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'Living brain implants' may restore stroke mobility
Researchers behind the ongoing Cortimo trial successfully performed a procedure on a patient 2 years removed from a stroke, in which microelectrode arrays were implanted into his brain to decode signals driving motor function. These signals then allowed him to operate a powered brace worn on his paralyzed arm.
This news organization spoke with the trial’s principal investigator, Mijail D. Serruya, MD, PhD, an assistant professor of neurology at Thomas Jefferson University Hospital, Philadelphia, about the trial’s initial findings, what this technology may ultimately look like, and the implications for stroke patients in knowing that restorative interventions may be on the horizon.
How did you first get involved with implanting electrodes to help stroke patients with recovery?
I was involved in the first human application of a microelectrode array in a young man who had quadriplegia because of a spinal cord injury. We showed that we could record signal directly from his motor cortex and use it to move a cursor on the screen, and open and close a prosthetic hand and arm.
I was naive and thought that this would soon be a widely available clinical medical device. Now it’s nearly 15 years later, and while it certainly has been safely used in multiple labs to record signals from people with spinal cord injury, amyotrophic lateral sclerosis (ALS), or locked-in syndrome from a brain stem stroke, it still requires a team of technicians and a percutaneous connector. It really has not gotten out of the university.
A few years ago I spoke with Robert Rosenwasser, MD, chairman of the department of neurosurgery at Thomas Jefferson, who runs a very busy stroke center and performed the surgery in this trial. We put our heads together and said: “Maybe the time is now to see whether we can move this technology to this much more prevalent condition of a hemispheric stroke.” And that’s what we did.
How did the idea of using computer brain electrode interfaces begin?
Around 20 years ago, if you had someone who had severe paralysis and you wanted to restore movement, the question was, where can you get a good control signal from? Obviously, if someone can talk, they can use a voice-actuated system with speech recognition and maybe you can track their eye gaze. But if they’re trying to move their limbs, you want a motor control signal.
In someone who has end-stage ALS or a brain stem stroke, you can’t even record residual muscle activity; you have almost nothing to work with. The only thing left is to try to record directly from the brain itself.
It’s important to clarify that brain-computer interfaces are not necessarily stimulating the brain to inject the signal. They’re just recording the endogenous activity that the brain makes. In comparison, a deep brain stimulator is usually not recording anything; it’s just delivering energy to the brain and hoping for the best.
But what we’re doing is asking, if the person is trying to move the paralyzed limb but can’t, can we get to the source of the signal and then do something with it?
What’s the process for measuring that in, for example, someone who has a localized lesion in the motor cortex?
The first step is a scan. People have been doing functional MRI on patients who have had a stroke as long as we’ve had fMRI. We know that people can actually activate on MRI areas of their brain around the stroke, but obviously not in the stroke because it’s been lesioned. However, we do know that the circuit adjacent to it and other regions do appear able to be modulated.
So by having a person either imagine trying to do what they want to do or doing what they can do, if they have some tiny residual movement, you can then identify a kind of hot spot on the fMRI where the brain gobbles up all the oxygen because it’s so active. Then that gives you an anatomical target for the surgeon to place the electrode arrays.
The Cortimo trial’s enticing findings
What are the most striking results that you’ve seen so far with the device?
The first thing is that we were able to get such recordings at all. We knew from fMRIs that there were fluctuations in oxygen changing when the person was trying to do something they couldn’t do. But nobody knew that you would see this whole population of individual neurons chattering away when you place these electrode arrays in the motor cortex right next to the stroke, and make sense of what we’re recording.
Obviously, that’s very encouraging and gives us hope that many months or years after a stroke, people’s brains are able to maintain this representation of all these different movements and plans. It’s almost like it’s trapped on the other side of the stroke and some of the signals can’t get out.
The other discovery we’re pleased with is that we can actually decode signals in real time and the person can use it to do something, such as trigger the brain to open and close the hand. That’s very different from all the prior research with brain array interfaces.
Furthermore, the gentleman who participated actually had strokes in other parts of his brain affecting his vision; he had homonymous hemianopia. That raised the question of what happens if you affect parts of the brain that have to do with attention and visual processing. Could a system like this work? And again, the answer appears to be yes.
What are the next steps for this technology before it can potentially become available in the clinic?
For this to work, the system clearly has to be fully implantable. What we used was percutaneous. The risk-benefit may be acceptable for someone who has quadriplegia because of, for example, spinal cord injury or end-stage ALS who may already have a tracheostomy and a percutaneous endoscopic gastrostomy. But for someone who is hemiparetic and ambulatory, that may not be acceptable. And a fully implantable system would also have much better patient compliance.
Also, when you’re recording from lots and lots of individual brain cells at many, many samples a second on many, many channels, it’s certainly an engineering challenge. It’s not just a single channel that you occasionally query; it’s hundreds of thousands of channels of this complicated data stream.
But these are solvable challenges. People have been making a lot of progress. It’s really a matter of funding and the engineering expertise, rather than some sort of fundamental scientific breakthrough.
With that said, I think it could be within the next 5-10 years that we could actually have a product that expands the toolbox of what can be done for patients who’ve had a stroke, if they’re motivated and there’s no real contraindication.
Creating a novel device
On that point, are you partnering with engineering and technology companies?
The hope is that we and other groups working on this can do for the interface sort of what Celera Genomics did for the Human Genome Project. By having enough interest and investment, you may be able to propel the field forward to widespread use rather than just a purely academic, lab-science type of project.
We are in discussion with different companies to see how we can move ahead with this, and we would be pleased to work with whomever is interested. It may be that different companies have different pieces of the puzzle – a better sensor or a better wireless transmitter.
The plan is to move as quickly as we can to a fully implantable system. And then the benchmark for any kind of clinical advancement is to do a prospective trial. With devices, if you can get a big enough effect size, then you sometimes don’t need quite as many patients to prove it. If paralysis is striking enough and you can reverse that, then you can convince the Food and Drug Administration of its safety and efficacy, and the various insurance companies, that it’s actually reasonable and necessary.
How long will an implantable device last?
That’s a key question and concern. If you have someone like our participant, who’s in his early 40s, will it keep working 10, 20, 30, 40 years? For the rest of his life? Deep brain stimulators and cochlear implants do function for those long durations, but their designs are quite different. There’s a macroelectrode that’s just delivering current, which is very different from listening in on this microscopic scale. There are different technical considerations.
One possible solution is to make the device out of living tissue, which is something I just wrote about with my colleague D. Kacy Cullen. Living electrodes and amplifiers may seem a bit like science fiction, but on the other hand, we have over a century of plastic surgeons, neurosurgeons, and orthopedic surgeons doing all kinds of complicated modifications of the body, moving nerves and vessels around. It makes you realize that, in a sense, they’ve already done living electrodes by doing a nerve transfer. So the question becomes whether we can refine that living electrode technology, which could then open up more possibilities.
Are there any final messages you’d like to share with clinician audience of this news organization?
Regardless of our specialty, we’re always telling our patients about the benefits of things like eating healthy, exercise, and sleep. Now we can point to the fact that, 2 years after stroke, all of these brain areas are still active, and devices that can potentially reverse and unparalyze your limbs may be available in the coming 5- or 10-plus years. That gives clinicians more justification to tell their patients to really stay on top of those things so that they can be in as optimal brain-mind health as possible to someday benefit from them.
Patients and their families need to be part of the conversation of where this is all going. That’s one thing that’s totally different for brain devices versus other devices, where a person’s psychological state doesn’t necessarily matter. But with a brain device, your mental state, psychosocial situation, exercise, sleep – the way you think about and approach it – actually changes to the structure of the brain pretty dramatically.
I don’t want to cause unreasonable hope that we’re going to snap our fingers and it’s going to be cured. But I do think it’s fair to raise a possibility as a way to say that keeping oneself really healthy is justified.
A version of this article first appeared on Medscape.com.
Researchers behind the ongoing Cortimo trial successfully performed a procedure on a patient 2 years removed from a stroke, in which microelectrode arrays were implanted into his brain to decode signals driving motor function. These signals then allowed him to operate a powered brace worn on his paralyzed arm.
This news organization spoke with the trial’s principal investigator, Mijail D. Serruya, MD, PhD, an assistant professor of neurology at Thomas Jefferson University Hospital, Philadelphia, about the trial’s initial findings, what this technology may ultimately look like, and the implications for stroke patients in knowing that restorative interventions may be on the horizon.
How did you first get involved with implanting electrodes to help stroke patients with recovery?
I was involved in the first human application of a microelectrode array in a young man who had quadriplegia because of a spinal cord injury. We showed that we could record signal directly from his motor cortex and use it to move a cursor on the screen, and open and close a prosthetic hand and arm.
I was naive and thought that this would soon be a widely available clinical medical device. Now it’s nearly 15 years later, and while it certainly has been safely used in multiple labs to record signals from people with spinal cord injury, amyotrophic lateral sclerosis (ALS), or locked-in syndrome from a brain stem stroke, it still requires a team of technicians and a percutaneous connector. It really has not gotten out of the university.
A few years ago I spoke with Robert Rosenwasser, MD, chairman of the department of neurosurgery at Thomas Jefferson, who runs a very busy stroke center and performed the surgery in this trial. We put our heads together and said: “Maybe the time is now to see whether we can move this technology to this much more prevalent condition of a hemispheric stroke.” And that’s what we did.
How did the idea of using computer brain electrode interfaces begin?
Around 20 years ago, if you had someone who had severe paralysis and you wanted to restore movement, the question was, where can you get a good control signal from? Obviously, if someone can talk, they can use a voice-actuated system with speech recognition and maybe you can track their eye gaze. But if they’re trying to move their limbs, you want a motor control signal.
In someone who has end-stage ALS or a brain stem stroke, you can’t even record residual muscle activity; you have almost nothing to work with. The only thing left is to try to record directly from the brain itself.
It’s important to clarify that brain-computer interfaces are not necessarily stimulating the brain to inject the signal. They’re just recording the endogenous activity that the brain makes. In comparison, a deep brain stimulator is usually not recording anything; it’s just delivering energy to the brain and hoping for the best.
But what we’re doing is asking, if the person is trying to move the paralyzed limb but can’t, can we get to the source of the signal and then do something with it?
What’s the process for measuring that in, for example, someone who has a localized lesion in the motor cortex?
The first step is a scan. People have been doing functional MRI on patients who have had a stroke as long as we’ve had fMRI. We know that people can actually activate on MRI areas of their brain around the stroke, but obviously not in the stroke because it’s been lesioned. However, we do know that the circuit adjacent to it and other regions do appear able to be modulated.
So by having a person either imagine trying to do what they want to do or doing what they can do, if they have some tiny residual movement, you can then identify a kind of hot spot on the fMRI where the brain gobbles up all the oxygen because it’s so active. Then that gives you an anatomical target for the surgeon to place the electrode arrays.
The Cortimo trial’s enticing findings
What are the most striking results that you’ve seen so far with the device?
The first thing is that we were able to get such recordings at all. We knew from fMRIs that there were fluctuations in oxygen changing when the person was trying to do something they couldn’t do. But nobody knew that you would see this whole population of individual neurons chattering away when you place these electrode arrays in the motor cortex right next to the stroke, and make sense of what we’re recording.
Obviously, that’s very encouraging and gives us hope that many months or years after a stroke, people’s brains are able to maintain this representation of all these different movements and plans. It’s almost like it’s trapped on the other side of the stroke and some of the signals can’t get out.
The other discovery we’re pleased with is that we can actually decode signals in real time and the person can use it to do something, such as trigger the brain to open and close the hand. That’s very different from all the prior research with brain array interfaces.
Furthermore, the gentleman who participated actually had strokes in other parts of his brain affecting his vision; he had homonymous hemianopia. That raised the question of what happens if you affect parts of the brain that have to do with attention and visual processing. Could a system like this work? And again, the answer appears to be yes.
What are the next steps for this technology before it can potentially become available in the clinic?
For this to work, the system clearly has to be fully implantable. What we used was percutaneous. The risk-benefit may be acceptable for someone who has quadriplegia because of, for example, spinal cord injury or end-stage ALS who may already have a tracheostomy and a percutaneous endoscopic gastrostomy. But for someone who is hemiparetic and ambulatory, that may not be acceptable. And a fully implantable system would also have much better patient compliance.
Also, when you’re recording from lots and lots of individual brain cells at many, many samples a second on many, many channels, it’s certainly an engineering challenge. It’s not just a single channel that you occasionally query; it’s hundreds of thousands of channels of this complicated data stream.
But these are solvable challenges. People have been making a lot of progress. It’s really a matter of funding and the engineering expertise, rather than some sort of fundamental scientific breakthrough.
With that said, I think it could be within the next 5-10 years that we could actually have a product that expands the toolbox of what can be done for patients who’ve had a stroke, if they’re motivated and there’s no real contraindication.
Creating a novel device
On that point, are you partnering with engineering and technology companies?
The hope is that we and other groups working on this can do for the interface sort of what Celera Genomics did for the Human Genome Project. By having enough interest and investment, you may be able to propel the field forward to widespread use rather than just a purely academic, lab-science type of project.
We are in discussion with different companies to see how we can move ahead with this, and we would be pleased to work with whomever is interested. It may be that different companies have different pieces of the puzzle – a better sensor or a better wireless transmitter.
The plan is to move as quickly as we can to a fully implantable system. And then the benchmark for any kind of clinical advancement is to do a prospective trial. With devices, if you can get a big enough effect size, then you sometimes don’t need quite as many patients to prove it. If paralysis is striking enough and you can reverse that, then you can convince the Food and Drug Administration of its safety and efficacy, and the various insurance companies, that it’s actually reasonable and necessary.
How long will an implantable device last?
That’s a key question and concern. If you have someone like our participant, who’s in his early 40s, will it keep working 10, 20, 30, 40 years? For the rest of his life? Deep brain stimulators and cochlear implants do function for those long durations, but their designs are quite different. There’s a macroelectrode that’s just delivering current, which is very different from listening in on this microscopic scale. There are different technical considerations.
One possible solution is to make the device out of living tissue, which is something I just wrote about with my colleague D. Kacy Cullen. Living electrodes and amplifiers may seem a bit like science fiction, but on the other hand, we have over a century of plastic surgeons, neurosurgeons, and orthopedic surgeons doing all kinds of complicated modifications of the body, moving nerves and vessels around. It makes you realize that, in a sense, they’ve already done living electrodes by doing a nerve transfer. So the question becomes whether we can refine that living electrode technology, which could then open up more possibilities.
Are there any final messages you’d like to share with clinician audience of this news organization?
Regardless of our specialty, we’re always telling our patients about the benefits of things like eating healthy, exercise, and sleep. Now we can point to the fact that, 2 years after stroke, all of these brain areas are still active, and devices that can potentially reverse and unparalyze your limbs may be available in the coming 5- or 10-plus years. That gives clinicians more justification to tell their patients to really stay on top of those things so that they can be in as optimal brain-mind health as possible to someday benefit from them.
Patients and their families need to be part of the conversation of where this is all going. That’s one thing that’s totally different for brain devices versus other devices, where a person’s psychological state doesn’t necessarily matter. But with a brain device, your mental state, psychosocial situation, exercise, sleep – the way you think about and approach it – actually changes to the structure of the brain pretty dramatically.
I don’t want to cause unreasonable hope that we’re going to snap our fingers and it’s going to be cured. But I do think it’s fair to raise a possibility as a way to say that keeping oneself really healthy is justified.
A version of this article first appeared on Medscape.com.
Researchers behind the ongoing Cortimo trial successfully performed a procedure on a patient 2 years removed from a stroke, in which microelectrode arrays were implanted into his brain to decode signals driving motor function. These signals then allowed him to operate a powered brace worn on his paralyzed arm.
This news organization spoke with the trial’s principal investigator, Mijail D. Serruya, MD, PhD, an assistant professor of neurology at Thomas Jefferson University Hospital, Philadelphia, about the trial’s initial findings, what this technology may ultimately look like, and the implications for stroke patients in knowing that restorative interventions may be on the horizon.
How did you first get involved with implanting electrodes to help stroke patients with recovery?
I was involved in the first human application of a microelectrode array in a young man who had quadriplegia because of a spinal cord injury. We showed that we could record signal directly from his motor cortex and use it to move a cursor on the screen, and open and close a prosthetic hand and arm.
I was naive and thought that this would soon be a widely available clinical medical device. Now it’s nearly 15 years later, and while it certainly has been safely used in multiple labs to record signals from people with spinal cord injury, amyotrophic lateral sclerosis (ALS), or locked-in syndrome from a brain stem stroke, it still requires a team of technicians and a percutaneous connector. It really has not gotten out of the university.
A few years ago I spoke with Robert Rosenwasser, MD, chairman of the department of neurosurgery at Thomas Jefferson, who runs a very busy stroke center and performed the surgery in this trial. We put our heads together and said: “Maybe the time is now to see whether we can move this technology to this much more prevalent condition of a hemispheric stroke.” And that’s what we did.
How did the idea of using computer brain electrode interfaces begin?
Around 20 years ago, if you had someone who had severe paralysis and you wanted to restore movement, the question was, where can you get a good control signal from? Obviously, if someone can talk, they can use a voice-actuated system with speech recognition and maybe you can track their eye gaze. But if they’re trying to move their limbs, you want a motor control signal.
In someone who has end-stage ALS or a brain stem stroke, you can’t even record residual muscle activity; you have almost nothing to work with. The only thing left is to try to record directly from the brain itself.
It’s important to clarify that brain-computer interfaces are not necessarily stimulating the brain to inject the signal. They’re just recording the endogenous activity that the brain makes. In comparison, a deep brain stimulator is usually not recording anything; it’s just delivering energy to the brain and hoping for the best.
But what we’re doing is asking, if the person is trying to move the paralyzed limb but can’t, can we get to the source of the signal and then do something with it?
What’s the process for measuring that in, for example, someone who has a localized lesion in the motor cortex?
The first step is a scan. People have been doing functional MRI on patients who have had a stroke as long as we’ve had fMRI. We know that people can actually activate on MRI areas of their brain around the stroke, but obviously not in the stroke because it’s been lesioned. However, we do know that the circuit adjacent to it and other regions do appear able to be modulated.
So by having a person either imagine trying to do what they want to do or doing what they can do, if they have some tiny residual movement, you can then identify a kind of hot spot on the fMRI where the brain gobbles up all the oxygen because it’s so active. Then that gives you an anatomical target for the surgeon to place the electrode arrays.
The Cortimo trial’s enticing findings
What are the most striking results that you’ve seen so far with the device?
The first thing is that we were able to get such recordings at all. We knew from fMRIs that there were fluctuations in oxygen changing when the person was trying to do something they couldn’t do. But nobody knew that you would see this whole population of individual neurons chattering away when you place these electrode arrays in the motor cortex right next to the stroke, and make sense of what we’re recording.
Obviously, that’s very encouraging and gives us hope that many months or years after a stroke, people’s brains are able to maintain this representation of all these different movements and plans. It’s almost like it’s trapped on the other side of the stroke and some of the signals can’t get out.
The other discovery we’re pleased with is that we can actually decode signals in real time and the person can use it to do something, such as trigger the brain to open and close the hand. That’s very different from all the prior research with brain array interfaces.
Furthermore, the gentleman who participated actually had strokes in other parts of his brain affecting his vision; he had homonymous hemianopia. That raised the question of what happens if you affect parts of the brain that have to do with attention and visual processing. Could a system like this work? And again, the answer appears to be yes.
What are the next steps for this technology before it can potentially become available in the clinic?
For this to work, the system clearly has to be fully implantable. What we used was percutaneous. The risk-benefit may be acceptable for someone who has quadriplegia because of, for example, spinal cord injury or end-stage ALS who may already have a tracheostomy and a percutaneous endoscopic gastrostomy. But for someone who is hemiparetic and ambulatory, that may not be acceptable. And a fully implantable system would also have much better patient compliance.
Also, when you’re recording from lots and lots of individual brain cells at many, many samples a second on many, many channels, it’s certainly an engineering challenge. It’s not just a single channel that you occasionally query; it’s hundreds of thousands of channels of this complicated data stream.
But these are solvable challenges. People have been making a lot of progress. It’s really a matter of funding and the engineering expertise, rather than some sort of fundamental scientific breakthrough.
With that said, I think it could be within the next 5-10 years that we could actually have a product that expands the toolbox of what can be done for patients who’ve had a stroke, if they’re motivated and there’s no real contraindication.
Creating a novel device
On that point, are you partnering with engineering and technology companies?
The hope is that we and other groups working on this can do for the interface sort of what Celera Genomics did for the Human Genome Project. By having enough interest and investment, you may be able to propel the field forward to widespread use rather than just a purely academic, lab-science type of project.
We are in discussion with different companies to see how we can move ahead with this, and we would be pleased to work with whomever is interested. It may be that different companies have different pieces of the puzzle – a better sensor or a better wireless transmitter.
The plan is to move as quickly as we can to a fully implantable system. And then the benchmark for any kind of clinical advancement is to do a prospective trial. With devices, if you can get a big enough effect size, then you sometimes don’t need quite as many patients to prove it. If paralysis is striking enough and you can reverse that, then you can convince the Food and Drug Administration of its safety and efficacy, and the various insurance companies, that it’s actually reasonable and necessary.
How long will an implantable device last?
That’s a key question and concern. If you have someone like our participant, who’s in his early 40s, will it keep working 10, 20, 30, 40 years? For the rest of his life? Deep brain stimulators and cochlear implants do function for those long durations, but their designs are quite different. There’s a macroelectrode that’s just delivering current, which is very different from listening in on this microscopic scale. There are different technical considerations.
One possible solution is to make the device out of living tissue, which is something I just wrote about with my colleague D. Kacy Cullen. Living electrodes and amplifiers may seem a bit like science fiction, but on the other hand, we have over a century of plastic surgeons, neurosurgeons, and orthopedic surgeons doing all kinds of complicated modifications of the body, moving nerves and vessels around. It makes you realize that, in a sense, they’ve already done living electrodes by doing a nerve transfer. So the question becomes whether we can refine that living electrode technology, which could then open up more possibilities.
Are there any final messages you’d like to share with clinician audience of this news organization?
Regardless of our specialty, we’re always telling our patients about the benefits of things like eating healthy, exercise, and sleep. Now we can point to the fact that, 2 years after stroke, all of these brain areas are still active, and devices that can potentially reverse and unparalyze your limbs may be available in the coming 5- or 10-plus years. That gives clinicians more justification to tell their patients to really stay on top of those things so that they can be in as optimal brain-mind health as possible to someday benefit from them.
Patients and their families need to be part of the conversation of where this is all going. That’s one thing that’s totally different for brain devices versus other devices, where a person’s psychological state doesn’t necessarily matter. But with a brain device, your mental state, psychosocial situation, exercise, sleep – the way you think about and approach it – actually changes to the structure of the brain pretty dramatically.
I don’t want to cause unreasonable hope that we’re going to snap our fingers and it’s going to be cured. But I do think it’s fair to raise a possibility as a way to say that keeping oneself really healthy is justified.
A version of this article first appeared on Medscape.com.
Core feature of frontotemporal dementia may aid diagnosis
(FTD) in findings that may help physicians make this difficult diagnosis that affects adults in their prime.
“The assessment of WMH can aid differential diagnosis of bvFTD [behavioral-variant FTD] against other neurodegenerative conditions in the absence of vascular risk factors, especially when considering their spatial distribution,” said senior author Ramón Landin-Romero, PhD, Appenzeller Neuroscience Fellow, Frontotemporal Dementia Research Group, University of Sydney.
“Clinicians can ask for specific sequences in routine MRI scans to visually detect WMH,” said Dr. Landin-Romero, who is also a senior lecturer in the School of Psychology and Brain and Mind Center.
The study was published online Feb. 17 in Neurology.
Difficult diagnosis
“FTD is a collection of unrecognized young-onset (before age 65) dementia syndromes that affect people in their prime,” said Dr. Landin-Romero. He added that heterogeneity in progression trajectories and symptoms, which can include changes in behavior and personality, language impairments, and psychosis, make it a difficult disease to diagnose.
“As such, our research was motivated by the need of sensitive and specific biomarkers of FTD, which are urgently needed to aid diagnosis, prognosis, and treatment development,” he said.
Previous research has been limited; there have only been a “handful” of cohort and case studies and studies involving individuals with mutations in one FTD-causative gene.
FTD is genetically and pathologically complex, and there has been no clear correlation between genetic mutations/underlying pathology and clinical presentation, Dr. Landin-Romero said.
WMH are common in older individuals and are linked to increased risk for cognitive impairment and dementia. Traditionally, they have been associated with vascular risk factors, such as smoking and diabetes. “But the presentation of WMH in FTD and its associations with the severity of symptoms and brain atrophy across FTD symptoms remains to be established,” said Dr. Landin-Romero.
Higher disease severity
To explore the possible association, the researchers studied 129 patients with either bvFTD (n = 64; mean age, 64 years) or Alzheimer’s disease (n = 65; mean age, 64.66 years).
Neuropsychological assessments, medical and neurologic examinations, clinical interview, and structural brain MRI were conducted for all patients, who were compared with 66 age-, sex-, and education-matched healthy control persons (mean age, 64.69 years).
Some participants in the FTD, Alzheimer’s disease, and healthy control groups (n = 54, 44, and 26, respectively) also underwent genetic screening. Postmortem pathology findings were available for a small number of FTD and Alzheimer’s disease participants (n = 13 and 5, respectively).
The medical history included lifestyle and cardiovascular risk factors, as well as other health and neurologic conditions and medication history. Hypertension, hypercholesterolemia, diabetes, and smoking were used to assess vascular risk.
The FTD and Alzheimer’s disease groups did not differ with regard to disease duration (3.55 years; standard deviation, 1.75, and 3.24 years; SD, 1.59, respectively). However, disease severity was significantly higher among those with FTD than among those with Alzheimer’s disease, as measured by the FTD Rating Scale Rasch score (–0.52; SD, 1.28, vs. 0.78; SD, 1.55; P < .001).
Compared with healthy controls, patients in the FTD and Alzheimer’s disease groups scored significantly lower on the Addenbrooke’s Cognitive Examination–Revised (ACE-R) or ACE-III scale. Patients with Alzheimer’s disease showed “disproportionately larger deficits” in memory and visuospatial processing, compared with those with FTD, whereas those with FTD performed significantly worse than those with Alzheimer’s disease in the fluency subdomain.
A larger number of patients in the FTD group screened positive for genetic abnormalities than in the Alzheimer’s disease group; no participants in the healthy control group had genetic mutations.
Unexpected findings
Mean WMH volume was significantly higher in participants with FTD than in participants with Alzheimer’s disease and in healthy controls (mean, 0.76 mL, 0.40 mL, and 0.12 mL respectively). These larger volumes contributed to greater disease severity and cortical atrophy. Moreover, disease severity was “found to be a strong predictor of WMH volume in FTD,” the authors stated. Among patients with FTD, WMH volumes did not differ significantly with regard to genetic mutation status or presence of strong family history.
After controlling for age, vascular risk did not significantly predict WMH volume in the FTD group (P = .16); however, that did not hold true in the Alzheimer’s disease group.
Increased WMH were associated with anterior brain regions in FTD and with posterior brain regions in Alzheimer’s disease. In both disorders, higher WMH volume in the corpus callosum was associated with poorer cognitive performance in the domain of attention.
“The spatial distribution of WMH mirrored patterns of brain atrophy in FTD and Alzheimer’s disease, was partially independent of cortical degeneration, and was correlated with cognitive deficits,” said Dr. Landin-Romero.
The findings were not what he and his research colleagues expected. “We were expecting that the amounts of WMH would be similar in FTD and Alzheimer’s disease, but we actually found higher levels in participants with FTD,” he said. Additionally, he anticipated that patients with either FTD or Alzheimer’s disease who had more severe disease would have more WMH, but that finding only held true for people with FTD.
“In sum, our findings show that WMH are a core feature of FTD and Alzheimer’s disease that can contribute to cognitive problems, and not simply as a marker of vascular disease,” said Dr. Landin-Romero.
Major research contribution
Commenting on the study, Jordi Matias-Guiu, PhD, MD, of the department of neurology, Hospital Clinico, San Carlos, Spain, considers the study to be a “great contribution to the field.” Dr. Matias-Guiu, who was not involved with the study, said that WMH “do not necessarily mean vascular pathology, and atrophy may partially explain these abnormalities and should be taken into account in the interpretation of brain MRI.
“WMH are present in both Alzheimer’s disease and FTD and are relevant to cognitive deficits found in these disorders,” he added.
The study was funded by grants from the National Health and Medical Research Council of Australia, the Dementia Research Team, and the ARC Center of Excellence in Cognition and Its Disorders. Dr. Landin-Romero is supported by the Appenzeller Neuroscience Fellowship in Alzheimer’s Disease and the ARC Center of Excellence in Cognition and Its Disorders Memory Program. The other authors’ disclosures are listed on the original article. Dr. Matias-Guiu reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
(FTD) in findings that may help physicians make this difficult diagnosis that affects adults in their prime.
“The assessment of WMH can aid differential diagnosis of bvFTD [behavioral-variant FTD] against other neurodegenerative conditions in the absence of vascular risk factors, especially when considering their spatial distribution,” said senior author Ramón Landin-Romero, PhD, Appenzeller Neuroscience Fellow, Frontotemporal Dementia Research Group, University of Sydney.
“Clinicians can ask for specific sequences in routine MRI scans to visually detect WMH,” said Dr. Landin-Romero, who is also a senior lecturer in the School of Psychology and Brain and Mind Center.
The study was published online Feb. 17 in Neurology.
Difficult diagnosis
“FTD is a collection of unrecognized young-onset (before age 65) dementia syndromes that affect people in their prime,” said Dr. Landin-Romero. He added that heterogeneity in progression trajectories and symptoms, which can include changes in behavior and personality, language impairments, and psychosis, make it a difficult disease to diagnose.
“As such, our research was motivated by the need of sensitive and specific biomarkers of FTD, which are urgently needed to aid diagnosis, prognosis, and treatment development,” he said.
Previous research has been limited; there have only been a “handful” of cohort and case studies and studies involving individuals with mutations in one FTD-causative gene.
FTD is genetically and pathologically complex, and there has been no clear correlation between genetic mutations/underlying pathology and clinical presentation, Dr. Landin-Romero said.
WMH are common in older individuals and are linked to increased risk for cognitive impairment and dementia. Traditionally, they have been associated with vascular risk factors, such as smoking and diabetes. “But the presentation of WMH in FTD and its associations with the severity of symptoms and brain atrophy across FTD symptoms remains to be established,” said Dr. Landin-Romero.
Higher disease severity
To explore the possible association, the researchers studied 129 patients with either bvFTD (n = 64; mean age, 64 years) or Alzheimer’s disease (n = 65; mean age, 64.66 years).
Neuropsychological assessments, medical and neurologic examinations, clinical interview, and structural brain MRI were conducted for all patients, who were compared with 66 age-, sex-, and education-matched healthy control persons (mean age, 64.69 years).
Some participants in the FTD, Alzheimer’s disease, and healthy control groups (n = 54, 44, and 26, respectively) also underwent genetic screening. Postmortem pathology findings were available for a small number of FTD and Alzheimer’s disease participants (n = 13 and 5, respectively).
The medical history included lifestyle and cardiovascular risk factors, as well as other health and neurologic conditions and medication history. Hypertension, hypercholesterolemia, diabetes, and smoking were used to assess vascular risk.
The FTD and Alzheimer’s disease groups did not differ with regard to disease duration (3.55 years; standard deviation, 1.75, and 3.24 years; SD, 1.59, respectively). However, disease severity was significantly higher among those with FTD than among those with Alzheimer’s disease, as measured by the FTD Rating Scale Rasch score (–0.52; SD, 1.28, vs. 0.78; SD, 1.55; P < .001).
Compared with healthy controls, patients in the FTD and Alzheimer’s disease groups scored significantly lower on the Addenbrooke’s Cognitive Examination–Revised (ACE-R) or ACE-III scale. Patients with Alzheimer’s disease showed “disproportionately larger deficits” in memory and visuospatial processing, compared with those with FTD, whereas those with FTD performed significantly worse than those with Alzheimer’s disease in the fluency subdomain.
A larger number of patients in the FTD group screened positive for genetic abnormalities than in the Alzheimer’s disease group; no participants in the healthy control group had genetic mutations.
Unexpected findings
Mean WMH volume was significantly higher in participants with FTD than in participants with Alzheimer’s disease and in healthy controls (mean, 0.76 mL, 0.40 mL, and 0.12 mL respectively). These larger volumes contributed to greater disease severity and cortical atrophy. Moreover, disease severity was “found to be a strong predictor of WMH volume in FTD,” the authors stated. Among patients with FTD, WMH volumes did not differ significantly with regard to genetic mutation status or presence of strong family history.
After controlling for age, vascular risk did not significantly predict WMH volume in the FTD group (P = .16); however, that did not hold true in the Alzheimer’s disease group.
Increased WMH were associated with anterior brain regions in FTD and with posterior brain regions in Alzheimer’s disease. In both disorders, higher WMH volume in the corpus callosum was associated with poorer cognitive performance in the domain of attention.
“The spatial distribution of WMH mirrored patterns of brain atrophy in FTD and Alzheimer’s disease, was partially independent of cortical degeneration, and was correlated with cognitive deficits,” said Dr. Landin-Romero.
The findings were not what he and his research colleagues expected. “We were expecting that the amounts of WMH would be similar in FTD and Alzheimer’s disease, but we actually found higher levels in participants with FTD,” he said. Additionally, he anticipated that patients with either FTD or Alzheimer’s disease who had more severe disease would have more WMH, but that finding only held true for people with FTD.
“In sum, our findings show that WMH are a core feature of FTD and Alzheimer’s disease that can contribute to cognitive problems, and not simply as a marker of vascular disease,” said Dr. Landin-Romero.
Major research contribution
Commenting on the study, Jordi Matias-Guiu, PhD, MD, of the department of neurology, Hospital Clinico, San Carlos, Spain, considers the study to be a “great contribution to the field.” Dr. Matias-Guiu, who was not involved with the study, said that WMH “do not necessarily mean vascular pathology, and atrophy may partially explain these abnormalities and should be taken into account in the interpretation of brain MRI.
“WMH are present in both Alzheimer’s disease and FTD and are relevant to cognitive deficits found in these disorders,” he added.
The study was funded by grants from the National Health and Medical Research Council of Australia, the Dementia Research Team, and the ARC Center of Excellence in Cognition and Its Disorders. Dr. Landin-Romero is supported by the Appenzeller Neuroscience Fellowship in Alzheimer’s Disease and the ARC Center of Excellence in Cognition and Its Disorders Memory Program. The other authors’ disclosures are listed on the original article. Dr. Matias-Guiu reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
(FTD) in findings that may help physicians make this difficult diagnosis that affects adults in their prime.
“The assessment of WMH can aid differential diagnosis of bvFTD [behavioral-variant FTD] against other neurodegenerative conditions in the absence of vascular risk factors, especially when considering their spatial distribution,” said senior author Ramón Landin-Romero, PhD, Appenzeller Neuroscience Fellow, Frontotemporal Dementia Research Group, University of Sydney.
“Clinicians can ask for specific sequences in routine MRI scans to visually detect WMH,” said Dr. Landin-Romero, who is also a senior lecturer in the School of Psychology and Brain and Mind Center.
The study was published online Feb. 17 in Neurology.
Difficult diagnosis
“FTD is a collection of unrecognized young-onset (before age 65) dementia syndromes that affect people in their prime,” said Dr. Landin-Romero. He added that heterogeneity in progression trajectories and symptoms, which can include changes in behavior and personality, language impairments, and psychosis, make it a difficult disease to diagnose.
“As such, our research was motivated by the need of sensitive and specific biomarkers of FTD, which are urgently needed to aid diagnosis, prognosis, and treatment development,” he said.
Previous research has been limited; there have only been a “handful” of cohort and case studies and studies involving individuals with mutations in one FTD-causative gene.
FTD is genetically and pathologically complex, and there has been no clear correlation between genetic mutations/underlying pathology and clinical presentation, Dr. Landin-Romero said.
WMH are common in older individuals and are linked to increased risk for cognitive impairment and dementia. Traditionally, they have been associated with vascular risk factors, such as smoking and diabetes. “But the presentation of WMH in FTD and its associations with the severity of symptoms and brain atrophy across FTD symptoms remains to be established,” said Dr. Landin-Romero.
Higher disease severity
To explore the possible association, the researchers studied 129 patients with either bvFTD (n = 64; mean age, 64 years) or Alzheimer’s disease (n = 65; mean age, 64.66 years).
Neuropsychological assessments, medical and neurologic examinations, clinical interview, and structural brain MRI were conducted for all patients, who were compared with 66 age-, sex-, and education-matched healthy control persons (mean age, 64.69 years).
Some participants in the FTD, Alzheimer’s disease, and healthy control groups (n = 54, 44, and 26, respectively) also underwent genetic screening. Postmortem pathology findings were available for a small number of FTD and Alzheimer’s disease participants (n = 13 and 5, respectively).
The medical history included lifestyle and cardiovascular risk factors, as well as other health and neurologic conditions and medication history. Hypertension, hypercholesterolemia, diabetes, and smoking were used to assess vascular risk.
The FTD and Alzheimer’s disease groups did not differ with regard to disease duration (3.55 years; standard deviation, 1.75, and 3.24 years; SD, 1.59, respectively). However, disease severity was significantly higher among those with FTD than among those with Alzheimer’s disease, as measured by the FTD Rating Scale Rasch score (–0.52; SD, 1.28, vs. 0.78; SD, 1.55; P < .001).
Compared with healthy controls, patients in the FTD and Alzheimer’s disease groups scored significantly lower on the Addenbrooke’s Cognitive Examination–Revised (ACE-R) or ACE-III scale. Patients with Alzheimer’s disease showed “disproportionately larger deficits” in memory and visuospatial processing, compared with those with FTD, whereas those with FTD performed significantly worse than those with Alzheimer’s disease in the fluency subdomain.
A larger number of patients in the FTD group screened positive for genetic abnormalities than in the Alzheimer’s disease group; no participants in the healthy control group had genetic mutations.
Unexpected findings
Mean WMH volume was significantly higher in participants with FTD than in participants with Alzheimer’s disease and in healthy controls (mean, 0.76 mL, 0.40 mL, and 0.12 mL respectively). These larger volumes contributed to greater disease severity and cortical atrophy. Moreover, disease severity was “found to be a strong predictor of WMH volume in FTD,” the authors stated. Among patients with FTD, WMH volumes did not differ significantly with regard to genetic mutation status or presence of strong family history.
After controlling for age, vascular risk did not significantly predict WMH volume in the FTD group (P = .16); however, that did not hold true in the Alzheimer’s disease group.
Increased WMH were associated with anterior brain regions in FTD and with posterior brain regions in Alzheimer’s disease. In both disorders, higher WMH volume in the corpus callosum was associated with poorer cognitive performance in the domain of attention.
“The spatial distribution of WMH mirrored patterns of brain atrophy in FTD and Alzheimer’s disease, was partially independent of cortical degeneration, and was correlated with cognitive deficits,” said Dr. Landin-Romero.
The findings were not what he and his research colleagues expected. “We were expecting that the amounts of WMH would be similar in FTD and Alzheimer’s disease, but we actually found higher levels in participants with FTD,” he said. Additionally, he anticipated that patients with either FTD or Alzheimer’s disease who had more severe disease would have more WMH, but that finding only held true for people with FTD.
“In sum, our findings show that WMH are a core feature of FTD and Alzheimer’s disease that can contribute to cognitive problems, and not simply as a marker of vascular disease,” said Dr. Landin-Romero.
Major research contribution
Commenting on the study, Jordi Matias-Guiu, PhD, MD, of the department of neurology, Hospital Clinico, San Carlos, Spain, considers the study to be a “great contribution to the field.” Dr. Matias-Guiu, who was not involved with the study, said that WMH “do not necessarily mean vascular pathology, and atrophy may partially explain these abnormalities and should be taken into account in the interpretation of brain MRI.
“WMH are present in both Alzheimer’s disease and FTD and are relevant to cognitive deficits found in these disorders,” he added.
The study was funded by grants from the National Health and Medical Research Council of Australia, the Dementia Research Team, and the ARC Center of Excellence in Cognition and Its Disorders. Dr. Landin-Romero is supported by the Appenzeller Neuroscience Fellowship in Alzheimer’s Disease and the ARC Center of Excellence in Cognition and Its Disorders Memory Program. The other authors’ disclosures are listed on the original article. Dr. Matias-Guiu reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Heroes: Nurses’ sacrifice in the age of COVID-19
This past year, the referrals to my private practice have taken a noticeable shift and caused me to pause.
More calls have come from nurses, many who work directly with COVID-19 patients, understandably seeking mental health treatment, or support. Especially in this time, nurses are facing trauma and stress that is unimaginable to many, myself included. Despite the collective efforts we have made as a society to recognize their work, I do not think we have given enough consideration to the enormous sacrifice nurses are currently undertaking to save our collective psyche.
As physicians and mental health providers, we have a glimpse into the complexities and stressors of medical treatment. In our line of work, we support patients with trauma on a regular basis. We feel deeply connected to patients, some of whom we have treated until the end of their lives. Despite that, I am not sure that I, or anyone, can truly comprehend what nurses face in today’s climate of care.
There is no denying that doctors are of value to our system, but our service has limits; nurses and doctors operate as two sides to a shared coin. As doctors, we diagnose and prescribe, while nurses explain and dispense. As doctors, we talk to patients, while nurses comfort them. Imagine spending an entire year working in a hospital diligently wiping endotracheal tubes that are responsible for maintaining someone’s life. Imagine spending an entire year laboring through the heavy task of lifting patients to prone them in a position that may save their lives. Imagine spending an entire year holding the hands of comatose patients in hopes of maintaining a sense of humanity.
And this only begins to describe the tasks bestowed upon nurses. While doctors answer pagers or complete insurance authorization forms, nurses empathize and reassure scared and isolated patients. Imagine spending an entire year updating crying family members who cannot see their loved ones. Imagine spending an entire year explaining and pleading to the outside world that wearing a mask and washing hands would reduce the suffering that takes place inside the hospital walls.
Despite the uncertainties, pressures, and demands, nurses have continued, and will continue, to show up for their patients, shift by shift. It takes a tragic number of deaths for the nurses I see in my practice to share that they have lost count. These numbers reflect people they held to feed, carried to prevent ulcers, wiped for decency, caressed for compassion, probed with IVs and tubes, monitored for signs of life, and warmed with blankets. If love were in any job description, it would fall under that of a nurse.
And we can’t ignore the fact that all the lives lost by COVID-19 had family. Family members who, without ever stepping foot in the hospital, needed a place to be heard, a place to receive explanation, and a place for reassurance. This invaluable place is cultivated by nurses. Through Zoom and phone calls, nurses share messages of hope, love, and fear between patients and family. Through Zoom and phone calls, nurses orchestrate visits and last goodbyes.
There is no denying that we have all been affected by this shared human experience. But the pause we owe our nurses feels long overdue, and of great importance. Nurses need a space to be heard, to be comforted, to be recognized. They come to our practices, trying to contain the world’s angst, while also navigating for themselves what it means to go through what they are going through. They hope that by coming to see us, they will find the strength to go back another day, another week, another month. Sometimes, they come to talk about everything but the job, in hopes that by talking about more mundane problems, they will feel “normal” and reconnected.
I hope that our empathy, congruence, and unconditional positive regard will allow them to feel heard.1 I hope that our warmth, concern, and hopefulness provide a welcoming place to voice sadness, anger, and fears.2 I hope that our processing of traumatic memory, our challenge to avoid inaccurate self-blaming beliefs, and our encouragement to create more thought-out conclusions will allow them to understand what is happening more accurately.3
Yet, I worry. I worry that society hasn’t been particularly successful with helping prior generations of heroes. From war veterans, to Sept. 11, 2001, firefighters, it seems that we have repeated mistakes. My experience with veterans in particular has taught me that for many who are suffering, it feels like society has broken its very fabric by being bystanders to the pain.
But suffering and tragedy are an inevitable part of the human experience that we share. What we can keep sight of is this: As physicians, we work with nurses. We are witnessing firsthand the impossible sacrifice they are taking and the limits of resilience. Let us not be too busy to stop and give recognition where and when it is due. Let us listen and learn from our past, and present, heroes. And let us never forget to extend our own hand to those who make a living extending theirs.
Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com.
References
1. Rogers CR. J Consult Psychol. 1957;21(2):95-103.
2. Mallo CJ, Mintz DL. Psychodyn Psychiatry. 2013 Mar;41(1):13-37.
3. Resick PA et al. Cognitive Processing Therapy for PTSD: A Comprehensive Manual. Guilford Publications, 2016.
This past year, the referrals to my private practice have taken a noticeable shift and caused me to pause.
More calls have come from nurses, many who work directly with COVID-19 patients, understandably seeking mental health treatment, or support. Especially in this time, nurses are facing trauma and stress that is unimaginable to many, myself included. Despite the collective efforts we have made as a society to recognize their work, I do not think we have given enough consideration to the enormous sacrifice nurses are currently undertaking to save our collective psyche.
As physicians and mental health providers, we have a glimpse into the complexities and stressors of medical treatment. In our line of work, we support patients with trauma on a regular basis. We feel deeply connected to patients, some of whom we have treated until the end of their lives. Despite that, I am not sure that I, or anyone, can truly comprehend what nurses face in today’s climate of care.
There is no denying that doctors are of value to our system, but our service has limits; nurses and doctors operate as two sides to a shared coin. As doctors, we diagnose and prescribe, while nurses explain and dispense. As doctors, we talk to patients, while nurses comfort them. Imagine spending an entire year working in a hospital diligently wiping endotracheal tubes that are responsible for maintaining someone’s life. Imagine spending an entire year laboring through the heavy task of lifting patients to prone them in a position that may save their lives. Imagine spending an entire year holding the hands of comatose patients in hopes of maintaining a sense of humanity.
And this only begins to describe the tasks bestowed upon nurses. While doctors answer pagers or complete insurance authorization forms, nurses empathize and reassure scared and isolated patients. Imagine spending an entire year updating crying family members who cannot see their loved ones. Imagine spending an entire year explaining and pleading to the outside world that wearing a mask and washing hands would reduce the suffering that takes place inside the hospital walls.
Despite the uncertainties, pressures, and demands, nurses have continued, and will continue, to show up for their patients, shift by shift. It takes a tragic number of deaths for the nurses I see in my practice to share that they have lost count. These numbers reflect people they held to feed, carried to prevent ulcers, wiped for decency, caressed for compassion, probed with IVs and tubes, monitored for signs of life, and warmed with blankets. If love were in any job description, it would fall under that of a nurse.
And we can’t ignore the fact that all the lives lost by COVID-19 had family. Family members who, without ever stepping foot in the hospital, needed a place to be heard, a place to receive explanation, and a place for reassurance. This invaluable place is cultivated by nurses. Through Zoom and phone calls, nurses share messages of hope, love, and fear between patients and family. Through Zoom and phone calls, nurses orchestrate visits and last goodbyes.
There is no denying that we have all been affected by this shared human experience. But the pause we owe our nurses feels long overdue, and of great importance. Nurses need a space to be heard, to be comforted, to be recognized. They come to our practices, trying to contain the world’s angst, while also navigating for themselves what it means to go through what they are going through. They hope that by coming to see us, they will find the strength to go back another day, another week, another month. Sometimes, they come to talk about everything but the job, in hopes that by talking about more mundane problems, they will feel “normal” and reconnected.
I hope that our empathy, congruence, and unconditional positive regard will allow them to feel heard.1 I hope that our warmth, concern, and hopefulness provide a welcoming place to voice sadness, anger, and fears.2 I hope that our processing of traumatic memory, our challenge to avoid inaccurate self-blaming beliefs, and our encouragement to create more thought-out conclusions will allow them to understand what is happening more accurately.3
Yet, I worry. I worry that society hasn’t been particularly successful with helping prior generations of heroes. From war veterans, to Sept. 11, 2001, firefighters, it seems that we have repeated mistakes. My experience with veterans in particular has taught me that for many who are suffering, it feels like society has broken its very fabric by being bystanders to the pain.
But suffering and tragedy are an inevitable part of the human experience that we share. What we can keep sight of is this: As physicians, we work with nurses. We are witnessing firsthand the impossible sacrifice they are taking and the limits of resilience. Let us not be too busy to stop and give recognition where and when it is due. Let us listen and learn from our past, and present, heroes. And let us never forget to extend our own hand to those who make a living extending theirs.
Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com.
References
1. Rogers CR. J Consult Psychol. 1957;21(2):95-103.
2. Mallo CJ, Mintz DL. Psychodyn Psychiatry. 2013 Mar;41(1):13-37.
3. Resick PA et al. Cognitive Processing Therapy for PTSD: A Comprehensive Manual. Guilford Publications, 2016.
This past year, the referrals to my private practice have taken a noticeable shift and caused me to pause.
More calls have come from nurses, many who work directly with COVID-19 patients, understandably seeking mental health treatment, or support. Especially in this time, nurses are facing trauma and stress that is unimaginable to many, myself included. Despite the collective efforts we have made as a society to recognize their work, I do not think we have given enough consideration to the enormous sacrifice nurses are currently undertaking to save our collective psyche.
As physicians and mental health providers, we have a glimpse into the complexities and stressors of medical treatment. In our line of work, we support patients with trauma on a regular basis. We feel deeply connected to patients, some of whom we have treated until the end of their lives. Despite that, I am not sure that I, or anyone, can truly comprehend what nurses face in today’s climate of care.
There is no denying that doctors are of value to our system, but our service has limits; nurses and doctors operate as two sides to a shared coin. As doctors, we diagnose and prescribe, while nurses explain and dispense. As doctors, we talk to patients, while nurses comfort them. Imagine spending an entire year working in a hospital diligently wiping endotracheal tubes that are responsible for maintaining someone’s life. Imagine spending an entire year laboring through the heavy task of lifting patients to prone them in a position that may save their lives. Imagine spending an entire year holding the hands of comatose patients in hopes of maintaining a sense of humanity.
And this only begins to describe the tasks bestowed upon nurses. While doctors answer pagers or complete insurance authorization forms, nurses empathize and reassure scared and isolated patients. Imagine spending an entire year updating crying family members who cannot see their loved ones. Imagine spending an entire year explaining and pleading to the outside world that wearing a mask and washing hands would reduce the suffering that takes place inside the hospital walls.
Despite the uncertainties, pressures, and demands, nurses have continued, and will continue, to show up for their patients, shift by shift. It takes a tragic number of deaths for the nurses I see in my practice to share that they have lost count. These numbers reflect people they held to feed, carried to prevent ulcers, wiped for decency, caressed for compassion, probed with IVs and tubes, monitored for signs of life, and warmed with blankets. If love were in any job description, it would fall under that of a nurse.
And we can’t ignore the fact that all the lives lost by COVID-19 had family. Family members who, without ever stepping foot in the hospital, needed a place to be heard, a place to receive explanation, and a place for reassurance. This invaluable place is cultivated by nurses. Through Zoom and phone calls, nurses share messages of hope, love, and fear between patients and family. Through Zoom and phone calls, nurses orchestrate visits and last goodbyes.
There is no denying that we have all been affected by this shared human experience. But the pause we owe our nurses feels long overdue, and of great importance. Nurses need a space to be heard, to be comforted, to be recognized. They come to our practices, trying to contain the world’s angst, while also navigating for themselves what it means to go through what they are going through. They hope that by coming to see us, they will find the strength to go back another day, another week, another month. Sometimes, they come to talk about everything but the job, in hopes that by talking about more mundane problems, they will feel “normal” and reconnected.
I hope that our empathy, congruence, and unconditional positive regard will allow them to feel heard.1 I hope that our warmth, concern, and hopefulness provide a welcoming place to voice sadness, anger, and fears.2 I hope that our processing of traumatic memory, our challenge to avoid inaccurate self-blaming beliefs, and our encouragement to create more thought-out conclusions will allow them to understand what is happening more accurately.3
Yet, I worry. I worry that society hasn’t been particularly successful with helping prior generations of heroes. From war veterans, to Sept. 11, 2001, firefighters, it seems that we have repeated mistakes. My experience with veterans in particular has taught me that for many who are suffering, it feels like society has broken its very fabric by being bystanders to the pain.
But suffering and tragedy are an inevitable part of the human experience that we share. What we can keep sight of is this: As physicians, we work with nurses. We are witnessing firsthand the impossible sacrifice they are taking and the limits of resilience. Let us not be too busy to stop and give recognition where and when it is due. Let us listen and learn from our past, and present, heroes. And let us never forget to extend our own hand to those who make a living extending theirs.
Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com.
References
1. Rogers CR. J Consult Psychol. 1957;21(2):95-103.
2. Mallo CJ, Mintz DL. Psychodyn Psychiatry. 2013 Mar;41(1):13-37.
3. Resick PA et al. Cognitive Processing Therapy for PTSD: A Comprehensive Manual. Guilford Publications, 2016.
Inflammatory immune findings likely in acute schizophrenia, MDD, bipolar
Researchers have come a long way in understanding the link between acute inflammation and treatment-resistant depression, but more work needs to be done, according to Mark Hyman Rapaport, MD.
“Inflammation has been a hot topic in the past decade, both because of its impact in medical disorders and in psychiatric disorders,” Dr. Rapaport, CEO of the Huntsman Mental Health Institute in Salt Lake City, Utah, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “We run into difficulty with chronic inflammation, which we see with rheumatic disorders, and when we think of metabolic syndrome and obesity.”
The immune system helps to control energy regulation and neuroendocrine function in acute inflammation and chronic inflammatory diseases. “We see a variety of effects on the central nervous system or liver function or on homeostasis of the body,” said Dr. Rapaport, who also chairs the department of psychiatry at the University of Utah, also in Salt Lake City. “These are all normal and necessary to channel energy to the immune system in order to fight what’s necessary in acute inflammatory response.”
A chronic state of inflammation can result in prolonged allocation of fuels to the immune system, tissue inflammation, and a chronically aberrant immune reaction, he continued. This can cause depressive symptoms/fatigue, anorexia, malnutrition, muscle wasting, cachectic obesity, insulin resistance, dyslipidemia, increased adipose tissue in the proximity of inflammatory lesion, alterations of steroid hormone axes, elevated sympathetic tone, hypertension, decreased parasympathetic tone, inflammation-related anemia, and osteopenia. “So, chronic inflammation has a lot of long-term sequelae that are detrimental,” he said.
Both physical stress and psychological stress also cause an inflammatory state. After looking at the medical literature, Dr. Rapaport and colleagues began to wonder whether inflammation and immune activation associated with psychiatric disorders are attributable to the stress of acute illness. To find out, they performed a meta-analysis of blood cytokine network alterations in psychiatric patients and evaluated comparisons between schizophrenia, bipolar disorder, and depression. A total of three meta-analyses were performed: one of acute/inpatient studies, one on the impact of acute treatment, and one of outpatient studies. The researchers hypothesized that inflammatory and immune findings in psychiatric illnesses were tied to two distinct etiologies: the acute stress of illness and intrinsic immune dysfunction.
The meta-analyses included 68 studies: 40 involving patients with schizophrenia, 18 involving those with major depressive disorder (MDD) and 10 involving those with bipolar disorder. The researchers found that levels of four cytokines were significantly increased in acutely ill patients with schizophrenia, bipolar mania, and MDD, compared with controls: interleukin-6, tumor necrosis factor–alpha (TNF-alpha), soluble IL-2 receptor (sIL-2R), and IL-1 receptor antagonist (IL-1RA). “There has not been a consistent blood panel used across studies, be it within a disorder itself like depression, or across disorders,” Dr. Rapaport noted. “This is a challenge that we face in looking at these data.”
Following treatment of acute illness, IL-6 levels significantly decreased in schizophrenia and MDD, but no significant changes in TNF-alpha levels were observed in patients with schizophrenia or MDD. In addition, sIL-2R levels increase in schizophrenia but remained unchanged in bipolar and MDD, while IL-1RA levels in bipolar mania decreased but remained unchanged in MDD. Meanwhile, assessment of the study’s 24 outpatient studies revealed that levels of IL-6 were significantly increased in outpatients with schizophrenia, euthymic bipolar disorder, and MDD, compared with controls (P < .01 for each). In addition, levels of IL-1 beta and sIL-2R were significantly increased in outpatients with schizophrenia and bipolar disorder.
According to Dr. Rapaport, these meta-analyses suggest that there are likely inflammatory immune findings present in acutely ill patients with MDD, schizophrenia, and bipolar disorder.
“Some of this activation decreases with effective acute treatment of the disorder,” he said. “The data suggest that immune changes are present in a subset of patients with all three disorders.”
“We also need to understand the regulatory role that microglia and astroglia play within the brain,” he said. “We need to identify changes in brain circuitry and function associated with inflammation and other immune changes. We also need to carefully scrutinize publications, understand the assumptions behind the statistics, and carry out more research beyond the protein level.”
He concluded his presentation by calling for research to help clinicians differentiate acute from chronic inflammation. “The study of both is important,” he said. “We need to understand the pathophysiology of immune changes in psychiatric disorders. We need to study both the triggers and pathways to resolution.”
Dr. Rapaport disclosed that he has received research support from the National Institutes of Health, the National Institute of Mental Health, and the National Center for Complementary and Integrative Health.
Researchers have come a long way in understanding the link between acute inflammation and treatment-resistant depression, but more work needs to be done, according to Mark Hyman Rapaport, MD.
“Inflammation has been a hot topic in the past decade, both because of its impact in medical disorders and in psychiatric disorders,” Dr. Rapaport, CEO of the Huntsman Mental Health Institute in Salt Lake City, Utah, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “We run into difficulty with chronic inflammation, which we see with rheumatic disorders, and when we think of metabolic syndrome and obesity.”
The immune system helps to control energy regulation and neuroendocrine function in acute inflammation and chronic inflammatory diseases. “We see a variety of effects on the central nervous system or liver function or on homeostasis of the body,” said Dr. Rapaport, who also chairs the department of psychiatry at the University of Utah, also in Salt Lake City. “These are all normal and necessary to channel energy to the immune system in order to fight what’s necessary in acute inflammatory response.”
A chronic state of inflammation can result in prolonged allocation of fuels to the immune system, tissue inflammation, and a chronically aberrant immune reaction, he continued. This can cause depressive symptoms/fatigue, anorexia, malnutrition, muscle wasting, cachectic obesity, insulin resistance, dyslipidemia, increased adipose tissue in the proximity of inflammatory lesion, alterations of steroid hormone axes, elevated sympathetic tone, hypertension, decreased parasympathetic tone, inflammation-related anemia, and osteopenia. “So, chronic inflammation has a lot of long-term sequelae that are detrimental,” he said.
Both physical stress and psychological stress also cause an inflammatory state. After looking at the medical literature, Dr. Rapaport and colleagues began to wonder whether inflammation and immune activation associated with psychiatric disorders are attributable to the stress of acute illness. To find out, they performed a meta-analysis of blood cytokine network alterations in psychiatric patients and evaluated comparisons between schizophrenia, bipolar disorder, and depression. A total of three meta-analyses were performed: one of acute/inpatient studies, one on the impact of acute treatment, and one of outpatient studies. The researchers hypothesized that inflammatory and immune findings in psychiatric illnesses were tied to two distinct etiologies: the acute stress of illness and intrinsic immune dysfunction.
The meta-analyses included 68 studies: 40 involving patients with schizophrenia, 18 involving those with major depressive disorder (MDD) and 10 involving those with bipolar disorder. The researchers found that levels of four cytokines were significantly increased in acutely ill patients with schizophrenia, bipolar mania, and MDD, compared with controls: interleukin-6, tumor necrosis factor–alpha (TNF-alpha), soluble IL-2 receptor (sIL-2R), and IL-1 receptor antagonist (IL-1RA). “There has not been a consistent blood panel used across studies, be it within a disorder itself like depression, or across disorders,” Dr. Rapaport noted. “This is a challenge that we face in looking at these data.”
Following treatment of acute illness, IL-6 levels significantly decreased in schizophrenia and MDD, but no significant changes in TNF-alpha levels were observed in patients with schizophrenia or MDD. In addition, sIL-2R levels increase in schizophrenia but remained unchanged in bipolar and MDD, while IL-1RA levels in bipolar mania decreased but remained unchanged in MDD. Meanwhile, assessment of the study’s 24 outpatient studies revealed that levels of IL-6 were significantly increased in outpatients with schizophrenia, euthymic bipolar disorder, and MDD, compared with controls (P < .01 for each). In addition, levels of IL-1 beta and sIL-2R were significantly increased in outpatients with schizophrenia and bipolar disorder.
According to Dr. Rapaport, these meta-analyses suggest that there are likely inflammatory immune findings present in acutely ill patients with MDD, schizophrenia, and bipolar disorder.
“Some of this activation decreases with effective acute treatment of the disorder,” he said. “The data suggest that immune changes are present in a subset of patients with all three disorders.”
“We also need to understand the regulatory role that microglia and astroglia play within the brain,” he said. “We need to identify changes in brain circuitry and function associated with inflammation and other immune changes. We also need to carefully scrutinize publications, understand the assumptions behind the statistics, and carry out more research beyond the protein level.”
He concluded his presentation by calling for research to help clinicians differentiate acute from chronic inflammation. “The study of both is important,” he said. “We need to understand the pathophysiology of immune changes in psychiatric disorders. We need to study both the triggers and pathways to resolution.”
Dr. Rapaport disclosed that he has received research support from the National Institutes of Health, the National Institute of Mental Health, and the National Center for Complementary and Integrative Health.
Researchers have come a long way in understanding the link between acute inflammation and treatment-resistant depression, but more work needs to be done, according to Mark Hyman Rapaport, MD.
“Inflammation has been a hot topic in the past decade, both because of its impact in medical disorders and in psychiatric disorders,” Dr. Rapaport, CEO of the Huntsman Mental Health Institute in Salt Lake City, Utah, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “We run into difficulty with chronic inflammation, which we see with rheumatic disorders, and when we think of metabolic syndrome and obesity.”
The immune system helps to control energy regulation and neuroendocrine function in acute inflammation and chronic inflammatory diseases. “We see a variety of effects on the central nervous system or liver function or on homeostasis of the body,” said Dr. Rapaport, who also chairs the department of psychiatry at the University of Utah, also in Salt Lake City. “These are all normal and necessary to channel energy to the immune system in order to fight what’s necessary in acute inflammatory response.”
A chronic state of inflammation can result in prolonged allocation of fuels to the immune system, tissue inflammation, and a chronically aberrant immune reaction, he continued. This can cause depressive symptoms/fatigue, anorexia, malnutrition, muscle wasting, cachectic obesity, insulin resistance, dyslipidemia, increased adipose tissue in the proximity of inflammatory lesion, alterations of steroid hormone axes, elevated sympathetic tone, hypertension, decreased parasympathetic tone, inflammation-related anemia, and osteopenia. “So, chronic inflammation has a lot of long-term sequelae that are detrimental,” he said.
Both physical stress and psychological stress also cause an inflammatory state. After looking at the medical literature, Dr. Rapaport and colleagues began to wonder whether inflammation and immune activation associated with psychiatric disorders are attributable to the stress of acute illness. To find out, they performed a meta-analysis of blood cytokine network alterations in psychiatric patients and evaluated comparisons between schizophrenia, bipolar disorder, and depression. A total of three meta-analyses were performed: one of acute/inpatient studies, one on the impact of acute treatment, and one of outpatient studies. The researchers hypothesized that inflammatory and immune findings in psychiatric illnesses were tied to two distinct etiologies: the acute stress of illness and intrinsic immune dysfunction.
The meta-analyses included 68 studies: 40 involving patients with schizophrenia, 18 involving those with major depressive disorder (MDD) and 10 involving those with bipolar disorder. The researchers found that levels of four cytokines were significantly increased in acutely ill patients with schizophrenia, bipolar mania, and MDD, compared with controls: interleukin-6, tumor necrosis factor–alpha (TNF-alpha), soluble IL-2 receptor (sIL-2R), and IL-1 receptor antagonist (IL-1RA). “There has not been a consistent blood panel used across studies, be it within a disorder itself like depression, or across disorders,” Dr. Rapaport noted. “This is a challenge that we face in looking at these data.”
Following treatment of acute illness, IL-6 levels significantly decreased in schizophrenia and MDD, but no significant changes in TNF-alpha levels were observed in patients with schizophrenia or MDD. In addition, sIL-2R levels increase in schizophrenia but remained unchanged in bipolar and MDD, while IL-1RA levels in bipolar mania decreased but remained unchanged in MDD. Meanwhile, assessment of the study’s 24 outpatient studies revealed that levels of IL-6 were significantly increased in outpatients with schizophrenia, euthymic bipolar disorder, and MDD, compared with controls (P < .01 for each). In addition, levels of IL-1 beta and sIL-2R were significantly increased in outpatients with schizophrenia and bipolar disorder.
According to Dr. Rapaport, these meta-analyses suggest that there are likely inflammatory immune findings present in acutely ill patients with MDD, schizophrenia, and bipolar disorder.
“Some of this activation decreases with effective acute treatment of the disorder,” he said. “The data suggest that immune changes are present in a subset of patients with all three disorders.”
“We also need to understand the regulatory role that microglia and astroglia play within the brain,” he said. “We need to identify changes in brain circuitry and function associated with inflammation and other immune changes. We also need to carefully scrutinize publications, understand the assumptions behind the statistics, and carry out more research beyond the protein level.”
He concluded his presentation by calling for research to help clinicians differentiate acute from chronic inflammation. “The study of both is important,” he said. “We need to understand the pathophysiology of immune changes in psychiatric disorders. We need to study both the triggers and pathways to resolution.”
Dr. Rapaport disclosed that he has received research support from the National Institutes of Health, the National Institute of Mental Health, and the National Center for Complementary and Integrative Health.
FROM NPA 2021
Janssen/J&J COVID-19 vaccine cuts transmission, new data show
The single-dose vaccine reduces the risk of asymptomatic transmission by 74% at 71 days, compared with placebo, according to documents released today by the U.S. Food and Drug Administration.
“The decrease in asymptomatic transmission is very welcome news too in curbing the spread of the virus,” Phyllis Tien, MD, told this news organization.
“While the earlier press release reported that the vaccine was effective against preventing severe COVID-19 disease, as well as hospitalizations and death, this new data shows that the vaccine can also decrease transmission, which is very important on a public health level,” said Dr. Tien, professor of medicine in the division of infectious diseases at the University of California, San Francisco.
“It is extremely important in terms of getting to herd immunity,” Paul Goepfert, MD, director of the Alabama Vaccine Research Clinic and infectious disease specialist at the University of Alabama, Birmingham, said in an interview. “It means that this vaccine is likely preventing subsequent transmission after a single dose, which could have huge implications once we get the majority of folks vaccinated.”
The FDA cautioned that the numbers of participants included in the study are relatively small and need to be verified. However, the Johnson & Johnson vaccine might not be the only product offering this advantage. Early data suggest that the Pfizer/BioNTech vaccine also decreases transmission, providing further evidence that the protection offered by immunization goes beyond the individual.
The new analyses were provided by the FDA in advance of its review of the Janssen/Johnson & Johnson vaccine. The agency plans to fully address the Ad26.COV2.S vaccine at its Vaccines and Related Biological Products Advisory Committee Meeting on Friday, including evaluating its safety and efficacy.
The agency’s decision on whether or not to grant emergency use authorization (EUA) to the Johnson & Johnson vaccine could come as early as Friday evening or Saturday.
In addition to the newly released data, officials are likely to discuss phase 3 data, released Jan. 29, that reveal an 85% efficacy for the vaccine against severe COVID-19 illness globally, including data from South America, South Africa, and the United States. When the analysis was restricted to data from U.S. participants, the trial showed a 73% efficacy against moderate to severe COVID-19.
If and when the FDA grants an EUA, it remains unclear how much of the new vaccine will be immediately available. Initially, Johnson & Johnson predicted 18 million doses would be ready by the end of February, but others stated the figure will be closer to 2-4 million. The manufacturer’s contract with the U.S. government stipulates production of 100-million doses by the end of June.
Dr. Tien received support from Johnson & Johnson to conduct the J&J COVID-19 vaccine trial in the SF VA HealthCare System. Dr. Goepfert has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The single-dose vaccine reduces the risk of asymptomatic transmission by 74% at 71 days, compared with placebo, according to documents released today by the U.S. Food and Drug Administration.
“The decrease in asymptomatic transmission is very welcome news too in curbing the spread of the virus,” Phyllis Tien, MD, told this news organization.
“While the earlier press release reported that the vaccine was effective against preventing severe COVID-19 disease, as well as hospitalizations and death, this new data shows that the vaccine can also decrease transmission, which is very important on a public health level,” said Dr. Tien, professor of medicine in the division of infectious diseases at the University of California, San Francisco.
“It is extremely important in terms of getting to herd immunity,” Paul Goepfert, MD, director of the Alabama Vaccine Research Clinic and infectious disease specialist at the University of Alabama, Birmingham, said in an interview. “It means that this vaccine is likely preventing subsequent transmission after a single dose, which could have huge implications once we get the majority of folks vaccinated.”
The FDA cautioned that the numbers of participants included in the study are relatively small and need to be verified. However, the Johnson & Johnson vaccine might not be the only product offering this advantage. Early data suggest that the Pfizer/BioNTech vaccine also decreases transmission, providing further evidence that the protection offered by immunization goes beyond the individual.
The new analyses were provided by the FDA in advance of its review of the Janssen/Johnson & Johnson vaccine. The agency plans to fully address the Ad26.COV2.S vaccine at its Vaccines and Related Biological Products Advisory Committee Meeting on Friday, including evaluating its safety and efficacy.
The agency’s decision on whether or not to grant emergency use authorization (EUA) to the Johnson & Johnson vaccine could come as early as Friday evening or Saturday.
In addition to the newly released data, officials are likely to discuss phase 3 data, released Jan. 29, that reveal an 85% efficacy for the vaccine against severe COVID-19 illness globally, including data from South America, South Africa, and the United States. When the analysis was restricted to data from U.S. participants, the trial showed a 73% efficacy against moderate to severe COVID-19.
If and when the FDA grants an EUA, it remains unclear how much of the new vaccine will be immediately available. Initially, Johnson & Johnson predicted 18 million doses would be ready by the end of February, but others stated the figure will be closer to 2-4 million. The manufacturer’s contract with the U.S. government stipulates production of 100-million doses by the end of June.
Dr. Tien received support from Johnson & Johnson to conduct the J&J COVID-19 vaccine trial in the SF VA HealthCare System. Dr. Goepfert has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The single-dose vaccine reduces the risk of asymptomatic transmission by 74% at 71 days, compared with placebo, according to documents released today by the U.S. Food and Drug Administration.
“The decrease in asymptomatic transmission is very welcome news too in curbing the spread of the virus,” Phyllis Tien, MD, told this news organization.
“While the earlier press release reported that the vaccine was effective against preventing severe COVID-19 disease, as well as hospitalizations and death, this new data shows that the vaccine can also decrease transmission, which is very important on a public health level,” said Dr. Tien, professor of medicine in the division of infectious diseases at the University of California, San Francisco.
“It is extremely important in terms of getting to herd immunity,” Paul Goepfert, MD, director of the Alabama Vaccine Research Clinic and infectious disease specialist at the University of Alabama, Birmingham, said in an interview. “It means that this vaccine is likely preventing subsequent transmission after a single dose, which could have huge implications once we get the majority of folks vaccinated.”
The FDA cautioned that the numbers of participants included in the study are relatively small and need to be verified. However, the Johnson & Johnson vaccine might not be the only product offering this advantage. Early data suggest that the Pfizer/BioNTech vaccine also decreases transmission, providing further evidence that the protection offered by immunization goes beyond the individual.
The new analyses were provided by the FDA in advance of its review of the Janssen/Johnson & Johnson vaccine. The agency plans to fully address the Ad26.COV2.S vaccine at its Vaccines and Related Biological Products Advisory Committee Meeting on Friday, including evaluating its safety and efficacy.
The agency’s decision on whether or not to grant emergency use authorization (EUA) to the Johnson & Johnson vaccine could come as early as Friday evening or Saturday.
In addition to the newly released data, officials are likely to discuss phase 3 data, released Jan. 29, that reveal an 85% efficacy for the vaccine against severe COVID-19 illness globally, including data from South America, South Africa, and the United States. When the analysis was restricted to data from U.S. participants, the trial showed a 73% efficacy against moderate to severe COVID-19.
If and when the FDA grants an EUA, it remains unclear how much of the new vaccine will be immediately available. Initially, Johnson & Johnson predicted 18 million doses would be ready by the end of February, but others stated the figure will be closer to 2-4 million. The manufacturer’s contract with the U.S. government stipulates production of 100-million doses by the end of June.
Dr. Tien received support from Johnson & Johnson to conduct the J&J COVID-19 vaccine trial in the SF VA HealthCare System. Dr. Goepfert has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Consider connections between depression, chronic medical comorbidities
For many adults, depression and chronic medical conditions are inextricably linked.
In fact, the prevalence of depression is 2-10 times higher among people with chronic medical conditions, particularly in people with chronic pain, where the prevalence reaches 40%-60%, according to Jonathan E. Alpert, MD, PhD.
“About 60% of adults over 65 have two or more chronic conditions, of which depression is the single most common comorbidity,” Dr. Alpert, chair of the department of psychiatry and behavioral sciences at the Montefiore Medical Center and Albert Einstein College of Medicine, both in New York, said during an annual psychopharmacology update held by the Nevada Psychiatric Association.
“Premorbid depression is a risk factor for a number of medical conditions, such as heart disease. We also know that medical illness is a risk factor for depression. Comorbid depression predicts poorer health outcomes, including disability, hospital readmission, and mortality. It is also associated with up to severalfold higher general medical costs.”
Despite the pervasive nature of depression on other medical conditions, a limited evidence base exists to guide clinicians on treatment approaches.
“Most major depressive disorder randomized clinical trials exclude individuals with active medical illness, but we do know that medical comorbidity is associated with poorer depression outcomes,” Dr. Alpert said. For example, the STAR*D trial found that people with major depressive disorder plus medical comorbidity had lower remission rates, compared with those who had MDD alone (P < .001), while a large analysis from University of Pittsburgh researchers found that people with medical comorbidities had higher depression recurrence rates.
An assessment of the relationship between medical conditions and depression should include thinking about the association between the medical illness itself and medications with depressive symptoms.
“Are the medications contributing to depressive symptoms?” he asked. “We also want to be thinking of the impact of medical illness and medications on antidepressant pharmacokinetics and pharmacodynamics. We also want to know about the evidence for antidepressant safety, tolerability, efficacy, and anticipated drug-drug interactions among individuals with the medical illness. You also want to enhance focus on treatment adherence and coordination of care.”
Nontraditional routes of antidepressant administration exist for patients who have difficulty swallowing pills. Food and Drug Administration–approved options include transdermal selegiline; intranasal esketamine; liquid forms of fluoxetine, escitalopram, paroxetine, nortriptyline, doxepin, imipramine, and lithium; and oral disintegrating tablet forms of mirtazapine and selegiline. As for non–FDA-approved forms of antidepressant administration, small studies or case reports have appeared in the medical literature regarding intravenous ketamine, citalopram, amitriptyline, mirtazapine, maprotiline, and lithium; intramuscular ketamine and amitriptyline; and rectal forms of antidepressants such as trazodone, amitriptyline, doxepin, fluoxetine, and lamotrigine.
“It’s good to keep in mind that, when you’re not able to use by mouth antidepressants or typical tablet forms of antidepressants, there are other options available,” said Dr. Alpert, who is also chair of the American Psychiatric Association’s Council on Research.
Metabolism of medications occurs primarily in the liver, he continued, but some metabolic enzymes also line the intestinal tract. The metabolism of a substrate may be inhibited or induced by other drugs.
“If someone is on drug A and we give drug B, and drug B is inhibiting the metabolism of drug A, there will be a very rapid impact – hours to just a few days,” Dr. Alpert said. “The substrate levels rise very quickly, so within hours or days of taking drug B, drug A levels can rise steeply.” On the other hand, if someone is on drug A and you give a drug B – which induces the enzymes that usually metabolize drug A – the impact will be gradual. “That’s because induction requires increased synthesis of the metabolic enzyme responsible for metabolizing drug A,” he said. “That happens over days to weeks.”
Medications that are potential inducers of metabolism include carbamazepine, phenobarbital, phenytoin, primidone, prednisone, ritonavir, rifampin, chronic alcohol use, chronic smoking, St. John’s wort, and consumption of large quantities of cruciferous vegetables and charbroiled meats.
On the other hand, potential inhibitors of metabolism include antifungals, macrolide antibiotics, fluoroquinolones, antiretrovirals, isoniazid, antimalarials, disulfiram, SSRIs, phenothiazines, valproic acid, nefazodone, duloxetine, bupropion, beta-blockers, acute alcohol use, cimetidine, quinidine, calcium channel blockers, grapefruit juice, propafenone, and amiodarone.
“When treating people with significant medical comorbidity, start low and go slow, but persevere,” Dr. Alpert advised. “We want to always think about the risk of treating versus the risk of not treating, or not treating actively enough. Often, people with comorbid medical illness require the same or even more assertive treatment with pharmacotherapy for their depression as people without medical illness. So, we don’t want to make the mistake of undertreating depression. We also want to anticipate and address challenges with adherence.”
He also recommended being mindful of the most salient side effects for a given condition, such as lowered seizure threshold or QT prolongation in populations with brain injury or with cardiovascular disease, and to leverage dual benefits when they might exist, such as using [selective norepinephrine reuptake inhibitors] for depression and pain or hot flashes, or bupropion for depression and smoking cessation, or mirtazapine, which is effective for nausea, cachexia, or insomnia, as well as depression itself.
“We want to collaborate closely and regularly with other treaters, sharing our notes and diagnostic impressions,” Dr. Alpert said. “We want to use all the tools in the box in addition to pharmacotherapy, thinking about psychotherapy, neuromodulation, and peer navigators. We want to strive for measurement-based care using rating scales when we can, to augment our treatment. And
Dr. Alpert reports having received speaker’s honoraria, consulting fees, and research support from numerous pharmaceutical companies.
For many adults, depression and chronic medical conditions are inextricably linked.
In fact, the prevalence of depression is 2-10 times higher among people with chronic medical conditions, particularly in people with chronic pain, where the prevalence reaches 40%-60%, according to Jonathan E. Alpert, MD, PhD.
“About 60% of adults over 65 have two or more chronic conditions, of which depression is the single most common comorbidity,” Dr. Alpert, chair of the department of psychiatry and behavioral sciences at the Montefiore Medical Center and Albert Einstein College of Medicine, both in New York, said during an annual psychopharmacology update held by the Nevada Psychiatric Association.
“Premorbid depression is a risk factor for a number of medical conditions, such as heart disease. We also know that medical illness is a risk factor for depression. Comorbid depression predicts poorer health outcomes, including disability, hospital readmission, and mortality. It is also associated with up to severalfold higher general medical costs.”
Despite the pervasive nature of depression on other medical conditions, a limited evidence base exists to guide clinicians on treatment approaches.
“Most major depressive disorder randomized clinical trials exclude individuals with active medical illness, but we do know that medical comorbidity is associated with poorer depression outcomes,” Dr. Alpert said. For example, the STAR*D trial found that people with major depressive disorder plus medical comorbidity had lower remission rates, compared with those who had MDD alone (P < .001), while a large analysis from University of Pittsburgh researchers found that people with medical comorbidities had higher depression recurrence rates.
An assessment of the relationship between medical conditions and depression should include thinking about the association between the medical illness itself and medications with depressive symptoms.
“Are the medications contributing to depressive symptoms?” he asked. “We also want to be thinking of the impact of medical illness and medications on antidepressant pharmacokinetics and pharmacodynamics. We also want to know about the evidence for antidepressant safety, tolerability, efficacy, and anticipated drug-drug interactions among individuals with the medical illness. You also want to enhance focus on treatment adherence and coordination of care.”
Nontraditional routes of antidepressant administration exist for patients who have difficulty swallowing pills. Food and Drug Administration–approved options include transdermal selegiline; intranasal esketamine; liquid forms of fluoxetine, escitalopram, paroxetine, nortriptyline, doxepin, imipramine, and lithium; and oral disintegrating tablet forms of mirtazapine and selegiline. As for non–FDA-approved forms of antidepressant administration, small studies or case reports have appeared in the medical literature regarding intravenous ketamine, citalopram, amitriptyline, mirtazapine, maprotiline, and lithium; intramuscular ketamine and amitriptyline; and rectal forms of antidepressants such as trazodone, amitriptyline, doxepin, fluoxetine, and lamotrigine.
“It’s good to keep in mind that, when you’re not able to use by mouth antidepressants or typical tablet forms of antidepressants, there are other options available,” said Dr. Alpert, who is also chair of the American Psychiatric Association’s Council on Research.
Metabolism of medications occurs primarily in the liver, he continued, but some metabolic enzymes also line the intestinal tract. The metabolism of a substrate may be inhibited or induced by other drugs.
“If someone is on drug A and we give drug B, and drug B is inhibiting the metabolism of drug A, there will be a very rapid impact – hours to just a few days,” Dr. Alpert said. “The substrate levels rise very quickly, so within hours or days of taking drug B, drug A levels can rise steeply.” On the other hand, if someone is on drug A and you give a drug B – which induces the enzymes that usually metabolize drug A – the impact will be gradual. “That’s because induction requires increased synthesis of the metabolic enzyme responsible for metabolizing drug A,” he said. “That happens over days to weeks.”
Medications that are potential inducers of metabolism include carbamazepine, phenobarbital, phenytoin, primidone, prednisone, ritonavir, rifampin, chronic alcohol use, chronic smoking, St. John’s wort, and consumption of large quantities of cruciferous vegetables and charbroiled meats.
On the other hand, potential inhibitors of metabolism include antifungals, macrolide antibiotics, fluoroquinolones, antiretrovirals, isoniazid, antimalarials, disulfiram, SSRIs, phenothiazines, valproic acid, nefazodone, duloxetine, bupropion, beta-blockers, acute alcohol use, cimetidine, quinidine, calcium channel blockers, grapefruit juice, propafenone, and amiodarone.
“When treating people with significant medical comorbidity, start low and go slow, but persevere,” Dr. Alpert advised. “We want to always think about the risk of treating versus the risk of not treating, or not treating actively enough. Often, people with comorbid medical illness require the same or even more assertive treatment with pharmacotherapy for their depression as people without medical illness. So, we don’t want to make the mistake of undertreating depression. We also want to anticipate and address challenges with adherence.”
He also recommended being mindful of the most salient side effects for a given condition, such as lowered seizure threshold or QT prolongation in populations with brain injury or with cardiovascular disease, and to leverage dual benefits when they might exist, such as using [selective norepinephrine reuptake inhibitors] for depression and pain or hot flashes, or bupropion for depression and smoking cessation, or mirtazapine, which is effective for nausea, cachexia, or insomnia, as well as depression itself.
“We want to collaborate closely and regularly with other treaters, sharing our notes and diagnostic impressions,” Dr. Alpert said. “We want to use all the tools in the box in addition to pharmacotherapy, thinking about psychotherapy, neuromodulation, and peer navigators. We want to strive for measurement-based care using rating scales when we can, to augment our treatment. And
Dr. Alpert reports having received speaker’s honoraria, consulting fees, and research support from numerous pharmaceutical companies.
For many adults, depression and chronic medical conditions are inextricably linked.
In fact, the prevalence of depression is 2-10 times higher among people with chronic medical conditions, particularly in people with chronic pain, where the prevalence reaches 40%-60%, according to Jonathan E. Alpert, MD, PhD.
“About 60% of adults over 65 have two or more chronic conditions, of which depression is the single most common comorbidity,” Dr. Alpert, chair of the department of psychiatry and behavioral sciences at the Montefiore Medical Center and Albert Einstein College of Medicine, both in New York, said during an annual psychopharmacology update held by the Nevada Psychiatric Association.
“Premorbid depression is a risk factor for a number of medical conditions, such as heart disease. We also know that medical illness is a risk factor for depression. Comorbid depression predicts poorer health outcomes, including disability, hospital readmission, and mortality. It is also associated with up to severalfold higher general medical costs.”
Despite the pervasive nature of depression on other medical conditions, a limited evidence base exists to guide clinicians on treatment approaches.
“Most major depressive disorder randomized clinical trials exclude individuals with active medical illness, but we do know that medical comorbidity is associated with poorer depression outcomes,” Dr. Alpert said. For example, the STAR*D trial found that people with major depressive disorder plus medical comorbidity had lower remission rates, compared with those who had MDD alone (P < .001), while a large analysis from University of Pittsburgh researchers found that people with medical comorbidities had higher depression recurrence rates.
An assessment of the relationship between medical conditions and depression should include thinking about the association between the medical illness itself and medications with depressive symptoms.
“Are the medications contributing to depressive symptoms?” he asked. “We also want to be thinking of the impact of medical illness and medications on antidepressant pharmacokinetics and pharmacodynamics. We also want to know about the evidence for antidepressant safety, tolerability, efficacy, and anticipated drug-drug interactions among individuals with the medical illness. You also want to enhance focus on treatment adherence and coordination of care.”
Nontraditional routes of antidepressant administration exist for patients who have difficulty swallowing pills. Food and Drug Administration–approved options include transdermal selegiline; intranasal esketamine; liquid forms of fluoxetine, escitalopram, paroxetine, nortriptyline, doxepin, imipramine, and lithium; and oral disintegrating tablet forms of mirtazapine and selegiline. As for non–FDA-approved forms of antidepressant administration, small studies or case reports have appeared in the medical literature regarding intravenous ketamine, citalopram, amitriptyline, mirtazapine, maprotiline, and lithium; intramuscular ketamine and amitriptyline; and rectal forms of antidepressants such as trazodone, amitriptyline, doxepin, fluoxetine, and lamotrigine.
“It’s good to keep in mind that, when you’re not able to use by mouth antidepressants or typical tablet forms of antidepressants, there are other options available,” said Dr. Alpert, who is also chair of the American Psychiatric Association’s Council on Research.
Metabolism of medications occurs primarily in the liver, he continued, but some metabolic enzymes also line the intestinal tract. The metabolism of a substrate may be inhibited or induced by other drugs.
“If someone is on drug A and we give drug B, and drug B is inhibiting the metabolism of drug A, there will be a very rapid impact – hours to just a few days,” Dr. Alpert said. “The substrate levels rise very quickly, so within hours or days of taking drug B, drug A levels can rise steeply.” On the other hand, if someone is on drug A and you give a drug B – which induces the enzymes that usually metabolize drug A – the impact will be gradual. “That’s because induction requires increased synthesis of the metabolic enzyme responsible for metabolizing drug A,” he said. “That happens over days to weeks.”
Medications that are potential inducers of metabolism include carbamazepine, phenobarbital, phenytoin, primidone, prednisone, ritonavir, rifampin, chronic alcohol use, chronic smoking, St. John’s wort, and consumption of large quantities of cruciferous vegetables and charbroiled meats.
On the other hand, potential inhibitors of metabolism include antifungals, macrolide antibiotics, fluoroquinolones, antiretrovirals, isoniazid, antimalarials, disulfiram, SSRIs, phenothiazines, valproic acid, nefazodone, duloxetine, bupropion, beta-blockers, acute alcohol use, cimetidine, quinidine, calcium channel blockers, grapefruit juice, propafenone, and amiodarone.
“When treating people with significant medical comorbidity, start low and go slow, but persevere,” Dr. Alpert advised. “We want to always think about the risk of treating versus the risk of not treating, or not treating actively enough. Often, people with comorbid medical illness require the same or even more assertive treatment with pharmacotherapy for their depression as people without medical illness. So, we don’t want to make the mistake of undertreating depression. We also want to anticipate and address challenges with adherence.”
He also recommended being mindful of the most salient side effects for a given condition, such as lowered seizure threshold or QT prolongation in populations with brain injury or with cardiovascular disease, and to leverage dual benefits when they might exist, such as using [selective norepinephrine reuptake inhibitors] for depression and pain or hot flashes, or bupropion for depression and smoking cessation, or mirtazapine, which is effective for nausea, cachexia, or insomnia, as well as depression itself.
“We want to collaborate closely and regularly with other treaters, sharing our notes and diagnostic impressions,” Dr. Alpert said. “We want to use all the tools in the box in addition to pharmacotherapy, thinking about psychotherapy, neuromodulation, and peer navigators. We want to strive for measurement-based care using rating scales when we can, to augment our treatment. And
Dr. Alpert reports having received speaker’s honoraria, consulting fees, and research support from numerous pharmaceutical companies.
FROM NPA 2021
Screening tool may help better predict suicide attempts in adolescents
Researchers have developed a proprietary computer adaptive screening tool that may help emergency departments more accurately predict suicide attempts in adolescents, according to a recent study in JAMA Psychiatry.
The computerized adaptive screen for suicidal youth (CASSY) had an area under the curve (AUC) of 0.87 in an independent validation cohort that predicted an adolescent suicide attempt within 3 months, according to Cheryl A. King, PhD, of the department of psychiatry at the University of Michigan in Ann Arbor, and colleagues. CASSY’s adaptive design, which presents different questions based on a respondent’s answers, means “an individual’s initial item responses are used to determine a provisional estimate of their standing on the measured trait,” the researchers said.
Dr. King and colleagues evaluated the CASSY algorithm in a first study that consisted of 2,845 adolescents who were mean 15.1 years old, mostly girls (63%) enrolled from 13 different emergency departments across the United States within the Pediatric Emergency Care Applied Research Network (PECARN) between June 2015 and July 2016. To develop the CASSY algorithm, the participants received a 92-item self-report survey at baseline with three “anchor” questions from the Ask Suicide-Screening Questions (ASQ) and Columbia–Suicide Severity Rating Scale (C-SSRS). Based on the answers to the baseline survey, the researchers categorized participants as being at low, medium, or high risk for a suicide attempt, and followed participants for 3 months to record suicide attempts reported by a patient or parent.
Retention of participants at 3 months was 72.9%, leaving data available for 2,075 adolescents for review. The researchers found that the AUC was 0.89 (95% confidence interval, 0.85-0.91) in the first study, with a sensitivity of 82.4% and a specificity of 80%. Participants answered a mean number of 11 items during an assessment (range, 5-21 items) administered in a median time of 1 minute, 24 seconds.
In a second study consisting of a validation cohort, 4,050 adolescents from 14 PECARN emergency departments and 1 Indian Health Service hospital were followed, with a retention of 2,754 participants (69.5%) at the end of 3 months. Of the adolescents available at the end of 3 months, 62.1% were girls with a mean age of 15.0 years. The AUC for this validation group was 0.87 (95% CI, 0.85-0.89). Of these participants, 71.5% reported no previous suicide attempts, 9% reported one prior attempt, 18.2% reported multiple attempts, and 1.2% had an unknown number of suicide attempts. During the 3-month window of the second study, 6.0% of participants had at least one suicide attempt.
The researchers said that while the CASSY instrument may be advantageous for some emergency departments, “a standard screen such as the ASQ, which consists of fewer items, may be preferred in some settings, particularly those in which the cost and technical setup of a computerized adaptive screen poses too high a barrier.”
Dr. King and colleagues concluded.
Climbing adolescent suicide rate
In an interview, Igor Galynker, MD, PhD, professor in the department of psychiatry, and director of the suicide lab and the Zirinsky Center for Bipolar Disorder at the Icahn School of Medicine at Mount Sinai, New York, said the study by Dr. King and colleagues is important during a time when the suicide rate for adolescents is substantially increasing.
According to data from the CDC’s Web-based Injury Statistics Query and Reporting System, 1,750 adolescents died of suicide in 2018, and the rate of deaths by suicide has increased by 62% since the year 2000. “The issue really needs to be addressed,” said Dr. Galynker, who was not involved with the study.
Some methods of screening suicidal ideation that open with a direct question can miss suicide attempts in individuals who do not express these suicidal ideations, he explained, and the problem can be magnified in adolescent patients. “This is particularly difficult with adolescents because they’re notoriously poor historians. They cannot describe their feelings as well. It’s even more important to have methods that work for suicide prevention for adolescents and to support those predictors which do not rely on self-report,” he said.
Dr. Galynker said that CASSY is innovative because asking whether the patient is suicidal is not the “gateway question” and does not categorize people into groups determined to be at low, medium, or high risk for a suicide attempt.
“When you categorize people – adolescents in this particular case – you remove clinical judgment from [the] clinician. You deprive [the] clinician of exercising their clinical judgment in terms of somebody is or is not likely to die by suicide. That’s a serious problem,” he said, noting it may be one reason why these screening tools have difficulty identifying patients at risk of suicide.
Regarding limitations, the 3-month follow-up window for patients in the study may be too long to be clinically meaningful.
“If somebody is in treatment, 3 months is a long time. You want to know whether somebody is going to attempt suicide before the next time you see them, which is usually a month or a week,” he said.
But a strength of the CASSY instrument, Dr. Galynker said, is its ability to capture the patient’s mental state in the moment, as opposed to relying only a patient’s electronic medical record. The study also demonstrates “it should be possible to introduce detailed suicide risk assessment in the emergency rooms, and [it] should be done,” he said.
This study was funded with support from the Health Resources and Services Administration, the Maternal and Child Health Bureau, and the Emergency Medical Services for Children Network Development Demonstration Program, and a grant by the National Institute of Mental Health for the Emergency Department Screen for Teens at Risk for Suicide. Twelve authors reported personal and institutional relationships in the form of fees, grants, consultancies, royalties, copyrighted work, founding of technologies, and scientific council memberships for a variety of agencies, societies, foundations, and other organizations inside and outside of the study. Dr. Galynker reported his work unrelated to the study is supported by the National Institute of Mental Health and the American Foundation for Suicide Prevention. But he has no proprietary interests.
Researchers have developed a proprietary computer adaptive screening tool that may help emergency departments more accurately predict suicide attempts in adolescents, according to a recent study in JAMA Psychiatry.
The computerized adaptive screen for suicidal youth (CASSY) had an area under the curve (AUC) of 0.87 in an independent validation cohort that predicted an adolescent suicide attempt within 3 months, according to Cheryl A. King, PhD, of the department of psychiatry at the University of Michigan in Ann Arbor, and colleagues. CASSY’s adaptive design, which presents different questions based on a respondent’s answers, means “an individual’s initial item responses are used to determine a provisional estimate of their standing on the measured trait,” the researchers said.
Dr. King and colleagues evaluated the CASSY algorithm in a first study that consisted of 2,845 adolescents who were mean 15.1 years old, mostly girls (63%) enrolled from 13 different emergency departments across the United States within the Pediatric Emergency Care Applied Research Network (PECARN) between June 2015 and July 2016. To develop the CASSY algorithm, the participants received a 92-item self-report survey at baseline with three “anchor” questions from the Ask Suicide-Screening Questions (ASQ) and Columbia–Suicide Severity Rating Scale (C-SSRS). Based on the answers to the baseline survey, the researchers categorized participants as being at low, medium, or high risk for a suicide attempt, and followed participants for 3 months to record suicide attempts reported by a patient or parent.
Retention of participants at 3 months was 72.9%, leaving data available for 2,075 adolescents for review. The researchers found that the AUC was 0.89 (95% confidence interval, 0.85-0.91) in the first study, with a sensitivity of 82.4% and a specificity of 80%. Participants answered a mean number of 11 items during an assessment (range, 5-21 items) administered in a median time of 1 minute, 24 seconds.
In a second study consisting of a validation cohort, 4,050 adolescents from 14 PECARN emergency departments and 1 Indian Health Service hospital were followed, with a retention of 2,754 participants (69.5%) at the end of 3 months. Of the adolescents available at the end of 3 months, 62.1% were girls with a mean age of 15.0 years. The AUC for this validation group was 0.87 (95% CI, 0.85-0.89). Of these participants, 71.5% reported no previous suicide attempts, 9% reported one prior attempt, 18.2% reported multiple attempts, and 1.2% had an unknown number of suicide attempts. During the 3-month window of the second study, 6.0% of participants had at least one suicide attempt.
The researchers said that while the CASSY instrument may be advantageous for some emergency departments, “a standard screen such as the ASQ, which consists of fewer items, may be preferred in some settings, particularly those in which the cost and technical setup of a computerized adaptive screen poses too high a barrier.”
Dr. King and colleagues concluded.
Climbing adolescent suicide rate
In an interview, Igor Galynker, MD, PhD, professor in the department of psychiatry, and director of the suicide lab and the Zirinsky Center for Bipolar Disorder at the Icahn School of Medicine at Mount Sinai, New York, said the study by Dr. King and colleagues is important during a time when the suicide rate for adolescents is substantially increasing.
According to data from the CDC’s Web-based Injury Statistics Query and Reporting System, 1,750 adolescents died of suicide in 2018, and the rate of deaths by suicide has increased by 62% since the year 2000. “The issue really needs to be addressed,” said Dr. Galynker, who was not involved with the study.
Some methods of screening suicidal ideation that open with a direct question can miss suicide attempts in individuals who do not express these suicidal ideations, he explained, and the problem can be magnified in adolescent patients. “This is particularly difficult with adolescents because they’re notoriously poor historians. They cannot describe their feelings as well. It’s even more important to have methods that work for suicide prevention for adolescents and to support those predictors which do not rely on self-report,” he said.
Dr. Galynker said that CASSY is innovative because asking whether the patient is suicidal is not the “gateway question” and does not categorize people into groups determined to be at low, medium, or high risk for a suicide attempt.
“When you categorize people – adolescents in this particular case – you remove clinical judgment from [the] clinician. You deprive [the] clinician of exercising their clinical judgment in terms of somebody is or is not likely to die by suicide. That’s a serious problem,” he said, noting it may be one reason why these screening tools have difficulty identifying patients at risk of suicide.
Regarding limitations, the 3-month follow-up window for patients in the study may be too long to be clinically meaningful.
“If somebody is in treatment, 3 months is a long time. You want to know whether somebody is going to attempt suicide before the next time you see them, which is usually a month or a week,” he said.
But a strength of the CASSY instrument, Dr. Galynker said, is its ability to capture the patient’s mental state in the moment, as opposed to relying only a patient’s electronic medical record. The study also demonstrates “it should be possible to introduce detailed suicide risk assessment in the emergency rooms, and [it] should be done,” he said.
This study was funded with support from the Health Resources and Services Administration, the Maternal and Child Health Bureau, and the Emergency Medical Services for Children Network Development Demonstration Program, and a grant by the National Institute of Mental Health for the Emergency Department Screen for Teens at Risk for Suicide. Twelve authors reported personal and institutional relationships in the form of fees, grants, consultancies, royalties, copyrighted work, founding of technologies, and scientific council memberships for a variety of agencies, societies, foundations, and other organizations inside and outside of the study. Dr. Galynker reported his work unrelated to the study is supported by the National Institute of Mental Health and the American Foundation for Suicide Prevention. But he has no proprietary interests.
Researchers have developed a proprietary computer adaptive screening tool that may help emergency departments more accurately predict suicide attempts in adolescents, according to a recent study in JAMA Psychiatry.
The computerized adaptive screen for suicidal youth (CASSY) had an area under the curve (AUC) of 0.87 in an independent validation cohort that predicted an adolescent suicide attempt within 3 months, according to Cheryl A. King, PhD, of the department of psychiatry at the University of Michigan in Ann Arbor, and colleagues. CASSY’s adaptive design, which presents different questions based on a respondent’s answers, means “an individual’s initial item responses are used to determine a provisional estimate of their standing on the measured trait,” the researchers said.
Dr. King and colleagues evaluated the CASSY algorithm in a first study that consisted of 2,845 adolescents who were mean 15.1 years old, mostly girls (63%) enrolled from 13 different emergency departments across the United States within the Pediatric Emergency Care Applied Research Network (PECARN) between June 2015 and July 2016. To develop the CASSY algorithm, the participants received a 92-item self-report survey at baseline with three “anchor” questions from the Ask Suicide-Screening Questions (ASQ) and Columbia–Suicide Severity Rating Scale (C-SSRS). Based on the answers to the baseline survey, the researchers categorized participants as being at low, medium, or high risk for a suicide attempt, and followed participants for 3 months to record suicide attempts reported by a patient or parent.
Retention of participants at 3 months was 72.9%, leaving data available for 2,075 adolescents for review. The researchers found that the AUC was 0.89 (95% confidence interval, 0.85-0.91) in the first study, with a sensitivity of 82.4% and a specificity of 80%. Participants answered a mean number of 11 items during an assessment (range, 5-21 items) administered in a median time of 1 minute, 24 seconds.
In a second study consisting of a validation cohort, 4,050 adolescents from 14 PECARN emergency departments and 1 Indian Health Service hospital were followed, with a retention of 2,754 participants (69.5%) at the end of 3 months. Of the adolescents available at the end of 3 months, 62.1% were girls with a mean age of 15.0 years. The AUC for this validation group was 0.87 (95% CI, 0.85-0.89). Of these participants, 71.5% reported no previous suicide attempts, 9% reported one prior attempt, 18.2% reported multiple attempts, and 1.2% had an unknown number of suicide attempts. During the 3-month window of the second study, 6.0% of participants had at least one suicide attempt.
The researchers said that while the CASSY instrument may be advantageous for some emergency departments, “a standard screen such as the ASQ, which consists of fewer items, may be preferred in some settings, particularly those in which the cost and technical setup of a computerized adaptive screen poses too high a barrier.”
Dr. King and colleagues concluded.
Climbing adolescent suicide rate
In an interview, Igor Galynker, MD, PhD, professor in the department of psychiatry, and director of the suicide lab and the Zirinsky Center for Bipolar Disorder at the Icahn School of Medicine at Mount Sinai, New York, said the study by Dr. King and colleagues is important during a time when the suicide rate for adolescents is substantially increasing.
According to data from the CDC’s Web-based Injury Statistics Query and Reporting System, 1,750 adolescents died of suicide in 2018, and the rate of deaths by suicide has increased by 62% since the year 2000. “The issue really needs to be addressed,” said Dr. Galynker, who was not involved with the study.
Some methods of screening suicidal ideation that open with a direct question can miss suicide attempts in individuals who do not express these suicidal ideations, he explained, and the problem can be magnified in adolescent patients. “This is particularly difficult with adolescents because they’re notoriously poor historians. They cannot describe their feelings as well. It’s even more important to have methods that work for suicide prevention for adolescents and to support those predictors which do not rely on self-report,” he said.
Dr. Galynker said that CASSY is innovative because asking whether the patient is suicidal is not the “gateway question” and does not categorize people into groups determined to be at low, medium, or high risk for a suicide attempt.
“When you categorize people – adolescents in this particular case – you remove clinical judgment from [the] clinician. You deprive [the] clinician of exercising their clinical judgment in terms of somebody is or is not likely to die by suicide. That’s a serious problem,” he said, noting it may be one reason why these screening tools have difficulty identifying patients at risk of suicide.
Regarding limitations, the 3-month follow-up window for patients in the study may be too long to be clinically meaningful.
“If somebody is in treatment, 3 months is a long time. You want to know whether somebody is going to attempt suicide before the next time you see them, which is usually a month or a week,” he said.
But a strength of the CASSY instrument, Dr. Galynker said, is its ability to capture the patient’s mental state in the moment, as opposed to relying only a patient’s electronic medical record. The study also demonstrates “it should be possible to introduce detailed suicide risk assessment in the emergency rooms, and [it] should be done,” he said.
This study was funded with support from the Health Resources and Services Administration, the Maternal and Child Health Bureau, and the Emergency Medical Services for Children Network Development Demonstration Program, and a grant by the National Institute of Mental Health for the Emergency Department Screen for Teens at Risk for Suicide. Twelve authors reported personal and institutional relationships in the form of fees, grants, consultancies, royalties, copyrighted work, founding of technologies, and scientific council memberships for a variety of agencies, societies, foundations, and other organizations inside and outside of the study. Dr. Galynker reported his work unrelated to the study is supported by the National Institute of Mental Health and the American Foundation for Suicide Prevention. But he has no proprietary interests.
FROM JAMA PSYCHIATRY
Being in the now
Mindfulness as an intervention in challenging, changing, and uncertain times
The COVID-19 pandemic, multiple national displays of racial and social injustice, and recent political strife have left many feeling uncertain, anxious, sad, angry, grief-stricken, and struggling to cope. Coping may be especially difficult for our clients already grappling with mental health concerns, and many are looking to mental health professionals to restore a sense of well-being.
As professionals, we may be unsure about the best approach; after all, we haven’t experienced anything like this before! We’re facing many unknowns and unanswered questions, but one thing we do know is that we’re dealing with constant change. And, in fact, the only certainty is continued change and uncertainty. The truth of uncertainty can be challenging to contend with, especially when so much, including our country’s future, is in question. In times like this, there is likely no perfect treatment, but mindfulness can serve as a powerful intervention for coping with uncertainty and change, and for managing a range of difficult reactions.
The ‘what’ of mindfulness: Awareness, being in the now, and nonattachment
It’s crucial that we understand what mindfulness really is. It’s become something of a buzzword in American society, complete with misconceptions. Mindfulness has roots in many faith traditions, but as it’s practiced in the Western world, it usually has roots in Hinduism and Buddhism.
Mindfulness roughly means “awareness”; this is an approximate translation of the Pali (an ancient Indian language) word “Sati.” Mindfulness is moment-to-moment awareness and acceptance of our present experiences, thoughts, and feelings, without judgment or attachment. Attachment relates to the continually changing nature of all thoughts, feelings, and situations. Because everything is continuously changing, we needn’t become attached; attachment can keep us from being in the now. Acceptance means facing the now, which is essential when we feel tempted to avoid or deny painful feelings or situations. Acceptance doesn’t mean that we’ve resigned to being in pain forever; it merely means that we’re willing to see things as they actually are right now. This honest assessment of the present can prepare us for next steps.
Being in touch with the now helps us reconnect with ourselves, promote clarity about our situation and choices, and increases our awareness of our thoughts and feelings, moment to moment. It can also help us realize when we’ve fallen into unhelpful or catastrophic thinking, the risk of which is high during intense stress and uncertainty like what we’re facing now. Mindfulness helps us catch ourselves so we have the opportunity to make different choices, and feel better.
The how of mindfulness: Symptom management and changes in the brain
Research on mindfulness suggests that it can improve coping with anxiety,1 regulate mood,2 improve depression,3 reduce rumination,4 and mitigate trauma symptom severity.
Because mindfulness can effectively address psychiatric concerns, mindfulness-based clinical interventions such as mindfulness-based stress reduction and mindfulness-based cognitive therapy have been developed. These may reduce anxiety,5 depression, and posttraumatic stress disorder.6 Mindfulness can have a powerful impact on the brain; it’s been shown to improve the functioning of the regions associated with emotional regulation7 and change the regions related to awareness and fear.8 So, whether mindfulness is practiced in our clients’ everyday lives or used as the basis of therapeutic programs, it can promote well-being.
The how of mindfulness: In everyday life and treatment
How can we help our clients enjoy mindfulness’ benefits? I suggest that we start with ourselves. We’ll be more effective at guiding our clients in using mindfulness if we have our own experience.
And, mindfulness may help us to be more attentive to and effective in treatment. There is research demonstrating that treatment providers can benefit from mindfulness practices,9 and that clinicians who practice mindfulness report higher levels of empathy toward their clients.10 Because mindfulness is about attention and nonjudgmental and nonattached observation, it can be incorporated into many aspects of everyday life. Many options are available; we might encourage our clients to begin their day with a mindful pause, simply breathing and observing thoughts, feelings, sensations, or anything else that comes up. If they find themselves fixated on negative thinking or feelings, nonjudgmentally recognizing these experiences as temporary can help to prevent immersion and overwhelm. , perhaps during tasks such as housekeeping, working, talking with others, exercising, and even eating.
It can be beneficial to practice mindfulness before, during, and after situations that our clients know may bring on increased stress, anxiety, negative mood, and other undesirable experiences, such as watching the news or using some forms of social media. For clients who want more structure or guidance, several mobile apps are available, such as InsightTimer, Ten Percent Happier, or for Black clients, Liberate, which may be especially helpful for the impacts of racial injustice. Apps may also help clients who want to establish a formal mindfulness meditation practice, which may decrease anxiety and depression in some clinical populations.11 And, of course, with training, we can incorporate mindfulness into treatment. We may encourage clients to start our treatment or therapy sessions with a mindful pause to help them attain calm and focus, and depending on their concerns and needs, during times at which they feel particularly strong emotions. Clients may consider taking a Mindfulness-Based Stress Reduction course if something more intensive is needed, or clinicians may consider becoming trained in mindfulness-based cognitive therapy. Because recognition is increasing that mindfulness can address many clinical concerns, and because we’re contending with unprecedented challenges, mindfulness training for clinicians has become widely available.
Calm, clarity, and choices
None of us as individuals can eliminate the strife our country is living through, and none of us as clinicians can completely prevent or alleviate our clients’ pain. But by employing mindfulness, we can help clients cope with change and uncertainty, gain greater awareness of themselves and their experiences, feel calmer, attain more clarity to make better choices, and ultimately, feel better.
References
1. Bernstein A et al. J Cogn Psychother. 2011;25(2):99-113.
2. Remmers C et al. Mindfulness. 2016;7(4):829-37.
3. Rodrigues MF et al. Trends Psychiatry Psychother. Jul-Sep 2017;39(3):207-15.
4. Chambers R et al. Cogn Ther Res. 2008;32(3):303-22.
5. Montero-Marin et al. Psychol Med. 2019 Oct;49(13)2118-33.
6. Khusid MA, Vythilingam M. Mil Med. 2016 Sep;181(9):961-8.
7. Kral TRA et al. Neuroimage. 2018 Nov 1;181:301-13.
8. Desbordes G et al. Front Hum Neurosci. 2012 Nov 1. doi: 10.33891/fnhum.2012.00292.
9. Escuriex BF, Labbé EE. Mindfulness. 2011;2(4):242-53.
10. Aiken GA. Dissertation Abstracts Int Sec B: Sci Eng. 2006;67(4-B),2212.
11. Goyal M et al. JAMA Intern Med. 2014 Mar;174:357-68.
Dr. Collins is a Brooklyn-based licensed counseling psychologist, educator, and speaker. She is experienced in addressing a wide range of mental health concerns within youth, adult, and family populations. Her work has a strong social justice emphasis, and she is particularly skilled at working with clients of color. She has been a mindfulness practitioner for 10 years and is passionate about sharing the practice with others. Dr. Collins has no conflicts of interest.
Mindfulness as an intervention in challenging, changing, and uncertain times
Mindfulness as an intervention in challenging, changing, and uncertain times
The COVID-19 pandemic, multiple national displays of racial and social injustice, and recent political strife have left many feeling uncertain, anxious, sad, angry, grief-stricken, and struggling to cope. Coping may be especially difficult for our clients already grappling with mental health concerns, and many are looking to mental health professionals to restore a sense of well-being.
As professionals, we may be unsure about the best approach; after all, we haven’t experienced anything like this before! We’re facing many unknowns and unanswered questions, but one thing we do know is that we’re dealing with constant change. And, in fact, the only certainty is continued change and uncertainty. The truth of uncertainty can be challenging to contend with, especially when so much, including our country’s future, is in question. In times like this, there is likely no perfect treatment, but mindfulness can serve as a powerful intervention for coping with uncertainty and change, and for managing a range of difficult reactions.
The ‘what’ of mindfulness: Awareness, being in the now, and nonattachment
It’s crucial that we understand what mindfulness really is. It’s become something of a buzzword in American society, complete with misconceptions. Mindfulness has roots in many faith traditions, but as it’s practiced in the Western world, it usually has roots in Hinduism and Buddhism.
Mindfulness roughly means “awareness”; this is an approximate translation of the Pali (an ancient Indian language) word “Sati.” Mindfulness is moment-to-moment awareness and acceptance of our present experiences, thoughts, and feelings, without judgment or attachment. Attachment relates to the continually changing nature of all thoughts, feelings, and situations. Because everything is continuously changing, we needn’t become attached; attachment can keep us from being in the now. Acceptance means facing the now, which is essential when we feel tempted to avoid or deny painful feelings or situations. Acceptance doesn’t mean that we’ve resigned to being in pain forever; it merely means that we’re willing to see things as they actually are right now. This honest assessment of the present can prepare us for next steps.
Being in touch with the now helps us reconnect with ourselves, promote clarity about our situation and choices, and increases our awareness of our thoughts and feelings, moment to moment. It can also help us realize when we’ve fallen into unhelpful or catastrophic thinking, the risk of which is high during intense stress and uncertainty like what we’re facing now. Mindfulness helps us catch ourselves so we have the opportunity to make different choices, and feel better.
The how of mindfulness: Symptom management and changes in the brain
Research on mindfulness suggests that it can improve coping with anxiety,1 regulate mood,2 improve depression,3 reduce rumination,4 and mitigate trauma symptom severity.
Because mindfulness can effectively address psychiatric concerns, mindfulness-based clinical interventions such as mindfulness-based stress reduction and mindfulness-based cognitive therapy have been developed. These may reduce anxiety,5 depression, and posttraumatic stress disorder.6 Mindfulness can have a powerful impact on the brain; it’s been shown to improve the functioning of the regions associated with emotional regulation7 and change the regions related to awareness and fear.8 So, whether mindfulness is practiced in our clients’ everyday lives or used as the basis of therapeutic programs, it can promote well-being.
The how of mindfulness: In everyday life and treatment
How can we help our clients enjoy mindfulness’ benefits? I suggest that we start with ourselves. We’ll be more effective at guiding our clients in using mindfulness if we have our own experience.
And, mindfulness may help us to be more attentive to and effective in treatment. There is research demonstrating that treatment providers can benefit from mindfulness practices,9 and that clinicians who practice mindfulness report higher levels of empathy toward their clients.10 Because mindfulness is about attention and nonjudgmental and nonattached observation, it can be incorporated into many aspects of everyday life. Many options are available; we might encourage our clients to begin their day with a mindful pause, simply breathing and observing thoughts, feelings, sensations, or anything else that comes up. If they find themselves fixated on negative thinking or feelings, nonjudgmentally recognizing these experiences as temporary can help to prevent immersion and overwhelm. , perhaps during tasks such as housekeeping, working, talking with others, exercising, and even eating.
It can be beneficial to practice mindfulness before, during, and after situations that our clients know may bring on increased stress, anxiety, negative mood, and other undesirable experiences, such as watching the news or using some forms of social media. For clients who want more structure or guidance, several mobile apps are available, such as InsightTimer, Ten Percent Happier, or for Black clients, Liberate, which may be especially helpful for the impacts of racial injustice. Apps may also help clients who want to establish a formal mindfulness meditation practice, which may decrease anxiety and depression in some clinical populations.11 And, of course, with training, we can incorporate mindfulness into treatment. We may encourage clients to start our treatment or therapy sessions with a mindful pause to help them attain calm and focus, and depending on their concerns and needs, during times at which they feel particularly strong emotions. Clients may consider taking a Mindfulness-Based Stress Reduction course if something more intensive is needed, or clinicians may consider becoming trained in mindfulness-based cognitive therapy. Because recognition is increasing that mindfulness can address many clinical concerns, and because we’re contending with unprecedented challenges, mindfulness training for clinicians has become widely available.
Calm, clarity, and choices
None of us as individuals can eliminate the strife our country is living through, and none of us as clinicians can completely prevent or alleviate our clients’ pain. But by employing mindfulness, we can help clients cope with change and uncertainty, gain greater awareness of themselves and their experiences, feel calmer, attain more clarity to make better choices, and ultimately, feel better.
References
1. Bernstein A et al. J Cogn Psychother. 2011;25(2):99-113.
2. Remmers C et al. Mindfulness. 2016;7(4):829-37.
3. Rodrigues MF et al. Trends Psychiatry Psychother. Jul-Sep 2017;39(3):207-15.
4. Chambers R et al. Cogn Ther Res. 2008;32(3):303-22.
5. Montero-Marin et al. Psychol Med. 2019 Oct;49(13)2118-33.
6. Khusid MA, Vythilingam M. Mil Med. 2016 Sep;181(9):961-8.
7. Kral TRA et al. Neuroimage. 2018 Nov 1;181:301-13.
8. Desbordes G et al. Front Hum Neurosci. 2012 Nov 1. doi: 10.33891/fnhum.2012.00292.
9. Escuriex BF, Labbé EE. Mindfulness. 2011;2(4):242-53.
10. Aiken GA. Dissertation Abstracts Int Sec B: Sci Eng. 2006;67(4-B),2212.
11. Goyal M et al. JAMA Intern Med. 2014 Mar;174:357-68.
Dr. Collins is a Brooklyn-based licensed counseling psychologist, educator, and speaker. She is experienced in addressing a wide range of mental health concerns within youth, adult, and family populations. Her work has a strong social justice emphasis, and she is particularly skilled at working with clients of color. She has been a mindfulness practitioner for 10 years and is passionate about sharing the practice with others. Dr. Collins has no conflicts of interest.
The COVID-19 pandemic, multiple national displays of racial and social injustice, and recent political strife have left many feeling uncertain, anxious, sad, angry, grief-stricken, and struggling to cope. Coping may be especially difficult for our clients already grappling with mental health concerns, and many are looking to mental health professionals to restore a sense of well-being.
As professionals, we may be unsure about the best approach; after all, we haven’t experienced anything like this before! We’re facing many unknowns and unanswered questions, but one thing we do know is that we’re dealing with constant change. And, in fact, the only certainty is continued change and uncertainty. The truth of uncertainty can be challenging to contend with, especially when so much, including our country’s future, is in question. In times like this, there is likely no perfect treatment, but mindfulness can serve as a powerful intervention for coping with uncertainty and change, and for managing a range of difficult reactions.
The ‘what’ of mindfulness: Awareness, being in the now, and nonattachment
It’s crucial that we understand what mindfulness really is. It’s become something of a buzzword in American society, complete with misconceptions. Mindfulness has roots in many faith traditions, but as it’s practiced in the Western world, it usually has roots in Hinduism and Buddhism.
Mindfulness roughly means “awareness”; this is an approximate translation of the Pali (an ancient Indian language) word “Sati.” Mindfulness is moment-to-moment awareness and acceptance of our present experiences, thoughts, and feelings, without judgment or attachment. Attachment relates to the continually changing nature of all thoughts, feelings, and situations. Because everything is continuously changing, we needn’t become attached; attachment can keep us from being in the now. Acceptance means facing the now, which is essential when we feel tempted to avoid or deny painful feelings or situations. Acceptance doesn’t mean that we’ve resigned to being in pain forever; it merely means that we’re willing to see things as they actually are right now. This honest assessment of the present can prepare us for next steps.
Being in touch with the now helps us reconnect with ourselves, promote clarity about our situation and choices, and increases our awareness of our thoughts and feelings, moment to moment. It can also help us realize when we’ve fallen into unhelpful or catastrophic thinking, the risk of which is high during intense stress and uncertainty like what we’re facing now. Mindfulness helps us catch ourselves so we have the opportunity to make different choices, and feel better.
The how of mindfulness: Symptom management and changes in the brain
Research on mindfulness suggests that it can improve coping with anxiety,1 regulate mood,2 improve depression,3 reduce rumination,4 and mitigate trauma symptom severity.
Because mindfulness can effectively address psychiatric concerns, mindfulness-based clinical interventions such as mindfulness-based stress reduction and mindfulness-based cognitive therapy have been developed. These may reduce anxiety,5 depression, and posttraumatic stress disorder.6 Mindfulness can have a powerful impact on the brain; it’s been shown to improve the functioning of the regions associated with emotional regulation7 and change the regions related to awareness and fear.8 So, whether mindfulness is practiced in our clients’ everyday lives or used as the basis of therapeutic programs, it can promote well-being.
The how of mindfulness: In everyday life and treatment
How can we help our clients enjoy mindfulness’ benefits? I suggest that we start with ourselves. We’ll be more effective at guiding our clients in using mindfulness if we have our own experience.
And, mindfulness may help us to be more attentive to and effective in treatment. There is research demonstrating that treatment providers can benefit from mindfulness practices,9 and that clinicians who practice mindfulness report higher levels of empathy toward their clients.10 Because mindfulness is about attention and nonjudgmental and nonattached observation, it can be incorporated into many aspects of everyday life. Many options are available; we might encourage our clients to begin their day with a mindful pause, simply breathing and observing thoughts, feelings, sensations, or anything else that comes up. If they find themselves fixated on negative thinking or feelings, nonjudgmentally recognizing these experiences as temporary can help to prevent immersion and overwhelm. , perhaps during tasks such as housekeeping, working, talking with others, exercising, and even eating.
It can be beneficial to practice mindfulness before, during, and after situations that our clients know may bring on increased stress, anxiety, negative mood, and other undesirable experiences, such as watching the news or using some forms of social media. For clients who want more structure or guidance, several mobile apps are available, such as InsightTimer, Ten Percent Happier, or for Black clients, Liberate, which may be especially helpful for the impacts of racial injustice. Apps may also help clients who want to establish a formal mindfulness meditation practice, which may decrease anxiety and depression in some clinical populations.11 And, of course, with training, we can incorporate mindfulness into treatment. We may encourage clients to start our treatment or therapy sessions with a mindful pause to help them attain calm and focus, and depending on their concerns and needs, during times at which they feel particularly strong emotions. Clients may consider taking a Mindfulness-Based Stress Reduction course if something more intensive is needed, or clinicians may consider becoming trained in mindfulness-based cognitive therapy. Because recognition is increasing that mindfulness can address many clinical concerns, and because we’re contending with unprecedented challenges, mindfulness training for clinicians has become widely available.
Calm, clarity, and choices
None of us as individuals can eliminate the strife our country is living through, and none of us as clinicians can completely prevent or alleviate our clients’ pain. But by employing mindfulness, we can help clients cope with change and uncertainty, gain greater awareness of themselves and their experiences, feel calmer, attain more clarity to make better choices, and ultimately, feel better.
References
1. Bernstein A et al. J Cogn Psychother. 2011;25(2):99-113.
2. Remmers C et al. Mindfulness. 2016;7(4):829-37.
3. Rodrigues MF et al. Trends Psychiatry Psychother. Jul-Sep 2017;39(3):207-15.
4. Chambers R et al. Cogn Ther Res. 2008;32(3):303-22.
5. Montero-Marin et al. Psychol Med. 2019 Oct;49(13)2118-33.
6. Khusid MA, Vythilingam M. Mil Med. 2016 Sep;181(9):961-8.
7. Kral TRA et al. Neuroimage. 2018 Nov 1;181:301-13.
8. Desbordes G et al. Front Hum Neurosci. 2012 Nov 1. doi: 10.33891/fnhum.2012.00292.
9. Escuriex BF, Labbé EE. Mindfulness. 2011;2(4):242-53.
10. Aiken GA. Dissertation Abstracts Int Sec B: Sci Eng. 2006;67(4-B),2212.
11. Goyal M et al. JAMA Intern Med. 2014 Mar;174:357-68.
Dr. Collins is a Brooklyn-based licensed counseling psychologist, educator, and speaker. She is experienced in addressing a wide range of mental health concerns within youth, adult, and family populations. Her work has a strong social justice emphasis, and she is particularly skilled at working with clients of color. She has been a mindfulness practitioner for 10 years and is passionate about sharing the practice with others. Dr. Collins has no conflicts of interest.
Psychiatrists’ happiness, well-being hit hard by COVID-19
Events of the past year have taken a huge toll on the happiness, wellness, and lifestyles of many, but especially those in the health care field, including psychiatrists.
The newly released Medscape Psychiatrist Lifestyle, Happiness & Burnout Report 2021 reveals how psychiatrists are coping with burnout and trying to maintain personal wellness, and how they view their workplaces and their futures amid the ongoing COVID-19 pandemic.
Before the pandemic hit in March 2020, 84% of psychiatrists who responded to the survey reported being happy outside of work, similar to the percentage (82%) of physicians overall.
But as the pandemic has worn on, feelings have shifted, and there are clear signs of strain on those in the health care field. Now, just over half (55%) of psychiatrists say they are happy outside of work, similar to the percentage (58%) of physicians overall.
Perhaps not surprising given the specific challenges of COVID-19, infectious disease physicians, pulmonologists, rheumatologists, and intensivists currently rank lowest in happiness outside of work.
Anxiety, depression, burnout
With the ongoing COVID-19 pandemic, more than three quarters (77%) of psychiatrists surveyed report experiencing some degree of anxiety about their future, the same percentage as for physicians overall.
This year, more psychiatrists reported being either burned out or burned out and depressed (41% vs. 35% last year). About two-thirds of psychiatrists said burnout has had at least a moderate impact on their lives; 5% consider the impact so severe that they are thinking of leaving medicine altogether.
The majority of burned-out psychiatrists (63%) said they felt that way even before the pandemic began; for about one-third (37%), burnout set in after the pandemic began.
in the workplace (39%) and spending too many hours at work (37%).
Psychiatrists’ top tactic to cope with burnout is talking with family or friends (53%), followed by isolating themselves from others (51%), sleeping (45%), and exercising (43%); 42% said they eat junk food to cope; 35% play music; and 25% drink alcohol.
Most psychiatrists (63%) suffering burnout and/or depression don’t plan on seeking professional help. About one-third are currently seeking help or plan to do so, the highest proportion among all specialties.
Considering their symptoms not severe enough (57%) and feeling that they could deal with the problem on their own (41%) are the top reasons for not seeking professional help; 36% said they were too busy to get help, and 17% said they didn’t want to risk disclosing a problem.
Fifteen percent of psychiatrists who are burned out, depressed, or both have contemplated suicide, and 2% have attempted suicide.
Striving for work-life balance
Work-life balance is the most pressing workplace issue for 45% of psychiatrists, and 44% would sacrifice some of their salary for better work-life balance. These figures are about the same for physicians overall.
Forty-seven percent of psychiatrists take 3-4 weeks of vacation each year; 16% take 5 or more weeks. In this there was no change from last year’s report.
About one-third (35%) of psychiatrists generally make time to focus on their own well-being, the same proportion as physicians overall.
About two-thirds (68%) of psychiatrists exercise two or more times per week. Half of psychiatrists said they are currently trying to lose weight; about one-quarter are trying to maintain their current weight.
About one-quarter (26%) of psychiatrists said they do not drink alcohol at all; 17% have five or more drinks per week.
Most psychiatrists are currently in a committed relationship, with 81% either married or living with a partner. Among psychiatrists who are married or living with a partner, 43% are with someone who also works in medicine. About 81% of psychiatrists say their marriages are very good or good. These percentages are similar to those of physicians overall (85%).
Most psychiatrists (58%) spend up to 10 hours per week online for personal reasons; 82% spend this amount of time online each week for work.
It’s likely that the amount of time spent online for work will increase, given the pandemic-fueled surge in telemedicine. Yet even when their personal and professional Internet use are combined, psychiatrists, on average, spend far less time online than the nearly 7 hours per day of the average Internet user, according to recent data.
Findings from the latest happiness, wellness, and lifestyle survey are based on 12,339 Medscape member physicians practicing in the United States who completed an online survey conducted between Aug. 30 and Nov. 5, 2020.
A version of this article first appeared on Medscape.com.
Events of the past year have taken a huge toll on the happiness, wellness, and lifestyles of many, but especially those in the health care field, including psychiatrists.
The newly released Medscape Psychiatrist Lifestyle, Happiness & Burnout Report 2021 reveals how psychiatrists are coping with burnout and trying to maintain personal wellness, and how they view their workplaces and their futures amid the ongoing COVID-19 pandemic.
Before the pandemic hit in March 2020, 84% of psychiatrists who responded to the survey reported being happy outside of work, similar to the percentage (82%) of physicians overall.
But as the pandemic has worn on, feelings have shifted, and there are clear signs of strain on those in the health care field. Now, just over half (55%) of psychiatrists say they are happy outside of work, similar to the percentage (58%) of physicians overall.
Perhaps not surprising given the specific challenges of COVID-19, infectious disease physicians, pulmonologists, rheumatologists, and intensivists currently rank lowest in happiness outside of work.
Anxiety, depression, burnout
With the ongoing COVID-19 pandemic, more than three quarters (77%) of psychiatrists surveyed report experiencing some degree of anxiety about their future, the same percentage as for physicians overall.
This year, more psychiatrists reported being either burned out or burned out and depressed (41% vs. 35% last year). About two-thirds of psychiatrists said burnout has had at least a moderate impact on their lives; 5% consider the impact so severe that they are thinking of leaving medicine altogether.
The majority of burned-out psychiatrists (63%) said they felt that way even before the pandemic began; for about one-third (37%), burnout set in after the pandemic began.
in the workplace (39%) and spending too many hours at work (37%).
Psychiatrists’ top tactic to cope with burnout is talking with family or friends (53%), followed by isolating themselves from others (51%), sleeping (45%), and exercising (43%); 42% said they eat junk food to cope; 35% play music; and 25% drink alcohol.
Most psychiatrists (63%) suffering burnout and/or depression don’t plan on seeking professional help. About one-third are currently seeking help or plan to do so, the highest proportion among all specialties.
Considering their symptoms not severe enough (57%) and feeling that they could deal with the problem on their own (41%) are the top reasons for not seeking professional help; 36% said they were too busy to get help, and 17% said they didn’t want to risk disclosing a problem.
Fifteen percent of psychiatrists who are burned out, depressed, or both have contemplated suicide, and 2% have attempted suicide.
Striving for work-life balance
Work-life balance is the most pressing workplace issue for 45% of psychiatrists, and 44% would sacrifice some of their salary for better work-life balance. These figures are about the same for physicians overall.
Forty-seven percent of psychiatrists take 3-4 weeks of vacation each year; 16% take 5 or more weeks. In this there was no change from last year’s report.
About one-third (35%) of psychiatrists generally make time to focus on their own well-being, the same proportion as physicians overall.
About two-thirds (68%) of psychiatrists exercise two or more times per week. Half of psychiatrists said they are currently trying to lose weight; about one-quarter are trying to maintain their current weight.
About one-quarter (26%) of psychiatrists said they do not drink alcohol at all; 17% have five or more drinks per week.
Most psychiatrists are currently in a committed relationship, with 81% either married or living with a partner. Among psychiatrists who are married or living with a partner, 43% are with someone who also works in medicine. About 81% of psychiatrists say their marriages are very good or good. These percentages are similar to those of physicians overall (85%).
Most psychiatrists (58%) spend up to 10 hours per week online for personal reasons; 82% spend this amount of time online each week for work.
It’s likely that the amount of time spent online for work will increase, given the pandemic-fueled surge in telemedicine. Yet even when their personal and professional Internet use are combined, psychiatrists, on average, spend far less time online than the nearly 7 hours per day of the average Internet user, according to recent data.
Findings from the latest happiness, wellness, and lifestyle survey are based on 12,339 Medscape member physicians practicing in the United States who completed an online survey conducted between Aug. 30 and Nov. 5, 2020.
A version of this article first appeared on Medscape.com.
Events of the past year have taken a huge toll on the happiness, wellness, and lifestyles of many, but especially those in the health care field, including psychiatrists.
The newly released Medscape Psychiatrist Lifestyle, Happiness & Burnout Report 2021 reveals how psychiatrists are coping with burnout and trying to maintain personal wellness, and how they view their workplaces and their futures amid the ongoing COVID-19 pandemic.
Before the pandemic hit in March 2020, 84% of psychiatrists who responded to the survey reported being happy outside of work, similar to the percentage (82%) of physicians overall.
But as the pandemic has worn on, feelings have shifted, and there are clear signs of strain on those in the health care field. Now, just over half (55%) of psychiatrists say they are happy outside of work, similar to the percentage (58%) of physicians overall.
Perhaps not surprising given the specific challenges of COVID-19, infectious disease physicians, pulmonologists, rheumatologists, and intensivists currently rank lowest in happiness outside of work.
Anxiety, depression, burnout
With the ongoing COVID-19 pandemic, more than three quarters (77%) of psychiatrists surveyed report experiencing some degree of anxiety about their future, the same percentage as for physicians overall.
This year, more psychiatrists reported being either burned out or burned out and depressed (41% vs. 35% last year). About two-thirds of psychiatrists said burnout has had at least a moderate impact on their lives; 5% consider the impact so severe that they are thinking of leaving medicine altogether.
The majority of burned-out psychiatrists (63%) said they felt that way even before the pandemic began; for about one-third (37%), burnout set in after the pandemic began.
in the workplace (39%) and spending too many hours at work (37%).
Psychiatrists’ top tactic to cope with burnout is talking with family or friends (53%), followed by isolating themselves from others (51%), sleeping (45%), and exercising (43%); 42% said they eat junk food to cope; 35% play music; and 25% drink alcohol.
Most psychiatrists (63%) suffering burnout and/or depression don’t plan on seeking professional help. About one-third are currently seeking help or plan to do so, the highest proportion among all specialties.
Considering their symptoms not severe enough (57%) and feeling that they could deal with the problem on their own (41%) are the top reasons for not seeking professional help; 36% said they were too busy to get help, and 17% said they didn’t want to risk disclosing a problem.
Fifteen percent of psychiatrists who are burned out, depressed, or both have contemplated suicide, and 2% have attempted suicide.
Striving for work-life balance
Work-life balance is the most pressing workplace issue for 45% of psychiatrists, and 44% would sacrifice some of their salary for better work-life balance. These figures are about the same for physicians overall.
Forty-seven percent of psychiatrists take 3-4 weeks of vacation each year; 16% take 5 or more weeks. In this there was no change from last year’s report.
About one-third (35%) of psychiatrists generally make time to focus on their own well-being, the same proportion as physicians overall.
About two-thirds (68%) of psychiatrists exercise two or more times per week. Half of psychiatrists said they are currently trying to lose weight; about one-quarter are trying to maintain their current weight.
About one-quarter (26%) of psychiatrists said they do not drink alcohol at all; 17% have five or more drinks per week.
Most psychiatrists are currently in a committed relationship, with 81% either married or living with a partner. Among psychiatrists who are married or living with a partner, 43% are with someone who also works in medicine. About 81% of psychiatrists say their marriages are very good or good. These percentages are similar to those of physicians overall (85%).
Most psychiatrists (58%) spend up to 10 hours per week online for personal reasons; 82% spend this amount of time online each week for work.
It’s likely that the amount of time spent online for work will increase, given the pandemic-fueled surge in telemedicine. Yet even when their personal and professional Internet use are combined, psychiatrists, on average, spend far less time online than the nearly 7 hours per day of the average Internet user, according to recent data.
Findings from the latest happiness, wellness, and lifestyle survey are based on 12,339 Medscape member physicians practicing in the United States who completed an online survey conducted between Aug. 30 and Nov. 5, 2020.
A version of this article first appeared on Medscape.com.
Variants spur new FDA guidance on COVID vaccines, tests, drugs
The United States is currently facing three main variant threats, according to the Centers for Disease Control and Prevention: B.1.1.7, which originated in the United Kingdom; B.1.351 from South Africa; and the P.1 variant, which originated in Brazil.
Acting FDA Commissioner Janet Woodcock, MD, said on a telephone press briefing call Feb. 22 that the FDA has already been communicating with individual manufacturers as they assess the variants’ effect on their products, but these guidelines are issued for the sake of transparency and to welcome scientific input.
Tailoring may be necessary
Dr. Woodcock emphasized that, “at this time, available data suggest the FDA-authorized vaccines are effective in protecting circulating strains of SARS-CoV-2.” However, in the event the strains start to show resistance, it may be necessary to tailor the vaccine to the variant.
In that case, effectiveness of a modified vaccine should be determined by data from clinical immunogenicity studies, which would compare a recipient’s immune response with virus variants induced by the modified vaccine against the immune response to the authorized vaccine, the guidance states.
Manufacturers should also study the vaccine in both nonvaccinated people and people fully vaccinated with the authorized vaccine, according to the guidance.
Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research, said on the call that the clinical immunogenicity data is needed to understand, for instance, whether a new vaccine strain is able to cover the new and old strain or whether it just covers the new strain. Information is also needed to understand whether the modified vaccine, when given to someone fully vaccinated, will still promote a positive response without introducing safety concerns.
Further discussions will be necessary to decide whether future modified vaccines may be authorized without the need for clinical studies.
Variants and testing
The FDA’s updated guidance for test developers, Policy for Evaluating Impact of Viral Mutations on COVID-19 Tests, includes information that test performance can be influenced by the sequence of the variant, prevalence of the variant in the population, or design of the test. For example, molecular tests designed to detect multiple SARS-CoV-2 genetic targets are less susceptible to genetic variants than tests designed to detect a single genetic target.
The FDA already issued a safety alert on Jan. 8 to caution that genetic mutations to the virus in a patient sample can potentially change the performance of a diagnostic test. The FDA identified three tests that had been granted emergency-use authorization (EUA) that are known to be affected.
However, Dr. Woodcock said on the call, “at this time the impact does not appear to be significant.”
Updated guidance for therapeutics
The FDA has issued new guidance on the effect of variants on monoclonal antibody treatments.
“The FDA is aware that some of the monoclonal antibodies that have been authorized are less active against some of the SARS-CoV-2 variants that have emerged,” the FDA noted in its press release. “This guidance provides recommendations on efficient approaches to the generation of ... manufacturing and controls data that could potentially support an EUA for monoclonal antibody products that may be effective against emerging variants.”
While the FDA is monitoring the effects of variants, manufacturers bear a lot of the responsibility as well.
The FDA added: “With these guidances, the FDA is encouraging developers of drugs or biological products targeting SARS-CoV-2 to continuously monitor genomic databases for emerging SARS-CoV-2 variants and evaluate phenotypically any specific variants in the product target that are becoming prevalent or could potentially impact its activity.”
Dr.Woodcock added that “we urge all Americans to continue to get tested, get their vaccines when available, and follow important heath measures such as handwashing, masking, and social distancing.”
A version of this article first appeared on Medscape.com.
The United States is currently facing three main variant threats, according to the Centers for Disease Control and Prevention: B.1.1.7, which originated in the United Kingdom; B.1.351 from South Africa; and the P.1 variant, which originated in Brazil.
Acting FDA Commissioner Janet Woodcock, MD, said on a telephone press briefing call Feb. 22 that the FDA has already been communicating with individual manufacturers as they assess the variants’ effect on their products, but these guidelines are issued for the sake of transparency and to welcome scientific input.
Tailoring may be necessary
Dr. Woodcock emphasized that, “at this time, available data suggest the FDA-authorized vaccines are effective in protecting circulating strains of SARS-CoV-2.” However, in the event the strains start to show resistance, it may be necessary to tailor the vaccine to the variant.
In that case, effectiveness of a modified vaccine should be determined by data from clinical immunogenicity studies, which would compare a recipient’s immune response with virus variants induced by the modified vaccine against the immune response to the authorized vaccine, the guidance states.
Manufacturers should also study the vaccine in both nonvaccinated people and people fully vaccinated with the authorized vaccine, according to the guidance.
Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research, said on the call that the clinical immunogenicity data is needed to understand, for instance, whether a new vaccine strain is able to cover the new and old strain or whether it just covers the new strain. Information is also needed to understand whether the modified vaccine, when given to someone fully vaccinated, will still promote a positive response without introducing safety concerns.
Further discussions will be necessary to decide whether future modified vaccines may be authorized without the need for clinical studies.
Variants and testing
The FDA’s updated guidance for test developers, Policy for Evaluating Impact of Viral Mutations on COVID-19 Tests, includes information that test performance can be influenced by the sequence of the variant, prevalence of the variant in the population, or design of the test. For example, molecular tests designed to detect multiple SARS-CoV-2 genetic targets are less susceptible to genetic variants than tests designed to detect a single genetic target.
The FDA already issued a safety alert on Jan. 8 to caution that genetic mutations to the virus in a patient sample can potentially change the performance of a diagnostic test. The FDA identified three tests that had been granted emergency-use authorization (EUA) that are known to be affected.
However, Dr. Woodcock said on the call, “at this time the impact does not appear to be significant.”
Updated guidance for therapeutics
The FDA has issued new guidance on the effect of variants on monoclonal antibody treatments.
“The FDA is aware that some of the monoclonal antibodies that have been authorized are less active against some of the SARS-CoV-2 variants that have emerged,” the FDA noted in its press release. “This guidance provides recommendations on efficient approaches to the generation of ... manufacturing and controls data that could potentially support an EUA for monoclonal antibody products that may be effective against emerging variants.”
While the FDA is monitoring the effects of variants, manufacturers bear a lot of the responsibility as well.
The FDA added: “With these guidances, the FDA is encouraging developers of drugs or biological products targeting SARS-CoV-2 to continuously monitor genomic databases for emerging SARS-CoV-2 variants and evaluate phenotypically any specific variants in the product target that are becoming prevalent or could potentially impact its activity.”
Dr.Woodcock added that “we urge all Americans to continue to get tested, get their vaccines when available, and follow important heath measures such as handwashing, masking, and social distancing.”
A version of this article first appeared on Medscape.com.
The United States is currently facing three main variant threats, according to the Centers for Disease Control and Prevention: B.1.1.7, which originated in the United Kingdom; B.1.351 from South Africa; and the P.1 variant, which originated in Brazil.
Acting FDA Commissioner Janet Woodcock, MD, said on a telephone press briefing call Feb. 22 that the FDA has already been communicating with individual manufacturers as they assess the variants’ effect on their products, but these guidelines are issued for the sake of transparency and to welcome scientific input.
Tailoring may be necessary
Dr. Woodcock emphasized that, “at this time, available data suggest the FDA-authorized vaccines are effective in protecting circulating strains of SARS-CoV-2.” However, in the event the strains start to show resistance, it may be necessary to tailor the vaccine to the variant.
In that case, effectiveness of a modified vaccine should be determined by data from clinical immunogenicity studies, which would compare a recipient’s immune response with virus variants induced by the modified vaccine against the immune response to the authorized vaccine, the guidance states.
Manufacturers should also study the vaccine in both nonvaccinated people and people fully vaccinated with the authorized vaccine, according to the guidance.
Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research, said on the call that the clinical immunogenicity data is needed to understand, for instance, whether a new vaccine strain is able to cover the new and old strain or whether it just covers the new strain. Information is also needed to understand whether the modified vaccine, when given to someone fully vaccinated, will still promote a positive response without introducing safety concerns.
Further discussions will be necessary to decide whether future modified vaccines may be authorized without the need for clinical studies.
Variants and testing
The FDA’s updated guidance for test developers, Policy for Evaluating Impact of Viral Mutations on COVID-19 Tests, includes information that test performance can be influenced by the sequence of the variant, prevalence of the variant in the population, or design of the test. For example, molecular tests designed to detect multiple SARS-CoV-2 genetic targets are less susceptible to genetic variants than tests designed to detect a single genetic target.
The FDA already issued a safety alert on Jan. 8 to caution that genetic mutations to the virus in a patient sample can potentially change the performance of a diagnostic test. The FDA identified three tests that had been granted emergency-use authorization (EUA) that are known to be affected.
However, Dr. Woodcock said on the call, “at this time the impact does not appear to be significant.”
Updated guidance for therapeutics
The FDA has issued new guidance on the effect of variants on monoclonal antibody treatments.
“The FDA is aware that some of the monoclonal antibodies that have been authorized are less active against some of the SARS-CoV-2 variants that have emerged,” the FDA noted in its press release. “This guidance provides recommendations on efficient approaches to the generation of ... manufacturing and controls data that could potentially support an EUA for monoclonal antibody products that may be effective against emerging variants.”
While the FDA is monitoring the effects of variants, manufacturers bear a lot of the responsibility as well.
The FDA added: “With these guidances, the FDA is encouraging developers of drugs or biological products targeting SARS-CoV-2 to continuously monitor genomic databases for emerging SARS-CoV-2 variants and evaluate phenotypically any specific variants in the product target that are becoming prevalent or could potentially impact its activity.”
Dr.Woodcock added that “we urge all Americans to continue to get tested, get their vaccines when available, and follow important heath measures such as handwashing, masking, and social distancing.”
A version of this article first appeared on Medscape.com.