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Neurology Reviews covers innovative and emerging news in neurology and neuroscience every month, with a focus on practical approaches to treating Parkinson's disease, epilepsy, headache, stroke, multiple sclerosis, Alzheimer's disease, and other neurologic disorders.
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Progressive multifocal leukoencephalopathy
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The leading independent newspaper covering neurology news and commentary.
FDA warns of potentially lethal reaction to seizure meds
that can be life threatening if not detected and treated promptly, the Food and Drug Administration warns in an alert.
Known as drug reaction with eosinophilia and systemic symptoms (DRESS), it may start as a rash but can quickly progress and cause injury to internal organs, the need for hospitalization, and death, the FDA notes.
A search of the FDA Adverse Event Reporting System (FAERS) and the medical literature through March 2023 identified 32 serious cases of DRESS worldwide that were associated with levetiracetam.
Three cases occurred in the United States, and 29 occurred abroad. In all 32 cases, the patients were hospitalized and received medical treatment; in 2 cases, the patients died.
The median time to onset of DRESS in the levetiracetam cases was 24 days; times ranged from 7 to 170 days. The reported signs and symptoms included skin rash (n = 22), fever (n = 20), eosinophilia (n = 17), lymph node swelling (n = 9), and atypical lymphocytes (n = 4).
Twenty-two levetiracetam-associated cases of DRESS involved injury to one or more organs, including the liver, lungs, kidneys, and gallbladder.
In 25 of the 29 cases for which information on treatment discontinuation was available, DRESS symptoms resolved when levetiracetam was discontinued.
As for clobazam, a search of FAERS and the medical literature through July 2023 identified 10 serious cases of DRESS worldwide – 1 in the United States and 9 abroad. All 10 patients were hospitalized and received medical treatment. No deaths were reported.
The median time to onset of clobazam-associated DRESS was 21.5 days (range, 7-103 days). The reported signs and symptoms included skin rash (n = 10), fever (n = 8), eosinophilia (n = 7), facial swelling (n = 7), leukocytosis (n = 4), lymph node swelling (n = 4), and leukopenia/thrombocytopenia (n = 1).
In nine cases, there was injury to one or more organs, including the liver, kidneys, and gastrointestinal tract.
DRESS symptoms resolved in all 10 cases when treatment with clobazam was stopped. DRESS and other serious skin reactions reported with clobazam, a benzodiazepine, have not generally been associated with other benzodiazepines, the FDA notes.
Label updates
As a result of these cases, warnings about the risk of DRESS will be added to the prescribing information and patient medication guides for these medicines, the FDA announced.
“Health care professionals should be aware that prompt recognition and early treatment is important for improving DRESS outcomes and decreasing mortality,” the FDA said.
They noted that diagnosis is often difficult because early signs and symptoms, such as fever and swollen lymph nodes, may be present without evidence of a rash.
DRESS may develop 2-8 weeks after starting levetiracetam or clobazam. Symptoms and intensity can vary widely.
DRESS can also be confused with other serious skin reactions, such as Stevens-Johnson syndrome and toxic epidermal necrolysis.
The FDA says patients should be advised of the signs and symptoms of DRESS and be told to stop taking the medicine and seek immediate medical attention if DRESS is suspected during treatment with levetiracetam or clobazam.
Adverse reactions with these medications should be reported to the FDA’s MedWatch program.
A version of this article appeared on Medscape.com.
that can be life threatening if not detected and treated promptly, the Food and Drug Administration warns in an alert.
Known as drug reaction with eosinophilia and systemic symptoms (DRESS), it may start as a rash but can quickly progress and cause injury to internal organs, the need for hospitalization, and death, the FDA notes.
A search of the FDA Adverse Event Reporting System (FAERS) and the medical literature through March 2023 identified 32 serious cases of DRESS worldwide that were associated with levetiracetam.
Three cases occurred in the United States, and 29 occurred abroad. In all 32 cases, the patients were hospitalized and received medical treatment; in 2 cases, the patients died.
The median time to onset of DRESS in the levetiracetam cases was 24 days; times ranged from 7 to 170 days. The reported signs and symptoms included skin rash (n = 22), fever (n = 20), eosinophilia (n = 17), lymph node swelling (n = 9), and atypical lymphocytes (n = 4).
Twenty-two levetiracetam-associated cases of DRESS involved injury to one or more organs, including the liver, lungs, kidneys, and gallbladder.
In 25 of the 29 cases for which information on treatment discontinuation was available, DRESS symptoms resolved when levetiracetam was discontinued.
As for clobazam, a search of FAERS and the medical literature through July 2023 identified 10 serious cases of DRESS worldwide – 1 in the United States and 9 abroad. All 10 patients were hospitalized and received medical treatment. No deaths were reported.
The median time to onset of clobazam-associated DRESS was 21.5 days (range, 7-103 days). The reported signs and symptoms included skin rash (n = 10), fever (n = 8), eosinophilia (n = 7), facial swelling (n = 7), leukocytosis (n = 4), lymph node swelling (n = 4), and leukopenia/thrombocytopenia (n = 1).
In nine cases, there was injury to one or more organs, including the liver, kidneys, and gastrointestinal tract.
DRESS symptoms resolved in all 10 cases when treatment with clobazam was stopped. DRESS and other serious skin reactions reported with clobazam, a benzodiazepine, have not generally been associated with other benzodiazepines, the FDA notes.
Label updates
As a result of these cases, warnings about the risk of DRESS will be added to the prescribing information and patient medication guides for these medicines, the FDA announced.
“Health care professionals should be aware that prompt recognition and early treatment is important for improving DRESS outcomes and decreasing mortality,” the FDA said.
They noted that diagnosis is often difficult because early signs and symptoms, such as fever and swollen lymph nodes, may be present without evidence of a rash.
DRESS may develop 2-8 weeks after starting levetiracetam or clobazam. Symptoms and intensity can vary widely.
DRESS can also be confused with other serious skin reactions, such as Stevens-Johnson syndrome and toxic epidermal necrolysis.
The FDA says patients should be advised of the signs and symptoms of DRESS and be told to stop taking the medicine and seek immediate medical attention if DRESS is suspected during treatment with levetiracetam or clobazam.
Adverse reactions with these medications should be reported to the FDA’s MedWatch program.
A version of this article appeared on Medscape.com.
that can be life threatening if not detected and treated promptly, the Food and Drug Administration warns in an alert.
Known as drug reaction with eosinophilia and systemic symptoms (DRESS), it may start as a rash but can quickly progress and cause injury to internal organs, the need for hospitalization, and death, the FDA notes.
A search of the FDA Adverse Event Reporting System (FAERS) and the medical literature through March 2023 identified 32 serious cases of DRESS worldwide that were associated with levetiracetam.
Three cases occurred in the United States, and 29 occurred abroad. In all 32 cases, the patients were hospitalized and received medical treatment; in 2 cases, the patients died.
The median time to onset of DRESS in the levetiracetam cases was 24 days; times ranged from 7 to 170 days. The reported signs and symptoms included skin rash (n = 22), fever (n = 20), eosinophilia (n = 17), lymph node swelling (n = 9), and atypical lymphocytes (n = 4).
Twenty-two levetiracetam-associated cases of DRESS involved injury to one or more organs, including the liver, lungs, kidneys, and gallbladder.
In 25 of the 29 cases for which information on treatment discontinuation was available, DRESS symptoms resolved when levetiracetam was discontinued.
As for clobazam, a search of FAERS and the medical literature through July 2023 identified 10 serious cases of DRESS worldwide – 1 in the United States and 9 abroad. All 10 patients were hospitalized and received medical treatment. No deaths were reported.
The median time to onset of clobazam-associated DRESS was 21.5 days (range, 7-103 days). The reported signs and symptoms included skin rash (n = 10), fever (n = 8), eosinophilia (n = 7), facial swelling (n = 7), leukocytosis (n = 4), lymph node swelling (n = 4), and leukopenia/thrombocytopenia (n = 1).
In nine cases, there was injury to one or more organs, including the liver, kidneys, and gastrointestinal tract.
DRESS symptoms resolved in all 10 cases when treatment with clobazam was stopped. DRESS and other serious skin reactions reported with clobazam, a benzodiazepine, have not generally been associated with other benzodiazepines, the FDA notes.
Label updates
As a result of these cases, warnings about the risk of DRESS will be added to the prescribing information and patient medication guides for these medicines, the FDA announced.
“Health care professionals should be aware that prompt recognition and early treatment is important for improving DRESS outcomes and decreasing mortality,” the FDA said.
They noted that diagnosis is often difficult because early signs and symptoms, such as fever and swollen lymph nodes, may be present without evidence of a rash.
DRESS may develop 2-8 weeks after starting levetiracetam or clobazam. Symptoms and intensity can vary widely.
DRESS can also be confused with other serious skin reactions, such as Stevens-Johnson syndrome and toxic epidermal necrolysis.
The FDA says patients should be advised of the signs and symptoms of DRESS and be told to stop taking the medicine and seek immediate medical attention if DRESS is suspected during treatment with levetiracetam or clobazam.
Adverse reactions with these medications should be reported to the FDA’s MedWatch program.
A version of this article appeared on Medscape.com.
New consensus guide on rare drug hypersensitivity reaction
TOPLINE:
).
METHODOLOGY:
Data on the evaluation, assessment, and treatment of the rare but potentially life-threatening drug hypersensitivity reaction are lacking.
To support clinicians in diagnosing and managing DRESS, a steering committee conducted a literature review to examine current research, identify evidence, and develop consensus statements. They invited experts from 21 countries across four continents to participate in a Delphi consensus process.
An international panel of 54 experts (including 45 dermatologists) initially assessed 100 statements related to baseline workup, severity of the condition, and treatment. Two more statements were added in the second round.
After revisions and the second round, the group reached consensus for 93 statements overall.
TAKEAWAY:
The statements generating the most disagreement involved diagnosis. The group ultimately supported the value of measuring the viral load of Epstein-Barr virus, cytomegalovirus, and human herpesvirus 6 in all patients with suspected DRESS. The group also agreed on screening for hepatitis A, B, and C in cases of liver involvement and screening for hepatitis B and C before starting systemic therapy.
The group agreed with previous severity criteria that differentiate between mild, moderate, and severe DRESS based on the extent of liver, kidney, and blood involvement and the damage of other organs.
Consensus on treatment was reached for all 12 relevant statements in the first Delphi round. Recommendations included the use of corticosteroids and immediate discontinuation of the drugs causing the reaction.
IN PRACTICE:
“This Delphi exercise aimed to provide a common ground of consensus,” the authors noted. However, “each of the addressed categories needs more in-depth follow-up studies to improve the clinical management of patients.”
SOURCE:
The DRESS Delphi consensus group conducted its exercise under the leadership of Marie-Charlotte Brüggen, MD, of the University Hospital of Zürich. The consensus was published online in the JAMA Dermatology.
LIMITATIONS:
Published evidence was limited because of the low prevalence of DRESS. The consensus statements should therefore be considered with caution and in the context of a clinician’s expertise and available resources. Research gaps also persist in how DRESS may vary with region and ethnicity. The severity thresholds need validation in a revised multicenter statement.
DISCLOSURES:
The consensus review received no outside funding. Dr. Brüggen disclosed relationships with the Swiss National Science Foundation, Christine Kühne – Center for Allergy Research and Education, FreeNovation, LEO Foundation, Olga Mayenfisch Foundation, University of Zürich, LEO Pharma, Pierre Fabre Eczema Foundation, Eli Lilly, AbbVie, GSK, and AstraZeneca. Coauthors disclosed relationships with multiple pharmaceutical companies, foundations, and medical publishing companies.
A version of this article appeared on Medscape.com.
TOPLINE:
).
METHODOLOGY:
Data on the evaluation, assessment, and treatment of the rare but potentially life-threatening drug hypersensitivity reaction are lacking.
To support clinicians in diagnosing and managing DRESS, a steering committee conducted a literature review to examine current research, identify evidence, and develop consensus statements. They invited experts from 21 countries across four continents to participate in a Delphi consensus process.
An international panel of 54 experts (including 45 dermatologists) initially assessed 100 statements related to baseline workup, severity of the condition, and treatment. Two more statements were added in the second round.
After revisions and the second round, the group reached consensus for 93 statements overall.
TAKEAWAY:
The statements generating the most disagreement involved diagnosis. The group ultimately supported the value of measuring the viral load of Epstein-Barr virus, cytomegalovirus, and human herpesvirus 6 in all patients with suspected DRESS. The group also agreed on screening for hepatitis A, B, and C in cases of liver involvement and screening for hepatitis B and C before starting systemic therapy.
The group agreed with previous severity criteria that differentiate between mild, moderate, and severe DRESS based on the extent of liver, kidney, and blood involvement and the damage of other organs.
Consensus on treatment was reached for all 12 relevant statements in the first Delphi round. Recommendations included the use of corticosteroids and immediate discontinuation of the drugs causing the reaction.
IN PRACTICE:
“This Delphi exercise aimed to provide a common ground of consensus,” the authors noted. However, “each of the addressed categories needs more in-depth follow-up studies to improve the clinical management of patients.”
SOURCE:
The DRESS Delphi consensus group conducted its exercise under the leadership of Marie-Charlotte Brüggen, MD, of the University Hospital of Zürich. The consensus was published online in the JAMA Dermatology.
LIMITATIONS:
Published evidence was limited because of the low prevalence of DRESS. The consensus statements should therefore be considered with caution and in the context of a clinician’s expertise and available resources. Research gaps also persist in how DRESS may vary with region and ethnicity. The severity thresholds need validation in a revised multicenter statement.
DISCLOSURES:
The consensus review received no outside funding. Dr. Brüggen disclosed relationships with the Swiss National Science Foundation, Christine Kühne – Center for Allergy Research and Education, FreeNovation, LEO Foundation, Olga Mayenfisch Foundation, University of Zürich, LEO Pharma, Pierre Fabre Eczema Foundation, Eli Lilly, AbbVie, GSK, and AstraZeneca. Coauthors disclosed relationships with multiple pharmaceutical companies, foundations, and medical publishing companies.
A version of this article appeared on Medscape.com.
TOPLINE:
).
METHODOLOGY:
Data on the evaluation, assessment, and treatment of the rare but potentially life-threatening drug hypersensitivity reaction are lacking.
To support clinicians in diagnosing and managing DRESS, a steering committee conducted a literature review to examine current research, identify evidence, and develop consensus statements. They invited experts from 21 countries across four continents to participate in a Delphi consensus process.
An international panel of 54 experts (including 45 dermatologists) initially assessed 100 statements related to baseline workup, severity of the condition, and treatment. Two more statements were added in the second round.
After revisions and the second round, the group reached consensus for 93 statements overall.
TAKEAWAY:
The statements generating the most disagreement involved diagnosis. The group ultimately supported the value of measuring the viral load of Epstein-Barr virus, cytomegalovirus, and human herpesvirus 6 in all patients with suspected DRESS. The group also agreed on screening for hepatitis A, B, and C in cases of liver involvement and screening for hepatitis B and C before starting systemic therapy.
The group agreed with previous severity criteria that differentiate between mild, moderate, and severe DRESS based on the extent of liver, kidney, and blood involvement and the damage of other organs.
Consensus on treatment was reached for all 12 relevant statements in the first Delphi round. Recommendations included the use of corticosteroids and immediate discontinuation of the drugs causing the reaction.
IN PRACTICE:
“This Delphi exercise aimed to provide a common ground of consensus,” the authors noted. However, “each of the addressed categories needs more in-depth follow-up studies to improve the clinical management of patients.”
SOURCE:
The DRESS Delphi consensus group conducted its exercise under the leadership of Marie-Charlotte Brüggen, MD, of the University Hospital of Zürich. The consensus was published online in the JAMA Dermatology.
LIMITATIONS:
Published evidence was limited because of the low prevalence of DRESS. The consensus statements should therefore be considered with caution and in the context of a clinician’s expertise and available resources. Research gaps also persist in how DRESS may vary with region and ethnicity. The severity thresholds need validation in a revised multicenter statement.
DISCLOSURES:
The consensus review received no outside funding. Dr. Brüggen disclosed relationships with the Swiss National Science Foundation, Christine Kühne – Center for Allergy Research and Education, FreeNovation, LEO Foundation, Olga Mayenfisch Foundation, University of Zürich, LEO Pharma, Pierre Fabre Eczema Foundation, Eli Lilly, AbbVie, GSK, and AstraZeneca. Coauthors disclosed relationships with multiple pharmaceutical companies, foundations, and medical publishing companies.
A version of this article appeared on Medscape.com.
In general, I’m happy
I’m a general neurologist. I consider myself a jack of all (or at least most) trades in my field, and a master of none.
In the April 2023 issue of JAMA Neurology there was an editorial about neurology training, with general neurology being renamed “comprehensive neurology” and a fellowship offered in practicing general neurology.
This seems rather silly to me. If 4 years of residency (1 of internship and 3 of neurology) don’t prepare you to practice general neurology, then what’s the point of residency at all? For that matter, what difference will renaming it do?
Imagine completing a 3-year internal medicine residency, then being told you need to do a fellowship in “comprehensive medicine” in order to practice. Or at least so you can add the word “comprehensive” to your shingle.
The authors bemoan the increasing number of neurology residents wanting to do fellowships and subspecialize, a situation that mirrors the general trend of people away from general medicine toward specialties.
While I agree we do need subspecialists in neurology (and currently there are at least 31 recognized, which is way more than I would have guessed), the fact is that patients, and sometimes their internists, aren’t going to be the best judge of who does or doesn’t need to see one, compared with a general neurologist.
Most of us general people can handle straightforward Parkinson’s disease, epilepsy, migraines, etc. Certainly, there are times where the condition is refractory to our care, or there’s something unusual about the case, that leads us to refer them to someone with more expertise. But isn’t that how it’s supposed to work? Like medicine in general, we need more general people than subspecialists.
Honestly, I can’t claim to be any different. Twenty-six years ago, when I finished residency, I did a clinical neurophysiology fellowship. From a practical view it was an epilepsy fellowship at my program. Some of this was an interest at the time in subspecializing, some of it was me putting off joining the “real world” of having to find a job for a year.
When I hung up my own shingle, my business card listed a subspecialty in epilepsy. Looking back years later, this wasn’t the best move. In solo practice I had no access to an epilepsy monitoring unit, vagus nerve stimulation capabilities, or epilepsy surgery at the hospital I rounded at. Not only that, I discovered it put me at a disadvantage, as internists were referring only epilepsy patients to me, and all the other stuff (which is the majority of patients) to the general (or comprehensive) neurologists around me. Which, financially, wasn’t a good thing when you’re young and starting out.
Not only that, but I discovered that I didn’t like only seeing one thing. I found it boring, and not for me.
So after a year or so, I took the word “epilepsy” off my card, left it at “general neurology,” and sent out letters reminding my referral base that I was willing to see the majority of things in my field (rare diseases, even today, I won’t attempt to handle).
So now my days are a mix of things, which I like. Neurology is enough of a specialty for me without going further up the pyramid. Having sub (and even sub-sub) specialists is important to maintain medical excellence, but we still need people willing to do general neurology, and I’m happy there.
Changing my title to “comprehensive” is unnecessary. I’m happy with what I am.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
I’m a general neurologist. I consider myself a jack of all (or at least most) trades in my field, and a master of none.
In the April 2023 issue of JAMA Neurology there was an editorial about neurology training, with general neurology being renamed “comprehensive neurology” and a fellowship offered in practicing general neurology.
This seems rather silly to me. If 4 years of residency (1 of internship and 3 of neurology) don’t prepare you to practice general neurology, then what’s the point of residency at all? For that matter, what difference will renaming it do?
Imagine completing a 3-year internal medicine residency, then being told you need to do a fellowship in “comprehensive medicine” in order to practice. Or at least so you can add the word “comprehensive” to your shingle.
The authors bemoan the increasing number of neurology residents wanting to do fellowships and subspecialize, a situation that mirrors the general trend of people away from general medicine toward specialties.
While I agree we do need subspecialists in neurology (and currently there are at least 31 recognized, which is way more than I would have guessed), the fact is that patients, and sometimes their internists, aren’t going to be the best judge of who does or doesn’t need to see one, compared with a general neurologist.
Most of us general people can handle straightforward Parkinson’s disease, epilepsy, migraines, etc. Certainly, there are times where the condition is refractory to our care, or there’s something unusual about the case, that leads us to refer them to someone with more expertise. But isn’t that how it’s supposed to work? Like medicine in general, we need more general people than subspecialists.
Honestly, I can’t claim to be any different. Twenty-six years ago, when I finished residency, I did a clinical neurophysiology fellowship. From a practical view it was an epilepsy fellowship at my program. Some of this was an interest at the time in subspecializing, some of it was me putting off joining the “real world” of having to find a job for a year.
When I hung up my own shingle, my business card listed a subspecialty in epilepsy. Looking back years later, this wasn’t the best move. In solo practice I had no access to an epilepsy monitoring unit, vagus nerve stimulation capabilities, or epilepsy surgery at the hospital I rounded at. Not only that, I discovered it put me at a disadvantage, as internists were referring only epilepsy patients to me, and all the other stuff (which is the majority of patients) to the general (or comprehensive) neurologists around me. Which, financially, wasn’t a good thing when you’re young and starting out.
Not only that, but I discovered that I didn’t like only seeing one thing. I found it boring, and not for me.
So after a year or so, I took the word “epilepsy” off my card, left it at “general neurology,” and sent out letters reminding my referral base that I was willing to see the majority of things in my field (rare diseases, even today, I won’t attempt to handle).
So now my days are a mix of things, which I like. Neurology is enough of a specialty for me without going further up the pyramid. Having sub (and even sub-sub) specialists is important to maintain medical excellence, but we still need people willing to do general neurology, and I’m happy there.
Changing my title to “comprehensive” is unnecessary. I’m happy with what I am.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
I’m a general neurologist. I consider myself a jack of all (or at least most) trades in my field, and a master of none.
In the April 2023 issue of JAMA Neurology there was an editorial about neurology training, with general neurology being renamed “comprehensive neurology” and a fellowship offered in practicing general neurology.
This seems rather silly to me. If 4 years of residency (1 of internship and 3 of neurology) don’t prepare you to practice general neurology, then what’s the point of residency at all? For that matter, what difference will renaming it do?
Imagine completing a 3-year internal medicine residency, then being told you need to do a fellowship in “comprehensive medicine” in order to practice. Or at least so you can add the word “comprehensive” to your shingle.
The authors bemoan the increasing number of neurology residents wanting to do fellowships and subspecialize, a situation that mirrors the general trend of people away from general medicine toward specialties.
While I agree we do need subspecialists in neurology (and currently there are at least 31 recognized, which is way more than I would have guessed), the fact is that patients, and sometimes their internists, aren’t going to be the best judge of who does or doesn’t need to see one, compared with a general neurologist.
Most of us general people can handle straightforward Parkinson’s disease, epilepsy, migraines, etc. Certainly, there are times where the condition is refractory to our care, or there’s something unusual about the case, that leads us to refer them to someone with more expertise. But isn’t that how it’s supposed to work? Like medicine in general, we need more general people than subspecialists.
Honestly, I can’t claim to be any different. Twenty-six years ago, when I finished residency, I did a clinical neurophysiology fellowship. From a practical view it was an epilepsy fellowship at my program. Some of this was an interest at the time in subspecializing, some of it was me putting off joining the “real world” of having to find a job for a year.
When I hung up my own shingle, my business card listed a subspecialty in epilepsy. Looking back years later, this wasn’t the best move. In solo practice I had no access to an epilepsy monitoring unit, vagus nerve stimulation capabilities, or epilepsy surgery at the hospital I rounded at. Not only that, I discovered it put me at a disadvantage, as internists were referring only epilepsy patients to me, and all the other stuff (which is the majority of patients) to the general (or comprehensive) neurologists around me. Which, financially, wasn’t a good thing when you’re young and starting out.
Not only that, but I discovered that I didn’t like only seeing one thing. I found it boring, and not for me.
So after a year or so, I took the word “epilepsy” off my card, left it at “general neurology,” and sent out letters reminding my referral base that I was willing to see the majority of things in my field (rare diseases, even today, I won’t attempt to handle).
So now my days are a mix of things, which I like. Neurology is enough of a specialty for me without going further up the pyramid. Having sub (and even sub-sub) specialists is important to maintain medical excellence, but we still need people willing to do general neurology, and I’m happy there.
Changing my title to “comprehensive” is unnecessary. I’m happy with what I am.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
PTSD symptoms in women tied to worse heart, brain health
TOPLINE:
METHODOLOGY:
- Researchers conducted a cross-sectional study of 274 women (mean age, 59 years) participating in the MsBrain study of menopause and brain health.
- As part of the study, the women completed the PTSD Checklist–Civilian Version and underwent physical and neuropsychological testing, as well as carotid artery ultrasonography and brain MRI.
- Outcomes of interest were associations of PTSD symptoms with carotid intima media thickness (IMT), brain white matter hyperintensity volume (WMHV), and cognition, assessed in linear regression models.
- Interactions by APOEε4 were assessed; covariates included age, race/ethnicity, education, and CVD risk factors.
TAKEAWAY:
- Higher PTSD symptoms were associated with greater carotid IMT (P = .03); associations of PTSD symptoms with neurocognitive outcomes varied significantly by APOEε4 status.
- Among APOEε4 carriers, PTSD symptoms were associated with greater whole-brain WMHV (P = .009), periventricular WMHV (P = .02), deep WMHV (P = .01), and frontal WMHV (P = .04) in multivariable models.
- APOEε4 carriers with PTSD symptoms also had poorer cognition, specifically attention and working memory (P = .02), semantic fluency (P = .01), perceptual speed (P = .002) and processing speed (P = .002), in multivariable models.
IN PRACTICE:
“This study sheds important insight on the implications of PTSD symptoms to women’s cardiovascular and neurocognitive health. Our findings indicate that the APOEε4 genotype may identify a group of women with PTSD symptoms at particular risk for poor neurocognitive health,” the authors wrote.
SOURCE:
The study, with first author Rebecca Thurston, PhD, of the department of psychiatry, University of Pittsburgh, was published online in JAMA Network Open.
LIMITATIONS:
No diagnostic clinical interviews were conducted, and PTSD treatment was not assessed. All participants identified as cisgender, and most were non-Hispanic Black or White. The study was observational and cross-sectional, precluding assertions about directionality or causality.
DISCLOSURES:
The study was funded by the National Institutes of Health, the University of Pittsburgh Clinical and Translational Science Institute, and the University of Pittsburgh Small Molecule Biomarker Core. Dr. Thurston reported receiving personal fees from Astellas Pharma, Bayer, Hello Therapeutics, Vira Health, and Happify Health outside the submitted work.
A version of this article first appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- Researchers conducted a cross-sectional study of 274 women (mean age, 59 years) participating in the MsBrain study of menopause and brain health.
- As part of the study, the women completed the PTSD Checklist–Civilian Version and underwent physical and neuropsychological testing, as well as carotid artery ultrasonography and brain MRI.
- Outcomes of interest were associations of PTSD symptoms with carotid intima media thickness (IMT), brain white matter hyperintensity volume (WMHV), and cognition, assessed in linear regression models.
- Interactions by APOEε4 were assessed; covariates included age, race/ethnicity, education, and CVD risk factors.
TAKEAWAY:
- Higher PTSD symptoms were associated with greater carotid IMT (P = .03); associations of PTSD symptoms with neurocognitive outcomes varied significantly by APOEε4 status.
- Among APOEε4 carriers, PTSD symptoms were associated with greater whole-brain WMHV (P = .009), periventricular WMHV (P = .02), deep WMHV (P = .01), and frontal WMHV (P = .04) in multivariable models.
- APOEε4 carriers with PTSD symptoms also had poorer cognition, specifically attention and working memory (P = .02), semantic fluency (P = .01), perceptual speed (P = .002) and processing speed (P = .002), in multivariable models.
IN PRACTICE:
“This study sheds important insight on the implications of PTSD symptoms to women’s cardiovascular and neurocognitive health. Our findings indicate that the APOEε4 genotype may identify a group of women with PTSD symptoms at particular risk for poor neurocognitive health,” the authors wrote.
SOURCE:
The study, with first author Rebecca Thurston, PhD, of the department of psychiatry, University of Pittsburgh, was published online in JAMA Network Open.
LIMITATIONS:
No diagnostic clinical interviews were conducted, and PTSD treatment was not assessed. All participants identified as cisgender, and most were non-Hispanic Black or White. The study was observational and cross-sectional, precluding assertions about directionality or causality.
DISCLOSURES:
The study was funded by the National Institutes of Health, the University of Pittsburgh Clinical and Translational Science Institute, and the University of Pittsburgh Small Molecule Biomarker Core. Dr. Thurston reported receiving personal fees from Astellas Pharma, Bayer, Hello Therapeutics, Vira Health, and Happify Health outside the submitted work.
A version of this article first appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- Researchers conducted a cross-sectional study of 274 women (mean age, 59 years) participating in the MsBrain study of menopause and brain health.
- As part of the study, the women completed the PTSD Checklist–Civilian Version and underwent physical and neuropsychological testing, as well as carotid artery ultrasonography and brain MRI.
- Outcomes of interest were associations of PTSD symptoms with carotid intima media thickness (IMT), brain white matter hyperintensity volume (WMHV), and cognition, assessed in linear regression models.
- Interactions by APOEε4 were assessed; covariates included age, race/ethnicity, education, and CVD risk factors.
TAKEAWAY:
- Higher PTSD symptoms were associated with greater carotid IMT (P = .03); associations of PTSD symptoms with neurocognitive outcomes varied significantly by APOEε4 status.
- Among APOEε4 carriers, PTSD symptoms were associated with greater whole-brain WMHV (P = .009), periventricular WMHV (P = .02), deep WMHV (P = .01), and frontal WMHV (P = .04) in multivariable models.
- APOEε4 carriers with PTSD symptoms also had poorer cognition, specifically attention and working memory (P = .02), semantic fluency (P = .01), perceptual speed (P = .002) and processing speed (P = .002), in multivariable models.
IN PRACTICE:
“This study sheds important insight on the implications of PTSD symptoms to women’s cardiovascular and neurocognitive health. Our findings indicate that the APOEε4 genotype may identify a group of women with PTSD symptoms at particular risk for poor neurocognitive health,” the authors wrote.
SOURCE:
The study, with first author Rebecca Thurston, PhD, of the department of psychiatry, University of Pittsburgh, was published online in JAMA Network Open.
LIMITATIONS:
No diagnostic clinical interviews were conducted, and PTSD treatment was not assessed. All participants identified as cisgender, and most were non-Hispanic Black or White. The study was observational and cross-sectional, precluding assertions about directionality or causality.
DISCLOSURES:
The study was funded by the National Institutes of Health, the University of Pittsburgh Clinical and Translational Science Institute, and the University of Pittsburgh Small Molecule Biomarker Core. Dr. Thurston reported receiving personal fees from Astellas Pharma, Bayer, Hello Therapeutics, Vira Health, and Happify Health outside the submitted work.
A version of this article first appeared on Medscape.com.
Drugs to prevent versus those to treat migraine might not share targets
, according to experts attempting to put these puzzle pieces together at the 2023 Scottsdale Headache Symposium.
As the details of the complex chain of molecular events become better understood, there is reason to believe that the targets for aborting events early in the process are not necessarily therapeutic at later stages or vice versa, according to Peter Goadsby, MBBS, MD, PhD, director of the National Institute for Health Research and professor of neurology, King’s College, London.
“I think this explains some of the frustration at trigger modulation. I think we are often trying to modulate a process that has already got started,” he said. The analogy might be closing the barn door after the animals have escaped.
Migraine phases might explain pathology
Given the progress in understanding each step that leads from one phase to the next in migraine onset, this premise is not surprising. Increased blood flow, trigeminal activation, and release of calcitonin gene–related peptide (CGRP) are early events in this process, according to Dr. Goadsby, but there is still uncertainty about the triggers of brainstem stimulation and cranial blood flow that precedes these events.
In his talk about the advances that led to the development of CGRP-targeted therapy, Dr. Goadsby explained how and why CGRP inhibition, along with triptans, pituitary adenylate cyclase–activating polypeptide (PACAP) inhibitors, and ditans, have been developed as treatment targets in migraine, while other once-promising targets, such as substance P inhibition and inducible nitric oxide synthase (INOS) inhibition, have not.
Much of this progress has been by trial and error through clinical studies in which efficacy has or has not been seen. Despite the progress in mapping the release of CGRP and its activity, Dr. Goadsby acknowledged that there is still much about its participation in migraine pathophysiology that remains poorly defined.
“Anyone who tells you that they know how CGRP works I think is blowing smoke, frankly,” Dr. Goadsby said. “Clearly these things are complex.”
CGRP is active in the CSF
This includes the site of action. Dr. Goadsby said that it is widely believed that CGRP inhibitors are active in the dura and not in the cerebrospinal fluid (CSF). However, Dr. Goadsby said that a study undertaken with monoclonal antibodies targeting CGRP have produced compelling evidence that CGRP is reduced in the CSF.
“They clearly get into the CSF,” said Dr. Goadsby, noting that the barrier between peripheral blood and the CSF “is different from the blood-brain barrier.”
Widely regarded as playing a pivotal role in the development of CGRP as a therapeutic target in migraine, Dr. Goadsby spent some time speculating about its potential for preventing the earliest steps in the process that leads from the premonitory state to allodynia, prodromal symptoms, migraine, and postdromal recovery.
Of triggers, “light is my favorite example,” he said. He noted that many patients are convinced that light initiates the subsequent steps that end in a migraine. This is fair assumption for those who have seen a sequence of events in which light in the absence of any other symptom always precedes prodromal symptoms and migraine.
“Why would you not think that?” he asked. “Unless you point out that the attack had already started and the reason that you are noticing the light is because of photophobia that started during the premonitory phase.”
It is increasingly clear that CGRP inhibition does have clinical benefit when started at early signs of a coming migraine, according to Dr. Goadsby. He cited a phase 3 study published just days before he spoke at the Scottsdale Headache Symposium. Called PRODROME, the study associated the CGRP receptor antagonist ubrogepant, which is already approved for treatment of migraine, with a significant reduction in the risk of moderate to severe headache relative to placebo when measured 24 hours after randomization (46% vs. 29%; P < .0001).
Brain activity monitoring supports phases
Citing imaging studies in his own laboratory, Todd J. Schwedt, MD, chair of neurology research, Mayo Clinic, Phoenix, substantiated several of the points made by Dr. Goadsby in a separate talk he made on migraine phases. By monitoring brain activity during each phase of migraine, he suggested his data support the role of CGRP in producing an inflammatory response as well as sensitizing the trigeminal cervical system in steps that appear to be important to the pain process.
Dr. Schwedt showed several pieces of evidence suggesting that CGRP is an early mediator even if it is not necessarily the first step in a process for every patient. However, like Dr. Goadsby, Dr. Schwedt also acknowledged that the interplay between events is complex and might differ between patients.
Yet, he says that brain activity on imaging is not the only evidence of the role of CGRP activation early in the process leading toward migraine.
“I am a little biased towards imaging, but it’s not just about imaging,” Dr. Schwedt said.
“If we look at preictal salivary CGRP levels and then follow them into the headache phase, we see the levels increase, but they go back to normal a couple of hours into the attack and then stay normal, presumably, until the patient gets closer to the next attack,” Dr. Schwedt said.
Despite progress there is more to be done to determine why CGRP is released and whether it can be inhibited early to abort migraine before the headache phase, but both Dr. Goadsby and Dr. Schwedt pointed to this as a very early event. This is not to say that others, such as cortical spreading depression, do not have an equally important role in the evolution of migraine, but each expert considers migraine phases to be useful divisions for tracing the sequence of pathogenic events.
The phase of a migraine attack and their corresponding symptoms “can be mapped to altered brain function and release of neuropeptides and neurotransmitters,” Dr. Schwedt said. The implication is that better targets for blocking migraine before it reaches the headache phase might be discovered in these early phases.
Dr. Goadsby and Dr. Schwedt listed more than 10 pharmaceutical companies to which they have financial relationships, but both claimed that none of these relationships posed a potential conflict of interest.
, according to experts attempting to put these puzzle pieces together at the 2023 Scottsdale Headache Symposium.
As the details of the complex chain of molecular events become better understood, there is reason to believe that the targets for aborting events early in the process are not necessarily therapeutic at later stages or vice versa, according to Peter Goadsby, MBBS, MD, PhD, director of the National Institute for Health Research and professor of neurology, King’s College, London.
“I think this explains some of the frustration at trigger modulation. I think we are often trying to modulate a process that has already got started,” he said. The analogy might be closing the barn door after the animals have escaped.
Migraine phases might explain pathology
Given the progress in understanding each step that leads from one phase to the next in migraine onset, this premise is not surprising. Increased blood flow, trigeminal activation, and release of calcitonin gene–related peptide (CGRP) are early events in this process, according to Dr. Goadsby, but there is still uncertainty about the triggers of brainstem stimulation and cranial blood flow that precedes these events.
In his talk about the advances that led to the development of CGRP-targeted therapy, Dr. Goadsby explained how and why CGRP inhibition, along with triptans, pituitary adenylate cyclase–activating polypeptide (PACAP) inhibitors, and ditans, have been developed as treatment targets in migraine, while other once-promising targets, such as substance P inhibition and inducible nitric oxide synthase (INOS) inhibition, have not.
Much of this progress has been by trial and error through clinical studies in which efficacy has or has not been seen. Despite the progress in mapping the release of CGRP and its activity, Dr. Goadsby acknowledged that there is still much about its participation in migraine pathophysiology that remains poorly defined.
“Anyone who tells you that they know how CGRP works I think is blowing smoke, frankly,” Dr. Goadsby said. “Clearly these things are complex.”
CGRP is active in the CSF
This includes the site of action. Dr. Goadsby said that it is widely believed that CGRP inhibitors are active in the dura and not in the cerebrospinal fluid (CSF). However, Dr. Goadsby said that a study undertaken with monoclonal antibodies targeting CGRP have produced compelling evidence that CGRP is reduced in the CSF.
“They clearly get into the CSF,” said Dr. Goadsby, noting that the barrier between peripheral blood and the CSF “is different from the blood-brain barrier.”
Widely regarded as playing a pivotal role in the development of CGRP as a therapeutic target in migraine, Dr. Goadsby spent some time speculating about its potential for preventing the earliest steps in the process that leads from the premonitory state to allodynia, prodromal symptoms, migraine, and postdromal recovery.
Of triggers, “light is my favorite example,” he said. He noted that many patients are convinced that light initiates the subsequent steps that end in a migraine. This is fair assumption for those who have seen a sequence of events in which light in the absence of any other symptom always precedes prodromal symptoms and migraine.
“Why would you not think that?” he asked. “Unless you point out that the attack had already started and the reason that you are noticing the light is because of photophobia that started during the premonitory phase.”
It is increasingly clear that CGRP inhibition does have clinical benefit when started at early signs of a coming migraine, according to Dr. Goadsby. He cited a phase 3 study published just days before he spoke at the Scottsdale Headache Symposium. Called PRODROME, the study associated the CGRP receptor antagonist ubrogepant, which is already approved for treatment of migraine, with a significant reduction in the risk of moderate to severe headache relative to placebo when measured 24 hours after randomization (46% vs. 29%; P < .0001).
Brain activity monitoring supports phases
Citing imaging studies in his own laboratory, Todd J. Schwedt, MD, chair of neurology research, Mayo Clinic, Phoenix, substantiated several of the points made by Dr. Goadsby in a separate talk he made on migraine phases. By monitoring brain activity during each phase of migraine, he suggested his data support the role of CGRP in producing an inflammatory response as well as sensitizing the trigeminal cervical system in steps that appear to be important to the pain process.
Dr. Schwedt showed several pieces of evidence suggesting that CGRP is an early mediator even if it is not necessarily the first step in a process for every patient. However, like Dr. Goadsby, Dr. Schwedt also acknowledged that the interplay between events is complex and might differ between patients.
Yet, he says that brain activity on imaging is not the only evidence of the role of CGRP activation early in the process leading toward migraine.
“I am a little biased towards imaging, but it’s not just about imaging,” Dr. Schwedt said.
“If we look at preictal salivary CGRP levels and then follow them into the headache phase, we see the levels increase, but they go back to normal a couple of hours into the attack and then stay normal, presumably, until the patient gets closer to the next attack,” Dr. Schwedt said.
Despite progress there is more to be done to determine why CGRP is released and whether it can be inhibited early to abort migraine before the headache phase, but both Dr. Goadsby and Dr. Schwedt pointed to this as a very early event. This is not to say that others, such as cortical spreading depression, do not have an equally important role in the evolution of migraine, but each expert considers migraine phases to be useful divisions for tracing the sequence of pathogenic events.
The phase of a migraine attack and their corresponding symptoms “can be mapped to altered brain function and release of neuropeptides and neurotransmitters,” Dr. Schwedt said. The implication is that better targets for blocking migraine before it reaches the headache phase might be discovered in these early phases.
Dr. Goadsby and Dr. Schwedt listed more than 10 pharmaceutical companies to which they have financial relationships, but both claimed that none of these relationships posed a potential conflict of interest.
, according to experts attempting to put these puzzle pieces together at the 2023 Scottsdale Headache Symposium.
As the details of the complex chain of molecular events become better understood, there is reason to believe that the targets for aborting events early in the process are not necessarily therapeutic at later stages or vice versa, according to Peter Goadsby, MBBS, MD, PhD, director of the National Institute for Health Research and professor of neurology, King’s College, London.
“I think this explains some of the frustration at trigger modulation. I think we are often trying to modulate a process that has already got started,” he said. The analogy might be closing the barn door after the animals have escaped.
Migraine phases might explain pathology
Given the progress in understanding each step that leads from one phase to the next in migraine onset, this premise is not surprising. Increased blood flow, trigeminal activation, and release of calcitonin gene–related peptide (CGRP) are early events in this process, according to Dr. Goadsby, but there is still uncertainty about the triggers of brainstem stimulation and cranial blood flow that precedes these events.
In his talk about the advances that led to the development of CGRP-targeted therapy, Dr. Goadsby explained how and why CGRP inhibition, along with triptans, pituitary adenylate cyclase–activating polypeptide (PACAP) inhibitors, and ditans, have been developed as treatment targets in migraine, while other once-promising targets, such as substance P inhibition and inducible nitric oxide synthase (INOS) inhibition, have not.
Much of this progress has been by trial and error through clinical studies in which efficacy has or has not been seen. Despite the progress in mapping the release of CGRP and its activity, Dr. Goadsby acknowledged that there is still much about its participation in migraine pathophysiology that remains poorly defined.
“Anyone who tells you that they know how CGRP works I think is blowing smoke, frankly,” Dr. Goadsby said. “Clearly these things are complex.”
CGRP is active in the CSF
This includes the site of action. Dr. Goadsby said that it is widely believed that CGRP inhibitors are active in the dura and not in the cerebrospinal fluid (CSF). However, Dr. Goadsby said that a study undertaken with monoclonal antibodies targeting CGRP have produced compelling evidence that CGRP is reduced in the CSF.
“They clearly get into the CSF,” said Dr. Goadsby, noting that the barrier between peripheral blood and the CSF “is different from the blood-brain barrier.”
Widely regarded as playing a pivotal role in the development of CGRP as a therapeutic target in migraine, Dr. Goadsby spent some time speculating about its potential for preventing the earliest steps in the process that leads from the premonitory state to allodynia, prodromal symptoms, migraine, and postdromal recovery.
Of triggers, “light is my favorite example,” he said. He noted that many patients are convinced that light initiates the subsequent steps that end in a migraine. This is fair assumption for those who have seen a sequence of events in which light in the absence of any other symptom always precedes prodromal symptoms and migraine.
“Why would you not think that?” he asked. “Unless you point out that the attack had already started and the reason that you are noticing the light is because of photophobia that started during the premonitory phase.”
It is increasingly clear that CGRP inhibition does have clinical benefit when started at early signs of a coming migraine, according to Dr. Goadsby. He cited a phase 3 study published just days before he spoke at the Scottsdale Headache Symposium. Called PRODROME, the study associated the CGRP receptor antagonist ubrogepant, which is already approved for treatment of migraine, with a significant reduction in the risk of moderate to severe headache relative to placebo when measured 24 hours after randomization (46% vs. 29%; P < .0001).
Brain activity monitoring supports phases
Citing imaging studies in his own laboratory, Todd J. Schwedt, MD, chair of neurology research, Mayo Clinic, Phoenix, substantiated several of the points made by Dr. Goadsby in a separate talk he made on migraine phases. By monitoring brain activity during each phase of migraine, he suggested his data support the role of CGRP in producing an inflammatory response as well as sensitizing the trigeminal cervical system in steps that appear to be important to the pain process.
Dr. Schwedt showed several pieces of evidence suggesting that CGRP is an early mediator even if it is not necessarily the first step in a process for every patient. However, like Dr. Goadsby, Dr. Schwedt also acknowledged that the interplay between events is complex and might differ between patients.
Yet, he says that brain activity on imaging is not the only evidence of the role of CGRP activation early in the process leading toward migraine.
“I am a little biased towards imaging, but it’s not just about imaging,” Dr. Schwedt said.
“If we look at preictal salivary CGRP levels and then follow them into the headache phase, we see the levels increase, but they go back to normal a couple of hours into the attack and then stay normal, presumably, until the patient gets closer to the next attack,” Dr. Schwedt said.
Despite progress there is more to be done to determine why CGRP is released and whether it can be inhibited early to abort migraine before the headache phase, but both Dr. Goadsby and Dr. Schwedt pointed to this as a very early event. This is not to say that others, such as cortical spreading depression, do not have an equally important role in the evolution of migraine, but each expert considers migraine phases to be useful divisions for tracing the sequence of pathogenic events.
The phase of a migraine attack and their corresponding symptoms “can be mapped to altered brain function and release of neuropeptides and neurotransmitters,” Dr. Schwedt said. The implication is that better targets for blocking migraine before it reaches the headache phase might be discovered in these early phases.
Dr. Goadsby and Dr. Schwedt listed more than 10 pharmaceutical companies to which they have financial relationships, but both claimed that none of these relationships posed a potential conflict of interest.
FROM THE 2023 SCOTTSDALE HEADACHE SYMPOSIUM
Patients with Parkinson’s at elevated risk for suicidal thoughts, behavior
Adults with Parkinson’s disease are twice as likely to engage in suicidal behavior as the general population, results of a large meta-analysis show.
Given that up to half of patients with PD suffer from depression and anxiety, physicians should maintain a “high index of suspicion” for early recognition and management of suicidality, write the investigators, led by Eng-King Tan, MD, of Duke-NUS Medical School, Singapore.
“Management of both medical, such as sleep disorders, and psychosocial risk factors, such as feelings of loneliness, hopelessness, and depressed mood, could be useful in lowering suicide risk in patients with PD,” they add.
The study was published online in JAMA Neurology.
Suicide risk neglected in PD?
The analysis included 505,950 patients with PD across 28 cross-sectional, case-control, and cohort studies.
Across 14 studies, the prevalence of suicidal ideation in patients with PD was 22.2% (95% confidence interval, 14.6-32.3). In a sensitivity analysis excluding three outliers, the prevalence of suicidal ideation was higher at 24% (95% CI, 19.1-29.7).
Across 21 studies, the prevalence of suicidal behavior was “substantial” at 1.25% (95% CI, 0.64-2.41), the authors report. The prevalence of suicidal behavior was significantly higher in prospective studies (1.75%; 95% CI, 1.03-2.95) than retrospective studies (0.50%; 95% CI, 0.24 to 1.01).
Across 10 studies, the likelihood of suicidal behavior was about twofold higher among patients with PD than general population controls (odds ratio, 2.15; 95% CI, 1.22-3.78; P = .01). Across nine studies, the hazard ratio for suicidal behavior was 1.73 (95% CI, 1.40-2.14; P < .001).
There was no evidence of sex-related differences in suicidal behavior, although the analysis was limited by the paucity of data, the researchers note.
They note the quality of included studies was generally high, although eight of them did not explicitly identify and adjust for confounders.
Higher rate of mood, anxiety disorders
Paul Nestadt, MD, with Johns Hopkins Bloomberg School of Public Health, Baltimore, said this analysis reiterates what several reviews have found over the past few years, including his own.
“In general, rates of mood and anxiety disorders are much higher in PD than in other dementias, such as Alzheimer’s disease. This is reason enough to allocate resources to the mental health care of those diagnosed with PD and to pay special attention to at risk periods, such as early in the diagnosis, when suicide rates seem to be higher in dementias in general,” said Dr. Nestadt, who wasn’t involved in the study.
He noted that research has shown that suicides among people with PD are more likely to involve a firearm – likely because people with PD are more likely to be over age 65 and to be male – “both huge risk factors for firearm suicide.”
“Therefore, it is essential that caregivers be aware of the risks posed by firearms in the homes of people suffering from Parkinson’s or other dementias. It is the clinician’s responsibility to inform families of this risk, but it is all too often neglected,” Dr. Nestadt said.
Support for the study was provided in part by the National Medical Research Council. Dr. Tan reported honoraria from Eisai and Elsevier outside the submitted work. Dr. Nestadt reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Adults with Parkinson’s disease are twice as likely to engage in suicidal behavior as the general population, results of a large meta-analysis show.
Given that up to half of patients with PD suffer from depression and anxiety, physicians should maintain a “high index of suspicion” for early recognition and management of suicidality, write the investigators, led by Eng-King Tan, MD, of Duke-NUS Medical School, Singapore.
“Management of both medical, such as sleep disorders, and psychosocial risk factors, such as feelings of loneliness, hopelessness, and depressed mood, could be useful in lowering suicide risk in patients with PD,” they add.
The study was published online in JAMA Neurology.
Suicide risk neglected in PD?
The analysis included 505,950 patients with PD across 28 cross-sectional, case-control, and cohort studies.
Across 14 studies, the prevalence of suicidal ideation in patients with PD was 22.2% (95% confidence interval, 14.6-32.3). In a sensitivity analysis excluding three outliers, the prevalence of suicidal ideation was higher at 24% (95% CI, 19.1-29.7).
Across 21 studies, the prevalence of suicidal behavior was “substantial” at 1.25% (95% CI, 0.64-2.41), the authors report. The prevalence of suicidal behavior was significantly higher in prospective studies (1.75%; 95% CI, 1.03-2.95) than retrospective studies (0.50%; 95% CI, 0.24 to 1.01).
Across 10 studies, the likelihood of suicidal behavior was about twofold higher among patients with PD than general population controls (odds ratio, 2.15; 95% CI, 1.22-3.78; P = .01). Across nine studies, the hazard ratio for suicidal behavior was 1.73 (95% CI, 1.40-2.14; P < .001).
There was no evidence of sex-related differences in suicidal behavior, although the analysis was limited by the paucity of data, the researchers note.
They note the quality of included studies was generally high, although eight of them did not explicitly identify and adjust for confounders.
Higher rate of mood, anxiety disorders
Paul Nestadt, MD, with Johns Hopkins Bloomberg School of Public Health, Baltimore, said this analysis reiterates what several reviews have found over the past few years, including his own.
“In general, rates of mood and anxiety disorders are much higher in PD than in other dementias, such as Alzheimer’s disease. This is reason enough to allocate resources to the mental health care of those diagnosed with PD and to pay special attention to at risk periods, such as early in the diagnosis, when suicide rates seem to be higher in dementias in general,” said Dr. Nestadt, who wasn’t involved in the study.
He noted that research has shown that suicides among people with PD are more likely to involve a firearm – likely because people with PD are more likely to be over age 65 and to be male – “both huge risk factors for firearm suicide.”
“Therefore, it is essential that caregivers be aware of the risks posed by firearms in the homes of people suffering from Parkinson’s or other dementias. It is the clinician’s responsibility to inform families of this risk, but it is all too often neglected,” Dr. Nestadt said.
Support for the study was provided in part by the National Medical Research Council. Dr. Tan reported honoraria from Eisai and Elsevier outside the submitted work. Dr. Nestadt reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Adults with Parkinson’s disease are twice as likely to engage in suicidal behavior as the general population, results of a large meta-analysis show.
Given that up to half of patients with PD suffer from depression and anxiety, physicians should maintain a “high index of suspicion” for early recognition and management of suicidality, write the investigators, led by Eng-King Tan, MD, of Duke-NUS Medical School, Singapore.
“Management of both medical, such as sleep disorders, and psychosocial risk factors, such as feelings of loneliness, hopelessness, and depressed mood, could be useful in lowering suicide risk in patients with PD,” they add.
The study was published online in JAMA Neurology.
Suicide risk neglected in PD?
The analysis included 505,950 patients with PD across 28 cross-sectional, case-control, and cohort studies.
Across 14 studies, the prevalence of suicidal ideation in patients with PD was 22.2% (95% confidence interval, 14.6-32.3). In a sensitivity analysis excluding three outliers, the prevalence of suicidal ideation was higher at 24% (95% CI, 19.1-29.7).
Across 21 studies, the prevalence of suicidal behavior was “substantial” at 1.25% (95% CI, 0.64-2.41), the authors report. The prevalence of suicidal behavior was significantly higher in prospective studies (1.75%; 95% CI, 1.03-2.95) than retrospective studies (0.50%; 95% CI, 0.24 to 1.01).
Across 10 studies, the likelihood of suicidal behavior was about twofold higher among patients with PD than general population controls (odds ratio, 2.15; 95% CI, 1.22-3.78; P = .01). Across nine studies, the hazard ratio for suicidal behavior was 1.73 (95% CI, 1.40-2.14; P < .001).
There was no evidence of sex-related differences in suicidal behavior, although the analysis was limited by the paucity of data, the researchers note.
They note the quality of included studies was generally high, although eight of them did not explicitly identify and adjust for confounders.
Higher rate of mood, anxiety disorders
Paul Nestadt, MD, with Johns Hopkins Bloomberg School of Public Health, Baltimore, said this analysis reiterates what several reviews have found over the past few years, including his own.
“In general, rates of mood and anxiety disorders are much higher in PD than in other dementias, such as Alzheimer’s disease. This is reason enough to allocate resources to the mental health care of those diagnosed with PD and to pay special attention to at risk periods, such as early in the diagnosis, when suicide rates seem to be higher in dementias in general,” said Dr. Nestadt, who wasn’t involved in the study.
He noted that research has shown that suicides among people with PD are more likely to involve a firearm – likely because people with PD are more likely to be over age 65 and to be male – “both huge risk factors for firearm suicide.”
“Therefore, it is essential that caregivers be aware of the risks posed by firearms in the homes of people suffering from Parkinson’s or other dementias. It is the clinician’s responsibility to inform families of this risk, but it is all too often neglected,” Dr. Nestadt said.
Support for the study was provided in part by the National Medical Research Council. Dr. Tan reported honoraria from Eisai and Elsevier outside the submitted work. Dr. Nestadt reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Yoga linked to seizure, anxiety reduction in epilepsy
TOPLINE:
in people with epilepsy, a new study shows.
METHODOLOGY:
- Investigators included participants aged 18-60 years with epilepsy who scored ≥ 4 on the Kilifi Stigma Scale of Epilepsy. A score greater than the 66th percentile indicates the presence of strongly felt stigma.
- Patients (n = 160) had an average of one seizure per week, and most took at least two antiseizure medications.
- The intervention group (n = 80) participated in a yoga module with muscle-loosening exercises, slow and synchronized breathing, meditation, and positive affirmations. The control group (n = 80) participated in sham yoga sessions with no instructions on the breathing exercises or attention to the body movements and sensations during practice.
- Both groups participated in seven 1-hour supervised group yoga sessions over 3 months, were asked to practice the interventions at home five times per week, and received a psychoeducation module on epilepsy.
TAKEAWAY:
- Participants practicing the intervention module had significant reductions in self-perceived stigma, compared with those in the control group (P = .01).
- The proportion of participants in the intervention group who had a more than 50% seizure reduction (odds ratio, 4.11; P = .01) and complete seizure remission (OR, 7.4; P = .005) at the end of the 6-month follow-up was significantly higher than in the control group.
- Compared with those in the control group, there were also significant improvements in anxiety (P = .032) and quality of life (P < .001) in the intervention group.
- The intervention group also experienced significant improvement in mindfulness (P < .001) and cognitive impairment, compared with the control group (P < .004).
IN PRACTICE:
“This stigma can affect a person’s life in many ways, including treatment, emergency department visits, and poor mental health,” study investigator Majari Tripathi, MD, of All India Institute of Medical Sciences, New Delhi, said in a press release. “Our study showed that doing yoga can alleviate the burden of epilepsy and improve the overall quality of life by reducing this perceived stigma.”
SOURCE:
Dr. Tripathi and Kirandeep Kaur, MD, also of All India Institute of Medical Sciences, conducted the study with their colleagues. It was published online in Neurology.
LIMITATIONS:
There was no passive control or treatment as usual group, which would indicate the effect size of the intervention. In addition, there was no monitoring of seizure frequency before the study began, which may have biased the change of seizure frequency as an outcome.
DISCLOSURES:
The study investigators reported no study funding or reported disclosures.
A version of this article appeared on Medscape.com.
TOPLINE:
in people with epilepsy, a new study shows.
METHODOLOGY:
- Investigators included participants aged 18-60 years with epilepsy who scored ≥ 4 on the Kilifi Stigma Scale of Epilepsy. A score greater than the 66th percentile indicates the presence of strongly felt stigma.
- Patients (n = 160) had an average of one seizure per week, and most took at least two antiseizure medications.
- The intervention group (n = 80) participated in a yoga module with muscle-loosening exercises, slow and synchronized breathing, meditation, and positive affirmations. The control group (n = 80) participated in sham yoga sessions with no instructions on the breathing exercises or attention to the body movements and sensations during practice.
- Both groups participated in seven 1-hour supervised group yoga sessions over 3 months, were asked to practice the interventions at home five times per week, and received a psychoeducation module on epilepsy.
TAKEAWAY:
- Participants practicing the intervention module had significant reductions in self-perceived stigma, compared with those in the control group (P = .01).
- The proportion of participants in the intervention group who had a more than 50% seizure reduction (odds ratio, 4.11; P = .01) and complete seizure remission (OR, 7.4; P = .005) at the end of the 6-month follow-up was significantly higher than in the control group.
- Compared with those in the control group, there were also significant improvements in anxiety (P = .032) and quality of life (P < .001) in the intervention group.
- The intervention group also experienced significant improvement in mindfulness (P < .001) and cognitive impairment, compared with the control group (P < .004).
IN PRACTICE:
“This stigma can affect a person’s life in many ways, including treatment, emergency department visits, and poor mental health,” study investigator Majari Tripathi, MD, of All India Institute of Medical Sciences, New Delhi, said in a press release. “Our study showed that doing yoga can alleviate the burden of epilepsy and improve the overall quality of life by reducing this perceived stigma.”
SOURCE:
Dr. Tripathi and Kirandeep Kaur, MD, also of All India Institute of Medical Sciences, conducted the study with their colleagues. It was published online in Neurology.
LIMITATIONS:
There was no passive control or treatment as usual group, which would indicate the effect size of the intervention. In addition, there was no monitoring of seizure frequency before the study began, which may have biased the change of seizure frequency as an outcome.
DISCLOSURES:
The study investigators reported no study funding or reported disclosures.
A version of this article appeared on Medscape.com.
TOPLINE:
in people with epilepsy, a new study shows.
METHODOLOGY:
- Investigators included participants aged 18-60 years with epilepsy who scored ≥ 4 on the Kilifi Stigma Scale of Epilepsy. A score greater than the 66th percentile indicates the presence of strongly felt stigma.
- Patients (n = 160) had an average of one seizure per week, and most took at least two antiseizure medications.
- The intervention group (n = 80) participated in a yoga module with muscle-loosening exercises, slow and synchronized breathing, meditation, and positive affirmations. The control group (n = 80) participated in sham yoga sessions with no instructions on the breathing exercises or attention to the body movements and sensations during practice.
- Both groups participated in seven 1-hour supervised group yoga sessions over 3 months, were asked to practice the interventions at home five times per week, and received a psychoeducation module on epilepsy.
TAKEAWAY:
- Participants practicing the intervention module had significant reductions in self-perceived stigma, compared with those in the control group (P = .01).
- The proportion of participants in the intervention group who had a more than 50% seizure reduction (odds ratio, 4.11; P = .01) and complete seizure remission (OR, 7.4; P = .005) at the end of the 6-month follow-up was significantly higher than in the control group.
- Compared with those in the control group, there were also significant improvements in anxiety (P = .032) and quality of life (P < .001) in the intervention group.
- The intervention group also experienced significant improvement in mindfulness (P < .001) and cognitive impairment, compared with the control group (P < .004).
IN PRACTICE:
“This stigma can affect a person’s life in many ways, including treatment, emergency department visits, and poor mental health,” study investigator Majari Tripathi, MD, of All India Institute of Medical Sciences, New Delhi, said in a press release. “Our study showed that doing yoga can alleviate the burden of epilepsy and improve the overall quality of life by reducing this perceived stigma.”
SOURCE:
Dr. Tripathi and Kirandeep Kaur, MD, also of All India Institute of Medical Sciences, conducted the study with their colleagues. It was published online in Neurology.
LIMITATIONS:
There was no passive control or treatment as usual group, which would indicate the effect size of the intervention. In addition, there was no monitoring of seizure frequency before the study began, which may have biased the change of seizure frequency as an outcome.
DISCLOSURES:
The study investigators reported no study funding or reported disclosures.
A version of this article appeared on Medscape.com.
Chronic pain in the United States: New data
data from the Centers for Disease Control and Prevention show.
Results from the annual National Health Interview Survey (NHIS) show that over-the-counter (OTC) pain relievers were the most commonly used pharmacologic treatment and exercise was the most common choice among nonpharmacologic options.
The results also revealed that prescription opioid use for chronic pain decreased from 15.2% in 2019 to 13.5% in 2020. However, there was no corresponding increase in nonpharmacologic therapies, despite current CDC guidelines that recommend maximizing the use of medication alternatives.
“Public health efforts may reduce health inequities by increasing access to pain management therapies so that all persons with chronic pain can receive safe and effective care,” S. Michaela Rikard, PhD, and colleagues wrote.
The findings were published online in a research letter in Annals of Internal Medicine.
Among 31,500 survey respondents, 7,400 indicated that they had pain on most days or every day for the past 3 months.
The survey collected data on self-reported opioid prescriptions in the past 3 months, as well as prescription and nonprescription opiate use during the same time period.
Among adult respondents, 60% used a combination of pharmacologic and nonpharmacologic treatments for pain and almost 27% used medications alone. Older adults, those with low incomes, uninsured individuals, and those living in the South were among those least likely to turn to nonpharmacologic treatment for pain.
After exercise, complementary therapies were the most commonly used nonpharmacologic options, including massage, meditation, or guided imagery, and spinal manipulation or other forms of chiropractic care.
For those taking medications, 76% self-reported using OTC pain relievers for pain, followed by prescription nonopioids (31%) and prescription opioids (13.5%).
Of those who used both pharmacologic and nonpharmacologic therapies, about half reported nonopioid and nonpharmacologic therapy use and 8% reported combined use of opioids, nonopioids, and nonpharmacologic therapy.
After adjustment for multiple factors, investigators found those who were older, had public insurance, or had more severe pain were more likely to use prescription opioids. They also reported severe pain (22%), but 4% reported only mild pain.
Study limitations included generalizability only to noninstitutionalized civilian adults, potential recall bias, and cross-sectional results that do not include patient or treatment history.
“Despite its limitations, this study identifies opportunities to improve guideline-concordant use of pharmacologic and nonpharmacologic therapies among adults with chronic pain,” the authors wrote.
There was no specific funding source for the study. The authors have reported no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
data from the Centers for Disease Control and Prevention show.
Results from the annual National Health Interview Survey (NHIS) show that over-the-counter (OTC) pain relievers were the most commonly used pharmacologic treatment and exercise was the most common choice among nonpharmacologic options.
The results also revealed that prescription opioid use for chronic pain decreased from 15.2% in 2019 to 13.5% in 2020. However, there was no corresponding increase in nonpharmacologic therapies, despite current CDC guidelines that recommend maximizing the use of medication alternatives.
“Public health efforts may reduce health inequities by increasing access to pain management therapies so that all persons with chronic pain can receive safe and effective care,” S. Michaela Rikard, PhD, and colleagues wrote.
The findings were published online in a research letter in Annals of Internal Medicine.
Among 31,500 survey respondents, 7,400 indicated that they had pain on most days or every day for the past 3 months.
The survey collected data on self-reported opioid prescriptions in the past 3 months, as well as prescription and nonprescription opiate use during the same time period.
Among adult respondents, 60% used a combination of pharmacologic and nonpharmacologic treatments for pain and almost 27% used medications alone. Older adults, those with low incomes, uninsured individuals, and those living in the South were among those least likely to turn to nonpharmacologic treatment for pain.
After exercise, complementary therapies were the most commonly used nonpharmacologic options, including massage, meditation, or guided imagery, and spinal manipulation or other forms of chiropractic care.
For those taking medications, 76% self-reported using OTC pain relievers for pain, followed by prescription nonopioids (31%) and prescription opioids (13.5%).
Of those who used both pharmacologic and nonpharmacologic therapies, about half reported nonopioid and nonpharmacologic therapy use and 8% reported combined use of opioids, nonopioids, and nonpharmacologic therapy.
After adjustment for multiple factors, investigators found those who were older, had public insurance, or had more severe pain were more likely to use prescription opioids. They also reported severe pain (22%), but 4% reported only mild pain.
Study limitations included generalizability only to noninstitutionalized civilian adults, potential recall bias, and cross-sectional results that do not include patient or treatment history.
“Despite its limitations, this study identifies opportunities to improve guideline-concordant use of pharmacologic and nonpharmacologic therapies among adults with chronic pain,” the authors wrote.
There was no specific funding source for the study. The authors have reported no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
data from the Centers for Disease Control and Prevention show.
Results from the annual National Health Interview Survey (NHIS) show that over-the-counter (OTC) pain relievers were the most commonly used pharmacologic treatment and exercise was the most common choice among nonpharmacologic options.
The results also revealed that prescription opioid use for chronic pain decreased from 15.2% in 2019 to 13.5% in 2020. However, there was no corresponding increase in nonpharmacologic therapies, despite current CDC guidelines that recommend maximizing the use of medication alternatives.
“Public health efforts may reduce health inequities by increasing access to pain management therapies so that all persons with chronic pain can receive safe and effective care,” S. Michaela Rikard, PhD, and colleagues wrote.
The findings were published online in a research letter in Annals of Internal Medicine.
Among 31,500 survey respondents, 7,400 indicated that they had pain on most days or every day for the past 3 months.
The survey collected data on self-reported opioid prescriptions in the past 3 months, as well as prescription and nonprescription opiate use during the same time period.
Among adult respondents, 60% used a combination of pharmacologic and nonpharmacologic treatments for pain and almost 27% used medications alone. Older adults, those with low incomes, uninsured individuals, and those living in the South were among those least likely to turn to nonpharmacologic treatment for pain.
After exercise, complementary therapies were the most commonly used nonpharmacologic options, including massage, meditation, or guided imagery, and spinal manipulation or other forms of chiropractic care.
For those taking medications, 76% self-reported using OTC pain relievers for pain, followed by prescription nonopioids (31%) and prescription opioids (13.5%).
Of those who used both pharmacologic and nonpharmacologic therapies, about half reported nonopioid and nonpharmacologic therapy use and 8% reported combined use of opioids, nonopioids, and nonpharmacologic therapy.
After adjustment for multiple factors, investigators found those who were older, had public insurance, or had more severe pain were more likely to use prescription opioids. They also reported severe pain (22%), but 4% reported only mild pain.
Study limitations included generalizability only to noninstitutionalized civilian adults, potential recall bias, and cross-sectional results that do not include patient or treatment history.
“Despite its limitations, this study identifies opportunities to improve guideline-concordant use of pharmacologic and nonpharmacologic therapies among adults with chronic pain,” the authors wrote.
There was no specific funding source for the study. The authors have reported no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
FROM ANNALS OF INTERNAL MEDICINE
Alzheimer’s blood test coming within 5 years, UK group pledges
Alzheimer’s Research UK, the Alzheimer’s Society, and the National Institute for Health and Care Research (NIHR) are collaborating and leading AD researchers to bring a diagnostic blood test to the UK’s National Health Service (NHS).
“Dementia affects around 900,000 people in the UK today, and that number is expected to rise to 1.4 million by 2040. It is the UK’s biggest killer,” Fiona Carragher, with the Alzheimer’s Society, said during a media briefing announcing the project.
Yet, many people face a very long wait of up to 2-4 years to get a dementia diagnosis, and many cases remain undiagnosed, she noted.
A chief reason is lack of access to specialized diagnostic testing. Currently, only 2% of people in the United Kingdom have access to advanced diagnostic tests such as PET scans and lumbar punctures owing to limited availability.
“Getting an early and accurate diagnosis is the pivotal first step to getting help today and unlocking hope for the future” and blood biomarkers provide a “real opportunity to disrupt the diagnostic paradigm,” Ms. Carragher said. It also offers greater opportunities to participate in research and clinical trials, she added.
Attitude shift
Susan Kohlhaas, PhD, with Alzheimer’s Research UK, noted that attitudes toward dementia diagnosis have changed in the past few years. The days when people may have not wanted to know if they have dementia are gone.
Data from the latest wave of the Alzheimer’s Research UK Dementia Attitudes Monitor survey show that 9 in 10 people would seek a diagnosis from their provider. “That’s been driven by awareness of treatments and things that people can proactively do to try and slow disease progression,” Dr. Kohlhaas said.
“As new treatments for dementia become available there will to be a surge in people seeking a diagnosis. At the moment, we don’t have adequate infrastructure to cope with that demand,” Dr. Kohlhaas added.
She noted that blood tests are starting to show their potential as an effective part of the diagnosis and are widely used in research.
“In some cases, they are similar in sensitivity to gold-standard PET scans and lumbar punctures, and they’re less expensive and potentially more scalable on the NHS. What we need to do over the next several years is to understand how they fit into the clinical pathway,” Dr. Kohlhaas said.
The project will involve working with leading dementia researchers to pilot the implementation of potential blood tests in the NHS that can give an early and accurate diagnose of dementia.
The project, which kicks off in January 2024, will receive £5 million ($6.13 million) awarded by the UK Postcode Dream Fund. Specific details regarding the leadership team, participating centers, and specific blood biomarker tests to be trialed will be announced then.
Ms. Carragher and Dr. Kohlhaas reported no relevant financial conflicts of interest.
A version of this article appeared on Medscape.com.
Alzheimer’s Research UK, the Alzheimer’s Society, and the National Institute for Health and Care Research (NIHR) are collaborating and leading AD researchers to bring a diagnostic blood test to the UK’s National Health Service (NHS).
“Dementia affects around 900,000 people in the UK today, and that number is expected to rise to 1.4 million by 2040. It is the UK’s biggest killer,” Fiona Carragher, with the Alzheimer’s Society, said during a media briefing announcing the project.
Yet, many people face a very long wait of up to 2-4 years to get a dementia diagnosis, and many cases remain undiagnosed, she noted.
A chief reason is lack of access to specialized diagnostic testing. Currently, only 2% of people in the United Kingdom have access to advanced diagnostic tests such as PET scans and lumbar punctures owing to limited availability.
“Getting an early and accurate diagnosis is the pivotal first step to getting help today and unlocking hope for the future” and blood biomarkers provide a “real opportunity to disrupt the diagnostic paradigm,” Ms. Carragher said. It also offers greater opportunities to participate in research and clinical trials, she added.
Attitude shift
Susan Kohlhaas, PhD, with Alzheimer’s Research UK, noted that attitudes toward dementia diagnosis have changed in the past few years. The days when people may have not wanted to know if they have dementia are gone.
Data from the latest wave of the Alzheimer’s Research UK Dementia Attitudes Monitor survey show that 9 in 10 people would seek a diagnosis from their provider. “That’s been driven by awareness of treatments and things that people can proactively do to try and slow disease progression,” Dr. Kohlhaas said.
“As new treatments for dementia become available there will to be a surge in people seeking a diagnosis. At the moment, we don’t have adequate infrastructure to cope with that demand,” Dr. Kohlhaas added.
She noted that blood tests are starting to show their potential as an effective part of the diagnosis and are widely used in research.
“In some cases, they are similar in sensitivity to gold-standard PET scans and lumbar punctures, and they’re less expensive and potentially more scalable on the NHS. What we need to do over the next several years is to understand how they fit into the clinical pathway,” Dr. Kohlhaas said.
The project will involve working with leading dementia researchers to pilot the implementation of potential blood tests in the NHS that can give an early and accurate diagnose of dementia.
The project, which kicks off in January 2024, will receive £5 million ($6.13 million) awarded by the UK Postcode Dream Fund. Specific details regarding the leadership team, participating centers, and specific blood biomarker tests to be trialed will be announced then.
Ms. Carragher and Dr. Kohlhaas reported no relevant financial conflicts of interest.
A version of this article appeared on Medscape.com.
Alzheimer’s Research UK, the Alzheimer’s Society, and the National Institute for Health and Care Research (NIHR) are collaborating and leading AD researchers to bring a diagnostic blood test to the UK’s National Health Service (NHS).
“Dementia affects around 900,000 people in the UK today, and that number is expected to rise to 1.4 million by 2040. It is the UK’s biggest killer,” Fiona Carragher, with the Alzheimer’s Society, said during a media briefing announcing the project.
Yet, many people face a very long wait of up to 2-4 years to get a dementia diagnosis, and many cases remain undiagnosed, she noted.
A chief reason is lack of access to specialized diagnostic testing. Currently, only 2% of people in the United Kingdom have access to advanced diagnostic tests such as PET scans and lumbar punctures owing to limited availability.
“Getting an early and accurate diagnosis is the pivotal first step to getting help today and unlocking hope for the future” and blood biomarkers provide a “real opportunity to disrupt the diagnostic paradigm,” Ms. Carragher said. It also offers greater opportunities to participate in research and clinical trials, she added.
Attitude shift
Susan Kohlhaas, PhD, with Alzheimer’s Research UK, noted that attitudes toward dementia diagnosis have changed in the past few years. The days when people may have not wanted to know if they have dementia are gone.
Data from the latest wave of the Alzheimer’s Research UK Dementia Attitudes Monitor survey show that 9 in 10 people would seek a diagnosis from their provider. “That’s been driven by awareness of treatments and things that people can proactively do to try and slow disease progression,” Dr. Kohlhaas said.
“As new treatments for dementia become available there will to be a surge in people seeking a diagnosis. At the moment, we don’t have adequate infrastructure to cope with that demand,” Dr. Kohlhaas added.
She noted that blood tests are starting to show their potential as an effective part of the diagnosis and are widely used in research.
“In some cases, they are similar in sensitivity to gold-standard PET scans and lumbar punctures, and they’re less expensive and potentially more scalable on the NHS. What we need to do over the next several years is to understand how they fit into the clinical pathway,” Dr. Kohlhaas said.
The project will involve working with leading dementia researchers to pilot the implementation of potential blood tests in the NHS that can give an early and accurate diagnose of dementia.
The project, which kicks off in January 2024, will receive £5 million ($6.13 million) awarded by the UK Postcode Dream Fund. Specific details regarding the leadership team, participating centers, and specific blood biomarker tests to be trialed will be announced then.
Ms. Carragher and Dr. Kohlhaas reported no relevant financial conflicts of interest.
A version of this article appeared on Medscape.com.
Military service linked to Alzheimer’s neuropathology
TOPLINE:
METHODOLOGY:
- The study included 597 male decedents who donated their brains to one of two Alzheimer’s Disease Research Center (ADRC) brain bank programs between 1986 and 2018.
- Researchers conducted public data tracing for historical information on military history, which included searching online commercial genealogical databases and paper archives.
- They evaluated tau tangles (using a B score of neurofibrillary tangle deposition in four stages: B0 [not present], B1 [transentorhinal stages], B2 [limbic stages], and B3 [isocortical stages]) and amyloid plaque pathology (using a C score that classifies neuritic amyloid plaque into four categories: no plaques, sparse, moderate, or frequent).
- The study involved three B score comparisons (1, 2, 3 vs. 0; 2, 3 vs. 0, 1; and 3 vs. 0, 1, 2) and two C score comparisons (sparse, moderate, or frequent vs. no plaques, and moderate or frequent vs. no plaque or sparse).
TAKEAWAY:
- Public record tracing determined that 60% of the sample of male decedents had a history of military service; the median year of birth was 1923 and the median year of death was 2007.
- After adjustment for age and year of death, those with a military service history had a 26% increased risk for a higher neuritic amyloid plaque C score compared with those without such history (odds ratio [OR], 1.26; 95% confidence interval [CI], 1.06-1.49), an increase that applied for both relevant comparisons.
- A history of military service was also associated with a 10% greater adjusted odds of a higher neurofibrillary tangle B score (OR, 1.10; 95% CI, 1.08-1.12), with the increase applying to all three comparisons.
- A sensitivity analysis that included both the male decedents and 556 female decedents (increasing the overall sample to 1,153) and was adjusted for sex in addition to age and year of death showed similar results to the male-only sample estimations for both B and C score comparisons.
IN PRACTICE:
Understanding how military service affects AD biological processes is “essential” from a research perspective, the investigators noted. These new findings “emphasize that targeted AD therapies in the veteran population are urgently needed.”
SOURCE:
The study was conducted by W. Ryan Powell, Center for Health Disparities Research and Department of Medicine, Geriatrics Division, University of Wisconsin School of Medicine and Public Health, and colleagues. It was published online in Alzheimer’s & Dementia.
LIMITATIONS:
Selection bias in brain donation is likely because ADRC cohorts are recruitment based. The study was unable to rigorously identify factors that may explain why individuals with military service are at greater risk of having amyloid and tau neuropathology (including the interplay between environmental and genetic risk factors such as apolipoprotein E status).
DISCLOSURES:
The study was supported by the National Institute on Aging. The authors reported no disclosures.
A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- The study included 597 male decedents who donated their brains to one of two Alzheimer’s Disease Research Center (ADRC) brain bank programs between 1986 and 2018.
- Researchers conducted public data tracing for historical information on military history, which included searching online commercial genealogical databases and paper archives.
- They evaluated tau tangles (using a B score of neurofibrillary tangle deposition in four stages: B0 [not present], B1 [transentorhinal stages], B2 [limbic stages], and B3 [isocortical stages]) and amyloid plaque pathology (using a C score that classifies neuritic amyloid plaque into four categories: no plaques, sparse, moderate, or frequent).
- The study involved three B score comparisons (1, 2, 3 vs. 0; 2, 3 vs. 0, 1; and 3 vs. 0, 1, 2) and two C score comparisons (sparse, moderate, or frequent vs. no plaques, and moderate or frequent vs. no plaque or sparse).
TAKEAWAY:
- Public record tracing determined that 60% of the sample of male decedents had a history of military service; the median year of birth was 1923 and the median year of death was 2007.
- After adjustment for age and year of death, those with a military service history had a 26% increased risk for a higher neuritic amyloid plaque C score compared with those without such history (odds ratio [OR], 1.26; 95% confidence interval [CI], 1.06-1.49), an increase that applied for both relevant comparisons.
- A history of military service was also associated with a 10% greater adjusted odds of a higher neurofibrillary tangle B score (OR, 1.10; 95% CI, 1.08-1.12), with the increase applying to all three comparisons.
- A sensitivity analysis that included both the male decedents and 556 female decedents (increasing the overall sample to 1,153) and was adjusted for sex in addition to age and year of death showed similar results to the male-only sample estimations for both B and C score comparisons.
IN PRACTICE:
Understanding how military service affects AD biological processes is “essential” from a research perspective, the investigators noted. These new findings “emphasize that targeted AD therapies in the veteran population are urgently needed.”
SOURCE:
The study was conducted by W. Ryan Powell, Center for Health Disparities Research and Department of Medicine, Geriatrics Division, University of Wisconsin School of Medicine and Public Health, and colleagues. It was published online in Alzheimer’s & Dementia.
LIMITATIONS:
Selection bias in brain donation is likely because ADRC cohorts are recruitment based. The study was unable to rigorously identify factors that may explain why individuals with military service are at greater risk of having amyloid and tau neuropathology (including the interplay between environmental and genetic risk factors such as apolipoprotein E status).
DISCLOSURES:
The study was supported by the National Institute on Aging. The authors reported no disclosures.
A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- The study included 597 male decedents who donated their brains to one of two Alzheimer’s Disease Research Center (ADRC) brain bank programs between 1986 and 2018.
- Researchers conducted public data tracing for historical information on military history, which included searching online commercial genealogical databases and paper archives.
- They evaluated tau tangles (using a B score of neurofibrillary tangle deposition in four stages: B0 [not present], B1 [transentorhinal stages], B2 [limbic stages], and B3 [isocortical stages]) and amyloid plaque pathology (using a C score that classifies neuritic amyloid plaque into four categories: no plaques, sparse, moderate, or frequent).
- The study involved three B score comparisons (1, 2, 3 vs. 0; 2, 3 vs. 0, 1; and 3 vs. 0, 1, 2) and two C score comparisons (sparse, moderate, or frequent vs. no plaques, and moderate or frequent vs. no plaque or sparse).
TAKEAWAY:
- Public record tracing determined that 60% of the sample of male decedents had a history of military service; the median year of birth was 1923 and the median year of death was 2007.
- After adjustment for age and year of death, those with a military service history had a 26% increased risk for a higher neuritic amyloid plaque C score compared with those without such history (odds ratio [OR], 1.26; 95% confidence interval [CI], 1.06-1.49), an increase that applied for both relevant comparisons.
- A history of military service was also associated with a 10% greater adjusted odds of a higher neurofibrillary tangle B score (OR, 1.10; 95% CI, 1.08-1.12), with the increase applying to all three comparisons.
- A sensitivity analysis that included both the male decedents and 556 female decedents (increasing the overall sample to 1,153) and was adjusted for sex in addition to age and year of death showed similar results to the male-only sample estimations for both B and C score comparisons.
IN PRACTICE:
Understanding how military service affects AD biological processes is “essential” from a research perspective, the investigators noted. These new findings “emphasize that targeted AD therapies in the veteran population are urgently needed.”
SOURCE:
The study was conducted by W. Ryan Powell, Center for Health Disparities Research and Department of Medicine, Geriatrics Division, University of Wisconsin School of Medicine and Public Health, and colleagues. It was published online in Alzheimer’s & Dementia.
LIMITATIONS:
Selection bias in brain donation is likely because ADRC cohorts are recruitment based. The study was unable to rigorously identify factors that may explain why individuals with military service are at greater risk of having amyloid and tau neuropathology (including the interplay between environmental and genetic risk factors such as apolipoprotein E status).
DISCLOSURES:
The study was supported by the National Institute on Aging. The authors reported no disclosures.
A version of this article appeared on Medscape.com.