Neurology Reviews

TOPLINE:

Migraine is associated with a significantly increased risk of developing inflammatory bowel disease (IBD), including both Crohn’s disease (CD) and ulcerative colitis (UC), a new nationwide, population-based cohort study showed.

METHODOLOGY:

• Investigators analyzed data from South Korea’s National Health Insurance Service (NHIS) database, which houses data for the nationwide obligatory health system for South Korean citizens.
• Individuals aged ≥ 20 years who had at least one national health screening in 2009 were enrolled in the study and followed until December 2019.
• Investigators searched the data for International Classification of Diseases (10th Revision) codes corresponding to migraine and IBD. IBD diagnoses were also based on clinical manifestation, endoscopic findings, and pathologic findings.

TAKEAWAY:

• More than 10 million people were enrolled in the study (55% male; mean age, 47 years), and of these, 2.8% were diagnosed with migraine during the study period.
• During a median follow-up of 10 years, the incidence of IBD was significantly higher in patients with migraine (adjusted hazard ratio [aHR], 1.31; P < .001), CD (aHR, 1.58; P < .001) and UC (aHR, 1.26; P < .001) than in those without migraine.
• in men vs women (aHR, 1.43 vs 1.12; P = .042).
• Investigators could only speculate about the mechanisms underlying the association between migraine and IBD but suggest pathological processes underlying both migraine and IBD, including proinflammatory cytokines and tumor necrosis factor alpha, may be involved.

IN PRACTICE:

“Clinicians should be aware of the potential risk of IBD in patients diagnosed with migraine especially in men for the development of UC and in migraineurs with a long disease duration for a further risk of CD,” the authors wrote.

SOURCE:

Hyunjung Lee, MD, of Seoul National University College of Medicine, Seoul, South Korea, led the study, which was published online on January 12, 2024, in Scientific Reports.

LIMITATIONS:

Disease severity of migraine and IBD was not available. In addition, certain medications taken to relieve migraine, such as nonsteroidal anti-inflammatory drugs like ibuprofen, could cause intestinal inflammation, but there was no medication information available.

DISCLOSURES:

There was no information about study funding nor disclosures from study authors.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Migraine is associated with a significantly increased risk of developing inflammatory bowel disease (IBD), including both Crohn’s disease (CD) and ulcerative colitis (UC), a new nationwide, population-based cohort study showed.

METHODOLOGY:

• Investigators analyzed data from South Korea’s National Health Insurance Service (NHIS) database, which houses data for the nationwide obligatory health system for South Korean citizens.
• Individuals aged ≥ 20 years who had at least one national health screening in 2009 were enrolled in the study and followed until December 2019.
• Investigators searched the data for International Classification of Diseases (10th Revision) codes corresponding to migraine and IBD. IBD diagnoses were also based on clinical manifestation, endoscopic findings, and pathologic findings.

TAKEAWAY:

• More than 10 million people were enrolled in the study (55% male; mean age, 47 years), and of these, 2.8% were diagnosed with migraine during the study period.
• During a median follow-up of 10 years, the incidence of IBD was significantly higher in patients with migraine (adjusted hazard ratio [aHR], 1.31; P < .001), CD (aHR, 1.58; P < .001) and UC (aHR, 1.26; P < .001) than in those without migraine.
• in men vs women (aHR, 1.43 vs 1.12; P = .042).
• Investigators could only speculate about the mechanisms underlying the association between migraine and IBD but suggest pathological processes underlying both migraine and IBD, including proinflammatory cytokines and tumor necrosis factor alpha, may be involved.

IN PRACTICE:

“Clinicians should be aware of the potential risk of IBD in patients diagnosed with migraine especially in men for the development of UC and in migraineurs with a long disease duration for a further risk of CD,” the authors wrote.

SOURCE:

Hyunjung Lee, MD, of Seoul National University College of Medicine, Seoul, South Korea, led the study, which was published online on January 12, 2024, in Scientific Reports.

LIMITATIONS:

Disease severity of migraine and IBD was not available. In addition, certain medications taken to relieve migraine, such as nonsteroidal anti-inflammatory drugs like ibuprofen, could cause intestinal inflammation, but there was no medication information available.

DISCLOSURES:

There was no information about study funding nor disclosures from study authors.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Migraine is associated with a significantly increased risk of developing inflammatory bowel disease (IBD), including both Crohn’s disease (CD) and ulcerative colitis (UC), a new nationwide, population-based cohort study showed.

METHODOLOGY:

• Investigators analyzed data from South Korea’s National Health Insurance Service (NHIS) database, which houses data for the nationwide obligatory health system for South Korean citizens.
• Individuals aged ≥ 20 years who had at least one national health screening in 2009 were enrolled in the study and followed until December 2019.
• Investigators searched the data for International Classification of Diseases (10th Revision) codes corresponding to migraine and IBD. IBD diagnoses were also based on clinical manifestation, endoscopic findings, and pathologic findings.

TAKEAWAY:

• More than 10 million people were enrolled in the study (55% male; mean age, 47 years), and of these, 2.8% were diagnosed with migraine during the study period.
• During a median follow-up of 10 years, the incidence of IBD was significantly higher in patients with migraine (adjusted hazard ratio [aHR], 1.31; P < .001), CD (aHR, 1.58; P < .001) and UC (aHR, 1.26; P < .001) than in those without migraine.
• in men vs women (aHR, 1.43 vs 1.12; P = .042).
• Investigators could only speculate about the mechanisms underlying the association between migraine and IBD but suggest pathological processes underlying both migraine and IBD, including proinflammatory cytokines and tumor necrosis factor alpha, may be involved.

IN PRACTICE:

“Clinicians should be aware of the potential risk of IBD in patients diagnosed with migraine especially in men for the development of UC and in migraineurs with a long disease duration for a further risk of CD,” the authors wrote.

SOURCE:

Hyunjung Lee, MD, of Seoul National University College of Medicine, Seoul, South Korea, led the study, which was published online on January 12, 2024, in Scientific Reports.

LIMITATIONS:

Disease severity of migraine and IBD was not available. In addition, certain medications taken to relieve migraine, such as nonsteroidal anti-inflammatory drugs like ibuprofen, could cause intestinal inflammation, but there was no medication information available.

DISCLOSURES:

There was no information about study funding nor disclosures from study authors.
 

A version of this article appeared on Medscape.com.

A recent study sheds light on the heightened risk for burnout among physicians who take infrequent vacations and engage in patient-related work during their time off.

Conducted by the American Medical Association (AMA), the study focuses on the United States, where labor regulations regarding vacation days and compensation differ from German norms. Despite this distinction, it provides valuable insights into the vacation behavior of doctors and its potential impact on burnout risk.

Christine A. Sinsky, MD, study author and senior physician advisor for physician satisfaction at the AMA, and her colleagues invited more than 90,000 physicians to participate in a survey that used postal and computer-based methods. In all, 3024 physicians, mainly those contacted by mail, filled out the questionnaire.
 

Limited Vacation Days

A significant proportion (59.6%) of respondents reported having taken fewer than 15 vacation days in the previous year, with nearly 20% taking fewer than 5 days off. Even when officially on vacation, most (70.4%) found themselves dealing with patient-related tasks. For one-third, these tasks consumed at least 30 minutes on a typical vacation day, often longer. This phenomenon was noted especially among female physicians.

Doctors who took less vacation and worked during their time off displayed higher emotional exhaustion and reported feeling less fulfilled in their profession.
 

Administrative Tasks 

Administrative tasks, though no longer confined to paper, significantly influenced physicians’ vacation behavior. In the United States, handling messages from patients through the electronic health records (EHR) inbox demands a considerable amount of time.

Courses and tutorials on EHR inbox management are on the rise. A 2023 review linked electronic health records management to an increased burnout risk in the US medical community.
 

Lack of Coverage 

Many physicians lack coverage for their EHR inbox during their absence. Less than half (49.1%) stated that someone else manages their inbox while they are on vacation.

Difficulty in finding coverage, whether for the EHR inbox or patient care, is a leading reason why many physicians seldom take more than 3 weeks of vacation per year. Financial considerations also contribute to this decision, as revealed in the survey.
 

Vacation Lowers Risk

Further analysis showed that doctors who took more than 3 weeks of vacation per year, which is not common, had a lower risk of developing burnout. Having coverage for vacation was also associated with reduced burnout risk and increased professional fulfillment.

However, these benefits applied only when physicians truly took a break during their vacation. Respondents who spent 30 minutes or more per day on patient-related work had a higher burnout risk. The risk was 1.58 times greater for 30-60 minutes, 1.97 times greater for 60-90 minutes, and 1.92 times greater for more than 90 minutes.
 

System-Level Interventions

The vacation behavior observed in this study likely exacerbates the effects of chronic workplace overload that are associated with long working hours, thus increasing the risk for burnout, according to the researchers.

“System-level measures must be implemented to ensure physicians take an appropriate number of vacation days,” wrote the researchers. “This includes having coverage available to handle clinical activities and administrative tasks, such as managing the EHR inbox. This could potentially reduce the burnout rate among physicians.”

This article was translated from the Medscape German edition. A version of this article appeared on Medscape.com.

A recent study sheds light on the heightened risk for burnout among physicians who take infrequent vacations and engage in patient-related work during their time off.

Conducted by the American Medical Association (AMA), the study focuses on the United States, where labor regulations regarding vacation days and compensation differ from German norms. Despite this distinction, it provides valuable insights into the vacation behavior of doctors and its potential impact on burnout risk.

Christine A. Sinsky, MD, study author and senior physician advisor for physician satisfaction at the AMA, and her colleagues invited more than 90,000 physicians to participate in a survey that used postal and computer-based methods. In all, 3024 physicians, mainly those contacted by mail, filled out the questionnaire.
 

Limited Vacation Days

A significant proportion (59.6%) of respondents reported having taken fewer than 15 vacation days in the previous year, with nearly 20% taking fewer than 5 days off. Even when officially on vacation, most (70.4%) found themselves dealing with patient-related tasks. For one-third, these tasks consumed at least 30 minutes on a typical vacation day, often longer. This phenomenon was noted especially among female physicians.

Doctors who took less vacation and worked during their time off displayed higher emotional exhaustion and reported feeling less fulfilled in their profession.
 

Administrative Tasks 

Administrative tasks, though no longer confined to paper, significantly influenced physicians’ vacation behavior. In the United States, handling messages from patients through the electronic health records (EHR) inbox demands a considerable amount of time.

Courses and tutorials on EHR inbox management are on the rise. A 2023 review linked electronic health records management to an increased burnout risk in the US medical community.
 

Lack of Coverage 

Many physicians lack coverage for their EHR inbox during their absence. Less than half (49.1%) stated that someone else manages their inbox while they are on vacation.

Difficulty in finding coverage, whether for the EHR inbox or patient care, is a leading reason why many physicians seldom take more than 3 weeks of vacation per year. Financial considerations also contribute to this decision, as revealed in the survey.
 

Vacation Lowers Risk

Further analysis showed that doctors who took more than 3 weeks of vacation per year, which is not common, had a lower risk of developing burnout. Having coverage for vacation was also associated with reduced burnout risk and increased professional fulfillment.

However, these benefits applied only when physicians truly took a break during their vacation. Respondents who spent 30 minutes or more per day on patient-related work had a higher burnout risk. The risk was 1.58 times greater for 30-60 minutes, 1.97 times greater for 60-90 minutes, and 1.92 times greater for more than 90 minutes.
 

System-Level Interventions

The vacation behavior observed in this study likely exacerbates the effects of chronic workplace overload that are associated with long working hours, thus increasing the risk for burnout, according to the researchers.

“System-level measures must be implemented to ensure physicians take an appropriate number of vacation days,” wrote the researchers. “This includes having coverage available to handle clinical activities and administrative tasks, such as managing the EHR inbox. This could potentially reduce the burnout rate among physicians.”

This article was translated from the Medscape German edition. A version of this article appeared on Medscape.com.

A recent study sheds light on the heightened risk for burnout among physicians who take infrequent vacations and engage in patient-related work during their time off.

Conducted by the American Medical Association (AMA), the study focuses on the United States, where labor regulations regarding vacation days and compensation differ from German norms. Despite this distinction, it provides valuable insights into the vacation behavior of doctors and its potential impact on burnout risk.

Christine A. Sinsky, MD, study author and senior physician advisor for physician satisfaction at the AMA, and her colleagues invited more than 90,000 physicians to participate in a survey that used postal and computer-based methods. In all, 3024 physicians, mainly those contacted by mail, filled out the questionnaire.
 

Limited Vacation Days

A significant proportion (59.6%) of respondents reported having taken fewer than 15 vacation days in the previous year, with nearly 20% taking fewer than 5 days off. Even when officially on vacation, most (70.4%) found themselves dealing with patient-related tasks. For one-third, these tasks consumed at least 30 minutes on a typical vacation day, often longer. This phenomenon was noted especially among female physicians.

Doctors who took less vacation and worked during their time off displayed higher emotional exhaustion and reported feeling less fulfilled in their profession.
 

Administrative Tasks 

Administrative tasks, though no longer confined to paper, significantly influenced physicians’ vacation behavior. In the United States, handling messages from patients through the electronic health records (EHR) inbox demands a considerable amount of time.

Courses and tutorials on EHR inbox management are on the rise. A 2023 review linked electronic health records management to an increased burnout risk in the US medical community.
 

Lack of Coverage 

Many physicians lack coverage for their EHR inbox during their absence. Less than half (49.1%) stated that someone else manages their inbox while they are on vacation.

Difficulty in finding coverage, whether for the EHR inbox or patient care, is a leading reason why many physicians seldom take more than 3 weeks of vacation per year. Financial considerations also contribute to this decision, as revealed in the survey.
 

Vacation Lowers Risk

Further analysis showed that doctors who took more than 3 weeks of vacation per year, which is not common, had a lower risk of developing burnout. Having coverage for vacation was also associated with reduced burnout risk and increased professional fulfillment.

However, these benefits applied only when physicians truly took a break during their vacation. Respondents who spent 30 minutes or more per day on patient-related work had a higher burnout risk. The risk was 1.58 times greater for 30-60 minutes, 1.97 times greater for 60-90 minutes, and 1.92 times greater for more than 90 minutes.
 

System-Level Interventions

The vacation behavior observed in this study likely exacerbates the effects of chronic workplace overload that are associated with long working hours, thus increasing the risk for burnout, according to the researchers.

“System-level measures must be implemented to ensure physicians take an appropriate number of vacation days,” wrote the researchers. “This includes having coverage available to handle clinical activities and administrative tasks, such as managing the EHR inbox. This could potentially reduce the burnout rate among physicians.”

This article was translated from the Medscape German edition. A version of this article appeared on Medscape.com.

Modern technology for recording deep-brain activity involves sharp metal electrodes that penetrate the tissue, causing damage that can compromise the signal and limiting how often they can be used. 

A rapidly growing area in materials science and engineering aims to fix the problem by designing electrodes that are softer, smaller, and flexible — safer for use inside the delicate tissues of the brain. On January 17, researchers from the University of California, San Diego, reported the development of a thin, flexible electrode that can be inserted deep within the brain and communicate with sensors on the surface. 

But what if you could record detailed deep-brain activity without piercing the brain? 

A team of researchers (as it happens, also from UC San Diego) have developed a thin, flexible implant that “resides on the brain’s surface” and “can infer neural activity from deeper layers,” said Duygu Kuzum, PhD, a professor of electrical and computer engineering, who led the research. 

By combining electrical and optical imaging methods, and artificial intelligence, the researchers used the device — a polymer strip packed with graphene electrodes — to predict deep calcium activity from surface signals, according to a proof-of-concept study published this month in Nature Nanotechnology. 

“Almost everything we know about how neurons behave in living brains comes from data collected with either electrophysiology or two-photon imaging,” said neuroscientist Joshua H. Siegle, PhD, of the Allen Institute for Neural Dynamics in Seattle , who not involved in the study. “ Until now, these two methods have rarely been used simultaneously.”

The technology, which has been tested in mice, could help advance our knowledge of how the brain works and may lead to new minimally invasive treatments for neurologic disorders. 
 

Multimodal Neurotech: The Power of 2-in-1

Electrical and optical methods for recording brain activity have been crucial in advancing neurophysiologic science, but each technique has its limits. Electrical recordings provide high “temporal resolution”; they reveal when activation is happening, but not really where. Optical imaging, on the other hand, offers high “spatial resolution,” showing which area of the brain is lighting up, but its measurements may not correspond with the activity’s timing. 

Research over the past decade has explored how to combine and harness the strengths of both methods. One potential solution is to use electrodes made of transparent materials such as graphene, allowing a clear field of view for a microscope during imaging. Recently, University of Pennsylvania scientists used graphene electrodes to illuminate the neural dynamics of seizures. 

But there are challenges. If graphene electrodes are very small — in this case, 20 µm in diameter — they become more resistant to the flow of electricity. Dr. Kuzum and colleagues addressed this by adding tiny platinum particles to improve electrical conductivity. Long graphene wires connect electrodes to the circuit board, but defects in graphene can interrupt the signal, so they made each wire with two layers; any defects in one wire could be hidden by the other.

By combining the two methods (microelectrode arrays and two-photon imaging), the researchers could see both when brain activity was happening and where, including in deeper layers. They discovered a correlation between electrical responses on the surface and cellular calcium activity deeper down. The team used these data to create a neural network (a type of artificial intelligence that learns to recognize patterns) that predicts deep calcium activity from surface-level readings.

The tech could help scientists study brain activity “in a way not possible with current single-function tools,” said Luyao Lu, PhD, professor of biomedical engineering at George Washington University in Washington, DC, who was not involved in the study. It could shed light on interactions between vascular and electrical activity, or explain how place cells (neurons in the hippocampus) are so efficient at creating spatial memory. 

It could also pave the way for minimally invasive neural prosthetics or targeted treatments for neurologic disorders, the researchers say. Implanting the device would be a “straightforward process” similar to placing electrocorticography grids in patients with epilepsy, said Dr. Kuzum. 

But first, the team plans to do more studies in animal models before testing the tech in clinical settings, Dr. Kuzum added.

A version of this article appeared on Medscape.com.

Modern technology for recording deep-brain activity involves sharp metal electrodes that penetrate the tissue, causing damage that can compromise the signal and limiting how often they can be used. 

A rapidly growing area in materials science and engineering aims to fix the problem by designing electrodes that are softer, smaller, and flexible — safer for use inside the delicate tissues of the brain. On January 17, researchers from the University of California, San Diego, reported the development of a thin, flexible electrode that can be inserted deep within the brain and communicate with sensors on the surface. 

But what if you could record detailed deep-brain activity without piercing the brain? 

A team of researchers (as it happens, also from UC San Diego) have developed a thin, flexible implant that “resides on the brain’s surface” and “can infer neural activity from deeper layers,” said Duygu Kuzum, PhD, a professor of electrical and computer engineering, who led the research. 

By combining electrical and optical imaging methods, and artificial intelligence, the researchers used the device — a polymer strip packed with graphene electrodes — to predict deep calcium activity from surface signals, according to a proof-of-concept study published this month in Nature Nanotechnology. 

“Almost everything we know about how neurons behave in living brains comes from data collected with either electrophysiology or two-photon imaging,” said neuroscientist Joshua H. Siegle, PhD, of the Allen Institute for Neural Dynamics in Seattle , who not involved in the study. “ Until now, these two methods have rarely been used simultaneously.”

The technology, which has been tested in mice, could help advance our knowledge of how the brain works and may lead to new minimally invasive treatments for neurologic disorders. 
 

Multimodal Neurotech: The Power of 2-in-1

Electrical and optical methods for recording brain activity have been crucial in advancing neurophysiologic science, but each technique has its limits. Electrical recordings provide high “temporal resolution”; they reveal when activation is happening, but not really where. Optical imaging, on the other hand, offers high “spatial resolution,” showing which area of the brain is lighting up, but its measurements may not correspond with the activity’s timing. 

Research over the past decade has explored how to combine and harness the strengths of both methods. One potential solution is to use electrodes made of transparent materials such as graphene, allowing a clear field of view for a microscope during imaging. Recently, University of Pennsylvania scientists used graphene electrodes to illuminate the neural dynamics of seizures. 

But there are challenges. If graphene electrodes are very small — in this case, 20 µm in diameter — they become more resistant to the flow of electricity. Dr. Kuzum and colleagues addressed this by adding tiny platinum particles to improve electrical conductivity. Long graphene wires connect electrodes to the circuit board, but defects in graphene can interrupt the signal, so they made each wire with two layers; any defects in one wire could be hidden by the other.

By combining the two methods (microelectrode arrays and two-photon imaging), the researchers could see both when brain activity was happening and where, including in deeper layers. They discovered a correlation between electrical responses on the surface and cellular calcium activity deeper down. The team used these data to create a neural network (a type of artificial intelligence that learns to recognize patterns) that predicts deep calcium activity from surface-level readings.

The tech could help scientists study brain activity “in a way not possible with current single-function tools,” said Luyao Lu, PhD, professor of biomedical engineering at George Washington University in Washington, DC, who was not involved in the study. It could shed light on interactions between vascular and electrical activity, or explain how place cells (neurons in the hippocampus) are so efficient at creating spatial memory. 

It could also pave the way for minimally invasive neural prosthetics or targeted treatments for neurologic disorders, the researchers say. Implanting the device would be a “straightforward process” similar to placing electrocorticography grids in patients with epilepsy, said Dr. Kuzum. 

But first, the team plans to do more studies in animal models before testing the tech in clinical settings, Dr. Kuzum added.

A version of this article appeared on Medscape.com.

Modern technology for recording deep-brain activity involves sharp metal electrodes that penetrate the tissue, causing damage that can compromise the signal and limiting how often they can be used. 

A rapidly growing area in materials science and engineering aims to fix the problem by designing electrodes that are softer, smaller, and flexible — safer for use inside the delicate tissues of the brain. On January 17, researchers from the University of California, San Diego, reported the development of a thin, flexible electrode that can be inserted deep within the brain and communicate with sensors on the surface. 

But what if you could record detailed deep-brain activity without piercing the brain? 

A team of researchers (as it happens, also from UC San Diego) have developed a thin, flexible implant that “resides on the brain’s surface” and “can infer neural activity from deeper layers,” said Duygu Kuzum, PhD, a professor of electrical and computer engineering, who led the research. 

By combining electrical and optical imaging methods, and artificial intelligence, the researchers used the device — a polymer strip packed with graphene electrodes — to predict deep calcium activity from surface signals, according to a proof-of-concept study published this month in Nature Nanotechnology. 

“Almost everything we know about how neurons behave in living brains comes from data collected with either electrophysiology or two-photon imaging,” said neuroscientist Joshua H. Siegle, PhD, of the Allen Institute for Neural Dynamics in Seattle , who not involved in the study. “ Until now, these two methods have rarely been used simultaneously.”

The technology, which has been tested in mice, could help advance our knowledge of how the brain works and may lead to new minimally invasive treatments for neurologic disorders. 
 

Multimodal Neurotech: The Power of 2-in-1

Electrical and optical methods for recording brain activity have been crucial in advancing neurophysiologic science, but each technique has its limits. Electrical recordings provide high “temporal resolution”; they reveal when activation is happening, but not really where. Optical imaging, on the other hand, offers high “spatial resolution,” showing which area of the brain is lighting up, but its measurements may not correspond with the activity’s timing. 

Research over the past decade has explored how to combine and harness the strengths of both methods. One potential solution is to use electrodes made of transparent materials such as graphene, allowing a clear field of view for a microscope during imaging. Recently, University of Pennsylvania scientists used graphene electrodes to illuminate the neural dynamics of seizures. 

But there are challenges. If graphene electrodes are very small — in this case, 20 µm in diameter — they become more resistant to the flow of electricity. Dr. Kuzum and colleagues addressed this by adding tiny platinum particles to improve electrical conductivity. Long graphene wires connect electrodes to the circuit board, but defects in graphene can interrupt the signal, so they made each wire with two layers; any defects in one wire could be hidden by the other.

By combining the two methods (microelectrode arrays and two-photon imaging), the researchers could see both when brain activity was happening and where, including in deeper layers. They discovered a correlation between electrical responses on the surface and cellular calcium activity deeper down. The team used these data to create a neural network (a type of artificial intelligence that learns to recognize patterns) that predicts deep calcium activity from surface-level readings.

The tech could help scientists study brain activity “in a way not possible with current single-function tools,” said Luyao Lu, PhD, professor of biomedical engineering at George Washington University in Washington, DC, who was not involved in the study. It could shed light on interactions between vascular and electrical activity, or explain how place cells (neurons in the hippocampus) are so efficient at creating spatial memory. 

It could also pave the way for minimally invasive neural prosthetics or targeted treatments for neurologic disorders, the researchers say. Implanting the device would be a “straightforward process” similar to placing electrocorticography grids in patients with epilepsy, said Dr. Kuzum. 

But first, the team plans to do more studies in animal models before testing the tech in clinical settings, Dr. Kuzum added.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Neha Pathak, MD: Hello. Today, we’re talking to Dr. Daniel Clauw, a professor at the University of Michigan in Ann Arbor, who is running a major trial on treatments for chronic back pain. We’re talking today about managing back pain in the post-opioid world. Thank you so much, Dr. Clauw, for taking the time to be our resident pain consultant today. Managing chronic pain can lead to a large amount of burnout and helplessness in the clinic setting. That’s the reality with some of the modalities that patients are requesting; there is still confusion about what is optimal for a particular type of patient, this feeling that we’re not really helping people get better, and whenever patients come in, that’s always still their chief complaint.

How would you advise providers to think about that and to settle into their role as communicators about better strategies without the burnout?

Daniel Clauw, MD: The first thing is to broaden the number of other providers that you get involved in these individuals’ care as the evidence base for all of these nonpharmacologic therapies being effective in chronic pain increases and increases. As third-party payers begin to reimburse for more and more of these therapies, it’s really difficult to manage chronic pain patients if you’re trying to do it alone on an island.

If you can, identify the good physical therapists in your community that are going to really work with people to give them an exercise program that they can use at home; find a pain psychologist that can offer some cognitive-behavioral therapy (CBT) for insomnia and some CBT for pain; and in the subset of patients with trauma, give them the emotional awareness of the neural reprocessing therapy for that specific subset.

As you start to identify more and more of these nonpharmacologic therapies that you want your patients to try, each of those has a set of providers and they can be incredibly helpful so that you, as the primary care provider (PCP), don’t really feel overwhelmed that you’re it, that you’re the only one.

Many of these individuals have more time to spend, and they have more one-on-one in-person time than you do as a primary care physician in the current healthcare system. Many of those providers have become really good at doing amateur CBT, goal-setting, and some of the other things that you need to do when you manage chronic pain patients. Try to find that other group of people that you can send your patients to that are going to be offering some of these nonpharmacologic therapies, and they’ll really help you manage these individuals.

Dr. Pathak: I think a couple of things come up for me. One is that we have to maybe broaden thinking about pain management, not only as multimodal strategies but also as multidisciplinary strategies. To your point, I think that’s really important. I also worry and wonder about health equity concerns, because just as overburdened as many PCPs are, we’re seeing it’s very difficult to get into physical therapy or to get into a setting where you’d be able to receive CBT for your pain. Any thoughts on those types of considerations?

Dr. Clauw: That’s a huge problem. Our group and many other groups in the pain space are developing websites, smartphone apps, and things like that to try to get some of these things directly to individuals with pain, not only for the reasons that you stated but also so that persons with pain don’t have to become patients. Our healthcare systems often make pain worse rather than better.

There were some great articles in The Lancet about 5 years ago talking about low back pain and that in different countries, the healthcare systems, for different reasons, have a tendency to actually make low back pain worse because they do too much surgery, immobilize people, or things like that rather than just not make them better. I think we’ve overmedicalized chronic pain in some settings, and much of what we’re trying to lead people to are things that are parts of wellness programs. The NIH National Center for Complementary and Integrative Health director talks about whole person health often.

I think that these interdisciplinary, integrative approaches are what we have to be using for chronic pain patients. I tell pain patients that, among acupuncture, acupressure, mindfulness, five different forms of CBT, yoga, and tai chi, I don’t know which of those is going to work, but I know that about 1 in 3 individuals that tries each of those therapies gets a benefit. What I really should be doing most is incentivizing people and motivating people to keep trying some of those nonpharmacologic approaches that they haven’t yet tried, because when they find one that works for them, then they will integrate it into their day-to-day life.

The other trick I would use for primary care physicians or anyone managing chronic pain patients is, don’t try to incentivize a pain patient to go try a new nonpharmacologic therapy or start an exercise program because you want their pain score to go from a 6 to a 3. Incentivize them by asking them, what are two or three things that you’re not able to do now because you have chronic pain that you’d really like to be able to do?

You’d like to play nine holes of golf; you’d like to be able to hug your grandchild; or you’d like to be able to do something else. Use those functional goals that are patient0driven to motivate your patients to do these things, because that will work much better. Again, any of us are inherently more likely to take the time and the effort to do some of these nonpharmacologic therapies if it’s for a reason that internally motivates us.

Dr. Pathak: I think that’s great. I’m very privileged to work within the Veterans Affairs (VA) healthcare system. I think that there’s been a huge shift within VA healthcare to provide these ancillary services, whether it’s yoga, tai chi, or acupuncture, as an adjunct to the pain management strategy.

Also, what comes up for me, as you’re saying, is grounding the point that instead of relying on a pain score — which can be objective and different from patient to patient and even within a patient — we should choose a smart goal that is almost more objective when it’s functional. Your goal is to walk two blocks to the mailbox. Can we achieve that as part of your pain control strategy?

I so appreciate your taking the time to be our pain consultant today. I really appreciate our discussion, and I’d like to hand it over to you for any final thoughts.

Dr. Clauw: I’d add that when you’re seeing chronic pain patients, many of them are going to have comorbid sleep problems. They’re going to have comorbid problems with fatigue and memory problems, especially the central nervous system–driven forms of pain that we now call nociplastic pain. Look at those as therapeutic targets.

If you’re befuddled because you’ve tried many different things for pain in this individual you’ve been seeing for a while, focus on their sleep and focus on getting them more active. Don’t use the word exercise — because that scares chronic pain patients — but focus on getting them more active.

There are many different tactics and strategies that you can use to motivate the patients to try some of these new nonpharmacologic approaches as the evidence base continues to increase.

Dr. Pathak: Thank you so much, again, to Dr. Clauw for joining us and being our pain consultant, really helping us to think about managing back pain in the postopioid world.
 

Dr. Pathak is Chief Physician Editor, Health and Lifestyle Medicine, WebMD. She has disclosed no relevant financial relationships. Dr. Clauw is Director, Chronic Pain and Fatigue Research Center, Department of Anesthesia, University of Michigan, Ann Arbor. He disclosed ties with Tonix and Viatris.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Neha Pathak, MD: Hello. Today, we’re talking to Dr. Daniel Clauw, a professor at the University of Michigan in Ann Arbor, who is running a major trial on treatments for chronic back pain. We’re talking today about managing back pain in the post-opioid world. Thank you so much, Dr. Clauw, for taking the time to be our resident pain consultant today. Managing chronic pain can lead to a large amount of burnout and helplessness in the clinic setting. That’s the reality with some of the modalities that patients are requesting; there is still confusion about what is optimal for a particular type of patient, this feeling that we’re not really helping people get better, and whenever patients come in, that’s always still their chief complaint.

How would you advise providers to think about that and to settle into their role as communicators about better strategies without the burnout?

Daniel Clauw, MD: The first thing is to broaden the number of other providers that you get involved in these individuals’ care as the evidence base for all of these nonpharmacologic therapies being effective in chronic pain increases and increases. As third-party payers begin to reimburse for more and more of these therapies, it’s really difficult to manage chronic pain patients if you’re trying to do it alone on an island.

If you can, identify the good physical therapists in your community that are going to really work with people to give them an exercise program that they can use at home; find a pain psychologist that can offer some cognitive-behavioral therapy (CBT) for insomnia and some CBT for pain; and in the subset of patients with trauma, give them the emotional awareness of the neural reprocessing therapy for that specific subset.

As you start to identify more and more of these nonpharmacologic therapies that you want your patients to try, each of those has a set of providers and they can be incredibly helpful so that you, as the primary care provider (PCP), don’t really feel overwhelmed that you’re it, that you’re the only one.

Many of these individuals have more time to spend, and they have more one-on-one in-person time than you do as a primary care physician in the current healthcare system. Many of those providers have become really good at doing amateur CBT, goal-setting, and some of the other things that you need to do when you manage chronic pain patients. Try to find that other group of people that you can send your patients to that are going to be offering some of these nonpharmacologic therapies, and they’ll really help you manage these individuals.

Dr. Pathak: I think a couple of things come up for me. One is that we have to maybe broaden thinking about pain management, not only as multimodal strategies but also as multidisciplinary strategies. To your point, I think that’s really important. I also worry and wonder about health equity concerns, because just as overburdened as many PCPs are, we’re seeing it’s very difficult to get into physical therapy or to get into a setting where you’d be able to receive CBT for your pain. Any thoughts on those types of considerations?

Dr. Clauw: That’s a huge problem. Our group and many other groups in the pain space are developing websites, smartphone apps, and things like that to try to get some of these things directly to individuals with pain, not only for the reasons that you stated but also so that persons with pain don’t have to become patients. Our healthcare systems often make pain worse rather than better.

There were some great articles in The Lancet about 5 years ago talking about low back pain and that in different countries, the healthcare systems, for different reasons, have a tendency to actually make low back pain worse because they do too much surgery, immobilize people, or things like that rather than just not make them better. I think we’ve overmedicalized chronic pain in some settings, and much of what we’re trying to lead people to are things that are parts of wellness programs. The NIH National Center for Complementary and Integrative Health director talks about whole person health often.

I think that these interdisciplinary, integrative approaches are what we have to be using for chronic pain patients. I tell pain patients that, among acupuncture, acupressure, mindfulness, five different forms of CBT, yoga, and tai chi, I don’t know which of those is going to work, but I know that about 1 in 3 individuals that tries each of those therapies gets a benefit. What I really should be doing most is incentivizing people and motivating people to keep trying some of those nonpharmacologic approaches that they haven’t yet tried, because when they find one that works for them, then they will integrate it into their day-to-day life.

The other trick I would use for primary care physicians or anyone managing chronic pain patients is, don’t try to incentivize a pain patient to go try a new nonpharmacologic therapy or start an exercise program because you want their pain score to go from a 6 to a 3. Incentivize them by asking them, what are two or three things that you’re not able to do now because you have chronic pain that you’d really like to be able to do?

You’d like to play nine holes of golf; you’d like to be able to hug your grandchild; or you’d like to be able to do something else. Use those functional goals that are patient0driven to motivate your patients to do these things, because that will work much better. Again, any of us are inherently more likely to take the time and the effort to do some of these nonpharmacologic therapies if it’s for a reason that internally motivates us.

Dr. Pathak: I think that’s great. I’m very privileged to work within the Veterans Affairs (VA) healthcare system. I think that there’s been a huge shift within VA healthcare to provide these ancillary services, whether it’s yoga, tai chi, or acupuncture, as an adjunct to the pain management strategy.

Also, what comes up for me, as you’re saying, is grounding the point that instead of relying on a pain score — which can be objective and different from patient to patient and even within a patient — we should choose a smart goal that is almost more objective when it’s functional. Your goal is to walk two blocks to the mailbox. Can we achieve that as part of your pain control strategy?

I so appreciate your taking the time to be our pain consultant today. I really appreciate our discussion, and I’d like to hand it over to you for any final thoughts.

Dr. Clauw: I’d add that when you’re seeing chronic pain patients, many of them are going to have comorbid sleep problems. They’re going to have comorbid problems with fatigue and memory problems, especially the central nervous system–driven forms of pain that we now call nociplastic pain. Look at those as therapeutic targets.

If you’re befuddled because you’ve tried many different things for pain in this individual you’ve been seeing for a while, focus on their sleep and focus on getting them more active. Don’t use the word exercise — because that scares chronic pain patients — but focus on getting them more active.

There are many different tactics and strategies that you can use to motivate the patients to try some of these new nonpharmacologic approaches as the evidence base continues to increase.

Dr. Pathak: Thank you so much, again, to Dr. Clauw for joining us and being our pain consultant, really helping us to think about managing back pain in the postopioid world.
 

Dr. Pathak is Chief Physician Editor, Health and Lifestyle Medicine, WebMD. She has disclosed no relevant financial relationships. Dr. Clauw is Director, Chronic Pain and Fatigue Research Center, Department of Anesthesia, University of Michigan, Ann Arbor. He disclosed ties with Tonix and Viatris.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Neha Pathak, MD: Hello. Today, we’re talking to Dr. Daniel Clauw, a professor at the University of Michigan in Ann Arbor, who is running a major trial on treatments for chronic back pain. We’re talking today about managing back pain in the post-opioid world. Thank you so much, Dr. Clauw, for taking the time to be our resident pain consultant today. Managing chronic pain can lead to a large amount of burnout and helplessness in the clinic setting. That’s the reality with some of the modalities that patients are requesting; there is still confusion about what is optimal for a particular type of patient, this feeling that we’re not really helping people get better, and whenever patients come in, that’s always still their chief complaint.

How would you advise providers to think about that and to settle into their role as communicators about better strategies without the burnout?

Daniel Clauw, MD: The first thing is to broaden the number of other providers that you get involved in these individuals’ care as the evidence base for all of these nonpharmacologic therapies being effective in chronic pain increases and increases. As third-party payers begin to reimburse for more and more of these therapies, it’s really difficult to manage chronic pain patients if you’re trying to do it alone on an island.

If you can, identify the good physical therapists in your community that are going to really work with people to give them an exercise program that they can use at home; find a pain psychologist that can offer some cognitive-behavioral therapy (CBT) for insomnia and some CBT for pain; and in the subset of patients with trauma, give them the emotional awareness of the neural reprocessing therapy for that specific subset.

As you start to identify more and more of these nonpharmacologic therapies that you want your patients to try, each of those has a set of providers and they can be incredibly helpful so that you, as the primary care provider (PCP), don’t really feel overwhelmed that you’re it, that you’re the only one.

Many of these individuals have more time to spend, and they have more one-on-one in-person time than you do as a primary care physician in the current healthcare system. Many of those providers have become really good at doing amateur CBT, goal-setting, and some of the other things that you need to do when you manage chronic pain patients. Try to find that other group of people that you can send your patients to that are going to be offering some of these nonpharmacologic therapies, and they’ll really help you manage these individuals.

Dr. Pathak: I think a couple of things come up for me. One is that we have to maybe broaden thinking about pain management, not only as multimodal strategies but also as multidisciplinary strategies. To your point, I think that’s really important. I also worry and wonder about health equity concerns, because just as overburdened as many PCPs are, we’re seeing it’s very difficult to get into physical therapy or to get into a setting where you’d be able to receive CBT for your pain. Any thoughts on those types of considerations?

Dr. Clauw: That’s a huge problem. Our group and many other groups in the pain space are developing websites, smartphone apps, and things like that to try to get some of these things directly to individuals with pain, not only for the reasons that you stated but also so that persons with pain don’t have to become patients. Our healthcare systems often make pain worse rather than better.

There were some great articles in The Lancet about 5 years ago talking about low back pain and that in different countries, the healthcare systems, for different reasons, have a tendency to actually make low back pain worse because they do too much surgery, immobilize people, or things like that rather than just not make them better. I think we’ve overmedicalized chronic pain in some settings, and much of what we’re trying to lead people to are things that are parts of wellness programs. The NIH National Center for Complementary and Integrative Health director talks about whole person health often.

I think that these interdisciplinary, integrative approaches are what we have to be using for chronic pain patients. I tell pain patients that, among acupuncture, acupressure, mindfulness, five different forms of CBT, yoga, and tai chi, I don’t know which of those is going to work, but I know that about 1 in 3 individuals that tries each of those therapies gets a benefit. What I really should be doing most is incentivizing people and motivating people to keep trying some of those nonpharmacologic approaches that they haven’t yet tried, because when they find one that works for them, then they will integrate it into their day-to-day life.

The other trick I would use for primary care physicians or anyone managing chronic pain patients is, don’t try to incentivize a pain patient to go try a new nonpharmacologic therapy or start an exercise program because you want their pain score to go from a 6 to a 3. Incentivize them by asking them, what are two or three things that you’re not able to do now because you have chronic pain that you’d really like to be able to do?

You’d like to play nine holes of golf; you’d like to be able to hug your grandchild; or you’d like to be able to do something else. Use those functional goals that are patient0driven to motivate your patients to do these things, because that will work much better. Again, any of us are inherently more likely to take the time and the effort to do some of these nonpharmacologic therapies if it’s for a reason that internally motivates us.

Dr. Pathak: I think that’s great. I’m very privileged to work within the Veterans Affairs (VA) healthcare system. I think that there’s been a huge shift within VA healthcare to provide these ancillary services, whether it’s yoga, tai chi, or acupuncture, as an adjunct to the pain management strategy.

Also, what comes up for me, as you’re saying, is grounding the point that instead of relying on a pain score — which can be objective and different from patient to patient and even within a patient — we should choose a smart goal that is almost more objective when it’s functional. Your goal is to walk two blocks to the mailbox. Can we achieve that as part of your pain control strategy?

I so appreciate your taking the time to be our pain consultant today. I really appreciate our discussion, and I’d like to hand it over to you for any final thoughts.

Dr. Clauw: I’d add that when you’re seeing chronic pain patients, many of them are going to have comorbid sleep problems. They’re going to have comorbid problems with fatigue and memory problems, especially the central nervous system–driven forms of pain that we now call nociplastic pain. Look at those as therapeutic targets.

If you’re befuddled because you’ve tried many different things for pain in this individual you’ve been seeing for a while, focus on their sleep and focus on getting them more active. Don’t use the word exercise — because that scares chronic pain patients — but focus on getting them more active.

There are many different tactics and strategies that you can use to motivate the patients to try some of these new nonpharmacologic approaches as the evidence base continues to increase.

Dr. Pathak: Thank you so much, again, to Dr. Clauw for joining us and being our pain consultant, really helping us to think about managing back pain in the postopioid world.
 

Dr. Pathak is Chief Physician Editor, Health and Lifestyle Medicine, WebMD. She has disclosed no relevant financial relationships. Dr. Clauw is Director, Chronic Pain and Fatigue Research Center, Department of Anesthesia, University of Michigan, Ann Arbor. He disclosed ties with Tonix and Viatris.

A version of this article appeared on Medscape.com.

When pediatric patients with epilepsy shift to adult care, inherent challenges are complicated by a near-total lack of efforts to smooth the transition, according to a recent survey. Many respondents received little to no information regarding the process, and many adults were still receiving care from family physicians or pediatric neurologists. The study was published online in Epilepsy & Behavior.

Room for Improvement

“We are not doing as good a job with planning for transition as we should,” said Elaine C. Wirrell, MD, who was not involved with the study. “It is not just a simple issue of sending your patient to an adult neurologist. Transition is a process that happens over time, so we need to do a better job getting our families ready for moving on to an adult provider.” Dr. Wirrell is director of pediatric epilepsy and professor of neurology at the Mayo Clinic in Rochester, Minnesota.

Mayo Clinic

Clumsy Transitions

Investigators distributed a 25-question survey to patients and caregivers who attended the 2019 Epilepsy Awareness Day at Disneyland, and through online support groups in North America. Among 58 responses, 32 came from patients between ages 12 and 17 years or their caregivers.

Despite attempts to recruit a diverse cross-section of respondents, most patients had severe epilepsy and comorbidities: 43% had daily or weekly seizures; 45% were on three or more antiseizure medications; and 74% had intellectual disabilities.

Many children with early-life epilepsies suffer from developmental and epileptic encephalopathy, which has associated non-seizure symptoms including learning challenges, behavioral issues, and other medical concerns, Dr. Wirrell said. Therefore, she said, finding a neurologist who treats adults — and has the expertise and interest to care for such patients — can be difficult.

“We’re seeing many patients not making that transition, or maybe not making it appropriately, so they’re not necessarily getting to the providers who have the most expertise in managing their epilepsy.” Among adults surveyed, 27% were still being followed by pediatric neurologists, and 35% were visiting family doctors for epilepsy-related treatment.

Because the needs of children with complex epilepsy can extend well beyond neurology, Dr. Wirrell added, managing such cases often requires multidisciplinary pediatric teams. “Finding that team on the adult side is more challenging.” As a result, she said, patients may transfer their neurology care without getting additional support for comorbidities such as mood disorders and learning disabilities.

The foregoing challenges are complicated by the fact that pediatric neurologists often lack the time (and in the United States, reimbursement) to adequately address the transition process, said Dr. Wirrell. Providers in freestanding children’s hospitals may face additional challenges coordinating with adult-care providers outside their facilities, she said.

“There’s also potentially a reluctance of both families and physicians to transition the patient on, because there’s concern that maybe there isn’t anybody on the adult side who is able to do as good a job as what they have on the pediatric side.”
 

Well-Coordinated Transitions Should Have No Surprises

Transition should be a planned, independence-promoting process that results in smooth, well-coordinated movement of pediatric patients into adult care — one without surprises or disconnections, the authors wrote. However, 55% of respondents never heard the term “transition” from any provider, even though 69% of patients were being treated in academic specialty centers.

Among 12- to 17-year-olds, 72% had never discussed transition with their healthcare team. That figure includes no 17-year-olds. Approximately 90% of respondents said they received sufficient time during healthcare visits, but 54% reported feeling stressed when moving from pediatric to adult care.

Given resource constraints in many pediatric epilepsy programs, the study authors recommended patient-empowerment tools such as a transition toolkit to help patients and families navigate the transition process even in places without formal transition programs.

“Many of these children are coming over with boatloads of medical records,” Dr. Wirrell said. “It’s not fair to the adult provider, who then has to go through all those records.” Instead, she said, pediatric teams should provide succinct summaries of relevant test results, medication side effects, prior treatments tried, and the like. “Those summaries are critically important so that we can get information to the person who needs it.”

Although successful transition requires significant coordination, she added, much of the process can often be handled by nonphysicians. “There are some very good nurse-led transition programs. Often, we can have a nurse providing education to the family and even potentially having a joint visit with an adult epilepsy nurse for complex patients.”

Pediatric providers also must know when to begin the transition process, Dr. Wirrell said. As soon as patients are 13 or 14 years old, she suggested discussing the process with them and their families every 6 to 12 months, covering specifics ranging from how to order medications to why adult patients may need power of attorney designees.

On a broader scale, said Dr. Wirrell, a smooth handoff requires planning. Fortunately, she said, the topic is becoming a significant priority for a growing number of children’s hospitals specific not only to epilepsy, but also to other chronic illnesses.

Dr. Wirrell is co–editor-in-chief for epilepsy.com. She reports no relevant financial interests.

When pediatric patients with epilepsy shift to adult care, inherent challenges are complicated by a near-total lack of efforts to smooth the transition, according to a recent survey. Many respondents received little to no information regarding the process, and many adults were still receiving care from family physicians or pediatric neurologists. The study was published online in Epilepsy & Behavior.

Room for Improvement

“We are not doing as good a job with planning for transition as we should,” said Elaine C. Wirrell, MD, who was not involved with the study. “It is not just a simple issue of sending your patient to an adult neurologist. Transition is a process that happens over time, so we need to do a better job getting our families ready for moving on to an adult provider.” Dr. Wirrell is director of pediatric epilepsy and professor of neurology at the Mayo Clinic in Rochester, Minnesota.

Mayo Clinic

Clumsy Transitions

Investigators distributed a 25-question survey to patients and caregivers who attended the 2019 Epilepsy Awareness Day at Disneyland, and through online support groups in North America. Among 58 responses, 32 came from patients between ages 12 and 17 years or their caregivers.

Despite attempts to recruit a diverse cross-section of respondents, most patients had severe epilepsy and comorbidities: 43% had daily or weekly seizures; 45% were on three or more antiseizure medications; and 74% had intellectual disabilities.

Many children with early-life epilepsies suffer from developmental and epileptic encephalopathy, which has associated non-seizure symptoms including learning challenges, behavioral issues, and other medical concerns, Dr. Wirrell said. Therefore, she said, finding a neurologist who treats adults — and has the expertise and interest to care for such patients — can be difficult.

“We’re seeing many patients not making that transition, or maybe not making it appropriately, so they’re not necessarily getting to the providers who have the most expertise in managing their epilepsy.” Among adults surveyed, 27% were still being followed by pediatric neurologists, and 35% were visiting family doctors for epilepsy-related treatment.

Because the needs of children with complex epilepsy can extend well beyond neurology, Dr. Wirrell added, managing such cases often requires multidisciplinary pediatric teams. “Finding that team on the adult side is more challenging.” As a result, she said, patients may transfer their neurology care without getting additional support for comorbidities such as mood disorders and learning disabilities.

The foregoing challenges are complicated by the fact that pediatric neurologists often lack the time (and in the United States, reimbursement) to adequately address the transition process, said Dr. Wirrell. Providers in freestanding children’s hospitals may face additional challenges coordinating with adult-care providers outside their facilities, she said.

“There’s also potentially a reluctance of both families and physicians to transition the patient on, because there’s concern that maybe there isn’t anybody on the adult side who is able to do as good a job as what they have on the pediatric side.”
 

Well-Coordinated Transitions Should Have No Surprises

Transition should be a planned, independence-promoting process that results in smooth, well-coordinated movement of pediatric patients into adult care — one without surprises or disconnections, the authors wrote. However, 55% of respondents never heard the term “transition” from any provider, even though 69% of patients were being treated in academic specialty centers.

Among 12- to 17-year-olds, 72% had never discussed transition with their healthcare team. That figure includes no 17-year-olds. Approximately 90% of respondents said they received sufficient time during healthcare visits, but 54% reported feeling stressed when moving from pediatric to adult care.

Given resource constraints in many pediatric epilepsy programs, the study authors recommended patient-empowerment tools such as a transition toolkit to help patients and families navigate the transition process even in places without formal transition programs.

“Many of these children are coming over with boatloads of medical records,” Dr. Wirrell said. “It’s not fair to the adult provider, who then has to go through all those records.” Instead, she said, pediatric teams should provide succinct summaries of relevant test results, medication side effects, prior treatments tried, and the like. “Those summaries are critically important so that we can get information to the person who needs it.”

Although successful transition requires significant coordination, she added, much of the process can often be handled by nonphysicians. “There are some very good nurse-led transition programs. Often, we can have a nurse providing education to the family and even potentially having a joint visit with an adult epilepsy nurse for complex patients.”

Pediatric providers also must know when to begin the transition process, Dr. Wirrell said. As soon as patients are 13 or 14 years old, she suggested discussing the process with them and their families every 6 to 12 months, covering specifics ranging from how to order medications to why adult patients may need power of attorney designees.

On a broader scale, said Dr. Wirrell, a smooth handoff requires planning. Fortunately, she said, the topic is becoming a significant priority for a growing number of children’s hospitals specific not only to epilepsy, but also to other chronic illnesses.

Dr. Wirrell is co–editor-in-chief for epilepsy.com. She reports no relevant financial interests.

When pediatric patients with epilepsy shift to adult care, inherent challenges are complicated by a near-total lack of efforts to smooth the transition, according to a recent survey. Many respondents received little to no information regarding the process, and many adults were still receiving care from family physicians or pediatric neurologists. The study was published online in Epilepsy & Behavior.

Room for Improvement

“We are not doing as good a job with planning for transition as we should,” said Elaine C. Wirrell, MD, who was not involved with the study. “It is not just a simple issue of sending your patient to an adult neurologist. Transition is a process that happens over time, so we need to do a better job getting our families ready for moving on to an adult provider.” Dr. Wirrell is director of pediatric epilepsy and professor of neurology at the Mayo Clinic in Rochester, Minnesota.

Mayo Clinic

Clumsy Transitions

Investigators distributed a 25-question survey to patients and caregivers who attended the 2019 Epilepsy Awareness Day at Disneyland, and through online support groups in North America. Among 58 responses, 32 came from patients between ages 12 and 17 years or their caregivers.

Despite attempts to recruit a diverse cross-section of respondents, most patients had severe epilepsy and comorbidities: 43% had daily or weekly seizures; 45% were on three or more antiseizure medications; and 74% had intellectual disabilities.

Many children with early-life epilepsies suffer from developmental and epileptic encephalopathy, which has associated non-seizure symptoms including learning challenges, behavioral issues, and other medical concerns, Dr. Wirrell said. Therefore, she said, finding a neurologist who treats adults — and has the expertise and interest to care for such patients — can be difficult.

“We’re seeing many patients not making that transition, or maybe not making it appropriately, so they’re not necessarily getting to the providers who have the most expertise in managing their epilepsy.” Among adults surveyed, 27% were still being followed by pediatric neurologists, and 35% were visiting family doctors for epilepsy-related treatment.

Because the needs of children with complex epilepsy can extend well beyond neurology, Dr. Wirrell added, managing such cases often requires multidisciplinary pediatric teams. “Finding that team on the adult side is more challenging.” As a result, she said, patients may transfer their neurology care without getting additional support for comorbidities such as mood disorders and learning disabilities.

The foregoing challenges are complicated by the fact that pediatric neurologists often lack the time (and in the United States, reimbursement) to adequately address the transition process, said Dr. Wirrell. Providers in freestanding children’s hospitals may face additional challenges coordinating with adult-care providers outside their facilities, she said.

“There’s also potentially a reluctance of both families and physicians to transition the patient on, because there’s concern that maybe there isn’t anybody on the adult side who is able to do as good a job as what they have on the pediatric side.”
 

Well-Coordinated Transitions Should Have No Surprises

Transition should be a planned, independence-promoting process that results in smooth, well-coordinated movement of pediatric patients into adult care — one without surprises or disconnections, the authors wrote. However, 55% of respondents never heard the term “transition” from any provider, even though 69% of patients were being treated in academic specialty centers.

Among 12- to 17-year-olds, 72% had never discussed transition with their healthcare team. That figure includes no 17-year-olds. Approximately 90% of respondents said they received sufficient time during healthcare visits, but 54% reported feeling stressed when moving from pediatric to adult care.

Given resource constraints in many pediatric epilepsy programs, the study authors recommended patient-empowerment tools such as a transition toolkit to help patients and families navigate the transition process even in places without formal transition programs.

“Many of these children are coming over with boatloads of medical records,” Dr. Wirrell said. “It’s not fair to the adult provider, who then has to go through all those records.” Instead, she said, pediatric teams should provide succinct summaries of relevant test results, medication side effects, prior treatments tried, and the like. “Those summaries are critically important so that we can get information to the person who needs it.”

Although successful transition requires significant coordination, she added, much of the process can often be handled by nonphysicians. “There are some very good nurse-led transition programs. Often, we can have a nurse providing education to the family and even potentially having a joint visit with an adult epilepsy nurse for complex patients.”

Pediatric providers also must know when to begin the transition process, Dr. Wirrell said. As soon as patients are 13 or 14 years old, she suggested discussing the process with them and their families every 6 to 12 months, covering specifics ranging from how to order medications to why adult patients may need power of attorney designees.

On a broader scale, said Dr. Wirrell, a smooth handoff requires planning. Fortunately, she said, the topic is becoming a significant priority for a growing number of children’s hospitals specific not only to epilepsy, but also to other chronic illnesses.

Dr. Wirrell is co–editor-in-chief for epilepsy.com. She reports no relevant financial interests.

Five people in the United Kingdom have been diagnosed with Alzheimer’s disease resulting from a medical treatment they received decades earlier, new research shows. 

Investigators say they are the first known cases of medically acquired AD in living people, but outside experts say the findings should be interpreted cautiously.

The individuals received treatment as children with human growth hormone extracted from pituitary glands of cadavers (c-hGH). Between 1958-1985, an estimated 30,000 people worldwide, mostly children, were treated with c-hGH for genetic disorders and growth hormone deficiencies. 

The therapy was halted in 1985 after three patients in the US who received the treatment later died of Creutzfeldt-Jakob disease (CJD) transmitted through batches of c-hGH that were contaminated with disease-causing prions. 

The new study builds on the investigators’ earlier work that showed the batches of c-hGH also contained amyloid-beta protein and that the protein could be transmitted decades later. These five cases were referred to or reviewed by researchers and clinicians at a prion clinic led by one of the lead researchers.

There are no reports of amyloid-beta transmission through any other medical or surgical procedures, researchers stress, and there is no evidence that amyloid-beta can be passed on during routine patient care or in daily activities. 

“However, the recognition of transmission of amyloid-beta pathology in these rare situations should lead us to review measures to prevent accidental transmission via other medical or surgical procedures, in order to prevent such cases occurring in future,” lead author John Collinge, MD, director of the University of College London Institute of Prion Diseases, London, England, and leader of the UK’s National Prion Clinic, said in a press release. 

“Importantly, our findings also suggest that Alzheimer’s and some other neurological conditions share similar disease processes to CJD, and this may have important implications for understanding and treating Alzheimer’s disease in the future,” Dr. Collinge continued.

The findings were published online January 29 in Nature Medicine. 
 

Building on Earlier Work

The research builds on investigators’ previous 2015 work that found archived samples of c-hGH were also contaminated with amyloid-beta protein. In 2018, mouse studies showed that c-hGH samples stored for decades could still transmit amyloid-beta via injection. 

Researchers said the findings suggested that individuals exposed to contaminated c-hGH who did not die from CJD might eventually develop AD.

Patients in the new study developed neurological symptoms consistent with AD between the ages of 38 and 55 years. The individual cases were either referred to or reviewed by experts in the National Prion Clinic in the UK between 2017 and 2022. The clinic coordinates the National Prion Monitoring Cohort, a longitudinal study of individuals with confirmed prion diseases. 

Of the eight cases, three were diagnosed with AD before referral to the clinic; two others met criteria for an AD diagnosis; and three did not meet the criteria. Three of the patients — two of whom had AD — are now deceased. 

All patients in the study received c-hGH prepared using a method called Wilhelmi or Hartree-modified Wilhelmi preparation (HWP).

Biomarker analyses confirmed the AD diagnosis in two patients. Other cases showed either progressive brain volume loss on brain imaging or elevated cerebrospinal fluid total tau and phosphorylated tau, or evidence of amyloid-beta deposits on autopsy. 
 

‘Potentially Transmissible’

The cases offered diverse presentations. Some were not symptomatic and some failed to meet current diagnostic criteria for sporadic Alzheimer’s disease. Treatment duration and frequency differed among those in the study, as did their age at treatment onset and completion. That and other factors could contribute to the diverse phenotype recorded in individuals, investigators note. 

Investigators examined and ruled out other factors that might explain the individuals’ cognitive symptoms, including childhood intellectual disability, which has been linked to dementia risk, the underlying condition that prompted their treatment with c-hGH, growth hormone deficiency, and cranial radiotherapy, which four of the individuals had received. They also ruled out inherited disease in all five of the cases with samples available for testing. 

“Taken together, the only factor common to all of the patients whom we describe is treatment with the HWP subtype of c-hGH,” the authors write. “Given the strong experimental evidence for A-beta transmission from relevant archived HWP c-hGH batches, we conclude that this is the most plausible explanation for the findings observed.”

Investigators say the findings show that, like other prion diseases, AD has three etiologies: sporadic, inherited, and rare acquired forms, or iatrogenic AD. 

“The clinical syndrome developed by these individuals can, therefore, be termed iatrogenic Alzheimer’s disease, and Alzheimer’s disease should now be recognized as a potentially transmissible disorder,” the authors write. 

“Our cases suggest that, similarly to what is observed in human prion diseases, iatrogenic forms of Alzheimer’s disease differ phenotypically from sporadic and inherited forms, with some individuals remaining asymptomatic despite exposure to A-beta seeds due to protective factors that, at present, are unknown,” they continue
 

‘Measure of Skepticism’

In an accompanying editorial, Mathias Jucker, PhD, of the Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany, and Lary C. Walker, PhD, in the Department of Neurology at Emory University, Atlanta, write that the findings should be considered “with a measure of skepticism.”

“The cases presented are diverse and complicated; the individuals had undergone a variety of medical interventions for various disorders earlier in life, and it is difficult to exclude a contribution of these circumstances to the complex disease phenotypes that appeared many years later,” they write. 

However, they continue, “there is good reason to take the findings seriously.”

“From a practical standpoint, this report reinforces the potential of amyloid-beta seeds as targets for early prevention, and it underscores the importance of informed caution in the preparation of surgical instruments, handling of tissues, and implementation of therapeutic biologics, particularly those derived from human sources,” Dr. Jucker and Dr. Walker write. 

Commenting on the findings for this news organization, Christopher Weber, PhD, director of global science initiatives for the Alzheimer’s Association, says the idea that amyloid-beta is transmissible between individuals has been shown before. 

“We’ve known for a long time that it is possible to create abnormal amyloid buildup — similar to that seen in Alzheimer’s – in the brain of an animal by injecting it with amyloid-beta. We also transfer human Alzheimer’s genes into animals to initiate abnormal, Alzheimer’s-like processes in their brains,” he said. “Thus, the idea that amyloid is transferable between individuals is not so novel as implied in the new paper.”

However, the study does highlight the importance of safety measures to prevent the accidental transmission of amyloid-beta, Weber added. 

“It is a reasonable and actionable caution that the scientific and clinical communities must understand the possible risks and ensure that all methods of transmission are eliminated — for example, with complete and conscientious sterilization of surgical instruments,” he said. “Bottom line: We shouldn’t put amyloid-beta into people’s brains, either accidentally or on purpose, and appropriate measures should be in place to ensure that doesn’t happen.”

The study was supported by the Medical Research Council, the National Institute for Health and Care Research (NIHR), the NIHR University College of London Hospital Biomedical Research Centre, Alzheimer’s Research UK, and the Stroke Association. Dr. Collinge is a shareholder and director of D-Gen, Ltd., an academic spin-out company working in the field of prion disease diagnosis, decontamination and therapeutics. Dr. Jucker and Dr. Walker report no conflicts of interest. 

A version of this article appeared on Medscape.com.

Five people in the United Kingdom have been diagnosed with Alzheimer’s disease resulting from a medical treatment they received decades earlier, new research shows. 

Investigators say they are the first known cases of medically acquired AD in living people, but outside experts say the findings should be interpreted cautiously.

The individuals received treatment as children with human growth hormone extracted from pituitary glands of cadavers (c-hGH). Between 1958-1985, an estimated 30,000 people worldwide, mostly children, were treated with c-hGH for genetic disorders and growth hormone deficiencies. 

The therapy was halted in 1985 after three patients in the US who received the treatment later died of Creutzfeldt-Jakob disease (CJD) transmitted through batches of c-hGH that were contaminated with disease-causing prions. 

The new study builds on the investigators’ earlier work that showed the batches of c-hGH also contained amyloid-beta protein and that the protein could be transmitted decades later. These five cases were referred to or reviewed by researchers and clinicians at a prion clinic led by one of the lead researchers.

There are no reports of amyloid-beta transmission through any other medical or surgical procedures, researchers stress, and there is no evidence that amyloid-beta can be passed on during routine patient care or in daily activities. 

“However, the recognition of transmission of amyloid-beta pathology in these rare situations should lead us to review measures to prevent accidental transmission via other medical or surgical procedures, in order to prevent such cases occurring in future,” lead author John Collinge, MD, director of the University of College London Institute of Prion Diseases, London, England, and leader of the UK’s National Prion Clinic, said in a press release. 

“Importantly, our findings also suggest that Alzheimer’s and some other neurological conditions share similar disease processes to CJD, and this may have important implications for understanding and treating Alzheimer’s disease in the future,” Dr. Collinge continued.

The findings were published online January 29 in Nature Medicine. 
 

Building on Earlier Work

The research builds on investigators’ previous 2015 work that found archived samples of c-hGH were also contaminated with amyloid-beta protein. In 2018, mouse studies showed that c-hGH samples stored for decades could still transmit amyloid-beta via injection. 

Researchers said the findings suggested that individuals exposed to contaminated c-hGH who did not die from CJD might eventually develop AD.

Patients in the new study developed neurological symptoms consistent with AD between the ages of 38 and 55 years. The individual cases were either referred to or reviewed by experts in the National Prion Clinic in the UK between 2017 and 2022. The clinic coordinates the National Prion Monitoring Cohort, a longitudinal study of individuals with confirmed prion diseases. 

Of the eight cases, three were diagnosed with AD before referral to the clinic; two others met criteria for an AD diagnosis; and three did not meet the criteria. Three of the patients — two of whom had AD — are now deceased. 

All patients in the study received c-hGH prepared using a method called Wilhelmi or Hartree-modified Wilhelmi preparation (HWP).

Biomarker analyses confirmed the AD diagnosis in two patients. Other cases showed either progressive brain volume loss on brain imaging or elevated cerebrospinal fluid total tau and phosphorylated tau, or evidence of amyloid-beta deposits on autopsy. 
 

‘Potentially Transmissible’

The cases offered diverse presentations. Some were not symptomatic and some failed to meet current diagnostic criteria for sporadic Alzheimer’s disease. Treatment duration and frequency differed among those in the study, as did their age at treatment onset and completion. That and other factors could contribute to the diverse phenotype recorded in individuals, investigators note. 

Investigators examined and ruled out other factors that might explain the individuals’ cognitive symptoms, including childhood intellectual disability, which has been linked to dementia risk, the underlying condition that prompted their treatment with c-hGH, growth hormone deficiency, and cranial radiotherapy, which four of the individuals had received. They also ruled out inherited disease in all five of the cases with samples available for testing. 

“Taken together, the only factor common to all of the patients whom we describe is treatment with the HWP subtype of c-hGH,” the authors write. “Given the strong experimental evidence for A-beta transmission from relevant archived HWP c-hGH batches, we conclude that this is the most plausible explanation for the findings observed.”

Investigators say the findings show that, like other prion diseases, AD has three etiologies: sporadic, inherited, and rare acquired forms, or iatrogenic AD. 

“The clinical syndrome developed by these individuals can, therefore, be termed iatrogenic Alzheimer’s disease, and Alzheimer’s disease should now be recognized as a potentially transmissible disorder,” the authors write. 

“Our cases suggest that, similarly to what is observed in human prion diseases, iatrogenic forms of Alzheimer’s disease differ phenotypically from sporadic and inherited forms, with some individuals remaining asymptomatic despite exposure to A-beta seeds due to protective factors that, at present, are unknown,” they continue
 

‘Measure of Skepticism’

In an accompanying editorial, Mathias Jucker, PhD, of the Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany, and Lary C. Walker, PhD, in the Department of Neurology at Emory University, Atlanta, write that the findings should be considered “with a measure of skepticism.”

“The cases presented are diverse and complicated; the individuals had undergone a variety of medical interventions for various disorders earlier in life, and it is difficult to exclude a contribution of these circumstances to the complex disease phenotypes that appeared many years later,” they write. 

However, they continue, “there is good reason to take the findings seriously.”

“From a practical standpoint, this report reinforces the potential of amyloid-beta seeds as targets for early prevention, and it underscores the importance of informed caution in the preparation of surgical instruments, handling of tissues, and implementation of therapeutic biologics, particularly those derived from human sources,” Dr. Jucker and Dr. Walker write. 

Commenting on the findings for this news organization, Christopher Weber, PhD, director of global science initiatives for the Alzheimer’s Association, says the idea that amyloid-beta is transmissible between individuals has been shown before. 

“We’ve known for a long time that it is possible to create abnormal amyloid buildup — similar to that seen in Alzheimer’s – in the brain of an animal by injecting it with amyloid-beta. We also transfer human Alzheimer’s genes into animals to initiate abnormal, Alzheimer’s-like processes in their brains,” he said. “Thus, the idea that amyloid is transferable between individuals is not so novel as implied in the new paper.”

However, the study does highlight the importance of safety measures to prevent the accidental transmission of amyloid-beta, Weber added. 

“It is a reasonable and actionable caution that the scientific and clinical communities must understand the possible risks and ensure that all methods of transmission are eliminated — for example, with complete and conscientious sterilization of surgical instruments,” he said. “Bottom line: We shouldn’t put amyloid-beta into people’s brains, either accidentally or on purpose, and appropriate measures should be in place to ensure that doesn’t happen.”

The study was supported by the Medical Research Council, the National Institute for Health and Care Research (NIHR), the NIHR University College of London Hospital Biomedical Research Centre, Alzheimer’s Research UK, and the Stroke Association. Dr. Collinge is a shareholder and director of D-Gen, Ltd., an academic spin-out company working in the field of prion disease diagnosis, decontamination and therapeutics. Dr. Jucker and Dr. Walker report no conflicts of interest. 

A version of this article appeared on Medscape.com.

Five people in the United Kingdom have been diagnosed with Alzheimer’s disease resulting from a medical treatment they received decades earlier, new research shows. 

Investigators say they are the first known cases of medically acquired AD in living people, but outside experts say the findings should be interpreted cautiously.

The individuals received treatment as children with human growth hormone extracted from pituitary glands of cadavers (c-hGH). Between 1958-1985, an estimated 30,000 people worldwide, mostly children, were treated with c-hGH for genetic disorders and growth hormone deficiencies. 

The therapy was halted in 1985 after three patients in the US who received the treatment later died of Creutzfeldt-Jakob disease (CJD) transmitted through batches of c-hGH that were contaminated with disease-causing prions. 

The new study builds on the investigators’ earlier work that showed the batches of c-hGH also contained amyloid-beta protein and that the protein could be transmitted decades later. These five cases were referred to or reviewed by researchers and clinicians at a prion clinic led by one of the lead researchers.

There are no reports of amyloid-beta transmission through any other medical or surgical procedures, researchers stress, and there is no evidence that amyloid-beta can be passed on during routine patient care or in daily activities. 

“However, the recognition of transmission of amyloid-beta pathology in these rare situations should lead us to review measures to prevent accidental transmission via other medical or surgical procedures, in order to prevent such cases occurring in future,” lead author John Collinge, MD, director of the University of College London Institute of Prion Diseases, London, England, and leader of the UK’s National Prion Clinic, said in a press release. 

“Importantly, our findings also suggest that Alzheimer’s and some other neurological conditions share similar disease processes to CJD, and this may have important implications for understanding and treating Alzheimer’s disease in the future,” Dr. Collinge continued.

The findings were published online January 29 in Nature Medicine. 
 

Building on Earlier Work

The research builds on investigators’ previous 2015 work that found archived samples of c-hGH were also contaminated with amyloid-beta protein. In 2018, mouse studies showed that c-hGH samples stored for decades could still transmit amyloid-beta via injection. 

Researchers said the findings suggested that individuals exposed to contaminated c-hGH who did not die from CJD might eventually develop AD.

Patients in the new study developed neurological symptoms consistent with AD between the ages of 38 and 55 years. The individual cases were either referred to or reviewed by experts in the National Prion Clinic in the UK between 2017 and 2022. The clinic coordinates the National Prion Monitoring Cohort, a longitudinal study of individuals with confirmed prion diseases. 

Of the eight cases, three were diagnosed with AD before referral to the clinic; two others met criteria for an AD diagnosis; and three did not meet the criteria. Three of the patients — two of whom had AD — are now deceased. 

All patients in the study received c-hGH prepared using a method called Wilhelmi or Hartree-modified Wilhelmi preparation (HWP).

Biomarker analyses confirmed the AD diagnosis in two patients. Other cases showed either progressive brain volume loss on brain imaging or elevated cerebrospinal fluid total tau and phosphorylated tau, or evidence of amyloid-beta deposits on autopsy. 
 

‘Potentially Transmissible’

The cases offered diverse presentations. Some were not symptomatic and some failed to meet current diagnostic criteria for sporadic Alzheimer’s disease. Treatment duration and frequency differed among those in the study, as did their age at treatment onset and completion. That and other factors could contribute to the diverse phenotype recorded in individuals, investigators note. 

Investigators examined and ruled out other factors that might explain the individuals’ cognitive symptoms, including childhood intellectual disability, which has been linked to dementia risk, the underlying condition that prompted their treatment with c-hGH, growth hormone deficiency, and cranial radiotherapy, which four of the individuals had received. They also ruled out inherited disease in all five of the cases with samples available for testing. 

“Taken together, the only factor common to all of the patients whom we describe is treatment with the HWP subtype of c-hGH,” the authors write. “Given the strong experimental evidence for A-beta transmission from relevant archived HWP c-hGH batches, we conclude that this is the most plausible explanation for the findings observed.”

Investigators say the findings show that, like other prion diseases, AD has three etiologies: sporadic, inherited, and rare acquired forms, or iatrogenic AD. 

“The clinical syndrome developed by these individuals can, therefore, be termed iatrogenic Alzheimer’s disease, and Alzheimer’s disease should now be recognized as a potentially transmissible disorder,” the authors write. 

“Our cases suggest that, similarly to what is observed in human prion diseases, iatrogenic forms of Alzheimer’s disease differ phenotypically from sporadic and inherited forms, with some individuals remaining asymptomatic despite exposure to A-beta seeds due to protective factors that, at present, are unknown,” they continue
 

‘Measure of Skepticism’

In an accompanying editorial, Mathias Jucker, PhD, of the Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany, and Lary C. Walker, PhD, in the Department of Neurology at Emory University, Atlanta, write that the findings should be considered “with a measure of skepticism.”

“The cases presented are diverse and complicated; the individuals had undergone a variety of medical interventions for various disorders earlier in life, and it is difficult to exclude a contribution of these circumstances to the complex disease phenotypes that appeared many years later,” they write. 

However, they continue, “there is good reason to take the findings seriously.”

“From a practical standpoint, this report reinforces the potential of amyloid-beta seeds as targets for early prevention, and it underscores the importance of informed caution in the preparation of surgical instruments, handling of tissues, and implementation of therapeutic biologics, particularly those derived from human sources,” Dr. Jucker and Dr. Walker write. 

Commenting on the findings for this news organization, Christopher Weber, PhD, director of global science initiatives for the Alzheimer’s Association, says the idea that amyloid-beta is transmissible between individuals has been shown before. 

“We’ve known for a long time that it is possible to create abnormal amyloid buildup — similar to that seen in Alzheimer’s – in the brain of an animal by injecting it with amyloid-beta. We also transfer human Alzheimer’s genes into animals to initiate abnormal, Alzheimer’s-like processes in their brains,” he said. “Thus, the idea that amyloid is transferable between individuals is not so novel as implied in the new paper.”

However, the study does highlight the importance of safety measures to prevent the accidental transmission of amyloid-beta, Weber added. 

“It is a reasonable and actionable caution that the scientific and clinical communities must understand the possible risks and ensure that all methods of transmission are eliminated — for example, with complete and conscientious sterilization of surgical instruments,” he said. “Bottom line: We shouldn’t put amyloid-beta into people’s brains, either accidentally or on purpose, and appropriate measures should be in place to ensure that doesn’t happen.”

The study was supported by the Medical Research Council, the National Institute for Health and Care Research (NIHR), the NIHR University College of London Hospital Biomedical Research Centre, Alzheimer’s Research UK, and the Stroke Association. Dr. Collinge is a shareholder and director of D-Gen, Ltd., an academic spin-out company working in the field of prion disease diagnosis, decontamination and therapeutics. Dr. Jucker and Dr. Walker report no conflicts of interest. 

A version of this article appeared on Medscape.com.

Veterans Administration (VA) hospitals are a stepchild in the bizarre mishmash of the U.S. healthcare system. They’re best known (often justifiably so) for rather cantankerous patients, rigid rules, and other oddities (such as patients being able to go on leave and come back).

The majority of American doctors, including myself, did at least part of our training at a VA and have no shortage of stories about them. One I worked at (Omaha VA) was powered by its own nuclear reactor in the basement (no, really, it was, though sadly it’s since been taken out).

VA hospitals, in general, are no-frills — linoleum floors, no piano player in the lobby, very few private rooms, and occasionally in the news for scandals like the one at my hometown Carl T. Hayden VA hospital (I trained there, too).

Yet, a recent study found VA hospitals to be surprisingly efficient compared with the private sector. Their focus on patient care, rather than profits, allows them to run with 8% fewer administrative staff since they generally don’t have to deal with insurance billings, denials, and other paperwork (they also don’t have to deal with shareholders and investor demands or ridiculous CEO salaries, though the study didn’t address that).

On a national scale, this would mean roughly 900,000 fewer administrative jobs in the private sector. Granted, that also would mean those people would have to find other jobs, but let’s look at the patient side. If you had 900,000 fewer desk workers, you’d have the money to hire more nurses, respiratory techs, therapists, and other people directly involved in patient care. You’d also need a lot less office space, which further brings down overhead.

Part of the problem is that a lot of the current medical business is in marketing — how many ads do you see each day for different hospitals in your area? — and upcoding to extract more money from each billing. Neither of these has any clinical value on the patient side of things.

You don’t have to look back too far (2020) for the study that found U.S. healthcare spent four times as much money ($812 billion) per capita than our northern neighbors.

And, for all the jokes we make about the VA (myself included), a study last year found its care was on par (or even better than) most hospitals .

I’m not saying the VA is perfect. All of us who worked there can think of times it wasn’t. But we also remember plenty of issues we’ve had at other places we’ve practiced, too.

Maybe it’s time to stop laughing at the VA and realize they’re doing something right — and learn from it to make healthcare better at the other 6,000 or so hospitals in the U.S.
 

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

Veterans Administration (VA) hospitals are a stepchild in the bizarre mishmash of the U.S. healthcare system. They’re best known (often justifiably so) for rather cantankerous patients, rigid rules, and other oddities (such as patients being able to go on leave and come back).

The majority of American doctors, including myself, did at least part of our training at a VA and have no shortage of stories about them. One I worked at (Omaha VA) was powered by its own nuclear reactor in the basement (no, really, it was, though sadly it’s since been taken out).

VA hospitals, in general, are no-frills — linoleum floors, no piano player in the lobby, very few private rooms, and occasionally in the news for scandals like the one at my hometown Carl T. Hayden VA hospital (I trained there, too).

Yet, a recent study found VA hospitals to be surprisingly efficient compared with the private sector. Their focus on patient care, rather than profits, allows them to run with 8% fewer administrative staff since they generally don’t have to deal with insurance billings, denials, and other paperwork (they also don’t have to deal with shareholders and investor demands or ridiculous CEO salaries, though the study didn’t address that).

On a national scale, this would mean roughly 900,000 fewer administrative jobs in the private sector. Granted, that also would mean those people would have to find other jobs, but let’s look at the patient side. If you had 900,000 fewer desk workers, you’d have the money to hire more nurses, respiratory techs, therapists, and other people directly involved in patient care. You’d also need a lot less office space, which further brings down overhead.

Part of the problem is that a lot of the current medical business is in marketing — how many ads do you see each day for different hospitals in your area? — and upcoding to extract more money from each billing. Neither of these has any clinical value on the patient side of things.

You don’t have to look back too far (2020) for the study that found U.S. healthcare spent four times as much money ($812 billion) per capita than our northern neighbors.

And, for all the jokes we make about the VA (myself included), a study last year found its care was on par (or even better than) most hospitals .

I’m not saying the VA is perfect. All of us who worked there can think of times it wasn’t. But we also remember plenty of issues we’ve had at other places we’ve practiced, too.

Maybe it’s time to stop laughing at the VA and realize they’re doing something right — and learn from it to make healthcare better at the other 6,000 or so hospitals in the U.S.
 

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

Veterans Administration (VA) hospitals are a stepchild in the bizarre mishmash of the U.S. healthcare system. They’re best known (often justifiably so) for rather cantankerous patients, rigid rules, and other oddities (such as patients being able to go on leave and come back).

The majority of American doctors, including myself, did at least part of our training at a VA and have no shortage of stories about them. One I worked at (Omaha VA) was powered by its own nuclear reactor in the basement (no, really, it was, though sadly it’s since been taken out).

VA hospitals, in general, are no-frills — linoleum floors, no piano player in the lobby, very few private rooms, and occasionally in the news for scandals like the one at my hometown Carl T. Hayden VA hospital (I trained there, too).

Yet, a recent study found VA hospitals to be surprisingly efficient compared with the private sector. Their focus on patient care, rather than profits, allows them to run with 8% fewer administrative staff since they generally don’t have to deal with insurance billings, denials, and other paperwork (they also don’t have to deal with shareholders and investor demands or ridiculous CEO salaries, though the study didn’t address that).

On a national scale, this would mean roughly 900,000 fewer administrative jobs in the private sector. Granted, that also would mean those people would have to find other jobs, but let’s look at the patient side. If you had 900,000 fewer desk workers, you’d have the money to hire more nurses, respiratory techs, therapists, and other people directly involved in patient care. You’d also need a lot less office space, which further brings down overhead.

Part of the problem is that a lot of the current medical business is in marketing — how many ads do you see each day for different hospitals in your area? — and upcoding to extract more money from each billing. Neither of these has any clinical value on the patient side of things.

You don’t have to look back too far (2020) for the study that found U.S. healthcare spent four times as much money ($812 billion) per capita than our northern neighbors.

And, for all the jokes we make about the VA (myself included), a study last year found its care was on par (or even better than) most hospitals .

I’m not saying the VA is perfect. All of us who worked there can think of times it wasn’t. But we also remember plenty of issues we’ve had at other places we’ve practiced, too.

Maybe it’s time to stop laughing at the VA and realize they’re doing something right — and learn from it to make healthcare better at the other 6,000 or so hospitals in the U.S.
 

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

Officials at Dana-Farber Cancer Institute are moving to retract at least six published research papers and correct 31 others amid allegations of data manipulation.

News of the investigation follows a blog post by British molecular biologist Sholto David, MD, who flagged almost 60 papers published between 1997 and 2017 that contained image manipulation and other errors. Some of the papers were published by Dana-Farber’s chief executive officer, Laurie Glimcher, MD, and chief operating officer, William Hahn, MD, on topics including multiple myeloma and immune cells.

Mr. David, who blogs about research integrity, highlighted numerous errors and irregularities, including copying and pasting images across multiple experiments to represent different days within the same experiment, sometimes rotating or stretching images.

In one case, Mr. David equated the manipulation with tactics used by “hapless Chinese papermills” and concluded that “a swathe of research coming out of [Dana-Farber] authored by the most senior researchers and managers appears to be hopelessly corrupt with errors that are obvious from just a cursory reading the papers.” 

“Imagine what mistakes might be found in the raw data if anyone was allowed to look!” he wrote.

Barrett Rollins, MD, PhD, Dana-Farber Cancer Institute’s research integrity officer, declined to comment on whether the errors represent scientific misconduct, according to STAT. Rollins told ScienceInsider that the “presence of image discrepancies in a paper is not evidence of an author’s intent to deceive.” 

Access to new artificial intelligence tools is making it easier for data sleuths, like Mr. David, to unearth data manipulation and errors. 

The current investigation closely follows two other investigations into the published work of Harvard University’s former president, Claudine Gay, and Stanford University’s former president, Marc Tessier-Lavigne, which led both to resign their posts. 

A version of this article appeared on Medscape.com.

Officials at Dana-Farber Cancer Institute are moving to retract at least six published research papers and correct 31 others amid allegations of data manipulation.

News of the investigation follows a blog post by British molecular biologist Sholto David, MD, who flagged almost 60 papers published between 1997 and 2017 that contained image manipulation and other errors. Some of the papers were published by Dana-Farber’s chief executive officer, Laurie Glimcher, MD, and chief operating officer, William Hahn, MD, on topics including multiple myeloma and immune cells.

Mr. David, who blogs about research integrity, highlighted numerous errors and irregularities, including copying and pasting images across multiple experiments to represent different days within the same experiment, sometimes rotating or stretching images.

In one case, Mr. David equated the manipulation with tactics used by “hapless Chinese papermills” and concluded that “a swathe of research coming out of [Dana-Farber] authored by the most senior researchers and managers appears to be hopelessly corrupt with errors that are obvious from just a cursory reading the papers.” 

“Imagine what mistakes might be found in the raw data if anyone was allowed to look!” he wrote.

Barrett Rollins, MD, PhD, Dana-Farber Cancer Institute’s research integrity officer, declined to comment on whether the errors represent scientific misconduct, according to STAT. Rollins told ScienceInsider that the “presence of image discrepancies in a paper is not evidence of an author’s intent to deceive.” 

Access to new artificial intelligence tools is making it easier for data sleuths, like Mr. David, to unearth data manipulation and errors. 

The current investigation closely follows two other investigations into the published work of Harvard University’s former president, Claudine Gay, and Stanford University’s former president, Marc Tessier-Lavigne, which led both to resign their posts. 

A version of this article appeared on Medscape.com.

Officials at Dana-Farber Cancer Institute are moving to retract at least six published research papers and correct 31 others amid allegations of data manipulation.

News of the investigation follows a blog post by British molecular biologist Sholto David, MD, who flagged almost 60 papers published between 1997 and 2017 that contained image manipulation and other errors. Some of the papers were published by Dana-Farber’s chief executive officer, Laurie Glimcher, MD, and chief operating officer, William Hahn, MD, on topics including multiple myeloma and immune cells.

Mr. David, who blogs about research integrity, highlighted numerous errors and irregularities, including copying and pasting images across multiple experiments to represent different days within the same experiment, sometimes rotating or stretching images.

In one case, Mr. David equated the manipulation with tactics used by “hapless Chinese papermills” and concluded that “a swathe of research coming out of [Dana-Farber] authored by the most senior researchers and managers appears to be hopelessly corrupt with errors that are obvious from just a cursory reading the papers.” 

“Imagine what mistakes might be found in the raw data if anyone was allowed to look!” he wrote.

Barrett Rollins, MD, PhD, Dana-Farber Cancer Institute’s research integrity officer, declined to comment on whether the errors represent scientific misconduct, according to STAT. Rollins told ScienceInsider that the “presence of image discrepancies in a paper is not evidence of an author’s intent to deceive.” 

Access to new artificial intelligence tools is making it easier for data sleuths, like Mr. David, to unearth data manipulation and errors. 

The current investigation closely follows two other investigations into the published work of Harvard University’s former president, Claudine Gay, and Stanford University’s former president, Marc Tessier-Lavigne, which led both to resign their posts. 

A version of this article appeared on Medscape.com.

Adults with posttraumatic stress disorder (PTSD) have smaller cerebellums than unaffected adults, suggesting that this part of the brain may be a potential therapeutic target.

According to recent research on more than 4000 adults, cerebellum volume was significantly smaller (by about 2%) in those with PTSD than in trauma-exposed and trauma-naive controls without PTSD.

“The differences were largely within the posterior lobe, where a lot of the more cognitive functions attributed to the cerebellum seem to localize, as well as the vermis, which is linked to a lot of emotional processing functions,” lead author Ashley Huggins, PhD, said in a news release.

“If we know what areas are implicated, then we can start to focus interventions like brain stimulation on the cerebellum and potentially improve treatment outcomes,” said Dr. Huggins, who worked on the study while a postdoctoral researcher in the lab of Rajendra A. Morey, MD, at Duke University, Durham, North Carolina, and is now at the University of Arizona, Tucson.

While the cerebellum is known for its role in coordinating movement and balance, it also plays a key role in emotions and memory, which are affected by PTSD.

Smaller cerebellar volume has been observed in some adult and pediatric populations with PTSD.

However, those studies have been limited by either small sample sizes, the failure to consider key neuroanatomical subdivisions of the cerebellum, or a focus on certain populations such as veterans of sexual assault victims with PTSD.

To overcome these limitations, the researchers conducted a mega-analysis of total and subregional cerebellar volumes in a large, multicohort dataset from the Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA)-Psychiatric Genomics Consortium PTSD workgroup that was published online on January 10, 2024, in Molecular Psychiatry.

They employed a novel, standardized ENIGMA cerebellum parcellation protocol to quantify cerebellar lobule volumes using structural MRI data from 1642 adults with PTSD and 2573 healthy controls without PTSD (88% trauma-exposed and 12% trauma-naive).

After adjustment for age, gender, and total intracranial volume, PTSD was associated with significant gray and white matter reductions of the cerebellum.

People with PTSD demonstrated smaller total cerebellum volume as well as reduced volume in subregions primarily within the posterior cerebellum, vermis, and flocculonodular cerebellum than controls.

In general, PTSD severity was more robustly associated with cerebellar volume differences than PTSD diagnosis.

Focusing purely on a “yes-or-no” categorical diagnosis didn’t always provide the clearest picture. “When we looked at PTSD severity, people who had more severe forms of the disorder had an even smaller cerebellar volume,” Dr. Huggins explained in the news release.

Novel Treatment Target

These findings add to “an emerging literature that underscores the relevance of cerebellar structure in the pathophysiology of PTSD,” the researchers noted.

They caution that despite the significant findings suggesting associations between PTSD and smaller cerebellar volumes, effect sizes were small. “As such, it is unlikely that structural cerebellar volumes alone will provide a clinically useful biomarker (eg, for individual-level prediction).”

Nonetheless, the study highlights the cerebellum as a “novel treatment target that may be leveraged to improve treatment outcomes for PTSD,” they wrote.

They noted that prior work has shown that the cerebellum is sensitive to external modulation. For example, noninvasive brain stimulation of the cerebellum has been shown to modulate cognitive, emotional, and social processes commonly disrupted in PTSD.

Commenting on this research, Cyrus A. Raji, MD, PhD, associate professor of radiology and neurology at Washington University in St. Louis, noted that this “large neuroimaging study links PTSD to cerebellar volume loss.”

“However, PTSD and traumatic brain injury frequently co-occur, and PTSD also frequently arises after TBI. Additionally, TBI is strongly linked to cerebellar volume loss,” Dr. Raji pointed out.

“Future studies need to better delineate volume loss from these conditions, especially when they are comorbid, though the expectation is these effects would be additive with TBI being the initial and most severe driving force,” Dr. Raji added.

The research had no commercial funding. Author disclosures are listed with the original article. Dr. Raji is a consultant for Brainreader, Apollo Health, Pacific Neuroscience Foundation, and Neurevolution Medicine LLC.
 

A version of this article appears on Medscape.com.

Adults with posttraumatic stress disorder (PTSD) have smaller cerebellums than unaffected adults, suggesting that this part of the brain may be a potential therapeutic target.

According to recent research on more than 4000 adults, cerebellum volume was significantly smaller (by about 2%) in those with PTSD than in trauma-exposed and trauma-naive controls without PTSD.

“The differences were largely within the posterior lobe, where a lot of the more cognitive functions attributed to the cerebellum seem to localize, as well as the vermis, which is linked to a lot of emotional processing functions,” lead author Ashley Huggins, PhD, said in a news release.

“If we know what areas are implicated, then we can start to focus interventions like brain stimulation on the cerebellum and potentially improve treatment outcomes,” said Dr. Huggins, who worked on the study while a postdoctoral researcher in the lab of Rajendra A. Morey, MD, at Duke University, Durham, North Carolina, and is now at the University of Arizona, Tucson.

While the cerebellum is known for its role in coordinating movement and balance, it also plays a key role in emotions and memory, which are affected by PTSD.

Smaller cerebellar volume has been observed in some adult and pediatric populations with PTSD.

However, those studies have been limited by either small sample sizes, the failure to consider key neuroanatomical subdivisions of the cerebellum, or a focus on certain populations such as veterans of sexual assault victims with PTSD.

To overcome these limitations, the researchers conducted a mega-analysis of total and subregional cerebellar volumes in a large, multicohort dataset from the Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA)-Psychiatric Genomics Consortium PTSD workgroup that was published online on January 10, 2024, in Molecular Psychiatry.

They employed a novel, standardized ENIGMA cerebellum parcellation protocol to quantify cerebellar lobule volumes using structural MRI data from 1642 adults with PTSD and 2573 healthy controls without PTSD (88% trauma-exposed and 12% trauma-naive).

After adjustment for age, gender, and total intracranial volume, PTSD was associated with significant gray and white matter reductions of the cerebellum.

People with PTSD demonstrated smaller total cerebellum volume as well as reduced volume in subregions primarily within the posterior cerebellum, vermis, and flocculonodular cerebellum than controls.

In general, PTSD severity was more robustly associated with cerebellar volume differences than PTSD diagnosis.

Focusing purely on a “yes-or-no” categorical diagnosis didn’t always provide the clearest picture. “When we looked at PTSD severity, people who had more severe forms of the disorder had an even smaller cerebellar volume,” Dr. Huggins explained in the news release.

Novel Treatment Target

These findings add to “an emerging literature that underscores the relevance of cerebellar structure in the pathophysiology of PTSD,” the researchers noted.

They caution that despite the significant findings suggesting associations between PTSD and smaller cerebellar volumes, effect sizes were small. “As such, it is unlikely that structural cerebellar volumes alone will provide a clinically useful biomarker (eg, for individual-level prediction).”

Nonetheless, the study highlights the cerebellum as a “novel treatment target that may be leveraged to improve treatment outcomes for PTSD,” they wrote.

They noted that prior work has shown that the cerebellum is sensitive to external modulation. For example, noninvasive brain stimulation of the cerebellum has been shown to modulate cognitive, emotional, and social processes commonly disrupted in PTSD.

Commenting on this research, Cyrus A. Raji, MD, PhD, associate professor of radiology and neurology at Washington University in St. Louis, noted that this “large neuroimaging study links PTSD to cerebellar volume loss.”

“However, PTSD and traumatic brain injury frequently co-occur, and PTSD also frequently arises after TBI. Additionally, TBI is strongly linked to cerebellar volume loss,” Dr. Raji pointed out.

“Future studies need to better delineate volume loss from these conditions, especially when they are comorbid, though the expectation is these effects would be additive with TBI being the initial and most severe driving force,” Dr. Raji added.

The research had no commercial funding. Author disclosures are listed with the original article. Dr. Raji is a consultant for Brainreader, Apollo Health, Pacific Neuroscience Foundation, and Neurevolution Medicine LLC.
 

A version of this article appears on Medscape.com.

Adults with posttraumatic stress disorder (PTSD) have smaller cerebellums than unaffected adults, suggesting that this part of the brain may be a potential therapeutic target.

According to recent research on more than 4000 adults, cerebellum volume was significantly smaller (by about 2%) in those with PTSD than in trauma-exposed and trauma-naive controls without PTSD.

“The differences were largely within the posterior lobe, where a lot of the more cognitive functions attributed to the cerebellum seem to localize, as well as the vermis, which is linked to a lot of emotional processing functions,” lead author Ashley Huggins, PhD, said in a news release.

“If we know what areas are implicated, then we can start to focus interventions like brain stimulation on the cerebellum and potentially improve treatment outcomes,” said Dr. Huggins, who worked on the study while a postdoctoral researcher in the lab of Rajendra A. Morey, MD, at Duke University, Durham, North Carolina, and is now at the University of Arizona, Tucson.

While the cerebellum is known for its role in coordinating movement and balance, it also plays a key role in emotions and memory, which are affected by PTSD.

Smaller cerebellar volume has been observed in some adult and pediatric populations with PTSD.

However, those studies have been limited by either small sample sizes, the failure to consider key neuroanatomical subdivisions of the cerebellum, or a focus on certain populations such as veterans of sexual assault victims with PTSD.

To overcome these limitations, the researchers conducted a mega-analysis of total and subregional cerebellar volumes in a large, multicohort dataset from the Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA)-Psychiatric Genomics Consortium PTSD workgroup that was published online on January 10, 2024, in Molecular Psychiatry.

They employed a novel, standardized ENIGMA cerebellum parcellation protocol to quantify cerebellar lobule volumes using structural MRI data from 1642 adults with PTSD and 2573 healthy controls without PTSD (88% trauma-exposed and 12% trauma-naive).

After adjustment for age, gender, and total intracranial volume, PTSD was associated with significant gray and white matter reductions of the cerebellum.

People with PTSD demonstrated smaller total cerebellum volume as well as reduced volume in subregions primarily within the posterior cerebellum, vermis, and flocculonodular cerebellum than controls.

In general, PTSD severity was more robustly associated with cerebellar volume differences than PTSD diagnosis.

Focusing purely on a “yes-or-no” categorical diagnosis didn’t always provide the clearest picture. “When we looked at PTSD severity, people who had more severe forms of the disorder had an even smaller cerebellar volume,” Dr. Huggins explained in the news release.

Novel Treatment Target

These findings add to “an emerging literature that underscores the relevance of cerebellar structure in the pathophysiology of PTSD,” the researchers noted.

They caution that despite the significant findings suggesting associations between PTSD and smaller cerebellar volumes, effect sizes were small. “As such, it is unlikely that structural cerebellar volumes alone will provide a clinically useful biomarker (eg, for individual-level prediction).”

Nonetheless, the study highlights the cerebellum as a “novel treatment target that may be leveraged to improve treatment outcomes for PTSD,” they wrote.

They noted that prior work has shown that the cerebellum is sensitive to external modulation. For example, noninvasive brain stimulation of the cerebellum has been shown to modulate cognitive, emotional, and social processes commonly disrupted in PTSD.

Commenting on this research, Cyrus A. Raji, MD, PhD, associate professor of radiology and neurology at Washington University in St. Louis, noted that this “large neuroimaging study links PTSD to cerebellar volume loss.”

“However, PTSD and traumatic brain injury frequently co-occur, and PTSD also frequently arises after TBI. Additionally, TBI is strongly linked to cerebellar volume loss,” Dr. Raji pointed out.

“Future studies need to better delineate volume loss from these conditions, especially when they are comorbid, though the expectation is these effects would be additive with TBI being the initial and most severe driving force,” Dr. Raji added.

The research had no commercial funding. Author disclosures are listed with the original article. Dr. Raji is a consultant for Brainreader, Apollo Health, Pacific Neuroscience Foundation, and Neurevolution Medicine LLC.
 

A version of this article appears on Medscape.com.

Mr. Smith was once a nice guy.

These days, unfortunately, he’s anything but. The ravages of a neurodegenerative disease have left him demented, impulsive, and agitated.

His family is trying to find placement for him, and in the meantime I’m doing my best to keep his behavior controlled. Like many things in medicine, this is as much art as science. A tablet of this, a capsule of that, increase this slightly, add something for PRN use ... a witch’s brew of modern medicine.

Because of his worsening, his wife was calling us several times a week with updates, not in an annoying way but in an “I need help” way. I began answering the phone myself if I saw her number come up, because it was easier and faster for me to deal with her directly, and I knew she wasn’t calling for fun.

A few months ago I stopped a medication that didn’t seem to be doing much and started a different one.

And then things went quiet. His wife’s calls went from 3-4 a week to none.

This worried me. I mean, maybe the new medicine was working. ... but the sudden silence was deafening.

One week went by, then two ... I did a Google search to make sure he and his wife hadn’t died or been in the news.

Of course, I could have picked up the phone and called his wife, but why tempt fate?

Three weeks ... I was sure my MA, who handles far more calls than I do, had probably noticed this, too.

It would have been easy to mention it, but even with 16 years of school and 5 years of medical training, not to mention 3,000-4,000 years of hard-earned science behind me, there was the old grade school notion of jinxing myself. To say something is to invite trouble.

Four weeks. Finally, his wife called in and reached my MA. The medication had been working, but now was wearing off and the dose needed to be adjusted. So we did that.

Afterward I mentioned the time lapse to my MA, that I’d been afraid of jinxing it by saying something to her, and she told me she’d been thinking the same thing.

Funny when you think about it. We’re both educated people, believers in science, and (I hope) intelligent. We’re living in a (by human standards) technologically advanced time.

Yet, the old superstitions are still there, the idea that we somehow have magical control over time, space, random chance, and the actions of others by not talking about a phone call (or the lack of one).

Surprisingly (or maybe not), this is pretty normal. When on call we never say “quiet,” for fear of enraging the mysterious Call Gods. If needed, we use “the Q word.”

We still try not to walk under ladders, avoid stepping on sidewalk cracks, carry good luck charms, cross fingers, and fight over wishbones.

Superstitions such as saying “bless you” or “gesundheit” when someone sneezes are so ingrained into us that they’re now part of good manners and polite society.

I’ve worked in quite a few hospitals over the years. Not one of them had a room on any floor that ended in 13, always jumping from 12 to 14.

Civilization is roughly 10,000-15,000 years old. We have the internet and can travel to (relatively nearby) space and back. We have probes exploring — and even leaving — our solar system.

But it’s one thing to say a superstition is silly. It’s another to actually convince your primeval self of it.

I’m going to knock on wood now.

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

Mr. Smith was once a nice guy.

These days, unfortunately, he’s anything but. The ravages of a neurodegenerative disease have left him demented, impulsive, and agitated.

His family is trying to find placement for him, and in the meantime I’m doing my best to keep his behavior controlled. Like many things in medicine, this is as much art as science. A tablet of this, a capsule of that, increase this slightly, add something for PRN use ... a witch’s brew of modern medicine.

Because of his worsening, his wife was calling us several times a week with updates, not in an annoying way but in an “I need help” way. I began answering the phone myself if I saw her number come up, because it was easier and faster for me to deal with her directly, and I knew she wasn’t calling for fun.

A few months ago I stopped a medication that didn’t seem to be doing much and started a different one.

And then things went quiet. His wife’s calls went from 3-4 a week to none.

This worried me. I mean, maybe the new medicine was working. ... but the sudden silence was deafening.

One week went by, then two ... I did a Google search to make sure he and his wife hadn’t died or been in the news.

Of course, I could have picked up the phone and called his wife, but why tempt fate?

Three weeks ... I was sure my MA, who handles far more calls than I do, had probably noticed this, too.

It would have been easy to mention it, but even with 16 years of school and 5 years of medical training, not to mention 3,000-4,000 years of hard-earned science behind me, there was the old grade school notion of jinxing myself. To say something is to invite trouble.

Four weeks. Finally, his wife called in and reached my MA. The medication had been working, but now was wearing off and the dose needed to be adjusted. So we did that.

Afterward I mentioned the time lapse to my MA, that I’d been afraid of jinxing it by saying something to her, and she told me she’d been thinking the same thing.

Funny when you think about it. We’re both educated people, believers in science, and (I hope) intelligent. We’re living in a (by human standards) technologically advanced time.

Yet, the old superstitions are still there, the idea that we somehow have magical control over time, space, random chance, and the actions of others by not talking about a phone call (or the lack of one).

Surprisingly (or maybe not), this is pretty normal. When on call we never say “quiet,” for fear of enraging the mysterious Call Gods. If needed, we use “the Q word.”

We still try not to walk under ladders, avoid stepping on sidewalk cracks, carry good luck charms, cross fingers, and fight over wishbones.

Superstitions such as saying “bless you” or “gesundheit” when someone sneezes are so ingrained into us that they’re now part of good manners and polite society.

I’ve worked in quite a few hospitals over the years. Not one of them had a room on any floor that ended in 13, always jumping from 12 to 14.

Civilization is roughly 10,000-15,000 years old. We have the internet and can travel to (relatively nearby) space and back. We have probes exploring — and even leaving — our solar system.

But it’s one thing to say a superstition is silly. It’s another to actually convince your primeval self of it.

I’m going to knock on wood now.

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

Mr. Smith was once a nice guy.

These days, unfortunately, he’s anything but. The ravages of a neurodegenerative disease have left him demented, impulsive, and agitated.

His family is trying to find placement for him, and in the meantime I’m doing my best to keep his behavior controlled. Like many things in medicine, this is as much art as science. A tablet of this, a capsule of that, increase this slightly, add something for PRN use ... a witch’s brew of modern medicine.

Because of his worsening, his wife was calling us several times a week with updates, not in an annoying way but in an “I need help” way. I began answering the phone myself if I saw her number come up, because it was easier and faster for me to deal with her directly, and I knew she wasn’t calling for fun.

A few months ago I stopped a medication that didn’t seem to be doing much and started a different one.

And then things went quiet. His wife’s calls went from 3-4 a week to none.

This worried me. I mean, maybe the new medicine was working. ... but the sudden silence was deafening.

One week went by, then two ... I did a Google search to make sure he and his wife hadn’t died or been in the news.

Of course, I could have picked up the phone and called his wife, but why tempt fate?

Three weeks ... I was sure my MA, who handles far more calls than I do, had probably noticed this, too.

It would have been easy to mention it, but even with 16 years of school and 5 years of medical training, not to mention 3,000-4,000 years of hard-earned science behind me, there was the old grade school notion of jinxing myself. To say something is to invite trouble.

Four weeks. Finally, his wife called in and reached my MA. The medication had been working, but now was wearing off and the dose needed to be adjusted. So we did that.

Afterward I mentioned the time lapse to my MA, that I’d been afraid of jinxing it by saying something to her, and she told me she’d been thinking the same thing.

Funny when you think about it. We’re both educated people, believers in science, and (I hope) intelligent. We’re living in a (by human standards) technologically advanced time.

Yet, the old superstitions are still there, the idea that we somehow have magical control over time, space, random chance, and the actions of others by not talking about a phone call (or the lack of one).

Surprisingly (or maybe not), this is pretty normal. When on call we never say “quiet,” for fear of enraging the mysterious Call Gods. If needed, we use “the Q word.”

We still try not to walk under ladders, avoid stepping on sidewalk cracks, carry good luck charms, cross fingers, and fight over wishbones.

Superstitions such as saying “bless you” or “gesundheit” when someone sneezes are so ingrained into us that they’re now part of good manners and polite society.

I’ve worked in quite a few hospitals over the years. Not one of them had a room on any floor that ended in 13, always jumping from 12 to 14.

Civilization is roughly 10,000-15,000 years old. We have the internet and can travel to (relatively nearby) space and back. We have probes exploring — and even leaving — our solar system.

But it’s one thing to say a superstition is silly. It’s another to actually convince your primeval self of it.

I’m going to knock on wood now.

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