, including in patients as young as 18. They also found that patients who developed multiple postinjury problems had higher mortality during the decade-long follow-up.

The findings suggest patients with TBI may require longer follow-up and proactive screening for multisystem disease, regardless of age or injury severity.

“The fact that both patients with mild and moderate to severe injuries both had long-term ongoing associations with comorbidities that continued over time and that they are cardiovascular, endocrine, neurologic, and behavioral health oriented was pretty striking,” study author Ross Zafonte, DO, PhD, president of Spaulding Rehab Hospital and professor and chair of physical medicine and rehab at Harvard Medical School, both in Boston, told this news organization.

The study was published online in JAMA Network Open.
 

Injury severity not a factor

An estimated 2.8 million individuals in the United States experience TBI every year. Worldwide, the figure may be as high as 74 million.

Studies have long suggested a link between brain injury and subsequent neurologic disorders, but research suggesting a possible link to cardiovascular and endocrine problems has recently gained attention.

Building on a 2021 study that showed increased incidence of cardiovascular issues following a concussion, the researchers examined medical records of previously healthy patients treated for TBI between 2000 and 2015 who also had at least 1 follow-up visit between 6 months and 10 years after the initial injury.

Researchers analyzed data from 13,053 individuals – 4,351 with mild injury (mTBI), 4351 with moderate to severe injury (msTBI), and 4351 with no TBI. The most common cause of injury was a fall. Patients with sports-related injuries were excluded.

Incidence of hypertension was significantly higher among patients with mTBI (hazard ratio, 2.5; 95% confidence interval, 2.1-2.9) and msTBI (HR, 2.4; 95% CI, 2.0-2.9), compared with the unaffected group. Risk for other cardiovascular problems, including hyperlipidemia, obesity, and coronary artery disease, were also higher in the affected groups.

TBI patients also reported higher incidence of endocrine diseases, including diabetes (mTBI: HR, 1.9; 95% CI, 1.4-2.7; msTBI: HR, 1.9; 95% CI, 1.4-2.6). Elevated risk for ischemic stroke or transient ischemic attack was also increased (mTBI: HR, 2.2; 95% CI, 1.4-3.3; msTBI: HR, 3.6; 95% CI, 2.4-5.3).

Regardless of injury severity, patients with TBI had a higher risk for neurologic and psychiatric diseases, particularly depression, dementia, and psychotic disorders. “This tells us that mild TBI is not clean of events,” Dr. Zafonte said.

Surprising rate of comorbidity in youth

Investigators found increased risk for posttrauma comorbidities in all age groups, but researchers were struck by the high rates in younger patients, aged 18-40. Compared with age-matched individuals with no TBI history, hypertension risk was nearly six times higher in those with mTBI (HR, 5.9; 95% CI, 3.9-9.1) and nearly four times higher in patients with msTBI (HR, 3.9; 95% CI, 2.5-6.1).

Rates of hyperlipidemia and diabetes were also higher in younger patients in the mTBI group and posttraumatic seizures and psychiatric disorders were elevated regardless of TBI severity.

Overall, patients with msTBI, but not those with mTBI, were at higher risk for mortality, compared with the unexposed group (432 deaths [9.9%] vs. 250 deaths [5.7%]; P < .001).

“It’s clear that what we may be dealing with is that it holds up even for the younger people,” Dr. Zafonte said. “We used to think brain injury risk is worse in the severe cases, which it is, and it’s worse later on among those who are older, which it is. But our younger folks don’t get away either.”

While the study offers associations between TBI and multisystem health problems, Dr. Zafonte said it’s impossible to say at this point whether the brain injury caused the increased risk for cardiovascular or endocrine problems. Other organ injuries sustained in the trauma may be a contributing factor.

“Further data is needed to elucidate the mechanism and the causative relationships, which we do not have here,” he said.

Many of the postinjury comorbidities emerged a median of 3.5 years after TBI, regardless of severity. But some of the cardiovascular and psychiatric conditions emerged far sooner than that.

That’s important because research suggests less than half of patients with TBI receive follow-up care.

“It does make sense for folks who are interacting with people who’ve had a TBI to be suspicious of medical comorbidities relatively early on, within the first couple of years,” Dr. Zafonte said.

In an invited commentary, Vijay Krishnamoorthy, MD, MPH, PhD, Duke University, Durham, N.C., and Monica S. Vavilala, MD, University of Washington, Seattle, highlight some of the study’s limitations, including a lack of information on comorbidity severity and the lack of a matched group of patients who experienced non-head trauma.

Despite those limitations, the study offers important information on how TBI may affect organs beyond the brain, they noted.

“These observations, if replicated in future studies, raise intriguing implications in the future care of patients with TBI, including heightened chronic disease-screening measures and possibly enhanced guidelines for chronic extracranial organ system care for patients who experience TBI,” Dr. Krishnamoorthy and Dr. Vavilala wrote.

The study received no specific funding. Dr. Zafonte reported having received personal fees from Springer/Demos, serving on scientific advisory boards for Myomo and OnCare and has received funding from the Football Players Health Study at Harvard, funded in part by the National Football League Players Association. Dr. Krishnamoorthy and Dr. Vavilala disclosed no relevant financial relationships.

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

Mild traumatic brain injury (TBI) is linked to a significantly increased risk for a host of subsequent cardiovascular, endocrine, neurologic, and psychiatric disorders, new research shows.

Incidence of hypertension, coronary heart disease, diabetes, stroke, depression, and dementia all began to increase soon after the brain injury and persisted over a decade in both mild and moderate to severe TBI.

Researchers found the multisystem comorbidities in all age groups, including in patients as young as 18. They also found that patients who developed multiple postinjury problems had higher mortality during the decade-long follow-up.

The findings suggest patients with TBI may require longer follow-up and proactive screening for multisystem disease, regardless of age or injury severity.

“The fact that both patients with mild and moderate to severe injuries both had long-term ongoing associations with comorbidities that continued over time and that they are cardiovascular, endocrine, neurologic, and behavioral health oriented was pretty striking,” study author Ross Zafonte, DO, PhD, president of Spaulding Rehab Hospital and professor and chair of physical medicine and rehab at Harvard Medical School, both in Boston, told this news organization.

The study was published online in JAMA Network Open.
 

Injury severity not a factor

An estimated 2.8 million individuals in the United States experience TBI every year. Worldwide, the figure may be as high as 74 million.

Studies have long suggested a link between brain injury and subsequent neurologic disorders, but research suggesting a possible link to cardiovascular and endocrine problems has recently gained attention.

Building on a 2021 study that showed increased incidence of cardiovascular issues following a concussion, the researchers examined medical records of previously healthy patients treated for TBI between 2000 and 2015 who also had at least 1 follow-up visit between 6 months and 10 years after the initial injury.

Researchers analyzed data from 13,053 individuals – 4,351 with mild injury (mTBI), 4351 with moderate to severe injury (msTBI), and 4351 with no TBI. The most common cause of injury was a fall. Patients with sports-related injuries were excluded.

Incidence of hypertension was significantly higher among patients with mTBI (hazard ratio, 2.5; 95% confidence interval, 2.1-2.9) and msTBI (HR, 2.4; 95% CI, 2.0-2.9), compared with the unaffected group. Risk for other cardiovascular problems, including hyperlipidemia, obesity, and coronary artery disease, were also higher in the affected groups.

TBI patients also reported higher incidence of endocrine diseases, including diabetes (mTBI: HR, 1.9; 95% CI, 1.4-2.7; msTBI: HR, 1.9; 95% CI, 1.4-2.6). Elevated risk for ischemic stroke or transient ischemic attack was also increased (mTBI: HR, 2.2; 95% CI, 1.4-3.3; msTBI: HR, 3.6; 95% CI, 2.4-5.3).

Regardless of injury severity, patients with TBI had a higher risk for neurologic and psychiatric diseases, particularly depression, dementia, and psychotic disorders. “This tells us that mild TBI is not clean of events,” Dr. Zafonte said.

Surprising rate of comorbidity in youth

Investigators found increased risk for posttrauma comorbidities in all age groups, but researchers were struck by the high rates in younger patients, aged 18-40. Compared with age-matched individuals with no TBI history, hypertension risk was nearly six times higher in those with mTBI (HR, 5.9; 95% CI, 3.9-9.1) and nearly four times higher in patients with msTBI (HR, 3.9; 95% CI, 2.5-6.1).

Rates of hyperlipidemia and diabetes were also higher in younger patients in the mTBI group and posttraumatic seizures and psychiatric disorders were elevated regardless of TBI severity.

Overall, patients with msTBI, but not those with mTBI, were at higher risk for mortality, compared with the unexposed group (432 deaths [9.9%] vs. 250 deaths [5.7%]; P < .001).

“It’s clear that what we may be dealing with is that it holds up even for the younger people,” Dr. Zafonte said. “We used to think brain injury risk is worse in the severe cases, which it is, and it’s worse later on among those who are older, which it is. But our younger folks don’t get away either.”

While the study offers associations between TBI and multisystem health problems, Dr. Zafonte said it’s impossible to say at this point whether the brain injury caused the increased risk for cardiovascular or endocrine problems. Other organ injuries sustained in the trauma may be a contributing factor.

“Further data is needed to elucidate the mechanism and the causative relationships, which we do not have here,” he said.

Many of the postinjury comorbidities emerged a median of 3.5 years after TBI, regardless of severity. But some of the cardiovascular and psychiatric conditions emerged far sooner than that.

That’s important because research suggests less than half of patients with TBI receive follow-up care.

“It does make sense for folks who are interacting with people who’ve had a TBI to be suspicious of medical comorbidities relatively early on, within the first couple of years,” Dr. Zafonte said.

In an invited commentary, Vijay Krishnamoorthy, MD, MPH, PhD, Duke University, Durham, N.C., and Monica S. Vavilala, MD, University of Washington, Seattle, highlight some of the study’s limitations, including a lack of information on comorbidity severity and the lack of a matched group of patients who experienced non-head trauma.

Despite those limitations, the study offers important information on how TBI may affect organs beyond the brain, they noted.

“These observations, if replicated in future studies, raise intriguing implications in the future care of patients with TBI, including heightened chronic disease-screening measures and possibly enhanced guidelines for chronic extracranial organ system care for patients who experience TBI,” Dr. Krishnamoorthy and Dr. Vavilala wrote.

The study received no specific funding. Dr. Zafonte reported having received personal fees from Springer/Demos, serving on scientific advisory boards for Myomo and OnCare and has received funding from the Football Players Health Study at Harvard, funded in part by the National Football League Players Association. Dr. Krishnamoorthy and Dr. Vavilala disclosed no relevant financial relationships.

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

“It was my wife’s walker, and I’ve never used one before. Sorry that I keep bumping into things.”

He was in his early 70s, recently widowed. He hadn’t needed a walker until yesterday, and his son had gotten it out of the garage where they’d just stowed it away. I showed him how to change the height setting on it so he didn’t have to lean so far over.

His daughter was a longstanding patient of mine, and now she and her brother were worried about their dad. He’d been so healthy for years, taking care of their mother as she declined with cancer. Now, 2 months since her death, he’d started going downhill. He’d been, understandably, depressed and had lost some weight. A few weeks ago he’d had some nonspecific upper respiratory crud, and now they were worried he wasn’t eating. He’d gotten progressively weaker in the last few days, leading to their getting out the walker.

I knew my patient for several years. She wasn’t given to panicking, and was worried about her dad. By this time, I was too. Twenty-eight years of neurology training and practice puts you on the edge for some things. The “Spidey Sense,” as I’ve always called it, was tingling.

It took a very quick neurologic exam to find what I needed. He was indeed weak, had decreased distal sensation, and was completely areflexic. It was time to take the most-dreaded outpatient neurology gamble: The direct office-to-ER admission.

I told his daughter to take him to the nearby ER and scribbled a note that said “Probable Guillain-Barré. Needs urgent workup.” They were somewhat taken aback, as they had dinner plans that night, but his daughter knew me well enough to know that I don’t pull fire alarms for fun.

As soon as they’d left I called the ER doctor and told her what was coming. My hospital days ended 2 years ago, but I wanted to do everything I could to make sure the right ball was rolling.

Then my part was over. I had other patients waiting, tests to review, phone calls to make.

This is where the anxiety began. Nobody wants to be the person who cries wolf, or admits “dumps.” I’ve been on both sides of admissions, and bashing outpatient docs for unnecessary hospital referrals is a perennial pastime of inpatient care.

I was sure of my actions, but as the hours crept by some doubt came in. What if he got to the hospital and suddenly wasn’t weak? Or it was all from a medication error he’d made at home?

No one wants to claim they saw a flare when there wasn’t one, or get the reputation of being past their game. I was worried about the patient, but also began to worry I’d screwed up and missed something else.

I finished the day and went home. After closing out my usual end-of-the-day stuff I logged into the hospital system to see what was going on.

Normal cervical spine MRI. Spinal fluid had zero cells and elevated protein.

I breathed a sigh of relief and relaxed back into my chair. I’d made the right call. The hospital neurologist had ordered IVIG. The patient would hopefully recover. No one would think I’d screwed up a potentially serious case. And, somewhere in the back of my mind, the Sherlock Holmes inside every neurologist tipped his deerstalker cap at me and gave a slight nod.

There’s the relief of having done the right thing for the patient, having made the correct diagnosis, and, at the end of the day, being reassured that (some days at least) I still know what I’m doing.

It’s those feelings that brought me here and still keep me going.

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

“It was my wife’s walker, and I’ve never used one before. Sorry that I keep bumping into things.”

He was in his early 70s, recently widowed. He hadn’t needed a walker until yesterday, and his son had gotten it out of the garage where they’d just stowed it away. I showed him how to change the height setting on it so he didn’t have to lean so far over.

His daughter was a longstanding patient of mine, and now she and her brother were worried about their dad. He’d been so healthy for years, taking care of their mother as she declined with cancer. Now, 2 months since her death, he’d started going downhill. He’d been, understandably, depressed and had lost some weight. A few weeks ago he’d had some nonspecific upper respiratory crud, and now they were worried he wasn’t eating. He’d gotten progressively weaker in the last few days, leading to their getting out the walker.

I knew my patient for several years. She wasn’t given to panicking, and was worried about her dad. By this time, I was too. Twenty-eight years of neurology training and practice puts you on the edge for some things. The “Spidey Sense,” as I’ve always called it, was tingling.

It took a very quick neurologic exam to find what I needed. He was indeed weak, had decreased distal sensation, and was completely areflexic. It was time to take the most-dreaded outpatient neurology gamble: The direct office-to-ER admission.

I told his daughter to take him to the nearby ER and scribbled a note that said “Probable Guillain-Barré. Needs urgent workup.” They were somewhat taken aback, as they had dinner plans that night, but his daughter knew me well enough to know that I don’t pull fire alarms for fun.

As soon as they’d left I called the ER doctor and told her what was coming. My hospital days ended 2 years ago, but I wanted to do everything I could to make sure the right ball was rolling.

Then my part was over. I had other patients waiting, tests to review, phone calls to make.

This is where the anxiety began. Nobody wants to be the person who cries wolf, or admits “dumps.” I’ve been on both sides of admissions, and bashing outpatient docs for unnecessary hospital referrals is a perennial pastime of inpatient care.

I was sure of my actions, but as the hours crept by some doubt came in. What if he got to the hospital and suddenly wasn’t weak? Or it was all from a medication error he’d made at home?

No one wants to claim they saw a flare when there wasn’t one, or get the reputation of being past their game. I was worried about the patient, but also began to worry I’d screwed up and missed something else.

I finished the day and went home. After closing out my usual end-of-the-day stuff I logged into the hospital system to see what was going on.

Normal cervical spine MRI. Spinal fluid had zero cells and elevated protein.

I breathed a sigh of relief and relaxed back into my chair. I’d made the right call. The hospital neurologist had ordered IVIG. The patient would hopefully recover. No one would think I’d screwed up a potentially serious case. And, somewhere in the back of my mind, the Sherlock Holmes inside every neurologist tipped his deerstalker cap at me and gave a slight nod.

There’s the relief of having done the right thing for the patient, having made the correct diagnosis, and, at the end of the day, being reassured that (some days at least) I still know what I’m doing.

It’s those feelings that brought me here and still keep me going.

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

“It was my wife’s walker, and I’ve never used one before. Sorry that I keep bumping into things.”

He was in his early 70s, recently widowed. He hadn’t needed a walker until yesterday, and his son had gotten it out of the garage where they’d just stowed it away. I showed him how to change the height setting on it so he didn’t have to lean so far over.

His daughter was a longstanding patient of mine, and now she and her brother were worried about their dad. He’d been so healthy for years, taking care of their mother as she declined with cancer. Now, 2 months since her death, he’d started going downhill. He’d been, understandably, depressed and had lost some weight. A few weeks ago he’d had some nonspecific upper respiratory crud, and now they were worried he wasn’t eating. He’d gotten progressively weaker in the last few days, leading to their getting out the walker.

I knew my patient for several years. She wasn’t given to panicking, and was worried about her dad. By this time, I was too. Twenty-eight years of neurology training and practice puts you on the edge for some things. The “Spidey Sense,” as I’ve always called it, was tingling.

It took a very quick neurologic exam to find what I needed. He was indeed weak, had decreased distal sensation, and was completely areflexic. It was time to take the most-dreaded outpatient neurology gamble: The direct office-to-ER admission.

I told his daughter to take him to the nearby ER and scribbled a note that said “Probable Guillain-Barré. Needs urgent workup.” They were somewhat taken aback, as they had dinner plans that night, but his daughter knew me well enough to know that I don’t pull fire alarms for fun.

As soon as they’d left I called the ER doctor and told her what was coming. My hospital days ended 2 years ago, but I wanted to do everything I could to make sure the right ball was rolling.

Then my part was over. I had other patients waiting, tests to review, phone calls to make.

This is where the anxiety began. Nobody wants to be the person who cries wolf, or admits “dumps.” I’ve been on both sides of admissions, and bashing outpatient docs for unnecessary hospital referrals is a perennial pastime of inpatient care.

I was sure of my actions, but as the hours crept by some doubt came in. What if he got to the hospital and suddenly wasn’t weak? Or it was all from a medication error he’d made at home?

No one wants to claim they saw a flare when there wasn’t one, or get the reputation of being past their game. I was worried about the patient, but also began to worry I’d screwed up and missed something else.

I finished the day and went home. After closing out my usual end-of-the-day stuff I logged into the hospital system to see what was going on.

Normal cervical spine MRI. Spinal fluid had zero cells and elevated protein.

I breathed a sigh of relief and relaxed back into my chair. I’d made the right call. The hospital neurologist had ordered IVIG. The patient would hopefully recover. No one would think I’d screwed up a potentially serious case. And, somewhere in the back of my mind, the Sherlock Holmes inside every neurologist tipped his deerstalker cap at me and gave a slight nod.

There’s the relief of having done the right thing for the patient, having made the correct diagnosis, and, at the end of the day, being reassured that (some days at least) I still know what I’m doing.

It’s those feelings that brought me here and still keep me going.

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

A unique ratio of metabolites measured in blood may help supplement a clinical diagnosis of early Alzheimer’s disease (AD), allowing for earlier intervention, early research suggests.

Investigators found that plasma concentrations of 2-aminoethyl dihydrogen phosphate and taurine could distinguish adults with early-stage Alzheimer’s disease from cognitively normal adults.

“Our biomarker for early-stage Alzheimer’s disease represents new thinking and is unique from the amyloid-beta and p-tau molecules that are currently being investigated to diagnose AD,” Sandra Banack, PhD, senior scientist, Brain Chemistry Labs, Jackson, Wyoming, told this news organization.

If further studies pan out, Dr. Banack said this biomarker could “easily be transformed into a test to aid clinical evaluations for Alzheimer’s disease.”

The study was published online in PLOS ONE.
 

New drug target?

The researchers measured concentrations of 2-aminoethyl dihydrogen phosphate and taurine in blood plasma samples in 25 patients (21 men; mean age, 71) with a clinical diagnosis of early-stage Alzheimer’s based on a Clinical Dementia Rating (CDR) score of 0.5, suggesting very mild cognitive impairment, and 25 healthy controls (20 men; mean age, 39).

The concentration of 2-aminoethyl dihydrogen phosphate, normalized by the concentration of taurine, reliably distinguished blood samples of early-stage Alzheimer’s patients from controls in a blinded analysis.

This biomarker “could lead to new understanding of [AD] and lead to new drug candidates,” Dr. Banack told this news organization.

The researchers note that 2-aminoethyl dihydrogen phosphate plays an important role in the structure and function of cellular membranes.

Physiologic effects of increased 2-aminoethyl dihydrogen phosphate concentrations in the blood are not known. However, in one study, concentrations of this molecule were found to be significantly lower in the temporal cortex, frontal cortex, and hippocampus (40%) in patients with Alzheimer’s disease, compared with controls.

“New biomarkers take time before they can be implemented in the clinic. The next step will be to repeat the experiments using a large sample size of AD patient blood samples,” Dr. Banack told this news organization.

The study team is looking to source a larger sample size of AD blood samples to replicate these findings. They are also examining this biomarker relative to other neurodegenerative diseases.

“If verified with larger sample sizes, the quantification of 2-aminoethyl dihydrogen phosphate could potentially assist in the diagnosis of early-stage Alzheimer’s disease when used in conjunction with the patient’s CDR score and other potential AD biomarkers,” Dr. Banack and colleagues say.
 

Caveats, cautionary notes

Commenting on the findings, Rebecca M. Edelmayer, PhD, Alzheimer’s Association senior director of scientific engagement, said the study is “interesting, though very small-scale and very preliminary.”

Dr. Edelmayer said one “major limitation” is that participants did not have their Alzheimer’s diagnosis confirmed with “gold standard biomarkers. They have been diagnosed based only on their cognitive and behavioral symptoms.”

She also cautioned that the study population is not representative – either of the general public or people living with Alzheimer’s disease.

For example, 41 out of all 50 samples are from men, “though we know women are disproportionately impacted by Alzheimer’s.”

“There is a mismatch in the age of the study groups,” Dr. Edelmayer noted. The mean age of controls in the study was 39 and the mean age of people with dementia was 71. Race or ethnicity and other demographic information is also unclear from the article.

“There is an urgent need for simple, inexpensive, noninvasive and easily available diagnostic tools for Alzheimer’s, such as a blood test. A simple blood test for Alzheimer’s would be a great advance for individuals with – and at risk for – the disease, families, doctors, and researchers,” Dr. Edelmayer said.

“Bottom line,” Dr. Edelmayer continued, “these results need to be further tested and verified in long-term, large-scale studies with diverse populations that are representative of those living with Alzheimer’s disease.”

This research was supported by the William Stamps Farish Fund and the Josephine P. & John J. Louis Foundation. Brain Chemistry Labs has applied for a patent related to this research. Dr. Edelmayer has no relevant disclosures.

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

A unique ratio of metabolites measured in blood may help supplement a clinical diagnosis of early Alzheimer’s disease (AD), allowing for earlier intervention, early research suggests.

Investigators found that plasma concentrations of 2-aminoethyl dihydrogen phosphate and taurine could distinguish adults with early-stage Alzheimer’s disease from cognitively normal adults.

“Our biomarker for early-stage Alzheimer’s disease represents new thinking and is unique from the amyloid-beta and p-tau molecules that are currently being investigated to diagnose AD,” Sandra Banack, PhD, senior scientist, Brain Chemistry Labs, Jackson, Wyoming, told this news organization.

If further studies pan out, Dr. Banack said this biomarker could “easily be transformed into a test to aid clinical evaluations for Alzheimer’s disease.”

The study was published online in PLOS ONE.
 

New drug target?

The researchers measured concentrations of 2-aminoethyl dihydrogen phosphate and taurine in blood plasma samples in 25 patients (21 men; mean age, 71) with a clinical diagnosis of early-stage Alzheimer’s based on a Clinical Dementia Rating (CDR) score of 0.5, suggesting very mild cognitive impairment, and 25 healthy controls (20 men; mean age, 39).

The concentration of 2-aminoethyl dihydrogen phosphate, normalized by the concentration of taurine, reliably distinguished blood samples of early-stage Alzheimer’s patients from controls in a blinded analysis.

This biomarker “could lead to new understanding of [AD] and lead to new drug candidates,” Dr. Banack told this news organization.

The researchers note that 2-aminoethyl dihydrogen phosphate plays an important role in the structure and function of cellular membranes.

Physiologic effects of increased 2-aminoethyl dihydrogen phosphate concentrations in the blood are not known. However, in one study, concentrations of this molecule were found to be significantly lower in the temporal cortex, frontal cortex, and hippocampus (40%) in patients with Alzheimer’s disease, compared with controls.

“New biomarkers take time before they can be implemented in the clinic. The next step will be to repeat the experiments using a large sample size of AD patient blood samples,” Dr. Banack told this news organization.

The study team is looking to source a larger sample size of AD blood samples to replicate these findings. They are also examining this biomarker relative to other neurodegenerative diseases.

“If verified with larger sample sizes, the quantification of 2-aminoethyl dihydrogen phosphate could potentially assist in the diagnosis of early-stage Alzheimer’s disease when used in conjunction with the patient’s CDR score and other potential AD biomarkers,” Dr. Banack and colleagues say.
 

Caveats, cautionary notes

Commenting on the findings, Rebecca M. Edelmayer, PhD, Alzheimer’s Association senior director of scientific engagement, said the study is “interesting, though very small-scale and very preliminary.”

Dr. Edelmayer said one “major limitation” is that participants did not have their Alzheimer’s diagnosis confirmed with “gold standard biomarkers. They have been diagnosed based only on their cognitive and behavioral symptoms.”

She also cautioned that the study population is not representative – either of the general public or people living with Alzheimer’s disease.

For example, 41 out of all 50 samples are from men, “though we know women are disproportionately impacted by Alzheimer’s.”

“There is a mismatch in the age of the study groups,” Dr. Edelmayer noted. The mean age of controls in the study was 39 and the mean age of people with dementia was 71. Race or ethnicity and other demographic information is also unclear from the article.

“There is an urgent need for simple, inexpensive, noninvasive and easily available diagnostic tools for Alzheimer’s, such as a blood test. A simple blood test for Alzheimer’s would be a great advance for individuals with – and at risk for – the disease, families, doctors, and researchers,” Dr. Edelmayer said.

“Bottom line,” Dr. Edelmayer continued, “these results need to be further tested and verified in long-term, large-scale studies with diverse populations that are representative of those living with Alzheimer’s disease.”

This research was supported by the William Stamps Farish Fund and the Josephine P. & John J. Louis Foundation. Brain Chemistry Labs has applied for a patent related to this research. Dr. Edelmayer has no relevant disclosures.

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

A unique ratio of metabolites measured in blood may help supplement a clinical diagnosis of early Alzheimer’s disease (AD), allowing for earlier intervention, early research suggests.

Investigators found that plasma concentrations of 2-aminoethyl dihydrogen phosphate and taurine could distinguish adults with early-stage Alzheimer’s disease from cognitively normal adults.

“Our biomarker for early-stage Alzheimer’s disease represents new thinking and is unique from the amyloid-beta and p-tau molecules that are currently being investigated to diagnose AD,” Sandra Banack, PhD, senior scientist, Brain Chemistry Labs, Jackson, Wyoming, told this news organization.

If further studies pan out, Dr. Banack said this biomarker could “easily be transformed into a test to aid clinical evaluations for Alzheimer’s disease.”

The study was published online in PLOS ONE.
 

New drug target?

The researchers measured concentrations of 2-aminoethyl dihydrogen phosphate and taurine in blood plasma samples in 25 patients (21 men; mean age, 71) with a clinical diagnosis of early-stage Alzheimer’s based on a Clinical Dementia Rating (CDR) score of 0.5, suggesting very mild cognitive impairment, and 25 healthy controls (20 men; mean age, 39).

The concentration of 2-aminoethyl dihydrogen phosphate, normalized by the concentration of taurine, reliably distinguished blood samples of early-stage Alzheimer’s patients from controls in a blinded analysis.

This biomarker “could lead to new understanding of [AD] and lead to new drug candidates,” Dr. Banack told this news organization.

The researchers note that 2-aminoethyl dihydrogen phosphate plays an important role in the structure and function of cellular membranes.

Physiologic effects of increased 2-aminoethyl dihydrogen phosphate concentrations in the blood are not known. However, in one study, concentrations of this molecule were found to be significantly lower in the temporal cortex, frontal cortex, and hippocampus (40%) in patients with Alzheimer’s disease, compared with controls.

“New biomarkers take time before they can be implemented in the clinic. The next step will be to repeat the experiments using a large sample size of AD patient blood samples,” Dr. Banack told this news organization.

The study team is looking to source a larger sample size of AD blood samples to replicate these findings. They are also examining this biomarker relative to other neurodegenerative diseases.

“If verified with larger sample sizes, the quantification of 2-aminoethyl dihydrogen phosphate could potentially assist in the diagnosis of early-stage Alzheimer’s disease when used in conjunction with the patient’s CDR score and other potential AD biomarkers,” Dr. Banack and colleagues say.
 

Caveats, cautionary notes

Commenting on the findings, Rebecca M. Edelmayer, PhD, Alzheimer’s Association senior director of scientific engagement, said the study is “interesting, though very small-scale and very preliminary.”

Dr. Edelmayer said one “major limitation” is that participants did not have their Alzheimer’s diagnosis confirmed with “gold standard biomarkers. They have been diagnosed based only on their cognitive and behavioral symptoms.”

She also cautioned that the study population is not representative – either of the general public or people living with Alzheimer’s disease.

For example, 41 out of all 50 samples are from men, “though we know women are disproportionately impacted by Alzheimer’s.”

“There is a mismatch in the age of the study groups,” Dr. Edelmayer noted. The mean age of controls in the study was 39 and the mean age of people with dementia was 71. Race or ethnicity and other demographic information is also unclear from the article.

“There is an urgent need for simple, inexpensive, noninvasive and easily available diagnostic tools for Alzheimer’s, such as a blood test. A simple blood test for Alzheimer’s would be a great advance for individuals with – and at risk for – the disease, families, doctors, and researchers,” Dr. Edelmayer said.

“Bottom line,” Dr. Edelmayer continued, “these results need to be further tested and verified in long-term, large-scale studies with diverse populations that are representative of those living with Alzheimer’s disease.”

This research was supported by the William Stamps Farish Fund and the Josephine P. & John J. Louis Foundation. Brain Chemistry Labs has applied for a patent related to this research. Dr. Edelmayer has no relevant disclosures.

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

Impaired vision in older adults is an underrecognized and modifiable dementia risk factor, new research suggests.

Investigators analyzed estimated population attributable fractions (PAFs) associated with dementia in more than 16,000 older adults. A PAF represents the number of dementia cases that could be prevented if a given risk factor were eliminated.

Results showed the PAF of vision impairment was 1.8%, suggesting that healthy vision had the potential to prevent more than 100,000 cases of dementia in the United States.

“Vision impairment and blindness disproportionately impact older adults, yet vision impairment is often preventable or even correctable,” study investigator Joshua Ehrlich MD, assistant professor of ophthalmology and visual sciences, University of Michigan, Ann Arbor, said in an interview.

Poor vision affects not only how individuals see the world, but also their systemic health and well-being, Dr. Ehrlich said.

“Accordingly, ensuring that older adults receive appropriate eye care is vital to promoting health, independence, and optimal aging,” he added.

The findings were published online in JAMA Neurology.
 

A surprising omission

There is an “urgent need to identify modifiable risk factors for dementia that can be targeted with interventions to slow cognitive decline and prevent dementia,” the investigators wrote.

In 2020, the Lancet Commission report on dementia prevention, intervention, and care proposed a life-course model of 12 potentially modifiable dementia risk factors. This included lower educational level, hearing loss, traumatic brain injury, hypertension, excessive alcohol consumption, obesity, smoking, depression, social isolation, physical inactivity, diabetes, and air pollution.

Together, these factors are associated with about 40% of dementia cases worldwide, the report notes.

Vision impairment was not included in this model, “despite considerable evidence that it is associated with an elevated risk of incident dementia and that it may operate through the same pathways as hearing loss,” the current researchers wrote.

“We have known for some time that vision impairment is a risk factor for dementia [and] we also know that a very large fraction of vision impairment, possibly in excess of 80%, is avoidable or has simply yet to be addressed,” Dr. Ehrlich said.

He and his colleagues found it “surprising that vision impairment had been ignored in key models of modifiable dementia risk factors that are used to shape health policy and resource allocation.” They set out to demonstrate that, “in fact, vision impairment is just as influential as a number of other long accepted modifiable dementia risk factors.”

The investigators assessed data from the Health and Retirement Study (HRS), a panel study that surveys more than 20,000 U.S. adults aged 50 years or older every 2 years.

The investigators applied the same methods used by the Lancet Commission to the HRS dataset and added vision impairment to the Lancet life-course model. Air pollution was excluded in their model “because those data were not readily available in the HRS,” the researchers wrote.

They noted the PAF is “based on the population prevalence and relative risk of dementia for each risk factor” and is “weighted, based on a principal components analysis, to account for communality (clustering of risk factors).”
 

A missed prevention opportunity

The sample included 16,690 participants (54% were women, 51.5% were at least age 65, 80.2% were White, 10.6% were Black, 9.2% were other).

In total, the 12 potentially modifiable risk factors used in the researchers’ model were associated with an estimated 62.4% of dementia cases in the United States, with hypertension as the most prevalent risk factor with the highest weighted PAF.
 

A new focus for prevention

Commenting for this article, Suzann Pershing, MD, associate professor of ophthalmology, Stanford (Calif.) University, called the study “particularly important because, despite growing recognition of its importance in relation to cognition, visual impairment is often an underrecognized risk factor.”

The current research “builds on increasingly robust medical literature linking visual impairment and dementia, applying analogous methods to those used for the life course model recently presented by the Lancet Commission to evaluate potentially modifiable dementia risk factors,” said Dr. Pershing, who was not involved with the study.

The investigators “make a compelling argument for inclusion of visual impairment as one of the potentially modifiable risk factors; practicing clinicians and health care systems may consider screening and targeted therapies to address visual impairment, with a goal of population health and contributing to a reduction in future dementia disease burden,” she added.

In an accompanying editorial), Jennifer Deal, PhD, department of epidemiology and Cochlear Center for Hearing and Public Health, Baltimore, and Julio Rojas, MD, PhD, Memory and Aging Center, department of neurology, Weill Institute for Neurosciences, University of California, San Francisco, call the findings “an important reminder that dementia is a social problem in which potentially treatable risk factors, including visual impairment, are highly prevalent in disadvantaged populations.”

The editorialists noted that 90% of cases of vision impairment are “preventable or have yet to be treated. The two “highly cost-effective interventions” of eyeglasses and/or cataract surgery “remain underused both in the U.S. and globally, especially in disadvantaged communities,” they wrote.

They added that more research is needed to “test the effectiveness of interventions to preserve cognitive health by promoting healthy vision.”

The study was supported by grants from the National Institute on Aging, the National Institutes of Health, and Research to Prevent Blindness. The investigators reported no relevant financial relationships. Dr. Deal reported having received grants from the National Institute on Aging. Dr. Rojas reported serving as site principal investigator on clinical trials for Eli Lilly and Eisai and receiving grants from the National Institute on Aging. Dr. Pershing is a consultant for Acumen, and Verana Health (as DigiSight Technologies).

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

Impaired vision in older adults is an underrecognized and modifiable dementia risk factor, new research suggests.

Investigators analyzed estimated population attributable fractions (PAFs) associated with dementia in more than 16,000 older adults. A PAF represents the number of dementia cases that could be prevented if a given risk factor were eliminated.

Results showed the PAF of vision impairment was 1.8%, suggesting that healthy vision had the potential to prevent more than 100,000 cases of dementia in the United States.

“Vision impairment and blindness disproportionately impact older adults, yet vision impairment is often preventable or even correctable,” study investigator Joshua Ehrlich MD, assistant professor of ophthalmology and visual sciences, University of Michigan, Ann Arbor, said in an interview.

Poor vision affects not only how individuals see the world, but also their systemic health and well-being, Dr. Ehrlich said.

“Accordingly, ensuring that older adults receive appropriate eye care is vital to promoting health, independence, and optimal aging,” he added.

The findings were published online in JAMA Neurology.
 

A surprising omission

There is an “urgent need to identify modifiable risk factors for dementia that can be targeted with interventions to slow cognitive decline and prevent dementia,” the investigators wrote.

In 2020, the Lancet Commission report on dementia prevention, intervention, and care proposed a life-course model of 12 potentially modifiable dementia risk factors. This included lower educational level, hearing loss, traumatic brain injury, hypertension, excessive alcohol consumption, obesity, smoking, depression, social isolation, physical inactivity, diabetes, and air pollution.

Together, these factors are associated with about 40% of dementia cases worldwide, the report notes.

Vision impairment was not included in this model, “despite considerable evidence that it is associated with an elevated risk of incident dementia and that it may operate through the same pathways as hearing loss,” the current researchers wrote.

“We have known for some time that vision impairment is a risk factor for dementia [and] we also know that a very large fraction of vision impairment, possibly in excess of 80%, is avoidable or has simply yet to be addressed,” Dr. Ehrlich said.

He and his colleagues found it “surprising that vision impairment had been ignored in key models of modifiable dementia risk factors that are used to shape health policy and resource allocation.” They set out to demonstrate that, “in fact, vision impairment is just as influential as a number of other long accepted modifiable dementia risk factors.”

The investigators assessed data from the Health and Retirement Study (HRS), a panel study that surveys more than 20,000 U.S. adults aged 50 years or older every 2 years.

The investigators applied the same methods used by the Lancet Commission to the HRS dataset and added vision impairment to the Lancet life-course model. Air pollution was excluded in their model “because those data were not readily available in the HRS,” the researchers wrote.

They noted the PAF is “based on the population prevalence and relative risk of dementia for each risk factor” and is “weighted, based on a principal components analysis, to account for communality (clustering of risk factors).”
 

A missed prevention opportunity

The sample included 16,690 participants (54% were women, 51.5% were at least age 65, 80.2% were White, 10.6% were Black, 9.2% were other).

In total, the 12 potentially modifiable risk factors used in the researchers’ model were associated with an estimated 62.4% of dementia cases in the United States, with hypertension as the most prevalent risk factor with the highest weighted PAF.
 

A new focus for prevention

Commenting for this article, Suzann Pershing, MD, associate professor of ophthalmology, Stanford (Calif.) University, called the study “particularly important because, despite growing recognition of its importance in relation to cognition, visual impairment is often an underrecognized risk factor.”

The current research “builds on increasingly robust medical literature linking visual impairment and dementia, applying analogous methods to those used for the life course model recently presented by the Lancet Commission to evaluate potentially modifiable dementia risk factors,” said Dr. Pershing, who was not involved with the study.

The investigators “make a compelling argument for inclusion of visual impairment as one of the potentially modifiable risk factors; practicing clinicians and health care systems may consider screening and targeted therapies to address visual impairment, with a goal of population health and contributing to a reduction in future dementia disease burden,” she added.

In an accompanying editorial), Jennifer Deal, PhD, department of epidemiology and Cochlear Center for Hearing and Public Health, Baltimore, and Julio Rojas, MD, PhD, Memory and Aging Center, department of neurology, Weill Institute for Neurosciences, University of California, San Francisco, call the findings “an important reminder that dementia is a social problem in which potentially treatable risk factors, including visual impairment, are highly prevalent in disadvantaged populations.”

The editorialists noted that 90% of cases of vision impairment are “preventable or have yet to be treated. The two “highly cost-effective interventions” of eyeglasses and/or cataract surgery “remain underused both in the U.S. and globally, especially in disadvantaged communities,” they wrote.

They added that more research is needed to “test the effectiveness of interventions to preserve cognitive health by promoting healthy vision.”

The study was supported by grants from the National Institute on Aging, the National Institutes of Health, and Research to Prevent Blindness. The investigators reported no relevant financial relationships. Dr. Deal reported having received grants from the National Institute on Aging. Dr. Rojas reported serving as site principal investigator on clinical trials for Eli Lilly and Eisai and receiving grants from the National Institute on Aging. Dr. Pershing is a consultant for Acumen, and Verana Health (as DigiSight Technologies).

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

Impaired vision in older adults is an underrecognized and modifiable dementia risk factor, new research suggests.

Investigators analyzed estimated population attributable fractions (PAFs) associated with dementia in more than 16,000 older adults. A PAF represents the number of dementia cases that could be prevented if a given risk factor were eliminated.

Results showed the PAF of vision impairment was 1.8%, suggesting that healthy vision had the potential to prevent more than 100,000 cases of dementia in the United States.

“Vision impairment and blindness disproportionately impact older adults, yet vision impairment is often preventable or even correctable,” study investigator Joshua Ehrlich MD, assistant professor of ophthalmology and visual sciences, University of Michigan, Ann Arbor, said in an interview.

Poor vision affects not only how individuals see the world, but also their systemic health and well-being, Dr. Ehrlich said.

“Accordingly, ensuring that older adults receive appropriate eye care is vital to promoting health, independence, and optimal aging,” he added.

The findings were published online in JAMA Neurology.
 

A surprising omission

There is an “urgent need to identify modifiable risk factors for dementia that can be targeted with interventions to slow cognitive decline and prevent dementia,” the investigators wrote.

In 2020, the Lancet Commission report on dementia prevention, intervention, and care proposed a life-course model of 12 potentially modifiable dementia risk factors. This included lower educational level, hearing loss, traumatic brain injury, hypertension, excessive alcohol consumption, obesity, smoking, depression, social isolation, physical inactivity, diabetes, and air pollution.

Together, these factors are associated with about 40% of dementia cases worldwide, the report notes.

Vision impairment was not included in this model, “despite considerable evidence that it is associated with an elevated risk of incident dementia and that it may operate through the same pathways as hearing loss,” the current researchers wrote.

“We have known for some time that vision impairment is a risk factor for dementia [and] we also know that a very large fraction of vision impairment, possibly in excess of 80%, is avoidable or has simply yet to be addressed,” Dr. Ehrlich said.

He and his colleagues found it “surprising that vision impairment had been ignored in key models of modifiable dementia risk factors that are used to shape health policy and resource allocation.” They set out to demonstrate that, “in fact, vision impairment is just as influential as a number of other long accepted modifiable dementia risk factors.”

The investigators assessed data from the Health and Retirement Study (HRS), a panel study that surveys more than 20,000 U.S. adults aged 50 years or older every 2 years.

The investigators applied the same methods used by the Lancet Commission to the HRS dataset and added vision impairment to the Lancet life-course model. Air pollution was excluded in their model “because those data were not readily available in the HRS,” the researchers wrote.

They noted the PAF is “based on the population prevalence and relative risk of dementia for each risk factor” and is “weighted, based on a principal components analysis, to account for communality (clustering of risk factors).”
 

A missed prevention opportunity

The sample included 16,690 participants (54% were women, 51.5% were at least age 65, 80.2% were White, 10.6% were Black, 9.2% were other).

In total, the 12 potentially modifiable risk factors used in the researchers’ model were associated with an estimated 62.4% of dementia cases in the United States, with hypertension as the most prevalent risk factor with the highest weighted PAF.
 

A new focus for prevention

Commenting for this article, Suzann Pershing, MD, associate professor of ophthalmology, Stanford (Calif.) University, called the study “particularly important because, despite growing recognition of its importance in relation to cognition, visual impairment is often an underrecognized risk factor.”

The current research “builds on increasingly robust medical literature linking visual impairment and dementia, applying analogous methods to those used for the life course model recently presented by the Lancet Commission to evaluate potentially modifiable dementia risk factors,” said Dr. Pershing, who was not involved with the study.

The investigators “make a compelling argument for inclusion of visual impairment as one of the potentially modifiable risk factors; practicing clinicians and health care systems may consider screening and targeted therapies to address visual impairment, with a goal of population health and contributing to a reduction in future dementia disease burden,” she added.

In an accompanying editorial), Jennifer Deal, PhD, department of epidemiology and Cochlear Center for Hearing and Public Health, Baltimore, and Julio Rojas, MD, PhD, Memory and Aging Center, department of neurology, Weill Institute for Neurosciences, University of California, San Francisco, call the findings “an important reminder that dementia is a social problem in which potentially treatable risk factors, including visual impairment, are highly prevalent in disadvantaged populations.”

The editorialists noted that 90% of cases of vision impairment are “preventable or have yet to be treated. The two “highly cost-effective interventions” of eyeglasses and/or cataract surgery “remain underused both in the U.S. and globally, especially in disadvantaged communities,” they wrote.

They added that more research is needed to “test the effectiveness of interventions to preserve cognitive health by promoting healthy vision.”

The study was supported by grants from the National Institute on Aging, the National Institutes of Health, and Research to Prevent Blindness. The investigators reported no relevant financial relationships. Dr. Deal reported having received grants from the National Institute on Aging. Dr. Rojas reported serving as site principal investigator on clinical trials for Eli Lilly and Eisai and receiving grants from the National Institute on Aging. Dr. Pershing is a consultant for Acumen, and Verana Health (as DigiSight Technologies).

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

Fat shaming doesn’t work. If it did, obesity as we know it wouldn’t exist because if the one thing society ensures isn’t lacking for people with obesity, it’s shame. We know that fat shaming doesn’t lead to weight loss and that it’s actually correlated with weight gain: More shame leads to more gain (Puhl and Suh; Sutin and Terracciano; Tomiyama et al).

Shaming and weight stigma have far more concerning associations than weight gain. People who report experiencing more weight stigma have an increased risk for depression, anxiety, low self-esteem, poor body image, substance abuse, suicidality, unhealthy eating behaviors, disordered eating, increased caloric intake, exercise avoidance, decreased exercise motivation potentially due to heightened cortisol reactivity, elevated C-reactive protein, and elevated blood pressure.

Meanwhile, people with obesity – likely in part owing to negative weight-biased experiences in health care – are reluctant to discuss weight with their health care providers and are less likely to seek care at all for any conditions. When care is sought, people with obesity are more likely to receive substandard treatment, including receiving fewer preventive health screenings, decreased health education, and decreased time spent in appointments.
 

Remember that obesity is not a conscious choice

A fact that is conveniently forgotten by those who are most prone to fat shaming is that obesity, like every chronic noncommunicable disease, isn’t a choice that is consciously made by patients.

And yes, though there are lifestyle means that might affect weight, there are lifestyle means that might affect all chronic diseases – yet obesity is the only one we seem to moralize about. It’s also worth noting that other chronic diseases’ lifestyle levers tend not to be governed by thousands of genes and dozens of hormones; those trying to “lifestyle” their way out of obesity are swimming against strong physiologic currents that influence our most seminally important survival drive: eating.

But forgetting about physiologic currents, there is also staggering privilege associated with intentional perpetual behavior change around food and fitness in the name of health.

Whereas medicine and the world are right and quick to embrace the fights against racism, sexism, and homophobia, the push to confront weight bias is far rarer, despite the fact that it’s been shown to be rampant among health care professionals.
 

Protecting the rights of people with obesity

Perhaps though, times are changing. Movements are popping up to protect the rights of people with obesity while combating hate.

Of note, Brazil seems to have embraced a campaign to fight gordofobia — the Portuguese term used to describe weight-based discrimination. For instance, laws are being passed to ensure appropriate seating is supplied in schools for children with obesity, an annual day was formalized to promote the rights of people with obesity, preferential seating is provided on subways for people with obesity, and fines have been levied against at least one comedian for making fat jokes on the grounds of the state’s duty to protect minorities.

We need to take this fight to medicine. Given the incredibly depressing prevalence of weight bias among trainees, medical schools and residency programs should ensure countering weight bias is not only part of the curriculum but that it’s explicitly examined. National medical licensing examinations should include weight bias as well.

Though we’re closer than ever before to widely effective treatment options for obesity, it’s likely to still be decades before pharmaceutical options to treat obesity are as effective, accepted, and encouraged as medications to treat hypertension, dyslipidemia, diabetes, and more are today.

If you’re curious about your own implicit weight biases, consider taking Harvard’s Implicit Association Test for Weight. You might also want to take a few moments and review the Strategies to Overcome and Prevent Obesity Alliances’ Weight Can’t Wait guide for advice on the management of obesity in primary care.

Treat patients with obesity the same as you would those with any chronic condition.

Also, consider your physical office space. Do you have chairs suitable for patients with obesity (wide base and with arms to help patients rise)? A scale that measures up to high weights that’s in a private location? Appropriately sized blood pressure cuffs?

If not, do you know who is deserving of shame?

Doctors who fat shame or who treat patients with obesity differently than they would any other patient with a chronic medical condition.

Examples include the family doctor who hadn’t checked my patient’s blood pressure in over a decade because he couldn’t be bothered buying an appropriately sized blood pressure cuff. Or the fertility doctor who told one of my patients that perhaps her weight reflected God’s will that she does not have children.

Finally, if reading this article about treating people with obesity the same as you would patients with other chronic, noncommunicable, lifestyle responsive diseases made you angry, there’s a great chance that you’re part of the problem.
 

Dr. Freedhoff, is associate professor of family medicine at the University of Ottawa and medical director of the Bariatric Medical Institute, a nonsurgical weight management center. He is one of Canada’s most outspoken obesity experts and the author of The Diet Fix: Why Diets Fail and How to Make Yours Work. He has disclosed the following: He served as a director, officer, partner, employee, adviser, consultant, or trustee for Bariatric Medical Institute and Constant Health; has received research grant from Novo Nordisk, and has publicly shared opinions via Weighty Matters and social media. A version of this article first appeared on Medscape.com.

Fat shaming doesn’t work. If it did, obesity as we know it wouldn’t exist because if the one thing society ensures isn’t lacking for people with obesity, it’s shame. We know that fat shaming doesn’t lead to weight loss and that it’s actually correlated with weight gain: More shame leads to more gain (Puhl and Suh; Sutin and Terracciano; Tomiyama et al).

Shaming and weight stigma have far more concerning associations than weight gain. People who report experiencing more weight stigma have an increased risk for depression, anxiety, low self-esteem, poor body image, substance abuse, suicidality, unhealthy eating behaviors, disordered eating, increased caloric intake, exercise avoidance, decreased exercise motivation potentially due to heightened cortisol reactivity, elevated C-reactive protein, and elevated blood pressure.

Meanwhile, people with obesity – likely in part owing to negative weight-biased experiences in health care – are reluctant to discuss weight with their health care providers and are less likely to seek care at all for any conditions. When care is sought, people with obesity are more likely to receive substandard treatment, including receiving fewer preventive health screenings, decreased health education, and decreased time spent in appointments.
 

Remember that obesity is not a conscious choice

A fact that is conveniently forgotten by those who are most prone to fat shaming is that obesity, like every chronic noncommunicable disease, isn’t a choice that is consciously made by patients.

And yes, though there are lifestyle means that might affect weight, there are lifestyle means that might affect all chronic diseases – yet obesity is the only one we seem to moralize about. It’s also worth noting that other chronic diseases’ lifestyle levers tend not to be governed by thousands of genes and dozens of hormones; those trying to “lifestyle” their way out of obesity are swimming against strong physiologic currents that influence our most seminally important survival drive: eating.

But forgetting about physiologic currents, there is also staggering privilege associated with intentional perpetual behavior change around food and fitness in the name of health.

Whereas medicine and the world are right and quick to embrace the fights against racism, sexism, and homophobia, the push to confront weight bias is far rarer, despite the fact that it’s been shown to be rampant among health care professionals.
 

Protecting the rights of people with obesity

Perhaps though, times are changing. Movements are popping up to protect the rights of people with obesity while combating hate.

Of note, Brazil seems to have embraced a campaign to fight gordofobia — the Portuguese term used to describe weight-based discrimination. For instance, laws are being passed to ensure appropriate seating is supplied in schools for children with obesity, an annual day was formalized to promote the rights of people with obesity, preferential seating is provided on subways for people with obesity, and fines have been levied against at least one comedian for making fat jokes on the grounds of the state’s duty to protect minorities.

We need to take this fight to medicine. Given the incredibly depressing prevalence of weight bias among trainees, medical schools and residency programs should ensure countering weight bias is not only part of the curriculum but that it’s explicitly examined. National medical licensing examinations should include weight bias as well.

Though we’re closer than ever before to widely effective treatment options for obesity, it’s likely to still be decades before pharmaceutical options to treat obesity are as effective, accepted, and encouraged as medications to treat hypertension, dyslipidemia, diabetes, and more are today.

If you’re curious about your own implicit weight biases, consider taking Harvard’s Implicit Association Test for Weight. You might also want to take a few moments and review the Strategies to Overcome and Prevent Obesity Alliances’ Weight Can’t Wait guide for advice on the management of obesity in primary care.

Treat patients with obesity the same as you would those with any chronic condition.

Also, consider your physical office space. Do you have chairs suitable for patients with obesity (wide base and with arms to help patients rise)? A scale that measures up to high weights that’s in a private location? Appropriately sized blood pressure cuffs?

If not, do you know who is deserving of shame?

Doctors who fat shame or who treat patients with obesity differently than they would any other patient with a chronic medical condition.

Examples include the family doctor who hadn’t checked my patient’s blood pressure in over a decade because he couldn’t be bothered buying an appropriately sized blood pressure cuff. Or the fertility doctor who told one of my patients that perhaps her weight reflected God’s will that she does not have children.

Finally, if reading this article about treating people with obesity the same as you would patients with other chronic, noncommunicable, lifestyle responsive diseases made you angry, there’s a great chance that you’re part of the problem.
 

Dr. Freedhoff, is associate professor of family medicine at the University of Ottawa and medical director of the Bariatric Medical Institute, a nonsurgical weight management center. He is one of Canada’s most outspoken obesity experts and the author of The Diet Fix: Why Diets Fail and How to Make Yours Work. He has disclosed the following: He served as a director, officer, partner, employee, adviser, consultant, or trustee for Bariatric Medical Institute and Constant Health; has received research grant from Novo Nordisk, and has publicly shared opinions via Weighty Matters and social media. A version of this article first appeared on Medscape.com.

Fat shaming doesn’t work. If it did, obesity as we know it wouldn’t exist because if the one thing society ensures isn’t lacking for people with obesity, it’s shame. We know that fat shaming doesn’t lead to weight loss and that it’s actually correlated with weight gain: More shame leads to more gain (Puhl and Suh; Sutin and Terracciano; Tomiyama et al).

Shaming and weight stigma have far more concerning associations than weight gain. People who report experiencing more weight stigma have an increased risk for depression, anxiety, low self-esteem, poor body image, substance abuse, suicidality, unhealthy eating behaviors, disordered eating, increased caloric intake, exercise avoidance, decreased exercise motivation potentially due to heightened cortisol reactivity, elevated C-reactive protein, and elevated blood pressure.

Meanwhile, people with obesity – likely in part owing to negative weight-biased experiences in health care – are reluctant to discuss weight with their health care providers and are less likely to seek care at all for any conditions. When care is sought, people with obesity are more likely to receive substandard treatment, including receiving fewer preventive health screenings, decreased health education, and decreased time spent in appointments.
 

Remember that obesity is not a conscious choice

A fact that is conveniently forgotten by those who are most prone to fat shaming is that obesity, like every chronic noncommunicable disease, isn’t a choice that is consciously made by patients.

And yes, though there are lifestyle means that might affect weight, there are lifestyle means that might affect all chronic diseases – yet obesity is the only one we seem to moralize about. It’s also worth noting that other chronic diseases’ lifestyle levers tend not to be governed by thousands of genes and dozens of hormones; those trying to “lifestyle” their way out of obesity are swimming against strong physiologic currents that influence our most seminally important survival drive: eating.

But forgetting about physiologic currents, there is also staggering privilege associated with intentional perpetual behavior change around food and fitness in the name of health.

Whereas medicine and the world are right and quick to embrace the fights against racism, sexism, and homophobia, the push to confront weight bias is far rarer, despite the fact that it’s been shown to be rampant among health care professionals.
 

Protecting the rights of people with obesity

Perhaps though, times are changing. Movements are popping up to protect the rights of people with obesity while combating hate.

Of note, Brazil seems to have embraced a campaign to fight gordofobia — the Portuguese term used to describe weight-based discrimination. For instance, laws are being passed to ensure appropriate seating is supplied in schools for children with obesity, an annual day was formalized to promote the rights of people with obesity, preferential seating is provided on subways for people with obesity, and fines have been levied against at least one comedian for making fat jokes on the grounds of the state’s duty to protect minorities.

We need to take this fight to medicine. Given the incredibly depressing prevalence of weight bias among trainees, medical schools and residency programs should ensure countering weight bias is not only part of the curriculum but that it’s explicitly examined. National medical licensing examinations should include weight bias as well.

Though we’re closer than ever before to widely effective treatment options for obesity, it’s likely to still be decades before pharmaceutical options to treat obesity are as effective, accepted, and encouraged as medications to treat hypertension, dyslipidemia, diabetes, and more are today.

If you’re curious about your own implicit weight biases, consider taking Harvard’s Implicit Association Test for Weight. You might also want to take a few moments and review the Strategies to Overcome and Prevent Obesity Alliances’ Weight Can’t Wait guide for advice on the management of obesity in primary care.

Treat patients with obesity the same as you would those with any chronic condition.

Also, consider your physical office space. Do you have chairs suitable for patients with obesity (wide base and with arms to help patients rise)? A scale that measures up to high weights that’s in a private location? Appropriately sized blood pressure cuffs?

If not, do you know who is deserving of shame?

Doctors who fat shame or who treat patients with obesity differently than they would any other patient with a chronic medical condition.

Examples include the family doctor who hadn’t checked my patient’s blood pressure in over a decade because he couldn’t be bothered buying an appropriately sized blood pressure cuff. Or the fertility doctor who told one of my patients that perhaps her weight reflected God’s will that she does not have children.

Finally, if reading this article about treating people with obesity the same as you would patients with other chronic, noncommunicable, lifestyle responsive diseases made you angry, there’s a great chance that you’re part of the problem.
 

Dr. Freedhoff, is associate professor of family medicine at the University of Ottawa and medical director of the Bariatric Medical Institute, a nonsurgical weight management center. He is one of Canada’s most outspoken obesity experts and the author of The Diet Fix: Why Diets Fail and How to Make Yours Work. He has disclosed the following: He served as a director, officer, partner, employee, adviser, consultant, or trustee for Bariatric Medical Institute and Constant Health; has received research grant from Novo Nordisk, and has publicly shared opinions via Weighty Matters and social media. A version of this article first appeared on Medscape.com.

Women with systemic lupus erythematosus (SLE) experience worse outcomes after an acute stroke than does the general population, but men with SLE do not, according to an analysis of the U.S. National Inpatient Sample presented at the annual meeting of the British Society for Rheumatology.

In a study of more than 1.5 million cases of acute stroke recorded in the United States between 2015 and 2018, women with SLE were more likely to be hospitalized for longer and less likely to be routinely discharged into their home environment than were those without SLE. No such association was found for men with SLE.

“The findings imply that primary stroke prevention is of utmost importance, especially in females with SLE,” said Sona Jesenakova, a fourth-year medical student at the University of Aberdeen (Scotland).

“There might be a need to explore more effective and targeted treatment strategies to try and minimize these excessive adverse acute stroke outcomes, especially in females with SLE suffering from stroke,” she suggested.

“Even though males form only a minority of the SLE patient population, some studies have shown that they are prone to suffer from worse disease outcomes,” Ms. Jesenakova said.

Importantly, “male sex has been identified as a risk factor for death early in the course of SLE,” she added, highlighting that sex differences do seem to exist in SLE.

Stroke is an important outcome to look at because people with SLE are known to be at higher risk for developing atherosclerosis, which is a widely known risk factor for ischemic stroke, and with antiphospholipid antibody positivity and uncontrolled disease activity, that risk can be increased. A meta-analysis of older studies has suggested that the risk for death after a stroke is 68% higher in people with SLE than in those without.

To examine the risk for death and other in-hospital outcomes in a more contemporary population, Ms. Jesenakova and associates used data from the National Inpatient Sample, a large, publicly available database that contains inpatient health care information from across the United States. Their sample population consisted of 1,581,430 individuals who had been hospitalized for stroke. Of these, there were 6,100 women and 940 men who had SLE; the remainder served as the ‘no-SLE’ control population.

As might be expected, patients with SLE were about 10 years younger than those without SLE; the median age of women and men with SLE and those without SLE were a respective 60, 61, and 71 years.

There was no difference in the type of stroke between the SLE and no-SLE groups; most had an ischemic stroke (around 89%) rather than a hemorrhagic stroke (around 11%).

The researchers analyzed three key outcomes: mortality at discharge, hospitalization prolonged to a stay of more than 4 days, and routine home discharge, meaning that the patient was able to be discharged home versus more specialist facilities such as a nursing home.

They conducted a multivariate analysis with adjustments made for potential confounding factors such as age, ethnicity, type of stroke, and revascularization treatment. Comorbidities, including major cardiovascular disease, were also accounted for.

Although women with SLE were 21% more likely to die than patients without SLE, men with SLE were 24% less likely to die than was the no-SLE population. However, these differences were not statistically significant.

Women with SLE were 20% more likely to have a prolonged hospital stay and 28% less likely to have a routine home discharge, compared with patients who did not have SLE. The 95% confidence intervals were statistically significant, which was not seen when comparing the same outcomes in men with SLE (odds ratios of 1.06 and 1.18, respectively).

“As for males, even though we didn’t find anything of statistical significance, we have to bear in mind that the sample we had was quite small, and thus these results need to be interpreted with caution,” Ms. Jesenakova said. “We also think that we identified a gap in the current knowledge, and as such, further research is needed to help us understand the influence of male sex on acute stroke outcomes in patients with comorbid SLE.”

The researchers performed a secondary analysis looking at the use of revascularization treatments for ischemic stroke and found that there were no differences between individuals with and without SLE. This analysis considered the use of intravenous thrombolysis and endovascular thrombectomy in just over 1.4 million cases but did not look at sex-specific differences.

Ms. Jesenakova had no conflicts of interest to disclose.

Women with systemic lupus erythematosus (SLE) experience worse outcomes after an acute stroke than does the general population, but men with SLE do not, according to an analysis of the U.S. National Inpatient Sample presented at the annual meeting of the British Society for Rheumatology.

In a study of more than 1.5 million cases of acute stroke recorded in the United States between 2015 and 2018, women with SLE were more likely to be hospitalized for longer and less likely to be routinely discharged into their home environment than were those without SLE. No such association was found for men with SLE.

“The findings imply that primary stroke prevention is of utmost importance, especially in females with SLE,” said Sona Jesenakova, a fourth-year medical student at the University of Aberdeen (Scotland).

“There might be a need to explore more effective and targeted treatment strategies to try and minimize these excessive adverse acute stroke outcomes, especially in females with SLE suffering from stroke,” she suggested.

“Even though males form only a minority of the SLE patient population, some studies have shown that they are prone to suffer from worse disease outcomes,” Ms. Jesenakova said.

Importantly, “male sex has been identified as a risk factor for death early in the course of SLE,” she added, highlighting that sex differences do seem to exist in SLE.

Stroke is an important outcome to look at because people with SLE are known to be at higher risk for developing atherosclerosis, which is a widely known risk factor for ischemic stroke, and with antiphospholipid antibody positivity and uncontrolled disease activity, that risk can be increased. A meta-analysis of older studies has suggested that the risk for death after a stroke is 68% higher in people with SLE than in those without.

To examine the risk for death and other in-hospital outcomes in a more contemporary population, Ms. Jesenakova and associates used data from the National Inpatient Sample, a large, publicly available database that contains inpatient health care information from across the United States. Their sample population consisted of 1,581,430 individuals who had been hospitalized for stroke. Of these, there were 6,100 women and 940 men who had SLE; the remainder served as the ‘no-SLE’ control population.

As might be expected, patients with SLE were about 10 years younger than those without SLE; the median age of women and men with SLE and those without SLE were a respective 60, 61, and 71 years.

There was no difference in the type of stroke between the SLE and no-SLE groups; most had an ischemic stroke (around 89%) rather than a hemorrhagic stroke (around 11%).

The researchers analyzed three key outcomes: mortality at discharge, hospitalization prolonged to a stay of more than 4 days, and routine home discharge, meaning that the patient was able to be discharged home versus more specialist facilities such as a nursing home.

They conducted a multivariate analysis with adjustments made for potential confounding factors such as age, ethnicity, type of stroke, and revascularization treatment. Comorbidities, including major cardiovascular disease, were also accounted for.

Although women with SLE were 21% more likely to die than patients without SLE, men with SLE were 24% less likely to die than was the no-SLE population. However, these differences were not statistically significant.

Women with SLE were 20% more likely to have a prolonged hospital stay and 28% less likely to have a routine home discharge, compared with patients who did not have SLE. The 95% confidence intervals were statistically significant, which was not seen when comparing the same outcomes in men with SLE (odds ratios of 1.06 and 1.18, respectively).

“As for males, even though we didn’t find anything of statistical significance, we have to bear in mind that the sample we had was quite small, and thus these results need to be interpreted with caution,” Ms. Jesenakova said. “We also think that we identified a gap in the current knowledge, and as such, further research is needed to help us understand the influence of male sex on acute stroke outcomes in patients with comorbid SLE.”

The researchers performed a secondary analysis looking at the use of revascularization treatments for ischemic stroke and found that there were no differences between individuals with and without SLE. This analysis considered the use of intravenous thrombolysis and endovascular thrombectomy in just over 1.4 million cases but did not look at sex-specific differences.

Ms. Jesenakova had no conflicts of interest to disclose.

Women with systemic lupus erythematosus (SLE) experience worse outcomes after an acute stroke than does the general population, but men with SLE do not, according to an analysis of the U.S. National Inpatient Sample presented at the annual meeting of the British Society for Rheumatology.

In a study of more than 1.5 million cases of acute stroke recorded in the United States between 2015 and 2018, women with SLE were more likely to be hospitalized for longer and less likely to be routinely discharged into their home environment than were those without SLE. No such association was found for men with SLE.

“The findings imply that primary stroke prevention is of utmost importance, especially in females with SLE,” said Sona Jesenakova, a fourth-year medical student at the University of Aberdeen (Scotland).

“There might be a need to explore more effective and targeted treatment strategies to try and minimize these excessive adverse acute stroke outcomes, especially in females with SLE suffering from stroke,” she suggested.

“Even though males form only a minority of the SLE patient population, some studies have shown that they are prone to suffer from worse disease outcomes,” Ms. Jesenakova said.

Importantly, “male sex has been identified as a risk factor for death early in the course of SLE,” she added, highlighting that sex differences do seem to exist in SLE.

Stroke is an important outcome to look at because people with SLE are known to be at higher risk for developing atherosclerosis, which is a widely known risk factor for ischemic stroke, and with antiphospholipid antibody positivity and uncontrolled disease activity, that risk can be increased. A meta-analysis of older studies has suggested that the risk for death after a stroke is 68% higher in people with SLE than in those without.

To examine the risk for death and other in-hospital outcomes in a more contemporary population, Ms. Jesenakova and associates used data from the National Inpatient Sample, a large, publicly available database that contains inpatient health care information from across the United States. Their sample population consisted of 1,581,430 individuals who had been hospitalized for stroke. Of these, there were 6,100 women and 940 men who had SLE; the remainder served as the ‘no-SLE’ control population.

As might be expected, patients with SLE were about 10 years younger than those without SLE; the median age of women and men with SLE and those without SLE were a respective 60, 61, and 71 years.

There was no difference in the type of stroke between the SLE and no-SLE groups; most had an ischemic stroke (around 89%) rather than a hemorrhagic stroke (around 11%).

The researchers analyzed three key outcomes: mortality at discharge, hospitalization prolonged to a stay of more than 4 days, and routine home discharge, meaning that the patient was able to be discharged home versus more specialist facilities such as a nursing home.

They conducted a multivariate analysis with adjustments made for potential confounding factors such as age, ethnicity, type of stroke, and revascularization treatment. Comorbidities, including major cardiovascular disease, were also accounted for.

Although women with SLE were 21% more likely to die than patients without SLE, men with SLE were 24% less likely to die than was the no-SLE population. However, these differences were not statistically significant.

Women with SLE were 20% more likely to have a prolonged hospital stay and 28% less likely to have a routine home discharge, compared with patients who did not have SLE. The 95% confidence intervals were statistically significant, which was not seen when comparing the same outcomes in men with SLE (odds ratios of 1.06 and 1.18, respectively).

“As for males, even though we didn’t find anything of statistical significance, we have to bear in mind that the sample we had was quite small, and thus these results need to be interpreted with caution,” Ms. Jesenakova said. “We also think that we identified a gap in the current knowledge, and as such, further research is needed to help us understand the influence of male sex on acute stroke outcomes in patients with comorbid SLE.”

The researchers performed a secondary analysis looking at the use of revascularization treatments for ischemic stroke and found that there were no differences between individuals with and without SLE. This analysis considered the use of intravenous thrombolysis and endovascular thrombectomy in just over 1.4 million cases but did not look at sex-specific differences.

Ms. Jesenakova had no conflicts of interest to disclose.