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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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Patient Navigators for Serious Illnesses Can Now Bill Under New Medicare Codes
In a move that acknowledges the gauntlet the US health system poses for people facing serious and fatal illnesses, Medicare will pay for a new class of workers to help patients manage treatments for conditions like cancer and heart failure.
The 2024 Medicare physician fee schedule includes new billing codes, including G0023, to pay for 60 minutes a month of care coordination by certified or trained auxiliary personnel working under the direction of a clinician.
A diagnosis of cancer or another serious illness takes a toll beyond the physical effects of the disease. Patients often scramble to make adjustments in family and work schedules to manage treatment, said Samyukta Mullangi, MD, MBA, medical director of oncology at Thyme Care, a Nashville, Tennessee–based firm that provides navigation and coordination services to oncology practices and insurers.
“It just really does create a bit of a pressure cooker for patients,” Dr. Mullangi told this news organization.
Medicare has for many years paid for medical professionals to help patients cope with the complexities of disease, such as chronic care management (CCM) provided by physicians, nurses, and physician assistants.
The new principal illness navigation (PIN) payments are intended to pay for work that to date typically has been done by people without medical degrees, including those involved in peer support networks and community health programs. The US Centers for Medicare and Medicaid Services(CMS) expects these navigators will undergo training and work under the supervision of clinicians.
The new navigators may coordinate care transitions between medical settings, follow up with patients after emergency department (ED) visits, or communicate with skilled nursing facilities regarding the psychosocial needs and functional deficits of a patient, among other functions.
CMS expects the new navigators may:
- Conduct assessments to understand a patient’s life story, strengths, needs, goals, preferences, and desired outcomes, including understanding cultural and linguistic factors.
- Provide support to accomplish the clinician’s treatment plan.
- Coordinate the receipt of needed services from healthcare facilities, home- and community-based service providers, and caregivers.
Peers as Navigators
The new navigators can be former patients who have undergone similar treatments for serious diseases, CMS said. This approach sets the new program apart from other care management services Medicare already covers, program officials wrote in the 2024 physician fee schedule.
“For some conditions, patients are best able to engage with the healthcare system and access care if they have assistance from a single, dedicated individual who has ‘lived experience,’ ” according to the rule.
The agency has taken a broad initial approach in defining what kinds of illnesses a patient may have to qualify for services. Patients must have a serious condition that is expected to last at least 3 months, such as cancer, heart failure, or substance use disorder.
But those without a definitive diagnosis may also qualify to receive navigator services.
In the rule, CMS cited a case in which a CT scan identified a suspicious mass in a patient’s colon. A clinician might decide this person would benefit from navigation services due to the potential risks for an undiagnosed illness.
“Regardless of the definitive diagnosis of the mass, presence of a colonic mass for that patient may be a serious high-risk condition that could, for example, cause obstruction and lead the patient to present to the emergency department, as well as be potentially indicative of an underlying life-threatening illness such as colon cancer,” CMS wrote in the rule.
Navigators often start their work when cancer patients are screened and guide them through initial diagnosis, potential surgery, radiation, or chemotherapy, said Sharon Gentry, MSN, RN, a former nurse navigator who is now the editor in chief of the Journal of the Academy of Oncology Nurse & Patient Navigators.
The navigators are meant to be a trusted and continual presence for patients, who otherwise might be left to start anew in finding help at each phase of care.
The navigators “see the whole picture. They see the whole journey the patient takes, from pre-diagnosis all the way through diagnosis care out through survival,” Ms. Gentry said.
Gaining a special Medicare payment for these kinds of services will elevate this work, she said.
Many newer drugs can target specific mechanisms and proteins of cancer. Often, oncology treatment involves testing to find out if mutations are allowing the cancer cells to evade a patient’s immune system.
Checking these biomarkers takes time, however. Patients sometimes become frustrated because they are anxious to begin treatment. Patients may receive inaccurate information from friends or family who went through treatment previously. Navigators can provide knowledge on the current state of care for a patient’s disease, helping them better manage anxieties.
“You have to explain to them that things have changed since the guy you drink coffee with was diagnosed with cancer, and there may be a drug that could target that,” Ms. Gentry said.
Potential Challenges
Initial uptake of the new PIN codes may be slow going, however, as clinicians and health systems may already use well-established codes. These include CCM and principal care management services, which may pay higher rates, Mullangi said.
“There might be sensitivity around not wanting to cannibalize existing programs with a new program,” Dr. Mullangi said.
In addition, many patients will have a copay for the services of principal illness navigators, Dr. Mullangi said.
While many patients have additional insurance that would cover the service, not all do. People with traditional Medicare coverage can sometimes pay 20% of the cost of some medical services.
“I think that may give patients pause, particularly if they’re already feeling the financial burden of a cancer treatment journey,” Dr. Mullangi said.
Pay rates for PIN services involve calculations of regional price differences, which are posted publicly by CMS, and potential added fees for services provided by hospital-affiliated organizations.
Consider payments for code G0023, covering 60 minutes of principal navigation services provided in a single month.
A set reimbursement for patients cared for in independent medical practices exists, with variation for local costs. Medicare’s non-facility price for G0023 would be $102.41 in some parts of Silicon Valley in California, including San Jose. In Arkansas, where costs are lower, reimbursement would be $73.14 for this same service.
Patients who get services covered by code G0023 in independent medical practices would have monthly copays of about $15-$20, depending on where they live.
The tab for patients tends to be higher for these same services if delivered through a medical practice owned by a hospital, as this would trigger the addition of facility fees to the payments made to cover the services. Facility fees are difficult for the public to ascertain before getting a treatment or service.
Dr. Mullangi and Ms. Gentry reported no relevant financial disclosures outside of their employers.
A version of this article first appeared on Medscape.com.
In a move that acknowledges the gauntlet the US health system poses for people facing serious and fatal illnesses, Medicare will pay for a new class of workers to help patients manage treatments for conditions like cancer and heart failure.
The 2024 Medicare physician fee schedule includes new billing codes, including G0023, to pay for 60 minutes a month of care coordination by certified or trained auxiliary personnel working under the direction of a clinician.
A diagnosis of cancer or another serious illness takes a toll beyond the physical effects of the disease. Patients often scramble to make adjustments in family and work schedules to manage treatment, said Samyukta Mullangi, MD, MBA, medical director of oncology at Thyme Care, a Nashville, Tennessee–based firm that provides navigation and coordination services to oncology practices and insurers.
“It just really does create a bit of a pressure cooker for patients,” Dr. Mullangi told this news organization.
Medicare has for many years paid for medical professionals to help patients cope with the complexities of disease, such as chronic care management (CCM) provided by physicians, nurses, and physician assistants.
The new principal illness navigation (PIN) payments are intended to pay for work that to date typically has been done by people without medical degrees, including those involved in peer support networks and community health programs. The US Centers for Medicare and Medicaid Services(CMS) expects these navigators will undergo training and work under the supervision of clinicians.
The new navigators may coordinate care transitions between medical settings, follow up with patients after emergency department (ED) visits, or communicate with skilled nursing facilities regarding the psychosocial needs and functional deficits of a patient, among other functions.
CMS expects the new navigators may:
- Conduct assessments to understand a patient’s life story, strengths, needs, goals, preferences, and desired outcomes, including understanding cultural and linguistic factors.
- Provide support to accomplish the clinician’s treatment plan.
- Coordinate the receipt of needed services from healthcare facilities, home- and community-based service providers, and caregivers.
Peers as Navigators
The new navigators can be former patients who have undergone similar treatments for serious diseases, CMS said. This approach sets the new program apart from other care management services Medicare already covers, program officials wrote in the 2024 physician fee schedule.
“For some conditions, patients are best able to engage with the healthcare system and access care if they have assistance from a single, dedicated individual who has ‘lived experience,’ ” according to the rule.
The agency has taken a broad initial approach in defining what kinds of illnesses a patient may have to qualify for services. Patients must have a serious condition that is expected to last at least 3 months, such as cancer, heart failure, or substance use disorder.
But those without a definitive diagnosis may also qualify to receive navigator services.
In the rule, CMS cited a case in which a CT scan identified a suspicious mass in a patient’s colon. A clinician might decide this person would benefit from navigation services due to the potential risks for an undiagnosed illness.
“Regardless of the definitive diagnosis of the mass, presence of a colonic mass for that patient may be a serious high-risk condition that could, for example, cause obstruction and lead the patient to present to the emergency department, as well as be potentially indicative of an underlying life-threatening illness such as colon cancer,” CMS wrote in the rule.
Navigators often start their work when cancer patients are screened and guide them through initial diagnosis, potential surgery, radiation, or chemotherapy, said Sharon Gentry, MSN, RN, a former nurse navigator who is now the editor in chief of the Journal of the Academy of Oncology Nurse & Patient Navigators.
The navigators are meant to be a trusted and continual presence for patients, who otherwise might be left to start anew in finding help at each phase of care.
The navigators “see the whole picture. They see the whole journey the patient takes, from pre-diagnosis all the way through diagnosis care out through survival,” Ms. Gentry said.
Gaining a special Medicare payment for these kinds of services will elevate this work, she said.
Many newer drugs can target specific mechanisms and proteins of cancer. Often, oncology treatment involves testing to find out if mutations are allowing the cancer cells to evade a patient’s immune system.
Checking these biomarkers takes time, however. Patients sometimes become frustrated because they are anxious to begin treatment. Patients may receive inaccurate information from friends or family who went through treatment previously. Navigators can provide knowledge on the current state of care for a patient’s disease, helping them better manage anxieties.
“You have to explain to them that things have changed since the guy you drink coffee with was diagnosed with cancer, and there may be a drug that could target that,” Ms. Gentry said.
Potential Challenges
Initial uptake of the new PIN codes may be slow going, however, as clinicians and health systems may already use well-established codes. These include CCM and principal care management services, which may pay higher rates, Mullangi said.
“There might be sensitivity around not wanting to cannibalize existing programs with a new program,” Dr. Mullangi said.
In addition, many patients will have a copay for the services of principal illness navigators, Dr. Mullangi said.
While many patients have additional insurance that would cover the service, not all do. People with traditional Medicare coverage can sometimes pay 20% of the cost of some medical services.
“I think that may give patients pause, particularly if they’re already feeling the financial burden of a cancer treatment journey,” Dr. Mullangi said.
Pay rates for PIN services involve calculations of regional price differences, which are posted publicly by CMS, and potential added fees for services provided by hospital-affiliated organizations.
Consider payments for code G0023, covering 60 minutes of principal navigation services provided in a single month.
A set reimbursement for patients cared for in independent medical practices exists, with variation for local costs. Medicare’s non-facility price for G0023 would be $102.41 in some parts of Silicon Valley in California, including San Jose. In Arkansas, where costs are lower, reimbursement would be $73.14 for this same service.
Patients who get services covered by code G0023 in independent medical practices would have monthly copays of about $15-$20, depending on where they live.
The tab for patients tends to be higher for these same services if delivered through a medical practice owned by a hospital, as this would trigger the addition of facility fees to the payments made to cover the services. Facility fees are difficult for the public to ascertain before getting a treatment or service.
Dr. Mullangi and Ms. Gentry reported no relevant financial disclosures outside of their employers.
A version of this article first appeared on Medscape.com.
In a move that acknowledges the gauntlet the US health system poses for people facing serious and fatal illnesses, Medicare will pay for a new class of workers to help patients manage treatments for conditions like cancer and heart failure.
The 2024 Medicare physician fee schedule includes new billing codes, including G0023, to pay for 60 minutes a month of care coordination by certified or trained auxiliary personnel working under the direction of a clinician.
A diagnosis of cancer or another serious illness takes a toll beyond the physical effects of the disease. Patients often scramble to make adjustments in family and work schedules to manage treatment, said Samyukta Mullangi, MD, MBA, medical director of oncology at Thyme Care, a Nashville, Tennessee–based firm that provides navigation and coordination services to oncology practices and insurers.
“It just really does create a bit of a pressure cooker for patients,” Dr. Mullangi told this news organization.
Medicare has for many years paid for medical professionals to help patients cope with the complexities of disease, such as chronic care management (CCM) provided by physicians, nurses, and physician assistants.
The new principal illness navigation (PIN) payments are intended to pay for work that to date typically has been done by people without medical degrees, including those involved in peer support networks and community health programs. The US Centers for Medicare and Medicaid Services(CMS) expects these navigators will undergo training and work under the supervision of clinicians.
The new navigators may coordinate care transitions between medical settings, follow up with patients after emergency department (ED) visits, or communicate with skilled nursing facilities regarding the psychosocial needs and functional deficits of a patient, among other functions.
CMS expects the new navigators may:
- Conduct assessments to understand a patient’s life story, strengths, needs, goals, preferences, and desired outcomes, including understanding cultural and linguistic factors.
- Provide support to accomplish the clinician’s treatment plan.
- Coordinate the receipt of needed services from healthcare facilities, home- and community-based service providers, and caregivers.
Peers as Navigators
The new navigators can be former patients who have undergone similar treatments for serious diseases, CMS said. This approach sets the new program apart from other care management services Medicare already covers, program officials wrote in the 2024 physician fee schedule.
“For some conditions, patients are best able to engage with the healthcare system and access care if they have assistance from a single, dedicated individual who has ‘lived experience,’ ” according to the rule.
The agency has taken a broad initial approach in defining what kinds of illnesses a patient may have to qualify for services. Patients must have a serious condition that is expected to last at least 3 months, such as cancer, heart failure, or substance use disorder.
But those without a definitive diagnosis may also qualify to receive navigator services.
In the rule, CMS cited a case in which a CT scan identified a suspicious mass in a patient’s colon. A clinician might decide this person would benefit from navigation services due to the potential risks for an undiagnosed illness.
“Regardless of the definitive diagnosis of the mass, presence of a colonic mass for that patient may be a serious high-risk condition that could, for example, cause obstruction and lead the patient to present to the emergency department, as well as be potentially indicative of an underlying life-threatening illness such as colon cancer,” CMS wrote in the rule.
Navigators often start their work when cancer patients are screened and guide them through initial diagnosis, potential surgery, radiation, or chemotherapy, said Sharon Gentry, MSN, RN, a former nurse navigator who is now the editor in chief of the Journal of the Academy of Oncology Nurse & Patient Navigators.
The navigators are meant to be a trusted and continual presence for patients, who otherwise might be left to start anew in finding help at each phase of care.
The navigators “see the whole picture. They see the whole journey the patient takes, from pre-diagnosis all the way through diagnosis care out through survival,” Ms. Gentry said.
Gaining a special Medicare payment for these kinds of services will elevate this work, she said.
Many newer drugs can target specific mechanisms and proteins of cancer. Often, oncology treatment involves testing to find out if mutations are allowing the cancer cells to evade a patient’s immune system.
Checking these biomarkers takes time, however. Patients sometimes become frustrated because they are anxious to begin treatment. Patients may receive inaccurate information from friends or family who went through treatment previously. Navigators can provide knowledge on the current state of care for a patient’s disease, helping them better manage anxieties.
“You have to explain to them that things have changed since the guy you drink coffee with was diagnosed with cancer, and there may be a drug that could target that,” Ms. Gentry said.
Potential Challenges
Initial uptake of the new PIN codes may be slow going, however, as clinicians and health systems may already use well-established codes. These include CCM and principal care management services, which may pay higher rates, Mullangi said.
“There might be sensitivity around not wanting to cannibalize existing programs with a new program,” Dr. Mullangi said.
In addition, many patients will have a copay for the services of principal illness navigators, Dr. Mullangi said.
While many patients have additional insurance that would cover the service, not all do. People with traditional Medicare coverage can sometimes pay 20% of the cost of some medical services.
“I think that may give patients pause, particularly if they’re already feeling the financial burden of a cancer treatment journey,” Dr. Mullangi said.
Pay rates for PIN services involve calculations of regional price differences, which are posted publicly by CMS, and potential added fees for services provided by hospital-affiliated organizations.
Consider payments for code G0023, covering 60 minutes of principal navigation services provided in a single month.
A set reimbursement for patients cared for in independent medical practices exists, with variation for local costs. Medicare’s non-facility price for G0023 would be $102.41 in some parts of Silicon Valley in California, including San Jose. In Arkansas, where costs are lower, reimbursement would be $73.14 for this same service.
Patients who get services covered by code G0023 in independent medical practices would have monthly copays of about $15-$20, depending on where they live.
The tab for patients tends to be higher for these same services if delivered through a medical practice owned by a hospital, as this would trigger the addition of facility fees to the payments made to cover the services. Facility fees are difficult for the public to ascertain before getting a treatment or service.
Dr. Mullangi and Ms. Gentry reported no relevant financial disclosures outside of their employers.
A version of this article first appeared on Medscape.com.
Updated Alzheimer’s Guidelines Chart the Full Diagnostic Journey
This is the first update since 2001 for specialists and the first guideline for primary care physicians. Executive summaries of the guidelines were published in three articles online on December 23 in a special issue of Alzheimer’s & Dementia.
What’s New?
“With this guideline, we expand the scope of prior guidelines by providing recommendations for practicing clinicians on the process from start to finish,” coauthor Brad Dickerson, MD, director of the Massachusetts General Hospital Frontotemporal Disorders Unit and professor of neurology at Harvard Medical School, Boston, said in a statement.
“If clinicians adopt these recommendations and healthcare systems provide adequate resources, outcomes should improve in most patients in most practice settings,” Dickerson added in an interview.
Through a modified-Delphi approach and guideline-development process, an expert workgroup representing primary and specialty care reviewed 7374 publications, of which 133 met inclusion criteria.
Based on the information, the workgroup outlined a three-step patient-centered evaluation process, which includes assessing cognitive functional status, identifying the cognitive-behavioral syndrome based on specific symptoms, and determining the likely brain diseases or conditions causing the symptoms.
What Are the Key Recommendations?
The guidelines include 19 “practical” recommendations that are applicable to any practice setting. They capture the core elements of a high-quality evaluation and disclosure process, the author said. Here is a brief summary of the recommendations:
Initial evaluation: Perform a multitiered evaluation for patients who self-report or whose care partner or clinician reports cognitive, behavioral, or functional changes.
Patient-centered communication: Partner with the patient and/or care partner to establish shared goals for the evaluation process; assess the patient’s capacity to engage in goal setting.
Diagnostic formulation: Use a tiered approach to assessments and tests based on individual presentation, risk factors, and profile, aiming to determine the level of impairment, cognitive-behavioral syndrome, and likely causes and contributing factors.
History taking: Gather reliable information from informants about changes in cognition, activities of daily living, mood, neuropsychiatric symptoms, and sensory/motor functions. Document individualized risk factors for cognitive decline.
Examination: Conduct a comprehensive examination of cognition, mood, behavior, and a dementia-focused neurologic evaluation using validated tools.
Laboratory tests: Perform tiered, individualized laboratory evaluations, starting with routine tests for all patients.
Structural imaging: Obtain structural brain imaging (MRI preferred, CT as an alternative) to help establish a cause.
Ongoing communication: Engage in ongoing dialogue with patient/care partner to guide them throughout the diagnostic process.
Diagnostic disclosure: Share findings honestly and compassionately, explaining the syndrome, its severity, probable cause, prognosis, treatment options and support resources.
Specialist referral: Refer patients with atypical, uncertain, early-onset, or rapidly progressing symptoms to a dementia subspecialist.
Neuropsychological testing: Use in instances of diagnostic uncertainty or patients with complex clinical profiles. At a minimum, the neuropsychological evaluation should include normed neuropsychological testing of the domains of learning and memory (in particular delayed free and cued recall/recognition), attention, executive function, visuospatial function, and language.
Advanced diagnostic testing: When diagnostic uncertainty remains, obtain additional laboratory tests tailored to individual patient profiles.
Molecular imaging: In a patient with an established cognitive-behavioral syndrome in whom there is continued diagnostic uncertainty regarding cause(s) after structural imaging, a dementia specialist can obtain molecular imaging with fluorodeoxyglucose PET to improve diagnostic accuracy.
Cerebrospinal fluid (CSF) analysis: Utilize CSF biomarkers to evaluate amyloid beta and tau profiles in cases with unresolved diagnostic uncertainty.
Amyloid PET imaging: Perform amyloid PET scans for patients with persistent diagnostic uncertainty after other assessments.
Genetic counseling and testing: Consider genetic testing for patients with strong autosomal dominant family histories and involve a genetic counselor.
Future Directions?
Maria C. Carrillo, PhD, chief science officer and medical affairs lead for the Alzheimer’s Association, encourages clinicians to incorporate these guidelines into their practice.
“These guidelines are important because they guide clinicians in the evaluation of memory complaints, which could have many underlying causes. That is the necessary start for an early and accurate Alzheimer’s diagnosis,” Carrillo said in a statement.
Dickerson said the new guidelines do not address blood-based biomarkers “because nobody really feels that they are ready for prime time yet, even though they’re getting rolled out as clinical products.”
However, the recommendations will be revised as needed. “That’s one of the values of setting this up as a process; whenever any new development occurs, it will be easy to update the guidelines to show where that new test or new biomarker fits in the overall process,” he said.
New Appropriate Use Guidance
A separate workgroup, jointly convened by the Alzheimer’s Association and the Society of Nuclear Medicine and Molecular Imaging, has revised appropriate use criteria (AUC) for amyloid PET imaging and developed AUC for tau PET imaging.
They were simultaneously published online in Alzheimer’s & Dementia and The Journal of Nuclear Medicine. They are the first revision since the initial AUC for amyloid PET was introduced in 2013.
“The updated amyloid/tau appropriate use criteria will help ensure these tracers are used in a cost-effective manner and the scan results will be used appropriately to add value to the diagnosis and management of dementia,” said workgroup members Kevin Donohoe, MD, with Beth Israel Deaconess Medical Center, Boston, and Phillip Kuo, MD, with City of Hope National Medical Center, Duarte, California.
The AUC include 17 real-world scenarios in which amyloid or tau PET may be considered, with the two tests considered separately and given their own rating for each scenario.
Overall, the strongest evidence for their use includes assessment and prognosis for people with mild cognitive impairment; assessment of people with dementia when the cause is not clearly known; and determining eligibility for treatment with new disease-modifying therapies, and monitoring response to these treatments, the workgroup said.
“Whereas the prior AUC was written at a time when only the deposition of amyloid could be documented, the new therapeutic agents allow us to demonstrate the actual clearance of amyloid during therapy,” Donohoe and Kuo explained.
“These new therapeutic agents are expensive and, as with most medications, may cause unwanted side effects. The most recent version of the AUC includes information about the appropriate use of amyloid imaging for both documenting the presence of amyloid deposits in the brain, making anti-amyloid therapy an option, as well as documenting the effectiveness of the therapeutic agents as amyloid is (or is not) cleared from the brain,” Donahoe and Kuo noted.
The revised AUC also state that, in most cases, amyloid and tau PET tests should not be used for people who do not have cognitive impairment, even if they carry the APOE4 risk-related gene for Alzheimer’s disease; nonmedical use such as for legal concerns, insurance coverage, or employment screening; and in place of genetic testing in patients suspected of carrying a disease-causing genetic mutation.
In a statement, lead author Gil D. Rabinovici, MD, with University of California, San Francisco, emphasized that the AUC “should be considered guidelines for clinicians, not a substitute for careful clinical judgment that considers the full clinical context for each patient with cognitive complaints.”
This research was funded by the Alzheimer’s Association. Disclosures for guideline authors are available with the original articles.
A version of this article first appeared on Medscape.com.
This is the first update since 2001 for specialists and the first guideline for primary care physicians. Executive summaries of the guidelines were published in three articles online on December 23 in a special issue of Alzheimer’s & Dementia.
What’s New?
“With this guideline, we expand the scope of prior guidelines by providing recommendations for practicing clinicians on the process from start to finish,” coauthor Brad Dickerson, MD, director of the Massachusetts General Hospital Frontotemporal Disorders Unit and professor of neurology at Harvard Medical School, Boston, said in a statement.
“If clinicians adopt these recommendations and healthcare systems provide adequate resources, outcomes should improve in most patients in most practice settings,” Dickerson added in an interview.
Through a modified-Delphi approach and guideline-development process, an expert workgroup representing primary and specialty care reviewed 7374 publications, of which 133 met inclusion criteria.
Based on the information, the workgroup outlined a three-step patient-centered evaluation process, which includes assessing cognitive functional status, identifying the cognitive-behavioral syndrome based on specific symptoms, and determining the likely brain diseases or conditions causing the symptoms.
What Are the Key Recommendations?
The guidelines include 19 “practical” recommendations that are applicable to any practice setting. They capture the core elements of a high-quality evaluation and disclosure process, the author said. Here is a brief summary of the recommendations:
Initial evaluation: Perform a multitiered evaluation for patients who self-report or whose care partner or clinician reports cognitive, behavioral, or functional changes.
Patient-centered communication: Partner with the patient and/or care partner to establish shared goals for the evaluation process; assess the patient’s capacity to engage in goal setting.
Diagnostic formulation: Use a tiered approach to assessments and tests based on individual presentation, risk factors, and profile, aiming to determine the level of impairment, cognitive-behavioral syndrome, and likely causes and contributing factors.
History taking: Gather reliable information from informants about changes in cognition, activities of daily living, mood, neuropsychiatric symptoms, and sensory/motor functions. Document individualized risk factors for cognitive decline.
Examination: Conduct a comprehensive examination of cognition, mood, behavior, and a dementia-focused neurologic evaluation using validated tools.
Laboratory tests: Perform tiered, individualized laboratory evaluations, starting with routine tests for all patients.
Structural imaging: Obtain structural brain imaging (MRI preferred, CT as an alternative) to help establish a cause.
Ongoing communication: Engage in ongoing dialogue with patient/care partner to guide them throughout the diagnostic process.
Diagnostic disclosure: Share findings honestly and compassionately, explaining the syndrome, its severity, probable cause, prognosis, treatment options and support resources.
Specialist referral: Refer patients with atypical, uncertain, early-onset, or rapidly progressing symptoms to a dementia subspecialist.
Neuropsychological testing: Use in instances of diagnostic uncertainty or patients with complex clinical profiles. At a minimum, the neuropsychological evaluation should include normed neuropsychological testing of the domains of learning and memory (in particular delayed free and cued recall/recognition), attention, executive function, visuospatial function, and language.
Advanced diagnostic testing: When diagnostic uncertainty remains, obtain additional laboratory tests tailored to individual patient profiles.
Molecular imaging: In a patient with an established cognitive-behavioral syndrome in whom there is continued diagnostic uncertainty regarding cause(s) after structural imaging, a dementia specialist can obtain molecular imaging with fluorodeoxyglucose PET to improve diagnostic accuracy.
Cerebrospinal fluid (CSF) analysis: Utilize CSF biomarkers to evaluate amyloid beta and tau profiles in cases with unresolved diagnostic uncertainty.
Amyloid PET imaging: Perform amyloid PET scans for patients with persistent diagnostic uncertainty after other assessments.
Genetic counseling and testing: Consider genetic testing for patients with strong autosomal dominant family histories and involve a genetic counselor.
Future Directions?
Maria C. Carrillo, PhD, chief science officer and medical affairs lead for the Alzheimer’s Association, encourages clinicians to incorporate these guidelines into their practice.
“These guidelines are important because they guide clinicians in the evaluation of memory complaints, which could have many underlying causes. That is the necessary start for an early and accurate Alzheimer’s diagnosis,” Carrillo said in a statement.
Dickerson said the new guidelines do not address blood-based biomarkers “because nobody really feels that they are ready for prime time yet, even though they’re getting rolled out as clinical products.”
However, the recommendations will be revised as needed. “That’s one of the values of setting this up as a process; whenever any new development occurs, it will be easy to update the guidelines to show where that new test or new biomarker fits in the overall process,” he said.
New Appropriate Use Guidance
A separate workgroup, jointly convened by the Alzheimer’s Association and the Society of Nuclear Medicine and Molecular Imaging, has revised appropriate use criteria (AUC) for amyloid PET imaging and developed AUC for tau PET imaging.
They were simultaneously published online in Alzheimer’s & Dementia and The Journal of Nuclear Medicine. They are the first revision since the initial AUC for amyloid PET was introduced in 2013.
“The updated amyloid/tau appropriate use criteria will help ensure these tracers are used in a cost-effective manner and the scan results will be used appropriately to add value to the diagnosis and management of dementia,” said workgroup members Kevin Donohoe, MD, with Beth Israel Deaconess Medical Center, Boston, and Phillip Kuo, MD, with City of Hope National Medical Center, Duarte, California.
The AUC include 17 real-world scenarios in which amyloid or tau PET may be considered, with the two tests considered separately and given their own rating for each scenario.
Overall, the strongest evidence for their use includes assessment and prognosis for people with mild cognitive impairment; assessment of people with dementia when the cause is not clearly known; and determining eligibility for treatment with new disease-modifying therapies, and monitoring response to these treatments, the workgroup said.
“Whereas the prior AUC was written at a time when only the deposition of amyloid could be documented, the new therapeutic agents allow us to demonstrate the actual clearance of amyloid during therapy,” Donohoe and Kuo explained.
“These new therapeutic agents are expensive and, as with most medications, may cause unwanted side effects. The most recent version of the AUC includes information about the appropriate use of amyloid imaging for both documenting the presence of amyloid deposits in the brain, making anti-amyloid therapy an option, as well as documenting the effectiveness of the therapeutic agents as amyloid is (or is not) cleared from the brain,” Donahoe and Kuo noted.
The revised AUC also state that, in most cases, amyloid and tau PET tests should not be used for people who do not have cognitive impairment, even if they carry the APOE4 risk-related gene for Alzheimer’s disease; nonmedical use such as for legal concerns, insurance coverage, or employment screening; and in place of genetic testing in patients suspected of carrying a disease-causing genetic mutation.
In a statement, lead author Gil D. Rabinovici, MD, with University of California, San Francisco, emphasized that the AUC “should be considered guidelines for clinicians, not a substitute for careful clinical judgment that considers the full clinical context for each patient with cognitive complaints.”
This research was funded by the Alzheimer’s Association. Disclosures for guideline authors are available with the original articles.
A version of this article first appeared on Medscape.com.
This is the first update since 2001 for specialists and the first guideline for primary care physicians. Executive summaries of the guidelines were published in three articles online on December 23 in a special issue of Alzheimer’s & Dementia.
What’s New?
“With this guideline, we expand the scope of prior guidelines by providing recommendations for practicing clinicians on the process from start to finish,” coauthor Brad Dickerson, MD, director of the Massachusetts General Hospital Frontotemporal Disorders Unit and professor of neurology at Harvard Medical School, Boston, said in a statement.
“If clinicians adopt these recommendations and healthcare systems provide adequate resources, outcomes should improve in most patients in most practice settings,” Dickerson added in an interview.
Through a modified-Delphi approach and guideline-development process, an expert workgroup representing primary and specialty care reviewed 7374 publications, of which 133 met inclusion criteria.
Based on the information, the workgroup outlined a three-step patient-centered evaluation process, which includes assessing cognitive functional status, identifying the cognitive-behavioral syndrome based on specific symptoms, and determining the likely brain diseases or conditions causing the symptoms.
What Are the Key Recommendations?
The guidelines include 19 “practical” recommendations that are applicable to any practice setting. They capture the core elements of a high-quality evaluation and disclosure process, the author said. Here is a brief summary of the recommendations:
Initial evaluation: Perform a multitiered evaluation for patients who self-report or whose care partner or clinician reports cognitive, behavioral, or functional changes.
Patient-centered communication: Partner with the patient and/or care partner to establish shared goals for the evaluation process; assess the patient’s capacity to engage in goal setting.
Diagnostic formulation: Use a tiered approach to assessments and tests based on individual presentation, risk factors, and profile, aiming to determine the level of impairment, cognitive-behavioral syndrome, and likely causes and contributing factors.
History taking: Gather reliable information from informants about changes in cognition, activities of daily living, mood, neuropsychiatric symptoms, and sensory/motor functions. Document individualized risk factors for cognitive decline.
Examination: Conduct a comprehensive examination of cognition, mood, behavior, and a dementia-focused neurologic evaluation using validated tools.
Laboratory tests: Perform tiered, individualized laboratory evaluations, starting with routine tests for all patients.
Structural imaging: Obtain structural brain imaging (MRI preferred, CT as an alternative) to help establish a cause.
Ongoing communication: Engage in ongoing dialogue with patient/care partner to guide them throughout the diagnostic process.
Diagnostic disclosure: Share findings honestly and compassionately, explaining the syndrome, its severity, probable cause, prognosis, treatment options and support resources.
Specialist referral: Refer patients with atypical, uncertain, early-onset, or rapidly progressing symptoms to a dementia subspecialist.
Neuropsychological testing: Use in instances of diagnostic uncertainty or patients with complex clinical profiles. At a minimum, the neuropsychological evaluation should include normed neuropsychological testing of the domains of learning and memory (in particular delayed free and cued recall/recognition), attention, executive function, visuospatial function, and language.
Advanced diagnostic testing: When diagnostic uncertainty remains, obtain additional laboratory tests tailored to individual patient profiles.
Molecular imaging: In a patient with an established cognitive-behavioral syndrome in whom there is continued diagnostic uncertainty regarding cause(s) after structural imaging, a dementia specialist can obtain molecular imaging with fluorodeoxyglucose PET to improve diagnostic accuracy.
Cerebrospinal fluid (CSF) analysis: Utilize CSF biomarkers to evaluate amyloid beta and tau profiles in cases with unresolved diagnostic uncertainty.
Amyloid PET imaging: Perform amyloid PET scans for patients with persistent diagnostic uncertainty after other assessments.
Genetic counseling and testing: Consider genetic testing for patients with strong autosomal dominant family histories and involve a genetic counselor.
Future Directions?
Maria C. Carrillo, PhD, chief science officer and medical affairs lead for the Alzheimer’s Association, encourages clinicians to incorporate these guidelines into their practice.
“These guidelines are important because they guide clinicians in the evaluation of memory complaints, which could have many underlying causes. That is the necessary start for an early and accurate Alzheimer’s diagnosis,” Carrillo said in a statement.
Dickerson said the new guidelines do not address blood-based biomarkers “because nobody really feels that they are ready for prime time yet, even though they’re getting rolled out as clinical products.”
However, the recommendations will be revised as needed. “That’s one of the values of setting this up as a process; whenever any new development occurs, it will be easy to update the guidelines to show where that new test or new biomarker fits in the overall process,” he said.
New Appropriate Use Guidance
A separate workgroup, jointly convened by the Alzheimer’s Association and the Society of Nuclear Medicine and Molecular Imaging, has revised appropriate use criteria (AUC) for amyloid PET imaging and developed AUC for tau PET imaging.
They were simultaneously published online in Alzheimer’s & Dementia and The Journal of Nuclear Medicine. They are the first revision since the initial AUC for amyloid PET was introduced in 2013.
“The updated amyloid/tau appropriate use criteria will help ensure these tracers are used in a cost-effective manner and the scan results will be used appropriately to add value to the diagnosis and management of dementia,” said workgroup members Kevin Donohoe, MD, with Beth Israel Deaconess Medical Center, Boston, and Phillip Kuo, MD, with City of Hope National Medical Center, Duarte, California.
The AUC include 17 real-world scenarios in which amyloid or tau PET may be considered, with the two tests considered separately and given their own rating for each scenario.
Overall, the strongest evidence for their use includes assessment and prognosis for people with mild cognitive impairment; assessment of people with dementia when the cause is not clearly known; and determining eligibility for treatment with new disease-modifying therapies, and monitoring response to these treatments, the workgroup said.
“Whereas the prior AUC was written at a time when only the deposition of amyloid could be documented, the new therapeutic agents allow us to demonstrate the actual clearance of amyloid during therapy,” Donohoe and Kuo explained.
“These new therapeutic agents are expensive and, as with most medications, may cause unwanted side effects. The most recent version of the AUC includes information about the appropriate use of amyloid imaging for both documenting the presence of amyloid deposits in the brain, making anti-amyloid therapy an option, as well as documenting the effectiveness of the therapeutic agents as amyloid is (or is not) cleared from the brain,” Donahoe and Kuo noted.
The revised AUC also state that, in most cases, amyloid and tau PET tests should not be used for people who do not have cognitive impairment, even if they carry the APOE4 risk-related gene for Alzheimer’s disease; nonmedical use such as for legal concerns, insurance coverage, or employment screening; and in place of genetic testing in patients suspected of carrying a disease-causing genetic mutation.
In a statement, lead author Gil D. Rabinovici, MD, with University of California, San Francisco, emphasized that the AUC “should be considered guidelines for clinicians, not a substitute for careful clinical judgment that considers the full clinical context for each patient with cognitive complaints.”
This research was funded by the Alzheimer’s Association. Disclosures for guideline authors are available with the original articles.
A version of this article first appeared on Medscape.com.
FROM ALZHEIMER’S & DEMENTIA
Losing Your Mind Trying to Understand the BP-Dementia Link
You could be forgiven if you are confused about how blood pressure (BP) affects dementia. First, you read an article extolling the benefits of BP lowering, then a study about how stopping antihypertensives slows cognitive decline in nursing home residents. It’s enough to make you lose your mind.
The Brain Benefits of BP Lowering
It should be stated unequivocally that you should absolutely treat high BP. It may have once been acceptable to state, “The greatest danger to a man with high blood pressure lies in its discovery, because then some fool is certain to try and reduce it.” But those dark days are long behind us.
In these divided times, at least we can agree that we should treat high BP. The cardiovascular (CV) benefits, in and of themselves, justify the decision. But BP’s relationship with dementia is more complex. There are different types of dementia even though we tend to lump them all into one category. Vascular dementia is driven by the same pathophysiology and risk factors as cardiac disease. It’s intuitive that treating hypertension, diabetes, hypercholesterolemia, and smoking will decrease the risk for stroke and limit the damage to the brain that we see with repeated vascular insults. For Alzheimer’s disease, high BP and other CV risk factors seem to increase the risk even if the mechanism is not fully elucidated.
Estimates suggest that if we could lower the prevalence of hypertension by 25%, there would be 160,000 fewer cases of Alzheimer’s disease. But the data are not as robust as one might hope. A 2021 Cochrane review found that hypertension treatment slowed cognitive decline, but the quality of the evidence was low. Short duration of follow-up, dropouts, crossovers, and other problems with the data precluded any certainty. What’s more, hypertension in midlife is associated with cognitive decline and dementia, but its impact in those over age 70 is less clear. Later in life, or once cognitive impairment has already developed, it may be too late for BP lowering to have any impact.
Potential Harms of Lowering BP
All this needs to be weighed against the potential harms of treating hypertension. I will reiterate that hypertension should be treated and treated aggressively for the prevention of CV events. But overtreatment, especially in older patients, is associated with hypotension, falls, and syncope. Older patients are also at risk for polypharmacy and drug-drug interactions.
A Korean nationwide survey showed a U-shaped association between BP and Alzheimer’s disease risk in adults (mean age, 67 years), with both high and low BPs associated with a higher risk for Alzheimer’s disease. Though not all studies agree. A post hoc analysis of SPRINT MIND did not find any negative impact of intensive BP lowering on cognitive outcomes or cerebral perfusion in older adults (mean age, 68 years). But it didn’t do much good either. Given the heterogeneity of the data, doubts remain on whether aggressive BP lowering might be detrimental in older patients with comorbidities and preexisting dementia. The obvious corollary then is whether deprescribing hypertensive medications could be beneficial.
A recent publication in JAMA Internal Medicine attempted to address this very question. The cohort study used data from Veterans Affairs nursing home residents (mean age, 78 years) to emulate a randomized trial on deprescribing antihypertensives and cognitive decline. Many of the residents’ cognitive scores worsened over the course of follow-up; however, the decline was less pronounced in the deprescribing group (10% vs 12%). The same group did a similar analysis looking at CV outcomes and found no increased risk for heart attack or stroke with deprescribing BP medications. Taken together, these nursing home data suggest that deprescribing may help slow cognitive decline without the expected trade-off of increased CV events.
Deprescribing, Yes or No?
However, randomized data would obviously be preferable, and these are in short supply. One such trial, the DANTE study, found no benefit to deprescribing in terms of cognition in adults aged 75 years or older with mild cognitive impairment. The study follow-up was only 16 weeks, however, which is hardly enough time to demonstrate any effect, positive or negative. The most that can be said is that it didn’t cause many short-term adverse events.
Perhaps the best conclusion to draw from this somewhat underwhelming collection of data is that lowering high BP is important, but less important the closer we get to the end of life. Hypotension is obviously bad, and overly aggressive BP lowering is going to lead to negative outcomes in older adults because gravity is an unforgiving mistress.
Deprescribing antihypertensives in older adults is probably not going to cause major negative outcomes, but whether it will do much good in nonhypotensive patients is debatable. The bigger problem is the millions of people with undiagnosed or undertreated hypertension. We would probably have less dementia if we treated hypertension when it does the most good: as a primary-prevention strategy in midlife.
Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal, Quebec, Canada. He disclosed no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
You could be forgiven if you are confused about how blood pressure (BP) affects dementia. First, you read an article extolling the benefits of BP lowering, then a study about how stopping antihypertensives slows cognitive decline in nursing home residents. It’s enough to make you lose your mind.
The Brain Benefits of BP Lowering
It should be stated unequivocally that you should absolutely treat high BP. It may have once been acceptable to state, “The greatest danger to a man with high blood pressure lies in its discovery, because then some fool is certain to try and reduce it.” But those dark days are long behind us.
In these divided times, at least we can agree that we should treat high BP. The cardiovascular (CV) benefits, in and of themselves, justify the decision. But BP’s relationship with dementia is more complex. There are different types of dementia even though we tend to lump them all into one category. Vascular dementia is driven by the same pathophysiology and risk factors as cardiac disease. It’s intuitive that treating hypertension, diabetes, hypercholesterolemia, and smoking will decrease the risk for stroke and limit the damage to the brain that we see with repeated vascular insults. For Alzheimer’s disease, high BP and other CV risk factors seem to increase the risk even if the mechanism is not fully elucidated.
Estimates suggest that if we could lower the prevalence of hypertension by 25%, there would be 160,000 fewer cases of Alzheimer’s disease. But the data are not as robust as one might hope. A 2021 Cochrane review found that hypertension treatment slowed cognitive decline, but the quality of the evidence was low. Short duration of follow-up, dropouts, crossovers, and other problems with the data precluded any certainty. What’s more, hypertension in midlife is associated with cognitive decline and dementia, but its impact in those over age 70 is less clear. Later in life, or once cognitive impairment has already developed, it may be too late for BP lowering to have any impact.
Potential Harms of Lowering BP
All this needs to be weighed against the potential harms of treating hypertension. I will reiterate that hypertension should be treated and treated aggressively for the prevention of CV events. But overtreatment, especially in older patients, is associated with hypotension, falls, and syncope. Older patients are also at risk for polypharmacy and drug-drug interactions.
A Korean nationwide survey showed a U-shaped association between BP and Alzheimer’s disease risk in adults (mean age, 67 years), with both high and low BPs associated with a higher risk for Alzheimer’s disease. Though not all studies agree. A post hoc analysis of SPRINT MIND did not find any negative impact of intensive BP lowering on cognitive outcomes or cerebral perfusion in older adults (mean age, 68 years). But it didn’t do much good either. Given the heterogeneity of the data, doubts remain on whether aggressive BP lowering might be detrimental in older patients with comorbidities and preexisting dementia. The obvious corollary then is whether deprescribing hypertensive medications could be beneficial.
A recent publication in JAMA Internal Medicine attempted to address this very question. The cohort study used data from Veterans Affairs nursing home residents (mean age, 78 years) to emulate a randomized trial on deprescribing antihypertensives and cognitive decline. Many of the residents’ cognitive scores worsened over the course of follow-up; however, the decline was less pronounced in the deprescribing group (10% vs 12%). The same group did a similar analysis looking at CV outcomes and found no increased risk for heart attack or stroke with deprescribing BP medications. Taken together, these nursing home data suggest that deprescribing may help slow cognitive decline without the expected trade-off of increased CV events.
Deprescribing, Yes or No?
However, randomized data would obviously be preferable, and these are in short supply. One such trial, the DANTE study, found no benefit to deprescribing in terms of cognition in adults aged 75 years or older with mild cognitive impairment. The study follow-up was only 16 weeks, however, which is hardly enough time to demonstrate any effect, positive or negative. The most that can be said is that it didn’t cause many short-term adverse events.
Perhaps the best conclusion to draw from this somewhat underwhelming collection of data is that lowering high BP is important, but less important the closer we get to the end of life. Hypotension is obviously bad, and overly aggressive BP lowering is going to lead to negative outcomes in older adults because gravity is an unforgiving mistress.
Deprescribing antihypertensives in older adults is probably not going to cause major negative outcomes, but whether it will do much good in nonhypotensive patients is debatable. The bigger problem is the millions of people with undiagnosed or undertreated hypertension. We would probably have less dementia if we treated hypertension when it does the most good: as a primary-prevention strategy in midlife.
Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal, Quebec, Canada. He disclosed no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
You could be forgiven if you are confused about how blood pressure (BP) affects dementia. First, you read an article extolling the benefits of BP lowering, then a study about how stopping antihypertensives slows cognitive decline in nursing home residents. It’s enough to make you lose your mind.
The Brain Benefits of BP Lowering
It should be stated unequivocally that you should absolutely treat high BP. It may have once been acceptable to state, “The greatest danger to a man with high blood pressure lies in its discovery, because then some fool is certain to try and reduce it.” But those dark days are long behind us.
In these divided times, at least we can agree that we should treat high BP. The cardiovascular (CV) benefits, in and of themselves, justify the decision. But BP’s relationship with dementia is more complex. There are different types of dementia even though we tend to lump them all into one category. Vascular dementia is driven by the same pathophysiology and risk factors as cardiac disease. It’s intuitive that treating hypertension, diabetes, hypercholesterolemia, and smoking will decrease the risk for stroke and limit the damage to the brain that we see with repeated vascular insults. For Alzheimer’s disease, high BP and other CV risk factors seem to increase the risk even if the mechanism is not fully elucidated.
Estimates suggest that if we could lower the prevalence of hypertension by 25%, there would be 160,000 fewer cases of Alzheimer’s disease. But the data are not as robust as one might hope. A 2021 Cochrane review found that hypertension treatment slowed cognitive decline, but the quality of the evidence was low. Short duration of follow-up, dropouts, crossovers, and other problems with the data precluded any certainty. What’s more, hypertension in midlife is associated with cognitive decline and dementia, but its impact in those over age 70 is less clear. Later in life, or once cognitive impairment has already developed, it may be too late for BP lowering to have any impact.
Potential Harms of Lowering BP
All this needs to be weighed against the potential harms of treating hypertension. I will reiterate that hypertension should be treated and treated aggressively for the prevention of CV events. But overtreatment, especially in older patients, is associated with hypotension, falls, and syncope. Older patients are also at risk for polypharmacy and drug-drug interactions.
A Korean nationwide survey showed a U-shaped association between BP and Alzheimer’s disease risk in adults (mean age, 67 years), with both high and low BPs associated with a higher risk for Alzheimer’s disease. Though not all studies agree. A post hoc analysis of SPRINT MIND did not find any negative impact of intensive BP lowering on cognitive outcomes or cerebral perfusion in older adults (mean age, 68 years). But it didn’t do much good either. Given the heterogeneity of the data, doubts remain on whether aggressive BP lowering might be detrimental in older patients with comorbidities and preexisting dementia. The obvious corollary then is whether deprescribing hypertensive medications could be beneficial.
A recent publication in JAMA Internal Medicine attempted to address this very question. The cohort study used data from Veterans Affairs nursing home residents (mean age, 78 years) to emulate a randomized trial on deprescribing antihypertensives and cognitive decline. Many of the residents’ cognitive scores worsened over the course of follow-up; however, the decline was less pronounced in the deprescribing group (10% vs 12%). The same group did a similar analysis looking at CV outcomes and found no increased risk for heart attack or stroke with deprescribing BP medications. Taken together, these nursing home data suggest that deprescribing may help slow cognitive decline without the expected trade-off of increased CV events.
Deprescribing, Yes or No?
However, randomized data would obviously be preferable, and these are in short supply. One such trial, the DANTE study, found no benefit to deprescribing in terms of cognition in adults aged 75 years or older with mild cognitive impairment. The study follow-up was only 16 weeks, however, which is hardly enough time to demonstrate any effect, positive or negative. The most that can be said is that it didn’t cause many short-term adverse events.
Perhaps the best conclusion to draw from this somewhat underwhelming collection of data is that lowering high BP is important, but less important the closer we get to the end of life. Hypotension is obviously bad, and overly aggressive BP lowering is going to lead to negative outcomes in older adults because gravity is an unforgiving mistress.
Deprescribing antihypertensives in older adults is probably not going to cause major negative outcomes, but whether it will do much good in nonhypotensive patients is debatable. The bigger problem is the millions of people with undiagnosed or undertreated hypertension. We would probably have less dementia if we treated hypertension when it does the most good: as a primary-prevention strategy in midlife.
Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal, Quebec, Canada. He disclosed no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
How Long Does It Take to See a Neurologist?
a cross-sectional analysis of Medicare data showed.
Wait times were not affected by the number of available neurologists. However, those with multiple sclerosis (MS), epilepsy, Parkinson’s disease, dementia, and sleep disorders had the longest wait times.
“In general, early referral to specialists has been shown to improve outcomes and increase patient satisfaction,” study author Chun Chieh Lin, PhD, MBA, of Ohio State University, Columbus, said in a press release. “Our findings underscore the need to develop new strategies to help people with neurological conditions see neurologists faster.”
The findings were published online in Neurology.
No National Benchmark for Wait Times
For this study, researchers analyzed a large sample of fee-for-service Medicare data from 2018 to 2019. Researchers identified patients with a year or less between their last referring physician visit and a new neurologist visit.
Exclusion criteria included enrollment in health maintenance organization plans without continuous enrollment in Medicare Part A and Part B for 2 years before the index neurologist visit, missing patient data, no physician referral at all, or referral by a different neurologist.
In addition to assessing wait times, investigators examined the availability of neurologists who provided medical services to Medicare beneficiaries in the 2018 dataset across 306 hospital referral regions in the United States, based on zip codes.
Results showed that 163,313 patients (average age, 74 years; 58% women; 85% White) were referred by 84,975 physicians to 10,250 neurologists across the United States.
Overall, the average wait time from physician referral to index neurologist visit was 34 days (range, 1-365 days), with longer wait times for White patients, women, and those aged 65-69 years. Overall, 18% waited longer than 90 days for an appointment.
The most common conditions diagnosed at the index neurologist visit were chronic pain/abnormality of gait (13%), sleep disorders (11%), and peripheral neuropathy (10%).
Using a linear mixed-effects statistical model, investigators found that patients with back pain waited an average of 30 days to see a neurologist, with longer waits for other conditions. Those with MS had an average wait that was 29 days longer, patients with epilepsy waited an average of 10 days longer, and those with Parkinson’s disease waited 9 days longer (P < .0001).
The number of available neurologists (range, 10-50 neurologists per 100,000 Medicare patients) did not affect wait times. However, there were differences in wait times across states because of different policies or regulations regarding healthcare access, with wait times ranging from a median high of 49 days in Idaho to a low of 24 days in Wyoming.
Notably, when patients saw a neurologist outside of their physician’s referral area, wait times were longer by an average of 11 days.
More than 40% of patients with new neurology referrals had prior office-based visits for the same neurologic diagnosis. For these patients, the median time between diagnosis and index neurologist visit was 342 days (range, 66-753 days).
Female patients in this category waited slightly longer (median, 353 days) than male patients (median, 328 days), and Black and Hispanic patients had longer median waits than White patients (389.5 days and 397 days respectively, vs 337 days; P = .0003).
“It is important to note that there is no national benchmark for determining appropriate wait times for specialist care, making it difficult to standardize expectations for timely access to specialists,” the authors noted.
The investigators suggested that a direct communication channel between primary care physicians and neurologists such as an eConsult service may hasten access to neurology consultation without the need for a formal appointment. Telemedicine in rural areas could also shorten wait times, they added.
Study limitations included the inability to determine if patients followed through with their index neurology visits or whether the last visit with the physician was the time of referral, as this could not be determined through the claims data.
This study was funded by the American Academy of Neurology. Lin reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
a cross-sectional analysis of Medicare data showed.
Wait times were not affected by the number of available neurologists. However, those with multiple sclerosis (MS), epilepsy, Parkinson’s disease, dementia, and sleep disorders had the longest wait times.
“In general, early referral to specialists has been shown to improve outcomes and increase patient satisfaction,” study author Chun Chieh Lin, PhD, MBA, of Ohio State University, Columbus, said in a press release. “Our findings underscore the need to develop new strategies to help people with neurological conditions see neurologists faster.”
The findings were published online in Neurology.
No National Benchmark for Wait Times
For this study, researchers analyzed a large sample of fee-for-service Medicare data from 2018 to 2019. Researchers identified patients with a year or less between their last referring physician visit and a new neurologist visit.
Exclusion criteria included enrollment in health maintenance organization plans without continuous enrollment in Medicare Part A and Part B for 2 years before the index neurologist visit, missing patient data, no physician referral at all, or referral by a different neurologist.
In addition to assessing wait times, investigators examined the availability of neurologists who provided medical services to Medicare beneficiaries in the 2018 dataset across 306 hospital referral regions in the United States, based on zip codes.
Results showed that 163,313 patients (average age, 74 years; 58% women; 85% White) were referred by 84,975 physicians to 10,250 neurologists across the United States.
Overall, the average wait time from physician referral to index neurologist visit was 34 days (range, 1-365 days), with longer wait times for White patients, women, and those aged 65-69 years. Overall, 18% waited longer than 90 days for an appointment.
The most common conditions diagnosed at the index neurologist visit were chronic pain/abnormality of gait (13%), sleep disorders (11%), and peripheral neuropathy (10%).
Using a linear mixed-effects statistical model, investigators found that patients with back pain waited an average of 30 days to see a neurologist, with longer waits for other conditions. Those with MS had an average wait that was 29 days longer, patients with epilepsy waited an average of 10 days longer, and those with Parkinson’s disease waited 9 days longer (P < .0001).
The number of available neurologists (range, 10-50 neurologists per 100,000 Medicare patients) did not affect wait times. However, there were differences in wait times across states because of different policies or regulations regarding healthcare access, with wait times ranging from a median high of 49 days in Idaho to a low of 24 days in Wyoming.
Notably, when patients saw a neurologist outside of their physician’s referral area, wait times were longer by an average of 11 days.
More than 40% of patients with new neurology referrals had prior office-based visits for the same neurologic diagnosis. For these patients, the median time between diagnosis and index neurologist visit was 342 days (range, 66-753 days).
Female patients in this category waited slightly longer (median, 353 days) than male patients (median, 328 days), and Black and Hispanic patients had longer median waits than White patients (389.5 days and 397 days respectively, vs 337 days; P = .0003).
“It is important to note that there is no national benchmark for determining appropriate wait times for specialist care, making it difficult to standardize expectations for timely access to specialists,” the authors noted.
The investigators suggested that a direct communication channel between primary care physicians and neurologists such as an eConsult service may hasten access to neurology consultation without the need for a formal appointment. Telemedicine in rural areas could also shorten wait times, they added.
Study limitations included the inability to determine if patients followed through with their index neurology visits or whether the last visit with the physician was the time of referral, as this could not be determined through the claims data.
This study was funded by the American Academy of Neurology. Lin reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
a cross-sectional analysis of Medicare data showed.
Wait times were not affected by the number of available neurologists. However, those with multiple sclerosis (MS), epilepsy, Parkinson’s disease, dementia, and sleep disorders had the longest wait times.
“In general, early referral to specialists has been shown to improve outcomes and increase patient satisfaction,” study author Chun Chieh Lin, PhD, MBA, of Ohio State University, Columbus, said in a press release. “Our findings underscore the need to develop new strategies to help people with neurological conditions see neurologists faster.”
The findings were published online in Neurology.
No National Benchmark for Wait Times
For this study, researchers analyzed a large sample of fee-for-service Medicare data from 2018 to 2019. Researchers identified patients with a year or less between their last referring physician visit and a new neurologist visit.
Exclusion criteria included enrollment in health maintenance organization plans without continuous enrollment in Medicare Part A and Part B for 2 years before the index neurologist visit, missing patient data, no physician referral at all, or referral by a different neurologist.
In addition to assessing wait times, investigators examined the availability of neurologists who provided medical services to Medicare beneficiaries in the 2018 dataset across 306 hospital referral regions in the United States, based on zip codes.
Results showed that 163,313 patients (average age, 74 years; 58% women; 85% White) were referred by 84,975 physicians to 10,250 neurologists across the United States.
Overall, the average wait time from physician referral to index neurologist visit was 34 days (range, 1-365 days), with longer wait times for White patients, women, and those aged 65-69 years. Overall, 18% waited longer than 90 days for an appointment.
The most common conditions diagnosed at the index neurologist visit were chronic pain/abnormality of gait (13%), sleep disorders (11%), and peripheral neuropathy (10%).
Using a linear mixed-effects statistical model, investigators found that patients with back pain waited an average of 30 days to see a neurologist, with longer waits for other conditions. Those with MS had an average wait that was 29 days longer, patients with epilepsy waited an average of 10 days longer, and those with Parkinson’s disease waited 9 days longer (P < .0001).
The number of available neurologists (range, 10-50 neurologists per 100,000 Medicare patients) did not affect wait times. However, there were differences in wait times across states because of different policies or regulations regarding healthcare access, with wait times ranging from a median high of 49 days in Idaho to a low of 24 days in Wyoming.
Notably, when patients saw a neurologist outside of their physician’s referral area, wait times were longer by an average of 11 days.
More than 40% of patients with new neurology referrals had prior office-based visits for the same neurologic diagnosis. For these patients, the median time between diagnosis and index neurologist visit was 342 days (range, 66-753 days).
Female patients in this category waited slightly longer (median, 353 days) than male patients (median, 328 days), and Black and Hispanic patients had longer median waits than White patients (389.5 days and 397 days respectively, vs 337 days; P = .0003).
“It is important to note that there is no national benchmark for determining appropriate wait times for specialist care, making it difficult to standardize expectations for timely access to specialists,” the authors noted.
The investigators suggested that a direct communication channel between primary care physicians and neurologists such as an eConsult service may hasten access to neurology consultation without the need for a formal appointment. Telemedicine in rural areas could also shorten wait times, they added.
Study limitations included the inability to determine if patients followed through with their index neurology visits or whether the last visit with the physician was the time of referral, as this could not be determined through the claims data.
This study was funded by the American Academy of Neurology. Lin reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM NEUROLOGY
Can Sea Lions Expand Our Knowledge of Epilepsy?
In 2022, the Journal of Neurosurgery took the unusual step of publishing a case report of a nonhuman subject, in this case an 8-year-old male sea lion named Cronutt, who had severe epilepsy that in many ways mirrored the common form seen in humans.
A 2020 xenotransplantation of interneuron progenitor cells in the sea lion’s hippocampus may have cured him. “He’s doing fantastic,” said Scott Baraban, PhD, a professor of neurological surgery at the University of California San Francisco Weill Institute for Neurosciences. The procedure offered a confirmation of success stories in mice and could serve as a bridge to human studies, although the science remains murky.
Cronutt’s story began the first time he was found stranded along the California coast in San Luis Obispo County, in November 2017, lethargic and disoriented. Nevertheless, he improved quickly under the care of the Marine Mammal Rescue Center in Sausalito, California, and they released him back into the wild 2 weeks later. Unfortunately, his troubles weren’t over. In the next 2 months, he came to the attention of the rehabilitation center two more times, and the resulting habituation to humans meant that he could not be re-released to the wild.
Things only got worse from there. He experienced a convulsive seizure and loss of consciousness in early 2018 and another seizure a year later. Despite anti-seizure medication, the episodes continued, and eventually, he stopped eating for long periods and lost a quarter of his body weight. It looked like euthanasia was the only alternative.
Neurosurgeons Take Notice
Baraban has devoted his career to animal models of epilepsy, focusing mainly on mice. He developed a method to transplant GABAergic interneurons from pigs, which can pick up the inhibitory role of endogenous neurons. In epileptic mice, mouse-derived progenitor cells mature into inhibitory synapses and dampen seizures, and even reverse behavioral problems.
Baraban was intrigued by the potential of the procedure to help sea lions and potentially bridge the gap between murine and human studies, and he was eager to try the approach after he learned of Cronutt’s case through his colleague Paul Buckmaster at Stanford University, California, who had collaborated with the Marine Mammal Rescue Center to demonstrate that sea lions suffer hippocampal damage that is very similar to human temporal lobe epilepsy.
It turns out that surgery on a sea lion is more complicated than on a mouse. The surgeon needs to conduct an MRI scan to locate the lesion and guide the placement of transplanted cells, and the big animals need to be sedated and intubated. Their caretakers are not enthusiastic about invasive procedures, but Cronutt had already been imaged as part of an earlier study of the effects of exposure to domoic acid on the sea lion brain, giving neurosurgeons at UCSF the information they needed.
In 2020, they transplanted GABAergic interneurons into Cronutt’s hippocampus in a last-ditch effort to save his life. He improved rapidly, and his caregivers eventually tapered off his anti-seizure medications. Today, Cronutt is living seizure-free at the Six Flags Discovery Kingdom in Vallejo, California. He even began participating in shows at Six Flags. “He is able to learn things and do things cognitively that he couldn’t do before,” said Baraban.
The researchers have not followed up with more imaging. “We just haven’t had any reason to bother him. It’s very invasive to get him to an MRI center,” said Baraban.
There haven’t been any more procedures on sea lions, in part because sea lions at rescue centers must be returned to the wild within 6-8 months, and animals with pig-based progenitor cells can’t be released. Any sea lion that would undergo such a procedure would have to live permanently in captivity, potentially for 20-30 years. “It’s a huge undertaking and expense,” said Baraban. There are also logistical challenges with the need to have MRI and other facilities close at hand to where the sea lion is kept.
Human Connections
As a veterinarian interested in human epilepsy, Buckmaster sought to find additional animal models for human temporal lobe epilepsy. He later met a veterinarian who worked with the Marine Mammal Center, who told him about temporal lobe epilepsy in sea lions.
Cronutt was just one of hundreds of California sea lions and other mammals rendered helpless by epileptic seizures induced by exposure to domoic acid, a chemical released by toxic algal blooms. Sea otters, whales, and even birds can likewise be affected. Humans, too, though it is rare: A domoic acid poisoning event in mussels from Prince Edward Island led to convulsions and an eventual diagnosis of temporal lobe epilepsy in an 84-year-old Canadian man, and three others died.
Most of Buckmaster’s work had been done in rats, but seizures are different than what are seen in humans. The damage isn’t unilateral, as in human epilepsy. The damage is unilateral in sea lions, and they suffer damage to similar neurons to those injured in humans. “In rats, you don’t see much loss of granule cells, which are the main neuron in the dentate gyrus, a region that’s really affected in temporal lobe epilepsy. In people, there’s a lot of variation, but [on average] you lose about half your granule cells, and that’s similar to sea lions. In rats, they just don’t lose them,” said Buckmaster.
That makes sea lions a useful model, but they hardly crack the case of human epilepsy. “To be humble about it, we don’t really know what’s causing the seizures. We have an idea of what region of the brain the seizures are coming from, but in terms of the cellular mechanisms, it’s still not clear,” said Buckmaster.
He also noted that, unlike sea lions, the vast majority of patients with human epilepsy have no exposure to domoic acid. That said, the case of sea lions and other marine animals makes researchers wonder. “This is speculative, but a lot of people with temporal epilepsy will have a history of some kind of precipitating event. Typically, it’s earlier in life, and a common one is prolonged febrile seizures. That could be a link to the domoic acid exposure in sea lions because the domoic acid exposure in sea lions frequently causes prolonged seizures. If the seizures are severe enough and long enough, they cause permanent brain damage, and that can cause temporal lobe epilepsy. That’s what we strongly believe is causing the temporal lobe epilepsy in sea lions. Prolonged, severe seizures can be caused by many things other than domoic acid, and that could be what causes it in many cases of human temporal lobe epilepsy,” said Buckmaster.
The approach taken with Cronutt makes sense to Buckmaster, who was not directly involved in the procedure. “The ideal treatment would be something that you would administer once, and it would cause cessation of seizures without any side effects. The transplantation of inhibitory cells is a treatment that would last and hopefully wouldn’t have any side effects and hopefully would provide complete control of seizures. It’s unlikely to reach all those goals, but it’s a step in the right direction, hopefully,” said Buckmaster.
He noted that Cronutt is only a single case and not proof that the procedure will work more generally. It’s possible the sea lion would have improved on his own without treatment, and the procedure itself could have influenced the brain. “That’s been the case with other neurological conditions that have attempted to be treated with cell transplantation,” said Buckmaster.
A phase 1/2 clinical trial, sponsored by Neurona Therapeutics, is currently recruiting patients to test transplant of human interneurons created from pluripotent stem cells into both temporal lobes of patients with drug-resistant bilateral mesial temporal lobe epilepsy.
Cronutt’s Course
Although he has improved dramatically, it’s possible that Cronutt continues to experience nonconvulsive seizures, which would not be easy to detect in an animal. “You don’t know if Cronutt’s seizures are controlled or not unless you can look at the electrical activity in Cronutt’s brain, and to my knowledge that has not been done,” said Buckmaster.
Previous studies in rats did repeatedly demonstrate the potential of the treatment approach. Despite the feel-good story of Cronutt, “that’s probably the most compelling evidence in support of that arm of treatment,” said Buckmaster.
Buckmaster and Barbaran had no relevant financial disclosures.
A version of this article appeared on Medscape.com.
In 2022, the Journal of Neurosurgery took the unusual step of publishing a case report of a nonhuman subject, in this case an 8-year-old male sea lion named Cronutt, who had severe epilepsy that in many ways mirrored the common form seen in humans.
A 2020 xenotransplantation of interneuron progenitor cells in the sea lion’s hippocampus may have cured him. “He’s doing fantastic,” said Scott Baraban, PhD, a professor of neurological surgery at the University of California San Francisco Weill Institute for Neurosciences. The procedure offered a confirmation of success stories in mice and could serve as a bridge to human studies, although the science remains murky.
Cronutt’s story began the first time he was found stranded along the California coast in San Luis Obispo County, in November 2017, lethargic and disoriented. Nevertheless, he improved quickly under the care of the Marine Mammal Rescue Center in Sausalito, California, and they released him back into the wild 2 weeks later. Unfortunately, his troubles weren’t over. In the next 2 months, he came to the attention of the rehabilitation center two more times, and the resulting habituation to humans meant that he could not be re-released to the wild.
Things only got worse from there. He experienced a convulsive seizure and loss of consciousness in early 2018 and another seizure a year later. Despite anti-seizure medication, the episodes continued, and eventually, he stopped eating for long periods and lost a quarter of his body weight. It looked like euthanasia was the only alternative.
Neurosurgeons Take Notice
Baraban has devoted his career to animal models of epilepsy, focusing mainly on mice. He developed a method to transplant GABAergic interneurons from pigs, which can pick up the inhibitory role of endogenous neurons. In epileptic mice, mouse-derived progenitor cells mature into inhibitory synapses and dampen seizures, and even reverse behavioral problems.
Baraban was intrigued by the potential of the procedure to help sea lions and potentially bridge the gap between murine and human studies, and he was eager to try the approach after he learned of Cronutt’s case through his colleague Paul Buckmaster at Stanford University, California, who had collaborated with the Marine Mammal Rescue Center to demonstrate that sea lions suffer hippocampal damage that is very similar to human temporal lobe epilepsy.
It turns out that surgery on a sea lion is more complicated than on a mouse. The surgeon needs to conduct an MRI scan to locate the lesion and guide the placement of transplanted cells, and the big animals need to be sedated and intubated. Their caretakers are not enthusiastic about invasive procedures, but Cronutt had already been imaged as part of an earlier study of the effects of exposure to domoic acid on the sea lion brain, giving neurosurgeons at UCSF the information they needed.
In 2020, they transplanted GABAergic interneurons into Cronutt’s hippocampus in a last-ditch effort to save his life. He improved rapidly, and his caregivers eventually tapered off his anti-seizure medications. Today, Cronutt is living seizure-free at the Six Flags Discovery Kingdom in Vallejo, California. He even began participating in shows at Six Flags. “He is able to learn things and do things cognitively that he couldn’t do before,” said Baraban.
The researchers have not followed up with more imaging. “We just haven’t had any reason to bother him. It’s very invasive to get him to an MRI center,” said Baraban.
There haven’t been any more procedures on sea lions, in part because sea lions at rescue centers must be returned to the wild within 6-8 months, and animals with pig-based progenitor cells can’t be released. Any sea lion that would undergo such a procedure would have to live permanently in captivity, potentially for 20-30 years. “It’s a huge undertaking and expense,” said Baraban. There are also logistical challenges with the need to have MRI and other facilities close at hand to where the sea lion is kept.
Human Connections
As a veterinarian interested in human epilepsy, Buckmaster sought to find additional animal models for human temporal lobe epilepsy. He later met a veterinarian who worked with the Marine Mammal Center, who told him about temporal lobe epilepsy in sea lions.
Cronutt was just one of hundreds of California sea lions and other mammals rendered helpless by epileptic seizures induced by exposure to domoic acid, a chemical released by toxic algal blooms. Sea otters, whales, and even birds can likewise be affected. Humans, too, though it is rare: A domoic acid poisoning event in mussels from Prince Edward Island led to convulsions and an eventual diagnosis of temporal lobe epilepsy in an 84-year-old Canadian man, and three others died.
Most of Buckmaster’s work had been done in rats, but seizures are different than what are seen in humans. The damage isn’t unilateral, as in human epilepsy. The damage is unilateral in sea lions, and they suffer damage to similar neurons to those injured in humans. “In rats, you don’t see much loss of granule cells, which are the main neuron in the dentate gyrus, a region that’s really affected in temporal lobe epilepsy. In people, there’s a lot of variation, but [on average] you lose about half your granule cells, and that’s similar to sea lions. In rats, they just don’t lose them,” said Buckmaster.
That makes sea lions a useful model, but they hardly crack the case of human epilepsy. “To be humble about it, we don’t really know what’s causing the seizures. We have an idea of what region of the brain the seizures are coming from, but in terms of the cellular mechanisms, it’s still not clear,” said Buckmaster.
He also noted that, unlike sea lions, the vast majority of patients with human epilepsy have no exposure to domoic acid. That said, the case of sea lions and other marine animals makes researchers wonder. “This is speculative, but a lot of people with temporal epilepsy will have a history of some kind of precipitating event. Typically, it’s earlier in life, and a common one is prolonged febrile seizures. That could be a link to the domoic acid exposure in sea lions because the domoic acid exposure in sea lions frequently causes prolonged seizures. If the seizures are severe enough and long enough, they cause permanent brain damage, and that can cause temporal lobe epilepsy. That’s what we strongly believe is causing the temporal lobe epilepsy in sea lions. Prolonged, severe seizures can be caused by many things other than domoic acid, and that could be what causes it in many cases of human temporal lobe epilepsy,” said Buckmaster.
The approach taken with Cronutt makes sense to Buckmaster, who was not directly involved in the procedure. “The ideal treatment would be something that you would administer once, and it would cause cessation of seizures without any side effects. The transplantation of inhibitory cells is a treatment that would last and hopefully wouldn’t have any side effects and hopefully would provide complete control of seizures. It’s unlikely to reach all those goals, but it’s a step in the right direction, hopefully,” said Buckmaster.
He noted that Cronutt is only a single case and not proof that the procedure will work more generally. It’s possible the sea lion would have improved on his own without treatment, and the procedure itself could have influenced the brain. “That’s been the case with other neurological conditions that have attempted to be treated with cell transplantation,” said Buckmaster.
A phase 1/2 clinical trial, sponsored by Neurona Therapeutics, is currently recruiting patients to test transplant of human interneurons created from pluripotent stem cells into both temporal lobes of patients with drug-resistant bilateral mesial temporal lobe epilepsy.
Cronutt’s Course
Although he has improved dramatically, it’s possible that Cronutt continues to experience nonconvulsive seizures, which would not be easy to detect in an animal. “You don’t know if Cronutt’s seizures are controlled or not unless you can look at the electrical activity in Cronutt’s brain, and to my knowledge that has not been done,” said Buckmaster.
Previous studies in rats did repeatedly demonstrate the potential of the treatment approach. Despite the feel-good story of Cronutt, “that’s probably the most compelling evidence in support of that arm of treatment,” said Buckmaster.
Buckmaster and Barbaran had no relevant financial disclosures.
A version of this article appeared on Medscape.com.
In 2022, the Journal of Neurosurgery took the unusual step of publishing a case report of a nonhuman subject, in this case an 8-year-old male sea lion named Cronutt, who had severe epilepsy that in many ways mirrored the common form seen in humans.
A 2020 xenotransplantation of interneuron progenitor cells in the sea lion’s hippocampus may have cured him. “He’s doing fantastic,” said Scott Baraban, PhD, a professor of neurological surgery at the University of California San Francisco Weill Institute for Neurosciences. The procedure offered a confirmation of success stories in mice and could serve as a bridge to human studies, although the science remains murky.
Cronutt’s story began the first time he was found stranded along the California coast in San Luis Obispo County, in November 2017, lethargic and disoriented. Nevertheless, he improved quickly under the care of the Marine Mammal Rescue Center in Sausalito, California, and they released him back into the wild 2 weeks later. Unfortunately, his troubles weren’t over. In the next 2 months, he came to the attention of the rehabilitation center two more times, and the resulting habituation to humans meant that he could not be re-released to the wild.
Things only got worse from there. He experienced a convulsive seizure and loss of consciousness in early 2018 and another seizure a year later. Despite anti-seizure medication, the episodes continued, and eventually, he stopped eating for long periods and lost a quarter of his body weight. It looked like euthanasia was the only alternative.
Neurosurgeons Take Notice
Baraban has devoted his career to animal models of epilepsy, focusing mainly on mice. He developed a method to transplant GABAergic interneurons from pigs, which can pick up the inhibitory role of endogenous neurons. In epileptic mice, mouse-derived progenitor cells mature into inhibitory synapses and dampen seizures, and even reverse behavioral problems.
Baraban was intrigued by the potential of the procedure to help sea lions and potentially bridge the gap between murine and human studies, and he was eager to try the approach after he learned of Cronutt’s case through his colleague Paul Buckmaster at Stanford University, California, who had collaborated with the Marine Mammal Rescue Center to demonstrate that sea lions suffer hippocampal damage that is very similar to human temporal lobe epilepsy.
It turns out that surgery on a sea lion is more complicated than on a mouse. The surgeon needs to conduct an MRI scan to locate the lesion and guide the placement of transplanted cells, and the big animals need to be sedated and intubated. Their caretakers are not enthusiastic about invasive procedures, but Cronutt had already been imaged as part of an earlier study of the effects of exposure to domoic acid on the sea lion brain, giving neurosurgeons at UCSF the information they needed.
In 2020, they transplanted GABAergic interneurons into Cronutt’s hippocampus in a last-ditch effort to save his life. He improved rapidly, and his caregivers eventually tapered off his anti-seizure medications. Today, Cronutt is living seizure-free at the Six Flags Discovery Kingdom in Vallejo, California. He even began participating in shows at Six Flags. “He is able to learn things and do things cognitively that he couldn’t do before,” said Baraban.
The researchers have not followed up with more imaging. “We just haven’t had any reason to bother him. It’s very invasive to get him to an MRI center,” said Baraban.
There haven’t been any more procedures on sea lions, in part because sea lions at rescue centers must be returned to the wild within 6-8 months, and animals with pig-based progenitor cells can’t be released. Any sea lion that would undergo such a procedure would have to live permanently in captivity, potentially for 20-30 years. “It’s a huge undertaking and expense,” said Baraban. There are also logistical challenges with the need to have MRI and other facilities close at hand to where the sea lion is kept.
Human Connections
As a veterinarian interested in human epilepsy, Buckmaster sought to find additional animal models for human temporal lobe epilepsy. He later met a veterinarian who worked with the Marine Mammal Center, who told him about temporal lobe epilepsy in sea lions.
Cronutt was just one of hundreds of California sea lions and other mammals rendered helpless by epileptic seizures induced by exposure to domoic acid, a chemical released by toxic algal blooms. Sea otters, whales, and even birds can likewise be affected. Humans, too, though it is rare: A domoic acid poisoning event in mussels from Prince Edward Island led to convulsions and an eventual diagnosis of temporal lobe epilepsy in an 84-year-old Canadian man, and three others died.
Most of Buckmaster’s work had been done in rats, but seizures are different than what are seen in humans. The damage isn’t unilateral, as in human epilepsy. The damage is unilateral in sea lions, and they suffer damage to similar neurons to those injured in humans. “In rats, you don’t see much loss of granule cells, which are the main neuron in the dentate gyrus, a region that’s really affected in temporal lobe epilepsy. In people, there’s a lot of variation, but [on average] you lose about half your granule cells, and that’s similar to sea lions. In rats, they just don’t lose them,” said Buckmaster.
That makes sea lions a useful model, but they hardly crack the case of human epilepsy. “To be humble about it, we don’t really know what’s causing the seizures. We have an idea of what region of the brain the seizures are coming from, but in terms of the cellular mechanisms, it’s still not clear,” said Buckmaster.
He also noted that, unlike sea lions, the vast majority of patients with human epilepsy have no exposure to domoic acid. That said, the case of sea lions and other marine animals makes researchers wonder. “This is speculative, but a lot of people with temporal epilepsy will have a history of some kind of precipitating event. Typically, it’s earlier in life, and a common one is prolonged febrile seizures. That could be a link to the domoic acid exposure in sea lions because the domoic acid exposure in sea lions frequently causes prolonged seizures. If the seizures are severe enough and long enough, they cause permanent brain damage, and that can cause temporal lobe epilepsy. That’s what we strongly believe is causing the temporal lobe epilepsy in sea lions. Prolonged, severe seizures can be caused by many things other than domoic acid, and that could be what causes it in many cases of human temporal lobe epilepsy,” said Buckmaster.
The approach taken with Cronutt makes sense to Buckmaster, who was not directly involved in the procedure. “The ideal treatment would be something that you would administer once, and it would cause cessation of seizures without any side effects. The transplantation of inhibitory cells is a treatment that would last and hopefully wouldn’t have any side effects and hopefully would provide complete control of seizures. It’s unlikely to reach all those goals, but it’s a step in the right direction, hopefully,” said Buckmaster.
He noted that Cronutt is only a single case and not proof that the procedure will work more generally. It’s possible the sea lion would have improved on his own without treatment, and the procedure itself could have influenced the brain. “That’s been the case with other neurological conditions that have attempted to be treated with cell transplantation,” said Buckmaster.
A phase 1/2 clinical trial, sponsored by Neurona Therapeutics, is currently recruiting patients to test transplant of human interneurons created from pluripotent stem cells into both temporal lobes of patients with drug-resistant bilateral mesial temporal lobe epilepsy.
Cronutt’s Course
Although he has improved dramatically, it’s possible that Cronutt continues to experience nonconvulsive seizures, which would not be easy to detect in an animal. “You don’t know if Cronutt’s seizures are controlled or not unless you can look at the electrical activity in Cronutt’s brain, and to my knowledge that has not been done,” said Buckmaster.
Previous studies in rats did repeatedly demonstrate the potential of the treatment approach. Despite the feel-good story of Cronutt, “that’s probably the most compelling evidence in support of that arm of treatment,” said Buckmaster.
Buckmaster and Barbaran had no relevant financial disclosures.
A version of this article appeared on Medscape.com.
Around 5% of US Population Diagnosed With Autoimmune Disease
TOPLINE:
In 2022, autoimmune diseases affected over 15 million individuals in the United States, with women nearly twice as likely to be affected as men and more than one third of affected individuals having more than one autoimmune condition.
METHODOLOGY:
- Researchers used electronic health record (EHR) data from six healthcare systems in the United States between 2011 and 2022 to estimate the prevalence of autoimmune diseases according to sex and age.
- They selected 105 autoimmune diseases from the textbook The Autoimmune Diseases and estimated their prevalence in more than 10 million individuals from these healthcare systems; these statistics were subsequently extrapolated to an estimated US population of 333.3 million.
- An individual was considered to have a diagnosis of an autoimmune disease if they had at least two diagnosis codes for the condition, with the codes being at least 30 days apart.
- A software program was developed to compute the prevalence of autoimmune diseases alone and in aggregate, enabling other researchers to replicate or modify the analysis over time.
TAKEAWAY:
- More than 15 million people, accounting for 4.6% of the US population, were diagnosed with at least one autoimmune disease from January 2011 to June 2022; 34% were diagnosed with more than one autoimmune disease.
- Sex-stratified analysis revealed that 63% of patients diagnosed with autoimmune disease were women, and only 37% were men, establishing a female-to-male ratio of 1.7:1; age-stratified analysis revealed increasing prevalence of autoimmune conditions with age, peaking in individuals aged ≥ 65 years.
- Among individuals with autoimmune diseases, 65% of patients had one condition, whereas 24% had two, 8% had three, and 2% had four or more autoimmune diseases (does not add to 100% due to rounding).
- Rheumatoid arthritis emerged as the most prevalent autoimmune disease, followed by psoriasis, type 1 diabetes, Grave’s disease, and autoimmune thyroiditis; 19 of the top 20 most prevalent autoimmune diseases occurred more frequently in women.
IN PRACTICE:
“Accurate data on the prevalence of autoimmune diseases as a category of disease and for individual autoimmune diseases are needed to further clinical and basic research to improve diagnosis, biomarkers, and therapies for these diseases, which significantly impact the US population,” the authors wrote.
SOURCE:
The study was led by Aaron H. Abend, Autoimmune Registry, Guilford, Connecticut, and was published online in The Journal of Clinical Investigation.
LIMITATIONS:
The use of EHR data presented several challenges, including potential inaccuracies in diagnosis codes and the possibility of missing patients with single diagnosis codes because of the two-code requirement. Certain autoimmune diseases evolve over time and involve nonspecific clinical signs and symptoms that can mimic other diseases, potentially resulting in underdiagnosis. Moreover, rare diseases lacking specific diagnosis codes may have been underrepresented.
DISCLOSURES:
The study received support from Autoimmune Registry; the National Institutes of Health National Center for Advancing Translational Sciences; the National Heart, Lung, and Blood Institute; and other sources. Information on potential conflicts of interest was not disclosed.
This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
In 2022, autoimmune diseases affected over 15 million individuals in the United States, with women nearly twice as likely to be affected as men and more than one third of affected individuals having more than one autoimmune condition.
METHODOLOGY:
- Researchers used electronic health record (EHR) data from six healthcare systems in the United States between 2011 and 2022 to estimate the prevalence of autoimmune diseases according to sex and age.
- They selected 105 autoimmune diseases from the textbook The Autoimmune Diseases and estimated their prevalence in more than 10 million individuals from these healthcare systems; these statistics were subsequently extrapolated to an estimated US population of 333.3 million.
- An individual was considered to have a diagnosis of an autoimmune disease if they had at least two diagnosis codes for the condition, with the codes being at least 30 days apart.
- A software program was developed to compute the prevalence of autoimmune diseases alone and in aggregate, enabling other researchers to replicate or modify the analysis over time.
TAKEAWAY:
- More than 15 million people, accounting for 4.6% of the US population, were diagnosed with at least one autoimmune disease from January 2011 to June 2022; 34% were diagnosed with more than one autoimmune disease.
- Sex-stratified analysis revealed that 63% of patients diagnosed with autoimmune disease were women, and only 37% were men, establishing a female-to-male ratio of 1.7:1; age-stratified analysis revealed increasing prevalence of autoimmune conditions with age, peaking in individuals aged ≥ 65 years.
- Among individuals with autoimmune diseases, 65% of patients had one condition, whereas 24% had two, 8% had three, and 2% had four or more autoimmune diseases (does not add to 100% due to rounding).
- Rheumatoid arthritis emerged as the most prevalent autoimmune disease, followed by psoriasis, type 1 diabetes, Grave’s disease, and autoimmune thyroiditis; 19 of the top 20 most prevalent autoimmune diseases occurred more frequently in women.
IN PRACTICE:
“Accurate data on the prevalence of autoimmune diseases as a category of disease and for individual autoimmune diseases are needed to further clinical and basic research to improve diagnosis, biomarkers, and therapies for these diseases, which significantly impact the US population,” the authors wrote.
SOURCE:
The study was led by Aaron H. Abend, Autoimmune Registry, Guilford, Connecticut, and was published online in The Journal of Clinical Investigation.
LIMITATIONS:
The use of EHR data presented several challenges, including potential inaccuracies in diagnosis codes and the possibility of missing patients with single diagnosis codes because of the two-code requirement. Certain autoimmune diseases evolve over time and involve nonspecific clinical signs and symptoms that can mimic other diseases, potentially resulting in underdiagnosis. Moreover, rare diseases lacking specific diagnosis codes may have been underrepresented.
DISCLOSURES:
The study received support from Autoimmune Registry; the National Institutes of Health National Center for Advancing Translational Sciences; the National Heart, Lung, and Blood Institute; and other sources. Information on potential conflicts of interest was not disclosed.
This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
In 2022, autoimmune diseases affected over 15 million individuals in the United States, with women nearly twice as likely to be affected as men and more than one third of affected individuals having more than one autoimmune condition.
METHODOLOGY:
- Researchers used electronic health record (EHR) data from six healthcare systems in the United States between 2011 and 2022 to estimate the prevalence of autoimmune diseases according to sex and age.
- They selected 105 autoimmune diseases from the textbook The Autoimmune Diseases and estimated their prevalence in more than 10 million individuals from these healthcare systems; these statistics were subsequently extrapolated to an estimated US population of 333.3 million.
- An individual was considered to have a diagnosis of an autoimmune disease if they had at least two diagnosis codes for the condition, with the codes being at least 30 days apart.
- A software program was developed to compute the prevalence of autoimmune diseases alone and in aggregate, enabling other researchers to replicate or modify the analysis over time.
TAKEAWAY:
- More than 15 million people, accounting for 4.6% of the US population, were diagnosed with at least one autoimmune disease from January 2011 to June 2022; 34% were diagnosed with more than one autoimmune disease.
- Sex-stratified analysis revealed that 63% of patients diagnosed with autoimmune disease were women, and only 37% were men, establishing a female-to-male ratio of 1.7:1; age-stratified analysis revealed increasing prevalence of autoimmune conditions with age, peaking in individuals aged ≥ 65 years.
- Among individuals with autoimmune diseases, 65% of patients had one condition, whereas 24% had two, 8% had three, and 2% had four or more autoimmune diseases (does not add to 100% due to rounding).
- Rheumatoid arthritis emerged as the most prevalent autoimmune disease, followed by psoriasis, type 1 diabetes, Grave’s disease, and autoimmune thyroiditis; 19 of the top 20 most prevalent autoimmune diseases occurred more frequently in women.
IN PRACTICE:
“Accurate data on the prevalence of autoimmune diseases as a category of disease and for individual autoimmune diseases are needed to further clinical and basic research to improve diagnosis, biomarkers, and therapies for these diseases, which significantly impact the US population,” the authors wrote.
SOURCE:
The study was led by Aaron H. Abend, Autoimmune Registry, Guilford, Connecticut, and was published online in The Journal of Clinical Investigation.
LIMITATIONS:
The use of EHR data presented several challenges, including potential inaccuracies in diagnosis codes and the possibility of missing patients with single diagnosis codes because of the two-code requirement. Certain autoimmune diseases evolve over time and involve nonspecific clinical signs and symptoms that can mimic other diseases, potentially resulting in underdiagnosis. Moreover, rare diseases lacking specific diagnosis codes may have been underrepresented.
DISCLOSURES:
The study received support from Autoimmune Registry; the National Institutes of Health National Center for Advancing Translational Sciences; the National Heart, Lung, and Blood Institute; and other sources. Information on potential conflicts of interest was not disclosed.
This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
Early-Onset Asthma May Slow Memory Development
Children with asthma scored significantly lower than those without asthma on measures of episodic memory, based on longitudinal data from nearly 500 individuals.
Animal models have shown associations between asthma and memory problems, but data for children are lacking, wrote Nicholas J. Christopher-Hayes, MA, of the University of California, Davis, and colleagues.
“Asthma is very frequent among children, and there is mounting evidence from rodent models that asthma may result in neural injury in the hippocampus, which in turn may cause memory loss,” Christopher-Hayes said in an interview. “Although there is also a good amount of research with older adults, very little research has been done with children, the period that is most frequently linked to asthma onset,” he said. Therefore, the researchers leveraged a large national study on child development to examine development of memory as a function of asthma exposure.
In this study published in JAMA Network Open, the researchers conducted both a longitudinal and cross-sectional analysis of data from the Adolescent Brain Cognitive Development Study, which began in 2015. Children were enrolled at ages 9-10 years with a follow-up assessment 1-2 years later.
The participants were categorized as early childhood-onset asthma (asthma at baseline and follow-up), later childhood-onset asthma (asthma at follow-up only), or no asthma history. The primary outcome of the longitudinal analysis was episodic memory. Approximately half of the participants were boys, and slightly more than half were White.
Overall, those with early-onset asthma showed significantly lower rates of longitudinal memory improvements at follow-up compared with the comparison group (P < .01).
Developmental memory improvement in children with later-onset asthma was not significantly different from the control individuals.
Secondary outcomes included processing speed and inhibition, and attention. In a cross-sectional analysis with a larger sample of 2062 children from the same database (1031 with any asthma), those with asthma scored significantly lower on measures not only of episodic memory but also processing speed and inhibition/attention than children with no asthma, with P values of .04, .01, and .02, respectively.
The results were limited by several factors, including the reliance on parent reports for indicators of asthma and the lack of data on the potential effect of prescription corticosteroid use on neurocognitive development, the researchers noted.
The mechanism behind the association remains unclear; the inflammation associated with asthma may disrupt neural processing and manifest as cognitive dysfunction, as has been seen in rodent models of asthma, the researchers wrote. “It is possible that associations between asthma and developmental trajectories emerge earlier for memory, perhaps due to its sensitivity to subtle hippocampal injury,” they noted.
Longer follow-up studies are needed to fully understand how childhood asthma predicts memory declines or difficulties in childhood and beyond, said Christopher-Hayes. “We also need additional studies to understand why children who were diagnosed earlier and had asthma for longer seem to be particularly affected,” he said.
The results of this study were consistent with previous findings and therefore not surprising, senior author Simona Ghetti, PhD, a professor of psychology at the University of California, Davis, said in an interview. However, the finding that the extent of exposure to asthma was associated with slower memory improvement in childhood was striking, she said. That children with an earlier asthma onset who had disease indicators for a longer period showed a slower development of memory over time, suggests that asthma exposure may affect the developmental trajectory of memory, Ghetti noted.
“Recommendations to clinicians are premature because we need a better understanding of the boundary conditions, such as the minimal level of asthma exposure that might generate memory difficulties,” said Ghetti.
“Nevertheless, our results underscore the importance of looking at asthma as a potential source of cognitive difficulty in children,” she said.
Asthma’s Extensive Effect
Evidence is mounting that a diagnosis of asthma may have implications outside the pulmonary system, Diego J. Maselli, MD, professor and chief of the Division of Pulmonary Diseases & Critical Care at UT Health, San Antonio, said in an interview.
“Asthmatics may be at risk of nasal polyps, allergic rhinitis, and other allergic conditions, but there is emerging of evidence inflammation associated with asthma may affect other organ systems,” said Maselli, who was not involved in the study.
“For example, chronic inflammation in asthmatics may increase the risk of cardiovascular disease,” he said.
Although less is known about the effects of asthma on the nervous system, animal models suggest that inflammation associated with asthma may result in neuronal injury and potential effects on memory, said Maselli.
The findings of this study provide evidence of potential detrimental effects on the memory of children with asthma but should be interpreted with caution, Maselli said. “Children with chronic medical conditions may have an inherent disadvantage compared with their peers due to the burden of their disease, medication utilization and side effects, absenteeism from school, physical limitations, and other disease-specific circumstances,” he noted.
“Uncontrolled asthma, in particular, has strong links to low socioeconomic factors that are closely tied to access to adequate medical care, nutrition, educational institutions, and other relevant contributors to normal cognitive development,” Maselli said. Although the authors account for some of these socioeconomic factors by evaluating income and race, other variables may have influenced the results, he added.
Overall, this study’s findings suggested that the diagnosis of asthma in children may be associated with memory deficits and may influence neurodevelopment; however, more research is needed to determine whether the findings are replicated in other cohorts, said Maselli. “In particular, evaluating the effects of the severity of asthma and different asthma endotypes would be crucial to identify children with a higher risk of memory or cognitive deficits and confirm these associations,” he said.
This study was funded by the Memory and Plasticity Program at the University of California, Davis, and by a Learning, Memory, and Plasticity Training Program Fellowship grant from the National Institutes of Health. The researchers and Maselli had no financial conflicts to disclose.
A version of this article appeared on Medscape.com.
Children with asthma scored significantly lower than those without asthma on measures of episodic memory, based on longitudinal data from nearly 500 individuals.
Animal models have shown associations between asthma and memory problems, but data for children are lacking, wrote Nicholas J. Christopher-Hayes, MA, of the University of California, Davis, and colleagues.
“Asthma is very frequent among children, and there is mounting evidence from rodent models that asthma may result in neural injury in the hippocampus, which in turn may cause memory loss,” Christopher-Hayes said in an interview. “Although there is also a good amount of research with older adults, very little research has been done with children, the period that is most frequently linked to asthma onset,” he said. Therefore, the researchers leveraged a large national study on child development to examine development of memory as a function of asthma exposure.
In this study published in JAMA Network Open, the researchers conducted both a longitudinal and cross-sectional analysis of data from the Adolescent Brain Cognitive Development Study, which began in 2015. Children were enrolled at ages 9-10 years with a follow-up assessment 1-2 years later.
The participants were categorized as early childhood-onset asthma (asthma at baseline and follow-up), later childhood-onset asthma (asthma at follow-up only), or no asthma history. The primary outcome of the longitudinal analysis was episodic memory. Approximately half of the participants were boys, and slightly more than half were White.
Overall, those with early-onset asthma showed significantly lower rates of longitudinal memory improvements at follow-up compared with the comparison group (P < .01).
Developmental memory improvement in children with later-onset asthma was not significantly different from the control individuals.
Secondary outcomes included processing speed and inhibition, and attention. In a cross-sectional analysis with a larger sample of 2062 children from the same database (1031 with any asthma), those with asthma scored significantly lower on measures not only of episodic memory but also processing speed and inhibition/attention than children with no asthma, with P values of .04, .01, and .02, respectively.
The results were limited by several factors, including the reliance on parent reports for indicators of asthma and the lack of data on the potential effect of prescription corticosteroid use on neurocognitive development, the researchers noted.
The mechanism behind the association remains unclear; the inflammation associated with asthma may disrupt neural processing and manifest as cognitive dysfunction, as has been seen in rodent models of asthma, the researchers wrote. “It is possible that associations between asthma and developmental trajectories emerge earlier for memory, perhaps due to its sensitivity to subtle hippocampal injury,” they noted.
Longer follow-up studies are needed to fully understand how childhood asthma predicts memory declines or difficulties in childhood and beyond, said Christopher-Hayes. “We also need additional studies to understand why children who were diagnosed earlier and had asthma for longer seem to be particularly affected,” he said.
The results of this study were consistent with previous findings and therefore not surprising, senior author Simona Ghetti, PhD, a professor of psychology at the University of California, Davis, said in an interview. However, the finding that the extent of exposure to asthma was associated with slower memory improvement in childhood was striking, she said. That children with an earlier asthma onset who had disease indicators for a longer period showed a slower development of memory over time, suggests that asthma exposure may affect the developmental trajectory of memory, Ghetti noted.
“Recommendations to clinicians are premature because we need a better understanding of the boundary conditions, such as the minimal level of asthma exposure that might generate memory difficulties,” said Ghetti.
“Nevertheless, our results underscore the importance of looking at asthma as a potential source of cognitive difficulty in children,” she said.
Asthma’s Extensive Effect
Evidence is mounting that a diagnosis of asthma may have implications outside the pulmonary system, Diego J. Maselli, MD, professor and chief of the Division of Pulmonary Diseases & Critical Care at UT Health, San Antonio, said in an interview.
“Asthmatics may be at risk of nasal polyps, allergic rhinitis, and other allergic conditions, but there is emerging of evidence inflammation associated with asthma may affect other organ systems,” said Maselli, who was not involved in the study.
“For example, chronic inflammation in asthmatics may increase the risk of cardiovascular disease,” he said.
Although less is known about the effects of asthma on the nervous system, animal models suggest that inflammation associated with asthma may result in neuronal injury and potential effects on memory, said Maselli.
The findings of this study provide evidence of potential detrimental effects on the memory of children with asthma but should be interpreted with caution, Maselli said. “Children with chronic medical conditions may have an inherent disadvantage compared with their peers due to the burden of their disease, medication utilization and side effects, absenteeism from school, physical limitations, and other disease-specific circumstances,” he noted.
“Uncontrolled asthma, in particular, has strong links to low socioeconomic factors that are closely tied to access to adequate medical care, nutrition, educational institutions, and other relevant contributors to normal cognitive development,” Maselli said. Although the authors account for some of these socioeconomic factors by evaluating income and race, other variables may have influenced the results, he added.
Overall, this study’s findings suggested that the diagnosis of asthma in children may be associated with memory deficits and may influence neurodevelopment; however, more research is needed to determine whether the findings are replicated in other cohorts, said Maselli. “In particular, evaluating the effects of the severity of asthma and different asthma endotypes would be crucial to identify children with a higher risk of memory or cognitive deficits and confirm these associations,” he said.
This study was funded by the Memory and Plasticity Program at the University of California, Davis, and by a Learning, Memory, and Plasticity Training Program Fellowship grant from the National Institutes of Health. The researchers and Maselli had no financial conflicts to disclose.
A version of this article appeared on Medscape.com.
Children with asthma scored significantly lower than those without asthma on measures of episodic memory, based on longitudinal data from nearly 500 individuals.
Animal models have shown associations between asthma and memory problems, but data for children are lacking, wrote Nicholas J. Christopher-Hayes, MA, of the University of California, Davis, and colleagues.
“Asthma is very frequent among children, and there is mounting evidence from rodent models that asthma may result in neural injury in the hippocampus, which in turn may cause memory loss,” Christopher-Hayes said in an interview. “Although there is also a good amount of research with older adults, very little research has been done with children, the period that is most frequently linked to asthma onset,” he said. Therefore, the researchers leveraged a large national study on child development to examine development of memory as a function of asthma exposure.
In this study published in JAMA Network Open, the researchers conducted both a longitudinal and cross-sectional analysis of data from the Adolescent Brain Cognitive Development Study, which began in 2015. Children were enrolled at ages 9-10 years with a follow-up assessment 1-2 years later.
The participants were categorized as early childhood-onset asthma (asthma at baseline and follow-up), later childhood-onset asthma (asthma at follow-up only), or no asthma history. The primary outcome of the longitudinal analysis was episodic memory. Approximately half of the participants were boys, and slightly more than half were White.
Overall, those with early-onset asthma showed significantly lower rates of longitudinal memory improvements at follow-up compared with the comparison group (P < .01).
Developmental memory improvement in children with later-onset asthma was not significantly different from the control individuals.
Secondary outcomes included processing speed and inhibition, and attention. In a cross-sectional analysis with a larger sample of 2062 children from the same database (1031 with any asthma), those with asthma scored significantly lower on measures not only of episodic memory but also processing speed and inhibition/attention than children with no asthma, with P values of .04, .01, and .02, respectively.
The results were limited by several factors, including the reliance on parent reports for indicators of asthma and the lack of data on the potential effect of prescription corticosteroid use on neurocognitive development, the researchers noted.
The mechanism behind the association remains unclear; the inflammation associated with asthma may disrupt neural processing and manifest as cognitive dysfunction, as has been seen in rodent models of asthma, the researchers wrote. “It is possible that associations between asthma and developmental trajectories emerge earlier for memory, perhaps due to its sensitivity to subtle hippocampal injury,” they noted.
Longer follow-up studies are needed to fully understand how childhood asthma predicts memory declines or difficulties in childhood and beyond, said Christopher-Hayes. “We also need additional studies to understand why children who were diagnosed earlier and had asthma for longer seem to be particularly affected,” he said.
The results of this study were consistent with previous findings and therefore not surprising, senior author Simona Ghetti, PhD, a professor of psychology at the University of California, Davis, said in an interview. However, the finding that the extent of exposure to asthma was associated with slower memory improvement in childhood was striking, she said. That children with an earlier asthma onset who had disease indicators for a longer period showed a slower development of memory over time, suggests that asthma exposure may affect the developmental trajectory of memory, Ghetti noted.
“Recommendations to clinicians are premature because we need a better understanding of the boundary conditions, such as the minimal level of asthma exposure that might generate memory difficulties,” said Ghetti.
“Nevertheless, our results underscore the importance of looking at asthma as a potential source of cognitive difficulty in children,” she said.
Asthma’s Extensive Effect
Evidence is mounting that a diagnosis of asthma may have implications outside the pulmonary system, Diego J. Maselli, MD, professor and chief of the Division of Pulmonary Diseases & Critical Care at UT Health, San Antonio, said in an interview.
“Asthmatics may be at risk of nasal polyps, allergic rhinitis, and other allergic conditions, but there is emerging of evidence inflammation associated with asthma may affect other organ systems,” said Maselli, who was not involved in the study.
“For example, chronic inflammation in asthmatics may increase the risk of cardiovascular disease,” he said.
Although less is known about the effects of asthma on the nervous system, animal models suggest that inflammation associated with asthma may result in neuronal injury and potential effects on memory, said Maselli.
The findings of this study provide evidence of potential detrimental effects on the memory of children with asthma but should be interpreted with caution, Maselli said. “Children with chronic medical conditions may have an inherent disadvantage compared with their peers due to the burden of their disease, medication utilization and side effects, absenteeism from school, physical limitations, and other disease-specific circumstances,” he noted.
“Uncontrolled asthma, in particular, has strong links to low socioeconomic factors that are closely tied to access to adequate medical care, nutrition, educational institutions, and other relevant contributors to normal cognitive development,” Maselli said. Although the authors account for some of these socioeconomic factors by evaluating income and race, other variables may have influenced the results, he added.
Overall, this study’s findings suggested that the diagnosis of asthma in children may be associated with memory deficits and may influence neurodevelopment; however, more research is needed to determine whether the findings are replicated in other cohorts, said Maselli. “In particular, evaluating the effects of the severity of asthma and different asthma endotypes would be crucial to identify children with a higher risk of memory or cognitive deficits and confirm these associations,” he said.
This study was funded by the Memory and Plasticity Program at the University of California, Davis, and by a Learning, Memory, and Plasticity Training Program Fellowship grant from the National Institutes of Health. The researchers and Maselli had no financial conflicts to disclose.
A version of this article appeared on Medscape.com.
Dementia Risk Higher for Stroke Survivors
TOPLINE:
Risk for dementia is nearly 80% higher in stroke survivors than in those without stroke, a new study reveals. The data suggest risk declines within 1 year after stroke but remains elevated for up to 20 years.
METHODOLOGY:
- Researchers conducted a population-wide analysis of over 15 million people in Canada between 2002 and 2022. The study focused on adults hospitalized for ischemic stroke, intracerebral hemorrhage, or acute myocardial infarction (AMI).
- Of 175,980 stroke survivors, 99% were matched 1:1 to residents without stroke on the basis of age, sex, rural residence, neighborhood deprivation, and vascular comorbidities. In addition, 90% of patients were matched to those with AMI.
- Incident dementia diagnoses were tracked starting 90 days after stroke until death, emigration, or the end of the study, using a validated algorithm based on hospitalization for dementia, prescriptions for cholinesterase inhibitors, or physician claims within 2 years.
- The mean follow-up duration was 5.6 years.
TAKEAWAY:
- Among stroke survivors, 19% were diagnosed with dementia vs 12.5% in the reference population. The dementia rate per 100 person-years was higher among stroke survivors than in the reference population over the entire follow-up period (3.34 vs 1.89).
- Over the entire study period, dementia was 76% more likely among stroke patients (hazard ratio [HR], 1.76; 95% CI, 1.73-1.79) and 82% more likely in the AMI cohort (HR, 1.82; 95% CI, 1.79-1.85) than in the reference population.
- Time-varying analysis revealed that dementia risk was highest within the first year after stroke, with a > 2.5-fold increase at 6 months (HR, 2.51; 95% CI, 2.42-2.59), which decreased to a 1.5-fold increase at 5 years (HR, 1.51; 95% CI, 1.48-1.56) but remained elevated compared with the reference population even 20 years after the index stroke.
- Recurrent stroke was associated with an approximately threefold increased risk for dementia (single recurrent stroke adjusted HR, 2.64; 95% CI, 2.54-2.74; multiple recurrent strokes adjusted HR, 3.05; 95% CI, 2.81-3.33).
IN PRACTICE:
“While much research has been focused on reducing the risk of a second stroke, our findings make it clear that more research also is needed on developing interventions to help prevent dementia after stroke,” lead author Raed A. Joundi, MD, DPhil, McMaster University, Hamilton, Ontario, Canada, said in a press release.
“There is a need to accelerate the implementation of promising interventions or multipronged approaches into large randomized controlled trials to lower the risk of dementia,” the investigators wrote.
SOURCE:
The study was published online on December 4 in Neurology.
LIMITATIONS:
The study’s limitations included reliance on administrative coding without imaging data, potential underestimation of mild dementia, and lack of granular information on stroke severity, disability, and prestroke cognitive decline. While adjustments were made for healthcare contact and secondary prevention medications, residual biases may have persisted.
DISCLOSURES:
This study received funding from the Canada Brain Research Fund, Heart & Stroke Foundation of Canada, and Canadian Stroke Consortium. Two authors hold awards and positions from national organizations and academic institutions in Canada. Additional details are provided in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Risk for dementia is nearly 80% higher in stroke survivors than in those without stroke, a new study reveals. The data suggest risk declines within 1 year after stroke but remains elevated for up to 20 years.
METHODOLOGY:
- Researchers conducted a population-wide analysis of over 15 million people in Canada between 2002 and 2022. The study focused on adults hospitalized for ischemic stroke, intracerebral hemorrhage, or acute myocardial infarction (AMI).
- Of 175,980 stroke survivors, 99% were matched 1:1 to residents without stroke on the basis of age, sex, rural residence, neighborhood deprivation, and vascular comorbidities. In addition, 90% of patients were matched to those with AMI.
- Incident dementia diagnoses were tracked starting 90 days after stroke until death, emigration, or the end of the study, using a validated algorithm based on hospitalization for dementia, prescriptions for cholinesterase inhibitors, or physician claims within 2 years.
- The mean follow-up duration was 5.6 years.
TAKEAWAY:
- Among stroke survivors, 19% were diagnosed with dementia vs 12.5% in the reference population. The dementia rate per 100 person-years was higher among stroke survivors than in the reference population over the entire follow-up period (3.34 vs 1.89).
- Over the entire study period, dementia was 76% more likely among stroke patients (hazard ratio [HR], 1.76; 95% CI, 1.73-1.79) and 82% more likely in the AMI cohort (HR, 1.82; 95% CI, 1.79-1.85) than in the reference population.
- Time-varying analysis revealed that dementia risk was highest within the first year after stroke, with a > 2.5-fold increase at 6 months (HR, 2.51; 95% CI, 2.42-2.59), which decreased to a 1.5-fold increase at 5 years (HR, 1.51; 95% CI, 1.48-1.56) but remained elevated compared with the reference population even 20 years after the index stroke.
- Recurrent stroke was associated with an approximately threefold increased risk for dementia (single recurrent stroke adjusted HR, 2.64; 95% CI, 2.54-2.74; multiple recurrent strokes adjusted HR, 3.05; 95% CI, 2.81-3.33).
IN PRACTICE:
“While much research has been focused on reducing the risk of a second stroke, our findings make it clear that more research also is needed on developing interventions to help prevent dementia after stroke,” lead author Raed A. Joundi, MD, DPhil, McMaster University, Hamilton, Ontario, Canada, said in a press release.
“There is a need to accelerate the implementation of promising interventions or multipronged approaches into large randomized controlled trials to lower the risk of dementia,” the investigators wrote.
SOURCE:
The study was published online on December 4 in Neurology.
LIMITATIONS:
The study’s limitations included reliance on administrative coding without imaging data, potential underestimation of mild dementia, and lack of granular information on stroke severity, disability, and prestroke cognitive decline. While adjustments were made for healthcare contact and secondary prevention medications, residual biases may have persisted.
DISCLOSURES:
This study received funding from the Canada Brain Research Fund, Heart & Stroke Foundation of Canada, and Canadian Stroke Consortium. Two authors hold awards and positions from national organizations and academic institutions in Canada. Additional details are provided in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Risk for dementia is nearly 80% higher in stroke survivors than in those without stroke, a new study reveals. The data suggest risk declines within 1 year after stroke but remains elevated for up to 20 years.
METHODOLOGY:
- Researchers conducted a population-wide analysis of over 15 million people in Canada between 2002 and 2022. The study focused on adults hospitalized for ischemic stroke, intracerebral hemorrhage, or acute myocardial infarction (AMI).
- Of 175,980 stroke survivors, 99% were matched 1:1 to residents without stroke on the basis of age, sex, rural residence, neighborhood deprivation, and vascular comorbidities. In addition, 90% of patients were matched to those with AMI.
- Incident dementia diagnoses were tracked starting 90 days after stroke until death, emigration, or the end of the study, using a validated algorithm based on hospitalization for dementia, prescriptions for cholinesterase inhibitors, or physician claims within 2 years.
- The mean follow-up duration was 5.6 years.
TAKEAWAY:
- Among stroke survivors, 19% were diagnosed with dementia vs 12.5% in the reference population. The dementia rate per 100 person-years was higher among stroke survivors than in the reference population over the entire follow-up period (3.34 vs 1.89).
- Over the entire study period, dementia was 76% more likely among stroke patients (hazard ratio [HR], 1.76; 95% CI, 1.73-1.79) and 82% more likely in the AMI cohort (HR, 1.82; 95% CI, 1.79-1.85) than in the reference population.
- Time-varying analysis revealed that dementia risk was highest within the first year after stroke, with a > 2.5-fold increase at 6 months (HR, 2.51; 95% CI, 2.42-2.59), which decreased to a 1.5-fold increase at 5 years (HR, 1.51; 95% CI, 1.48-1.56) but remained elevated compared with the reference population even 20 years after the index stroke.
- Recurrent stroke was associated with an approximately threefold increased risk for dementia (single recurrent stroke adjusted HR, 2.64; 95% CI, 2.54-2.74; multiple recurrent strokes adjusted HR, 3.05; 95% CI, 2.81-3.33).
IN PRACTICE:
“While much research has been focused on reducing the risk of a second stroke, our findings make it clear that more research also is needed on developing interventions to help prevent dementia after stroke,” lead author Raed A. Joundi, MD, DPhil, McMaster University, Hamilton, Ontario, Canada, said in a press release.
“There is a need to accelerate the implementation of promising interventions or multipronged approaches into large randomized controlled trials to lower the risk of dementia,” the investigators wrote.
SOURCE:
The study was published online on December 4 in Neurology.
LIMITATIONS:
The study’s limitations included reliance on administrative coding without imaging data, potential underestimation of mild dementia, and lack of granular information on stroke severity, disability, and prestroke cognitive decline. While adjustments were made for healthcare contact and secondary prevention medications, residual biases may have persisted.
DISCLOSURES:
This study received funding from the Canada Brain Research Fund, Heart & Stroke Foundation of Canada, and Canadian Stroke Consortium. Two authors hold awards and positions from national organizations and academic institutions in Canada. Additional details are provided in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
New Proposed Health Cybersecurity Rule: What Physicians Should Know
A new federal rule could force hospitals and doctors’ groups to boost health cybersecurity measures to better protect patients’ health information and prevent ransomware attacks.
The proposed rule, issued by the US Department of Health & Human Services (HHS) and published on January 6 in the Federal Register, marks the first time in a decade that the federal government has updated regulations governing the security of private health information (PHI) that’s kept or shared online. Comments on the rule are due on March 6.
Because the risks for cyberattacks have increased exponentially, “there is a greater need to invest than ever before in both people and technologies to secure patient information,” Adam Greene, an attorney at Davis Wright Tremaine in Washington, DC, who advises healthcare clients on cybersecurity, said in an interview.
Bad actors continue to evolve and are often far ahead of their targets, added Mark Fox, privacy and research compliance officer for the American College of Cardiology.
In the proposed rule, HHS noted that breaches have risen by more than 50% since 2020. Damages from health data breaches are more expensive than in any other sector, averaging $10 million per incident, said HHS.
The damage can continue for years, as much of the data — such as date of birth — in PHI are “immutable,” unlike a credit card number, the agency said. A review of breach reports made to HHS’ Office for Civil Rights shows near-daily data breaches affecting hundreds to tens of thousands of patients. Since December 1 alone, healthcare providers reported breaches affecting nearly 3 million US patients, according to federal data.
Debi Carr, a Florida-based cybersecurity consultant for small physician and dental practices, welcomed the new proposal. “Many practices are clinging to doing things the way they have always done it, and hackers are taking full advantage of that mindset,” she said in an interview. “We have to change our mindset.”
Among the proposal’s recommendations:
- A shift away from making security specifications “addressable” to required. Fox said that many interpreted addressable to mean optional. The clarification is important. The government will require greater accountability, including a requirement to annually revise the risk analysis, to review policies and procedures and implementation, and to perform penetration testing, said Greene.
- Requiring multifactor authentication (MFA) and encryption of PHI at rest and in transit. “A reasonable person who does security will tell you that should be a requirement,” said Fox. Carr added that the February 2024 Change Healthcare ransomware attack happened because workers at the payment processing company were not using MFA.
- Requiring all entities to verify at least once a year that “business associates” have put into place the required safeguards; the associates would need to provide a written analysis of relevant electronic information systems by a subject matter expert and a written certification that the analysis has been performed and is accurate. In the past, the rule “only required that you sign a business associate agreement” with the associate, which could be a payer, a pharmacy, or another physician practice, said Fox. The rule would require all entities to get certification that the controls are in place.
- Requiring a detailed map of an electronic network. For a physician practice, that means creating an inventory of all the technology assets, including devices, applications, and anything that would touch electronic PHI, and then creating a map of how it comes into the office, flows through it, and departs, said Greene.
- Having a plan of action in the case of a breach. The rule will require written procedures to restore certain relevant systems and data within 72 hours and written incident response plans.
Some physician practices — especially those still relying on passwords instead of more sophisticated MFA or encryption — may have to invest significantly to strengthen their information security, said Greene. Smaller organizations, for example, may need to upgrade systems to ensure that user access is terminated within an hour after someone’s employment ends.
Carr said practices should not view the investments as a burden. The regulation “will force practices to implement best cybersecurity practices,” she said.
Implementing those best practices serves as insurance, said Fox. He suggests that anyone in doubt “talk to someone who’s actually lived through a breach and had to recover.”
Tampa General Hospital in Florida, for instance, recently settled a class action suit, agreeing to pay $6.8 million to patients whose PHI was compromised.
It is not certain whether or when the health cybersecurity rule will be made final.
The incoming Trump administration could cancel or delay the rulemaking process.
Even if it continues, “I would not expect a final rule in 2025,” said Greene. He estimates that the rule would not take effect until at least 2026; healthcare entities would have 180 days to comply. Still, those 180 days can go by fast.
“I would say don’t panic, but don’t ignore it either,” he said.
A version of this article first appeared on Medscape.com.
A new federal rule could force hospitals and doctors’ groups to boost health cybersecurity measures to better protect patients’ health information and prevent ransomware attacks.
The proposed rule, issued by the US Department of Health & Human Services (HHS) and published on January 6 in the Federal Register, marks the first time in a decade that the federal government has updated regulations governing the security of private health information (PHI) that’s kept or shared online. Comments on the rule are due on March 6.
Because the risks for cyberattacks have increased exponentially, “there is a greater need to invest than ever before in both people and technologies to secure patient information,” Adam Greene, an attorney at Davis Wright Tremaine in Washington, DC, who advises healthcare clients on cybersecurity, said in an interview.
Bad actors continue to evolve and are often far ahead of their targets, added Mark Fox, privacy and research compliance officer for the American College of Cardiology.
In the proposed rule, HHS noted that breaches have risen by more than 50% since 2020. Damages from health data breaches are more expensive than in any other sector, averaging $10 million per incident, said HHS.
The damage can continue for years, as much of the data — such as date of birth — in PHI are “immutable,” unlike a credit card number, the agency said. A review of breach reports made to HHS’ Office for Civil Rights shows near-daily data breaches affecting hundreds to tens of thousands of patients. Since December 1 alone, healthcare providers reported breaches affecting nearly 3 million US patients, according to federal data.
Debi Carr, a Florida-based cybersecurity consultant for small physician and dental practices, welcomed the new proposal. “Many practices are clinging to doing things the way they have always done it, and hackers are taking full advantage of that mindset,” she said in an interview. “We have to change our mindset.”
Among the proposal’s recommendations:
- A shift away from making security specifications “addressable” to required. Fox said that many interpreted addressable to mean optional. The clarification is important. The government will require greater accountability, including a requirement to annually revise the risk analysis, to review policies and procedures and implementation, and to perform penetration testing, said Greene.
- Requiring multifactor authentication (MFA) and encryption of PHI at rest and in transit. “A reasonable person who does security will tell you that should be a requirement,” said Fox. Carr added that the February 2024 Change Healthcare ransomware attack happened because workers at the payment processing company were not using MFA.
- Requiring all entities to verify at least once a year that “business associates” have put into place the required safeguards; the associates would need to provide a written analysis of relevant electronic information systems by a subject matter expert and a written certification that the analysis has been performed and is accurate. In the past, the rule “only required that you sign a business associate agreement” with the associate, which could be a payer, a pharmacy, or another physician practice, said Fox. The rule would require all entities to get certification that the controls are in place.
- Requiring a detailed map of an electronic network. For a physician practice, that means creating an inventory of all the technology assets, including devices, applications, and anything that would touch electronic PHI, and then creating a map of how it comes into the office, flows through it, and departs, said Greene.
- Having a plan of action in the case of a breach. The rule will require written procedures to restore certain relevant systems and data within 72 hours and written incident response plans.
Some physician practices — especially those still relying on passwords instead of more sophisticated MFA or encryption — may have to invest significantly to strengthen their information security, said Greene. Smaller organizations, for example, may need to upgrade systems to ensure that user access is terminated within an hour after someone’s employment ends.
Carr said practices should not view the investments as a burden. The regulation “will force practices to implement best cybersecurity practices,” she said.
Implementing those best practices serves as insurance, said Fox. He suggests that anyone in doubt “talk to someone who’s actually lived through a breach and had to recover.”
Tampa General Hospital in Florida, for instance, recently settled a class action suit, agreeing to pay $6.8 million to patients whose PHI was compromised.
It is not certain whether or when the health cybersecurity rule will be made final.
The incoming Trump administration could cancel or delay the rulemaking process.
Even if it continues, “I would not expect a final rule in 2025,” said Greene. He estimates that the rule would not take effect until at least 2026; healthcare entities would have 180 days to comply. Still, those 180 days can go by fast.
“I would say don’t panic, but don’t ignore it either,” he said.
A version of this article first appeared on Medscape.com.
A new federal rule could force hospitals and doctors’ groups to boost health cybersecurity measures to better protect patients’ health information and prevent ransomware attacks.
The proposed rule, issued by the US Department of Health & Human Services (HHS) and published on January 6 in the Federal Register, marks the first time in a decade that the federal government has updated regulations governing the security of private health information (PHI) that’s kept or shared online. Comments on the rule are due on March 6.
Because the risks for cyberattacks have increased exponentially, “there is a greater need to invest than ever before in both people and technologies to secure patient information,” Adam Greene, an attorney at Davis Wright Tremaine in Washington, DC, who advises healthcare clients on cybersecurity, said in an interview.
Bad actors continue to evolve and are often far ahead of their targets, added Mark Fox, privacy and research compliance officer for the American College of Cardiology.
In the proposed rule, HHS noted that breaches have risen by more than 50% since 2020. Damages from health data breaches are more expensive than in any other sector, averaging $10 million per incident, said HHS.
The damage can continue for years, as much of the data — such as date of birth — in PHI are “immutable,” unlike a credit card number, the agency said. A review of breach reports made to HHS’ Office for Civil Rights shows near-daily data breaches affecting hundreds to tens of thousands of patients. Since December 1 alone, healthcare providers reported breaches affecting nearly 3 million US patients, according to federal data.
Debi Carr, a Florida-based cybersecurity consultant for small physician and dental practices, welcomed the new proposal. “Many practices are clinging to doing things the way they have always done it, and hackers are taking full advantage of that mindset,” she said in an interview. “We have to change our mindset.”
Among the proposal’s recommendations:
- A shift away from making security specifications “addressable” to required. Fox said that many interpreted addressable to mean optional. The clarification is important. The government will require greater accountability, including a requirement to annually revise the risk analysis, to review policies and procedures and implementation, and to perform penetration testing, said Greene.
- Requiring multifactor authentication (MFA) and encryption of PHI at rest and in transit. “A reasonable person who does security will tell you that should be a requirement,” said Fox. Carr added that the February 2024 Change Healthcare ransomware attack happened because workers at the payment processing company were not using MFA.
- Requiring all entities to verify at least once a year that “business associates” have put into place the required safeguards; the associates would need to provide a written analysis of relevant electronic information systems by a subject matter expert and a written certification that the analysis has been performed and is accurate. In the past, the rule “only required that you sign a business associate agreement” with the associate, which could be a payer, a pharmacy, or another physician practice, said Fox. The rule would require all entities to get certification that the controls are in place.
- Requiring a detailed map of an electronic network. For a physician practice, that means creating an inventory of all the technology assets, including devices, applications, and anything that would touch electronic PHI, and then creating a map of how it comes into the office, flows through it, and departs, said Greene.
- Having a plan of action in the case of a breach. The rule will require written procedures to restore certain relevant systems and data within 72 hours and written incident response plans.
Some physician practices — especially those still relying on passwords instead of more sophisticated MFA or encryption — may have to invest significantly to strengthen their information security, said Greene. Smaller organizations, for example, may need to upgrade systems to ensure that user access is terminated within an hour after someone’s employment ends.
Carr said practices should not view the investments as a burden. The regulation “will force practices to implement best cybersecurity practices,” she said.
Implementing those best practices serves as insurance, said Fox. He suggests that anyone in doubt “talk to someone who’s actually lived through a breach and had to recover.”
Tampa General Hospital in Florida, for instance, recently settled a class action suit, agreeing to pay $6.8 million to patients whose PHI was compromised.
It is not certain whether or when the health cybersecurity rule will be made final.
The incoming Trump administration could cancel or delay the rulemaking process.
Even if it continues, “I would not expect a final rule in 2025,” said Greene. He estimates that the rule would not take effect until at least 2026; healthcare entities would have 180 days to comply. Still, those 180 days can go by fast.
“I would say don’t panic, but don’t ignore it either,” he said.
A version of this article first appeared on Medscape.com.
Leaving ED Without Being Seen Entails Increasing Risks
Higher rates of leaving the emergency department (ED) without being seen are linked to increased short-term mortality or hospitalization, according to a cohort study in Ontario, Canada.
“We found that after 2020, there was a 14% higher risk for death or hospitalization within 7 days” among patients who left without being seen (LWBS), Candace McNaughton, MD, PhD, associate professor of medicine at the University of Toronto and scientist at Sunnybrook Research Institute, both in Toronto, Ontario, Canada, told this news organization.
“When we looked at death by itself, there was a 46% higher risk after 2020,” she said. “Even 30 days after a LWBS ED visit, there was still a 5% increased risk for death/hospitalization and a 24% increased risk for death.”
The study was published in the Journal of the American College of Emergency Physicians Open.
LWBS Rates Increased
Researchers used linked administrative data to analyze temporal trends in monthly rates of ED and LWBS visits for adults in Ontario from 2014 to 2023.
They compared the composite outcome of 7-day all-cause mortality or hospitalization following an LWBS ED visit in April 2022‒March 2023 (recent period) with that following an LWBS ED visit in April 2014‒March 2020 (baseline period), after adjustment for age, sex, and Charlson Comorbidity Index (CCI).
In the two periods, patient characteristics were similar across age, sex, neighborhood-level income quartile, history of being unhoused, rurality, CCI, day, time, and mode of arrival. The median age was 40 years for the baseline period and 42 years for the recent period.
Temporal trends showed sustained increases in monthly LWBS rates after 2020, despite fewer monthly ED visits. The rate of LWBS ED visits after April 1, 2020, exceeded the baseline period’s single-month LWBS maximum of 4% in 15 of 36 months.
The rate of 7-day all-cause mortality or hospitalization was 3.4% in the recent period vs 2.9% in the baseline period (adjusted risk ratio [aRR], 1.14), despite similar rates of post-ED outpatient visits (7-day recent and baseline, 38.9% and 39.7%, respectively).
Similar trends were seen at 30 days for all-cause mortality or hospitalization (6.2% in the recent period vs 5.8% at baseline; aRR, 1.05) despite similar rates of post-ED outpatient visits (59.4% and 59.7%, respectively).
After April 1, 2020, monthly ED visits and the proportion of patients who LWBS varied widely.
The proportion of LWBS visits categorized as emergent on the Canadian Triage and Acuity Scale was higher during the recent period (12.9% vs 9.2% in the baseline period), and fewer visits were categorized as semiurgent (22.6% vs 31.9%, respectively). This finding suggested a higher acuity of illness among patients who LWBS in the recent period.
LWBS Visits ‘Not Benign’
Results of a preplanned subgroup analysis examining the risk for all-cause mortality after an LWBS visit were “particularly notable,” the authors wrote, with a 46% higher adjusted risk for death at 7 days and 24% higher adjusted risk at 30 days.
The observational study had several limitations, however. The authors could not draw conclusions regarding direct causes of the increased risk for severe short-term adverse health outcomes after an LWBS ED visit, and residual confounding is possible. Cause-of-death information was not available to generate hypotheses for future studies of potential causes. Furthermore, the findings may not be generalizable to systems without universal access to healthcare.
Nevertheless, the findings are a “concerning signal [and] should prompt interventions to address system- and population-level causes,” the authors wrote.
“Unfortunately, because of politics, since 2020, ED closures in Ontario have become more and more common and seem to be affecting more and more Ontarians,” said McNaughton. “It would be surprising if ED closure didn’t play some role in our findings.”
She added, “It is important to note that people in our study were relatively young, with a median age in their 40s; this makes our findings all the more concerning. Clinicians should be aware that LWBS ED visits are not necessarily benign, particularly when rates of LWBS ED visits are high.”
Unanswered Questions
The study raised the following questions that the authors are or will be investigating, according to McNaughton:
- Which patients are at greatest risk for bad outcomes if they leave the ED without being seen, and why?
- How much of the findings might be related to recent ED closures, longer ED wait times, or other factors? Are there geographic variations in risk?
- What can be done in the ED to prevent LWBS ED visits, and what can be changed outside the ED to prevent LWBS ED visits? For example, what can hospitals do to reduce boarding in the ED? If patients leave without being seen, should they be contacted to try to meet their health needs in other ways?
- What worked in terms of maintaining access to outpatient medical care, despite the considerable disruptions starting in 2020, and how can continued success be ensured?
To address the current situation, McNaughton said, “We need consistent, predictable, and sustained investment in our public healthcare system. We need long-term, consistent funding for primary care, ED care, as well as hospital and long-term care.”
“It takes years to recruit and train the teams of people necessary to provide the high-quality medical care that Canadians have a right to. There are no shortcuts,” she concluded.
‘Tragic Situation’
American College of Emergency Physicians (ACEP) spokesperson Jesse Pines, MD, chief of clinical innovation at US Acute Care Solutions; clinical professor of emergency medicine at George Washington University in Washington, DC; and professor of emergency medicine at Drexel University in Philadelphia, commented on the study for this news organization.
“Similar to what the authors found in their report, LWBS and other metrics — specifically boarding — have progressively increased in the United States, in particular, since the early part of 2021,” he said. “The primary factor in the US driving this, and one that ACEP is trying to address on a national scale, is the boarding of admitted patients.”
When the number of boarded patients increases, there is less space in the ED for new patients, and waits increase, Pines explained. Some patients leave without being seen, and a subset of those patients experience poor outcomes. “It’s a tragic situation that is worsening.”
“Emergency physicians like me always worry when patients leave without being seen,” he said. While some of those patients have self-limited conditions that will improve on their own, “some have critical life-threatening conditions that require care and hospitalization. The worry is that these patients experience poorer outcomes,” Pines said. “The authors showed that this is increasingly the case in Canada. The same is likely true in the US.”
The study was funded by the Canadian Institutes of Health Research. McNaughton and Pines declared no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Higher rates of leaving the emergency department (ED) without being seen are linked to increased short-term mortality or hospitalization, according to a cohort study in Ontario, Canada.
“We found that after 2020, there was a 14% higher risk for death or hospitalization within 7 days” among patients who left without being seen (LWBS), Candace McNaughton, MD, PhD, associate professor of medicine at the University of Toronto and scientist at Sunnybrook Research Institute, both in Toronto, Ontario, Canada, told this news organization.
“When we looked at death by itself, there was a 46% higher risk after 2020,” she said. “Even 30 days after a LWBS ED visit, there was still a 5% increased risk for death/hospitalization and a 24% increased risk for death.”
The study was published in the Journal of the American College of Emergency Physicians Open.
LWBS Rates Increased
Researchers used linked administrative data to analyze temporal trends in monthly rates of ED and LWBS visits for adults in Ontario from 2014 to 2023.
They compared the composite outcome of 7-day all-cause mortality or hospitalization following an LWBS ED visit in April 2022‒March 2023 (recent period) with that following an LWBS ED visit in April 2014‒March 2020 (baseline period), after adjustment for age, sex, and Charlson Comorbidity Index (CCI).
In the two periods, patient characteristics were similar across age, sex, neighborhood-level income quartile, history of being unhoused, rurality, CCI, day, time, and mode of arrival. The median age was 40 years for the baseline period and 42 years for the recent period.
Temporal trends showed sustained increases in monthly LWBS rates after 2020, despite fewer monthly ED visits. The rate of LWBS ED visits after April 1, 2020, exceeded the baseline period’s single-month LWBS maximum of 4% in 15 of 36 months.
The rate of 7-day all-cause mortality or hospitalization was 3.4% in the recent period vs 2.9% in the baseline period (adjusted risk ratio [aRR], 1.14), despite similar rates of post-ED outpatient visits (7-day recent and baseline, 38.9% and 39.7%, respectively).
Similar trends were seen at 30 days for all-cause mortality or hospitalization (6.2% in the recent period vs 5.8% at baseline; aRR, 1.05) despite similar rates of post-ED outpatient visits (59.4% and 59.7%, respectively).
After April 1, 2020, monthly ED visits and the proportion of patients who LWBS varied widely.
The proportion of LWBS visits categorized as emergent on the Canadian Triage and Acuity Scale was higher during the recent period (12.9% vs 9.2% in the baseline period), and fewer visits were categorized as semiurgent (22.6% vs 31.9%, respectively). This finding suggested a higher acuity of illness among patients who LWBS in the recent period.
LWBS Visits ‘Not Benign’
Results of a preplanned subgroup analysis examining the risk for all-cause mortality after an LWBS visit were “particularly notable,” the authors wrote, with a 46% higher adjusted risk for death at 7 days and 24% higher adjusted risk at 30 days.
The observational study had several limitations, however. The authors could not draw conclusions regarding direct causes of the increased risk for severe short-term adverse health outcomes after an LWBS ED visit, and residual confounding is possible. Cause-of-death information was not available to generate hypotheses for future studies of potential causes. Furthermore, the findings may not be generalizable to systems without universal access to healthcare.
Nevertheless, the findings are a “concerning signal [and] should prompt interventions to address system- and population-level causes,” the authors wrote.
“Unfortunately, because of politics, since 2020, ED closures in Ontario have become more and more common and seem to be affecting more and more Ontarians,” said McNaughton. “It would be surprising if ED closure didn’t play some role in our findings.”
She added, “It is important to note that people in our study were relatively young, with a median age in their 40s; this makes our findings all the more concerning. Clinicians should be aware that LWBS ED visits are not necessarily benign, particularly when rates of LWBS ED visits are high.”
Unanswered Questions
The study raised the following questions that the authors are or will be investigating, according to McNaughton:
- Which patients are at greatest risk for bad outcomes if they leave the ED without being seen, and why?
- How much of the findings might be related to recent ED closures, longer ED wait times, or other factors? Are there geographic variations in risk?
- What can be done in the ED to prevent LWBS ED visits, and what can be changed outside the ED to prevent LWBS ED visits? For example, what can hospitals do to reduce boarding in the ED? If patients leave without being seen, should they be contacted to try to meet their health needs in other ways?
- What worked in terms of maintaining access to outpatient medical care, despite the considerable disruptions starting in 2020, and how can continued success be ensured?
To address the current situation, McNaughton said, “We need consistent, predictable, and sustained investment in our public healthcare system. We need long-term, consistent funding for primary care, ED care, as well as hospital and long-term care.”
“It takes years to recruit and train the teams of people necessary to provide the high-quality medical care that Canadians have a right to. There are no shortcuts,” she concluded.
‘Tragic Situation’
American College of Emergency Physicians (ACEP) spokesperson Jesse Pines, MD, chief of clinical innovation at US Acute Care Solutions; clinical professor of emergency medicine at George Washington University in Washington, DC; and professor of emergency medicine at Drexel University in Philadelphia, commented on the study for this news organization.
“Similar to what the authors found in their report, LWBS and other metrics — specifically boarding — have progressively increased in the United States, in particular, since the early part of 2021,” he said. “The primary factor in the US driving this, and one that ACEP is trying to address on a national scale, is the boarding of admitted patients.”
When the number of boarded patients increases, there is less space in the ED for new patients, and waits increase, Pines explained. Some patients leave without being seen, and a subset of those patients experience poor outcomes. “It’s a tragic situation that is worsening.”
“Emergency physicians like me always worry when patients leave without being seen,” he said. While some of those patients have self-limited conditions that will improve on their own, “some have critical life-threatening conditions that require care and hospitalization. The worry is that these patients experience poorer outcomes,” Pines said. “The authors showed that this is increasingly the case in Canada. The same is likely true in the US.”
The study was funded by the Canadian Institutes of Health Research. McNaughton and Pines declared no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Higher rates of leaving the emergency department (ED) without being seen are linked to increased short-term mortality or hospitalization, according to a cohort study in Ontario, Canada.
“We found that after 2020, there was a 14% higher risk for death or hospitalization within 7 days” among patients who left without being seen (LWBS), Candace McNaughton, MD, PhD, associate professor of medicine at the University of Toronto and scientist at Sunnybrook Research Institute, both in Toronto, Ontario, Canada, told this news organization.
“When we looked at death by itself, there was a 46% higher risk after 2020,” she said. “Even 30 days after a LWBS ED visit, there was still a 5% increased risk for death/hospitalization and a 24% increased risk for death.”
The study was published in the Journal of the American College of Emergency Physicians Open.
LWBS Rates Increased
Researchers used linked administrative data to analyze temporal trends in monthly rates of ED and LWBS visits for adults in Ontario from 2014 to 2023.
They compared the composite outcome of 7-day all-cause mortality or hospitalization following an LWBS ED visit in April 2022‒March 2023 (recent period) with that following an LWBS ED visit in April 2014‒March 2020 (baseline period), after adjustment for age, sex, and Charlson Comorbidity Index (CCI).
In the two periods, patient characteristics were similar across age, sex, neighborhood-level income quartile, history of being unhoused, rurality, CCI, day, time, and mode of arrival. The median age was 40 years for the baseline period and 42 years for the recent period.
Temporal trends showed sustained increases in monthly LWBS rates after 2020, despite fewer monthly ED visits. The rate of LWBS ED visits after April 1, 2020, exceeded the baseline period’s single-month LWBS maximum of 4% in 15 of 36 months.
The rate of 7-day all-cause mortality or hospitalization was 3.4% in the recent period vs 2.9% in the baseline period (adjusted risk ratio [aRR], 1.14), despite similar rates of post-ED outpatient visits (7-day recent and baseline, 38.9% and 39.7%, respectively).
Similar trends were seen at 30 days for all-cause mortality or hospitalization (6.2% in the recent period vs 5.8% at baseline; aRR, 1.05) despite similar rates of post-ED outpatient visits (59.4% and 59.7%, respectively).
After April 1, 2020, monthly ED visits and the proportion of patients who LWBS varied widely.
The proportion of LWBS visits categorized as emergent on the Canadian Triage and Acuity Scale was higher during the recent period (12.9% vs 9.2% in the baseline period), and fewer visits were categorized as semiurgent (22.6% vs 31.9%, respectively). This finding suggested a higher acuity of illness among patients who LWBS in the recent period.
LWBS Visits ‘Not Benign’
Results of a preplanned subgroup analysis examining the risk for all-cause mortality after an LWBS visit were “particularly notable,” the authors wrote, with a 46% higher adjusted risk for death at 7 days and 24% higher adjusted risk at 30 days.
The observational study had several limitations, however. The authors could not draw conclusions regarding direct causes of the increased risk for severe short-term adverse health outcomes after an LWBS ED visit, and residual confounding is possible. Cause-of-death information was not available to generate hypotheses for future studies of potential causes. Furthermore, the findings may not be generalizable to systems without universal access to healthcare.
Nevertheless, the findings are a “concerning signal [and] should prompt interventions to address system- and population-level causes,” the authors wrote.
“Unfortunately, because of politics, since 2020, ED closures in Ontario have become more and more common and seem to be affecting more and more Ontarians,” said McNaughton. “It would be surprising if ED closure didn’t play some role in our findings.”
She added, “It is important to note that people in our study were relatively young, with a median age in their 40s; this makes our findings all the more concerning. Clinicians should be aware that LWBS ED visits are not necessarily benign, particularly when rates of LWBS ED visits are high.”
Unanswered Questions
The study raised the following questions that the authors are or will be investigating, according to McNaughton:
- Which patients are at greatest risk for bad outcomes if they leave the ED without being seen, and why?
- How much of the findings might be related to recent ED closures, longer ED wait times, or other factors? Are there geographic variations in risk?
- What can be done in the ED to prevent LWBS ED visits, and what can be changed outside the ED to prevent LWBS ED visits? For example, what can hospitals do to reduce boarding in the ED? If patients leave without being seen, should they be contacted to try to meet their health needs in other ways?
- What worked in terms of maintaining access to outpatient medical care, despite the considerable disruptions starting in 2020, and how can continued success be ensured?
To address the current situation, McNaughton said, “We need consistent, predictable, and sustained investment in our public healthcare system. We need long-term, consistent funding for primary care, ED care, as well as hospital and long-term care.”
“It takes years to recruit and train the teams of people necessary to provide the high-quality medical care that Canadians have a right to. There are no shortcuts,” she concluded.
‘Tragic Situation’
American College of Emergency Physicians (ACEP) spokesperson Jesse Pines, MD, chief of clinical innovation at US Acute Care Solutions; clinical professor of emergency medicine at George Washington University in Washington, DC; and professor of emergency medicine at Drexel University in Philadelphia, commented on the study for this news organization.
“Similar to what the authors found in their report, LWBS and other metrics — specifically boarding — have progressively increased in the United States, in particular, since the early part of 2021,” he said. “The primary factor in the US driving this, and one that ACEP is trying to address on a national scale, is the boarding of admitted patients.”
When the number of boarded patients increases, there is less space in the ED for new patients, and waits increase, Pines explained. Some patients leave without being seen, and a subset of those patients experience poor outcomes. “It’s a tragic situation that is worsening.”
“Emergency physicians like me always worry when patients leave without being seen,” he said. While some of those patients have self-limited conditions that will improve on their own, “some have critical life-threatening conditions that require care and hospitalization. The worry is that these patients experience poorer outcomes,” Pines said. “The authors showed that this is increasingly the case in Canada. The same is likely true in the US.”
The study was funded by the Canadian Institutes of Health Research. McNaughton and Pines declared no relevant financial relationships.
A version of this article first appeared on Medscape.com.