Commentary

Emergencies happen anywhere, anytime, and sometimes medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series telling these stories.

In December 2017, I was a second-year urology resident at Cleveland Clinic. I’d gone to New Delhi to attend my best friend’s wedding. My flight back was New Delhi to Paris to JFK via Air France. I didn’t sleep on the first flight. So, on the second, I wanted to get some rest, because I had to go back to work the next day. I put on a movie and tried to snooze. As the saying goes in residency, you sleep when you can.

About 3 hours later, a flight attendant made an announcement in French, but I didn’t really hear it. Then they announced in English that they needed a physician. I noticed some flight attendants walking frantically around the economy cabin asking, “Is there a doctor on the plane?” Turns out there were two – the woman sitting next to me happened to be a pediatrician with Doctors Without Borders. I volunteered.

The flight attendant told me a woman was having abdominal pain. I thought it would be something straightforward. Usually, medical emergencies on planes involve chest pain or a panic attack or a vasovagal syncopal episode. Well, I was in for a ride that day.

The woman in pain was traveling from Nigeria. She told me about the abdominal pain. Then she lifted her blanket – she was pregnant. She said she was 37 or 38 weeks in. I said, “Okay, if you’re having this significant abdominal pain, then I need to examine you.” So we decided to move her to the first-class cabin, which was empty (I never did ask why – but it was good we had room to work).

Next step, I went back to my seat and asked the pediatrician if she could assist. My plan was to simply get the passenger through the flight, and as soon as we landed, she would go to the hospital.

There was room to lie down in first class. The pediatrician and I examined her, and she appeared fine. She was traveling with her 4-year-old daughter, and the flight attendants were taking care of her. Everything was okay.

The pilot came back and asked if we would need an emergency landing. I asked him how far it was to JFK – 4 hours. He said the closest place to land would be the Azores Islands, which is Portuguese territory, 2 hours away.

The problem: Even if we made it to the Azores, the hospital there was a very basic facility with no obstetric care available. And by the time the ambulance picked her up and got her there, it would still be 2 or 3 hours total. I said, “No, let’s just observe and continue our course.” Inside my head, I was hoping and praying to God that was the right decision.

Within an hour, everything changed.

The woman’s pain got worse, and she started having contractions. Then her water broke.

Things progressed quickly from there. The contractions progressively got worse and worse. The interval between them got smaller and smaller. The next time we examined her, we could see the baby’s head beginning to crown.

At that point, we had to decide – are we going to deliver? We were in the middle of the North Atlantic Ocean. There was nothing around us. We were 35,000 feet in the air, surrounded by blue.

The crew wanted us to sign a Good Samaritan agreement. So, we did that. And then I said, “Okay, let’s just go for it.”

We got the plane’s medical kit. They had IV fluids, so I started an IV. I was able to monitor the woman’s blood pressure. They had the usual drugs for doing ACLS [advanced cardiac life support], running the code, and things like that. But they didn’t have a suturing kit or a laceration kit. They didn’t have a scalpel. There was nothing else.

Honestly, there was a lot of panic going through my head. I started thinking about what could go wrong. I’d done an ob.gyn. rotation in medical school and delivered seven babies before it was over. But a plane – even the first-class cabin – is in no way, shape, or form like a delivery room. I was really scared she would hemorrhage out or something.

So, internally, I was having a meltdown. Sij, you have to keep it together right now, because there’s no one else that’s going to do this. Just give it your best shot. And that’s what I did.

I asked the pilot to go to an altitude that would minimize any turbulence, and we were very lucky that the notorious North Atlantic air wasn’t choppy.

More luck: This was the passenger’s second baby, and I was counting on second deliveries being easier. The pediatrician, the flight attendants, and I came together as a team. Two flight attendants had given birth before, so they held the patient’s hand and guided her to push. I was “downstairs” waiting to catch.

She was in some pain. At this point, usually people get an epidural. I kept thinking about what drugs were safe in pregnancy, but I wasn’t sure. I don’t know if they even had morphine or anything on the plane. We gave her some Tylenol.

It didn’t take long. After about 30 minutes, the baby’s head emerged. I was able to navigate it out, avoiding any shoulder dystocia. There’s a certain technique that you learn in medical school, which thankfully came back to me. I caught it – it was a boy born right there in a first-class seat.

I gave him to the pediatrician, and she did the Apgar score, calculating his breathing and appearance. Then my job was to make sure there were no postpartum complications.

I ended up using a piece of string in the kit to tie around the umbilical cord, and then I cut it with scissors. After that, the woman was able to deliver the placenta. She did have some vaginal bleeding, but that resolved by just holding pressure.

The baby was fine. Mom was doing great. No complications. It was a miracle. I was the right person at the right place at the right time. I just think it was something from God.

The pilot made an announcement, “We’re en route to JFK, and there’s an additional passenger on this plane now.”

When we landed, I had very little time because I had to catch my flight to Cleveland. I didn’t even process what had happened.

A few days later, I got this package from Air France with a very expensive bottle of champagne along with a travel voucher. I heard from the mom by email – she and baby were doing fine.

Eventually, the media relations people at Cleveland Clinic heard about the incident, and it became a story that went viral. That was very weird, because I’m usually someone who’s private. All through my residency, people would introduce me with, “Remember that guy who delivered a baby on a plane? That’s him.”

I’m so thankful for everyone who was on that team. It was very beautiful because it was people from different cultures, backgrounds, and faiths who came together to achieve something so miraculous. The patient was Nigerian. The flight attendants were French. The pediatrician and I were American.

That just shows you the power of teamwork and how humanity can come together. Medicine, surgery – everything, in fact – is a team sport.

Sij Hemal, MD, graduated from urology residency at the Cleveland Clinic and is currently a robotic urologic oncology and minimally invasive surgery fellow at the University of Southern California, Los Angeles.

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

Emergencies happen anywhere, anytime, and sometimes medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series telling these stories.

In December 2017, I was a second-year urology resident at Cleveland Clinic. I’d gone to New Delhi to attend my best friend’s wedding. My flight back was New Delhi to Paris to JFK via Air France. I didn’t sleep on the first flight. So, on the second, I wanted to get some rest, because I had to go back to work the next day. I put on a movie and tried to snooze. As the saying goes in residency, you sleep when you can.

About 3 hours later, a flight attendant made an announcement in French, but I didn’t really hear it. Then they announced in English that they needed a physician. I noticed some flight attendants walking frantically around the economy cabin asking, “Is there a doctor on the plane?” Turns out there were two – the woman sitting next to me happened to be a pediatrician with Doctors Without Borders. I volunteered.

The flight attendant told me a woman was having abdominal pain. I thought it would be something straightforward. Usually, medical emergencies on planes involve chest pain or a panic attack or a vasovagal syncopal episode. Well, I was in for a ride that day.

The woman in pain was traveling from Nigeria. She told me about the abdominal pain. Then she lifted her blanket – she was pregnant. She said she was 37 or 38 weeks in. I said, “Okay, if you’re having this significant abdominal pain, then I need to examine you.” So we decided to move her to the first-class cabin, which was empty (I never did ask why – but it was good we had room to work).

Next step, I went back to my seat and asked the pediatrician if she could assist. My plan was to simply get the passenger through the flight, and as soon as we landed, she would go to the hospital.

There was room to lie down in first class. The pediatrician and I examined her, and she appeared fine. She was traveling with her 4-year-old daughter, and the flight attendants were taking care of her. Everything was okay.

The pilot came back and asked if we would need an emergency landing. I asked him how far it was to JFK – 4 hours. He said the closest place to land would be the Azores Islands, which is Portuguese territory, 2 hours away.

The problem: Even if we made it to the Azores, the hospital there was a very basic facility with no obstetric care available. And by the time the ambulance picked her up and got her there, it would still be 2 or 3 hours total. I said, “No, let’s just observe and continue our course.” Inside my head, I was hoping and praying to God that was the right decision.

Within an hour, everything changed.

The woman’s pain got worse, and she started having contractions. Then her water broke.

Things progressed quickly from there. The contractions progressively got worse and worse. The interval between them got smaller and smaller. The next time we examined her, we could see the baby’s head beginning to crown.

At that point, we had to decide – are we going to deliver? We were in the middle of the North Atlantic Ocean. There was nothing around us. We were 35,000 feet in the air, surrounded by blue.

The crew wanted us to sign a Good Samaritan agreement. So, we did that. And then I said, “Okay, let’s just go for it.”

We got the plane’s medical kit. They had IV fluids, so I started an IV. I was able to monitor the woman’s blood pressure. They had the usual drugs for doing ACLS [advanced cardiac life support], running the code, and things like that. But they didn’t have a suturing kit or a laceration kit. They didn’t have a scalpel. There was nothing else.

Honestly, there was a lot of panic going through my head. I started thinking about what could go wrong. I’d done an ob.gyn. rotation in medical school and delivered seven babies before it was over. But a plane – even the first-class cabin – is in no way, shape, or form like a delivery room. I was really scared she would hemorrhage out or something.

So, internally, I was having a meltdown. Sij, you have to keep it together right now, because there’s no one else that’s going to do this. Just give it your best shot. And that’s what I did.

I asked the pilot to go to an altitude that would minimize any turbulence, and we were very lucky that the notorious North Atlantic air wasn’t choppy.

More luck: This was the passenger’s second baby, and I was counting on second deliveries being easier. The pediatrician, the flight attendants, and I came together as a team. Two flight attendants had given birth before, so they held the patient’s hand and guided her to push. I was “downstairs” waiting to catch.

She was in some pain. At this point, usually people get an epidural. I kept thinking about what drugs were safe in pregnancy, but I wasn’t sure. I don’t know if they even had morphine or anything on the plane. We gave her some Tylenol.

It didn’t take long. After about 30 minutes, the baby’s head emerged. I was able to navigate it out, avoiding any shoulder dystocia. There’s a certain technique that you learn in medical school, which thankfully came back to me. I caught it – it was a boy born right there in a first-class seat.

I gave him to the pediatrician, and she did the Apgar score, calculating his breathing and appearance. Then my job was to make sure there were no postpartum complications.

I ended up using a piece of string in the kit to tie around the umbilical cord, and then I cut it with scissors. After that, the woman was able to deliver the placenta. She did have some vaginal bleeding, but that resolved by just holding pressure.

The baby was fine. Mom was doing great. No complications. It was a miracle. I was the right person at the right place at the right time. I just think it was something from God.

The pilot made an announcement, “We’re en route to JFK, and there’s an additional passenger on this plane now.”

When we landed, I had very little time because I had to catch my flight to Cleveland. I didn’t even process what had happened.

A few days later, I got this package from Air France with a very expensive bottle of champagne along with a travel voucher. I heard from the mom by email – she and baby were doing fine.

Eventually, the media relations people at Cleveland Clinic heard about the incident, and it became a story that went viral. That was very weird, because I’m usually someone who’s private. All through my residency, people would introduce me with, “Remember that guy who delivered a baby on a plane? That’s him.”

I’m so thankful for everyone who was on that team. It was very beautiful because it was people from different cultures, backgrounds, and faiths who came together to achieve something so miraculous. The patient was Nigerian. The flight attendants were French. The pediatrician and I were American.

That just shows you the power of teamwork and how humanity can come together. Medicine, surgery – everything, in fact – is a team sport.

Sij Hemal, MD, graduated from urology residency at the Cleveland Clinic and is currently a robotic urologic oncology and minimally invasive surgery fellow at the University of Southern California, Los Angeles.

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

Emergencies happen anywhere, anytime, and sometimes medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series telling these stories.

In December 2017, I was a second-year urology resident at Cleveland Clinic. I’d gone to New Delhi to attend my best friend’s wedding. My flight back was New Delhi to Paris to JFK via Air France. I didn’t sleep on the first flight. So, on the second, I wanted to get some rest, because I had to go back to work the next day. I put on a movie and tried to snooze. As the saying goes in residency, you sleep when you can.

About 3 hours later, a flight attendant made an announcement in French, but I didn’t really hear it. Then they announced in English that they needed a physician. I noticed some flight attendants walking frantically around the economy cabin asking, “Is there a doctor on the plane?” Turns out there were two – the woman sitting next to me happened to be a pediatrician with Doctors Without Borders. I volunteered.

The flight attendant told me a woman was having abdominal pain. I thought it would be something straightforward. Usually, medical emergencies on planes involve chest pain or a panic attack or a vasovagal syncopal episode. Well, I was in for a ride that day.

The woman in pain was traveling from Nigeria. She told me about the abdominal pain. Then she lifted her blanket – she was pregnant. She said she was 37 or 38 weeks in. I said, “Okay, if you’re having this significant abdominal pain, then I need to examine you.” So we decided to move her to the first-class cabin, which was empty (I never did ask why – but it was good we had room to work).

Next step, I went back to my seat and asked the pediatrician if she could assist. My plan was to simply get the passenger through the flight, and as soon as we landed, she would go to the hospital.

There was room to lie down in first class. The pediatrician and I examined her, and she appeared fine. She was traveling with her 4-year-old daughter, and the flight attendants were taking care of her. Everything was okay.

The pilot came back and asked if we would need an emergency landing. I asked him how far it was to JFK – 4 hours. He said the closest place to land would be the Azores Islands, which is Portuguese territory, 2 hours away.

The problem: Even if we made it to the Azores, the hospital there was a very basic facility with no obstetric care available. And by the time the ambulance picked her up and got her there, it would still be 2 or 3 hours total. I said, “No, let’s just observe and continue our course.” Inside my head, I was hoping and praying to God that was the right decision.

Within an hour, everything changed.

The woman’s pain got worse, and she started having contractions. Then her water broke.

Things progressed quickly from there. The contractions progressively got worse and worse. The interval between them got smaller and smaller. The next time we examined her, we could see the baby’s head beginning to crown.

At that point, we had to decide – are we going to deliver? We were in the middle of the North Atlantic Ocean. There was nothing around us. We were 35,000 feet in the air, surrounded by blue.

The crew wanted us to sign a Good Samaritan agreement. So, we did that. And then I said, “Okay, let’s just go for it.”

We got the plane’s medical kit. They had IV fluids, so I started an IV. I was able to monitor the woman’s blood pressure. They had the usual drugs for doing ACLS [advanced cardiac life support], running the code, and things like that. But they didn’t have a suturing kit or a laceration kit. They didn’t have a scalpel. There was nothing else.

Honestly, there was a lot of panic going through my head. I started thinking about what could go wrong. I’d done an ob.gyn. rotation in medical school and delivered seven babies before it was over. But a plane – even the first-class cabin – is in no way, shape, or form like a delivery room. I was really scared she would hemorrhage out or something.

So, internally, I was having a meltdown. Sij, you have to keep it together right now, because there’s no one else that’s going to do this. Just give it your best shot. And that’s what I did.

I asked the pilot to go to an altitude that would minimize any turbulence, and we were very lucky that the notorious North Atlantic air wasn’t choppy.

More luck: This was the passenger’s second baby, and I was counting on second deliveries being easier. The pediatrician, the flight attendants, and I came together as a team. Two flight attendants had given birth before, so they held the patient’s hand and guided her to push. I was “downstairs” waiting to catch.

She was in some pain. At this point, usually people get an epidural. I kept thinking about what drugs were safe in pregnancy, but I wasn’t sure. I don’t know if they even had morphine or anything on the plane. We gave her some Tylenol.

It didn’t take long. After about 30 minutes, the baby’s head emerged. I was able to navigate it out, avoiding any shoulder dystocia. There’s a certain technique that you learn in medical school, which thankfully came back to me. I caught it – it was a boy born right there in a first-class seat.

I gave him to the pediatrician, and she did the Apgar score, calculating his breathing and appearance. Then my job was to make sure there were no postpartum complications.

I ended up using a piece of string in the kit to tie around the umbilical cord, and then I cut it with scissors. After that, the woman was able to deliver the placenta. She did have some vaginal bleeding, but that resolved by just holding pressure.

The baby was fine. Mom was doing great. No complications. It was a miracle. I was the right person at the right place at the right time. I just think it was something from God.

The pilot made an announcement, “We’re en route to JFK, and there’s an additional passenger on this plane now.”

When we landed, I had very little time because I had to catch my flight to Cleveland. I didn’t even process what had happened.

A few days later, I got this package from Air France with a very expensive bottle of champagne along with a travel voucher. I heard from the mom by email – she and baby were doing fine.

Eventually, the media relations people at Cleveland Clinic heard about the incident, and it became a story that went viral. That was very weird, because I’m usually someone who’s private. All through my residency, people would introduce me with, “Remember that guy who delivered a baby on a plane? That’s him.”

I’m so thankful for everyone who was on that team. It was very beautiful because it was people from different cultures, backgrounds, and faiths who came together to achieve something so miraculous. The patient was Nigerian. The flight attendants were French. The pediatrician and I were American.

That just shows you the power of teamwork and how humanity can come together. Medicine, surgery – everything, in fact – is a team sport.

Sij Hemal, MD, graduated from urology residency at the Cleveland Clinic and is currently a robotic urologic oncology and minimally invasive surgery fellow at the University of Southern California, Los Angeles.

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

This transcript has been edited for clarity.

Matthew F. Watto, MD: Welcome back to The Curbsiders. On tonight’s episode, we are going to be talking about back pain. This is based on an interview, Back Pain Update with Dr. Austin Baraki. He gave us some great pearls about how to manage back pain, which we see so much of in primary care. I’ll use one of my famous teaching techniques: If the patient has any kind of back pain, they should just not move. Right?

Paul N. Williams, MD: That’s right, Matt – we should recommend bedrest until they get better for anyone who has any back pain? No. For back pain, early activity and exercise are great. Patients are often concerned that physical therapy will make their pain worse, so they don’t exercise. This misunderstanding is not surprising. They believe that if they are experiencing pain, it’s facilitating more damage, which is not necessarily the case. It will get better, and a little bit of anticipatory guidance goes a long way in terms of managing patient expectations related to early mobilization, early exercise, and physical therapy.

Dr. Watto: Absolutely. One of the goals of treatment is symptom relief to the extent that we’re able to achieve. We’re not expecting the pain to go to zero. That just doesn’t happen, especially if someone’s on a medication long term. Another goal is return to function. We want them sleeping. We want them to be able to tolerate movement.

We have medications – NSAIDs and muscle relaxants, which are actually tranquilizers. But most therapy for back pain doesn’t involve medications. It involves active movement, so we have to find movement that the patient enjoys doing. Passive treatments, things being done to patients, just don’t work as well.
 

Dr. Williams: We should be clear – we’re talking primarily about chronic back pain here. For acute back pain, we actually have some decent medications, but acute back pain tends to improve no matter what you do. We don’t have much to offer pharmacologically for chronic low back pain. The best modalities usually involve physical activity of some kind.

Dr. Watto: Let’s discuss the evaluation of back pain. Something that always comes up: Should we order imaging, and is there a right time to get it? Dr. Baraki was very clear about when to do imaging. Two big buckets of patients might need imaging.

First, a patient who has a serious underlying condition and you’re using imaging to try to diagnose it; or in a chronic setting, a patient who needs surgery, and imaging is part of the presurgical evaluation. We talked about red flags.

The red flags are major trauma, where we have reason to believe there might be something going on – if we strongly suspect infection, or the patient is injecting drugs. If the patient has a history of cancer, we would be worried that they might have a recurrence. Those are some of the main red flags. With a patient who has osteoporosis or is on chronic steroids, you might even be able to get by with plain films instead of an MRI to look for fracture.

The other thing I wanted to ask you about is, when should we get imaging? Are there any pitfalls we need to worry about?
 

Dr. Williams: I always like podcasts I’m not on because I enjoy listening to them much more. Dr. Baraki talked about the very specific language that is used in radiology reports, such as spondylitis, spondylolysis, and multilevel degenerative disease. They sound bad, but if they are just reframed as age-related degenerative changes, that sounds so much more benign. When discussing with patients, we should avoid medical jargon and say that we saw some changes that we would expect for someone of your age. That sounds so much better than saying we saw multilevel degenerative disease, which sounds like an alarming pathology if you’re not a physician. Without being inaccurate, we should frame the discussion such that we aren’t providing a very specific diagnosis, because that is rarely the case with chronic low back pain. Typically, many things are going on and you may never identify a single unifying diagnosis, which doesn’t tend to help anyway.

Dr. Watto: There’s evidence showing that if the radiology report uses clinical terminology that both clinician and patient think of as less serious, they are less likely to proceed to more invasive treatments. Calling an episode of back pain a “lumbar strain” helps the patient understand that this is a pretty common thing. Almost everyone is going to have an episode of back pain at some point in their life, and almost all of them will get better. Most of the time there’s no serious underlying condition.

This was a great discussion with Dr. Baraki. Click on Back Pain Update with Dr Austin Baraki to hear the full discussion. Until next time, I’ve been Dr. Matthew Frank Watto.
 

Dr. Williams: And I’m Dr. Paul Nelson Williams.

Dr. Watto is Clinical Assistant Professor, Department of Medicine, University of Pennsylvania, Philadelphia. Dr. Williams is Associate Professor of Clinical Medicine, Department of General Internal Medicine, Temple University, Philadelphia. Neither reported any conflicts of interest.

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

This transcript has been edited for clarity.

Matthew F. Watto, MD: Welcome back to The Curbsiders. On tonight’s episode, we are going to be talking about back pain. This is based on an interview, Back Pain Update with Dr. Austin Baraki. He gave us some great pearls about how to manage back pain, which we see so much of in primary care. I’ll use one of my famous teaching techniques: If the patient has any kind of back pain, they should just not move. Right?

Paul N. Williams, MD: That’s right, Matt – we should recommend bedrest until they get better for anyone who has any back pain? No. For back pain, early activity and exercise are great. Patients are often concerned that physical therapy will make their pain worse, so they don’t exercise. This misunderstanding is not surprising. They believe that if they are experiencing pain, it’s facilitating more damage, which is not necessarily the case. It will get better, and a little bit of anticipatory guidance goes a long way in terms of managing patient expectations related to early mobilization, early exercise, and physical therapy.

Dr. Watto: Absolutely. One of the goals of treatment is symptom relief to the extent that we’re able to achieve. We’re not expecting the pain to go to zero. That just doesn’t happen, especially if someone’s on a medication long term. Another goal is return to function. We want them sleeping. We want them to be able to tolerate movement.

We have medications – NSAIDs and muscle relaxants, which are actually tranquilizers. But most therapy for back pain doesn’t involve medications. It involves active movement, so we have to find movement that the patient enjoys doing. Passive treatments, things being done to patients, just don’t work as well.
 

Dr. Williams: We should be clear – we’re talking primarily about chronic back pain here. For acute back pain, we actually have some decent medications, but acute back pain tends to improve no matter what you do. We don’t have much to offer pharmacologically for chronic low back pain. The best modalities usually involve physical activity of some kind.

Dr. Watto: Let’s discuss the evaluation of back pain. Something that always comes up: Should we order imaging, and is there a right time to get it? Dr. Baraki was very clear about when to do imaging. Two big buckets of patients might need imaging.

First, a patient who has a serious underlying condition and you’re using imaging to try to diagnose it; or in a chronic setting, a patient who needs surgery, and imaging is part of the presurgical evaluation. We talked about red flags.

The red flags are major trauma, where we have reason to believe there might be something going on – if we strongly suspect infection, or the patient is injecting drugs. If the patient has a history of cancer, we would be worried that they might have a recurrence. Those are some of the main red flags. With a patient who has osteoporosis or is on chronic steroids, you might even be able to get by with plain films instead of an MRI to look for fracture.

The other thing I wanted to ask you about is, when should we get imaging? Are there any pitfalls we need to worry about?
 

Dr. Williams: I always like podcasts I’m not on because I enjoy listening to them much more. Dr. Baraki talked about the very specific language that is used in radiology reports, such as spondylitis, spondylolysis, and multilevel degenerative disease. They sound bad, but if they are just reframed as age-related degenerative changes, that sounds so much more benign. When discussing with patients, we should avoid medical jargon and say that we saw some changes that we would expect for someone of your age. That sounds so much better than saying we saw multilevel degenerative disease, which sounds like an alarming pathology if you’re not a physician. Without being inaccurate, we should frame the discussion such that we aren’t providing a very specific diagnosis, because that is rarely the case with chronic low back pain. Typically, many things are going on and you may never identify a single unifying diagnosis, which doesn’t tend to help anyway.

Dr. Watto: There’s evidence showing that if the radiology report uses clinical terminology that both clinician and patient think of as less serious, they are less likely to proceed to more invasive treatments. Calling an episode of back pain a “lumbar strain” helps the patient understand that this is a pretty common thing. Almost everyone is going to have an episode of back pain at some point in their life, and almost all of them will get better. Most of the time there’s no serious underlying condition.

This was a great discussion with Dr. Baraki. Click on Back Pain Update with Dr Austin Baraki to hear the full discussion. Until next time, I’ve been Dr. Matthew Frank Watto.
 

Dr. Williams: And I’m Dr. Paul Nelson Williams.

Dr. Watto is Clinical Assistant Professor, Department of Medicine, University of Pennsylvania, Philadelphia. Dr. Williams is Associate Professor of Clinical Medicine, Department of General Internal Medicine, Temple University, Philadelphia. Neither reported any conflicts of interest.

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

This transcript has been edited for clarity.

Matthew F. Watto, MD: Welcome back to The Curbsiders. On tonight’s episode, we are going to be talking about back pain. This is based on an interview, Back Pain Update with Dr. Austin Baraki. He gave us some great pearls about how to manage back pain, which we see so much of in primary care. I’ll use one of my famous teaching techniques: If the patient has any kind of back pain, they should just not move. Right?

Paul N. Williams, MD: That’s right, Matt – we should recommend bedrest until they get better for anyone who has any back pain? No. For back pain, early activity and exercise are great. Patients are often concerned that physical therapy will make their pain worse, so they don’t exercise. This misunderstanding is not surprising. They believe that if they are experiencing pain, it’s facilitating more damage, which is not necessarily the case. It will get better, and a little bit of anticipatory guidance goes a long way in terms of managing patient expectations related to early mobilization, early exercise, and physical therapy.

Dr. Watto: Absolutely. One of the goals of treatment is symptom relief to the extent that we’re able to achieve. We’re not expecting the pain to go to zero. That just doesn’t happen, especially if someone’s on a medication long term. Another goal is return to function. We want them sleeping. We want them to be able to tolerate movement.

We have medications – NSAIDs and muscle relaxants, which are actually tranquilizers. But most therapy for back pain doesn’t involve medications. It involves active movement, so we have to find movement that the patient enjoys doing. Passive treatments, things being done to patients, just don’t work as well.
 

Dr. Williams: We should be clear – we’re talking primarily about chronic back pain here. For acute back pain, we actually have some decent medications, but acute back pain tends to improve no matter what you do. We don’t have much to offer pharmacologically for chronic low back pain. The best modalities usually involve physical activity of some kind.

Dr. Watto: Let’s discuss the evaluation of back pain. Something that always comes up: Should we order imaging, and is there a right time to get it? Dr. Baraki was very clear about when to do imaging. Two big buckets of patients might need imaging.

First, a patient who has a serious underlying condition and you’re using imaging to try to diagnose it; or in a chronic setting, a patient who needs surgery, and imaging is part of the presurgical evaluation. We talked about red flags.

The red flags are major trauma, where we have reason to believe there might be something going on – if we strongly suspect infection, or the patient is injecting drugs. If the patient has a history of cancer, we would be worried that they might have a recurrence. Those are some of the main red flags. With a patient who has osteoporosis or is on chronic steroids, you might even be able to get by with plain films instead of an MRI to look for fracture.

The other thing I wanted to ask you about is, when should we get imaging? Are there any pitfalls we need to worry about?
 

Dr. Williams: I always like podcasts I’m not on because I enjoy listening to them much more. Dr. Baraki talked about the very specific language that is used in radiology reports, such as spondylitis, spondylolysis, and multilevel degenerative disease. They sound bad, but if they are just reframed as age-related degenerative changes, that sounds so much more benign. When discussing with patients, we should avoid medical jargon and say that we saw some changes that we would expect for someone of your age. That sounds so much better than saying we saw multilevel degenerative disease, which sounds like an alarming pathology if you’re not a physician. Without being inaccurate, we should frame the discussion such that we aren’t providing a very specific diagnosis, because that is rarely the case with chronic low back pain. Typically, many things are going on and you may never identify a single unifying diagnosis, which doesn’t tend to help anyway.

Dr. Watto: There’s evidence showing that if the radiology report uses clinical terminology that both clinician and patient think of as less serious, they are less likely to proceed to more invasive treatments. Calling an episode of back pain a “lumbar strain” helps the patient understand that this is a pretty common thing. Almost everyone is going to have an episode of back pain at some point in their life, and almost all of them will get better. Most of the time there’s no serious underlying condition.

This was a great discussion with Dr. Baraki. Click on Back Pain Update with Dr Austin Baraki to hear the full discussion. Until next time, I’ve been Dr. Matthew Frank Watto.
 

Dr. Williams: And I’m Dr. Paul Nelson Williams.

Dr. Watto is Clinical Assistant Professor, Department of Medicine, University of Pennsylvania, Philadelphia. Dr. Williams is Associate Professor of Clinical Medicine, Department of General Internal Medicine, Temple University, Philadelphia. Neither reported any conflicts of interest.

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

This transcript has been edited for clarity.

I’m David Kerr, professor of cancer medicine at the University of Oxford. I’d like to talk to you today about something specific and generic around guidelines.

Annals of Oncology, my old journal, has just published an outstanding set of guidelines delivered by the ESMO (European Society for Medical Oncology) guidelines group. It’s around the management of toxicities from immunotherapy, and it’s the ESMO Clinical Practice Guideline for diagnosis, treatment, and follow-up, delivered by Dr. Haanen and, of course, a number of colleagues on behalf of the wider committee.

Have a look at it. I’m not going to talk about the details of it. It’s very well written. It’s very clear and evidence based, of course. There are many helpful hints and a very clear blueprint as to how we should better manage the myriad of potential side effects from immunotherapy.

It tells us a little about the basis of the science, some of the mechanistic work that’s going on in allowing us to understand why some people react in such different ways, almost as if the immune systems are primed to overreact. It gives a very helpful, stepwise look at how we best diagnose, manage, and, in the longer term, follow up patients who have problems with these very important drugs.

All of us recognize the extraordinary impact they’ve made across a wide range of different tumor types, and therefore, as practicing oncologists and health care professionals in the field, all of us need to understand better the details as to how we better care for our patients on these drugs.

Have a look at it. It’s well written and useful, and I think it’s a document that I’ll turn to when I’m looking for a refresher or advice in the future.

The generic focus is about guidelines. Many years ago, I was one of the architects of the British National Cancer Plan, and for me, there were four simple principles at that stage in our development of how we would improve the delivery of cancer control in the United Kingdom. It was around site specialization, particularly of our surgical colleagues who embraced this with vigor. God bless them.

It was using guidelines to help level up the quality of treatment that we were giving, of course underpinned by research, and using – one would hope – modern IT and telecommunications to improve the networking that we use to deliver multidisciplinary cancer care, one of the key elements. Guidelines were embedded in that.

A couple of years ago, we did a survey of cancer physicians around the world. Almost 30 different countries were represented, and we asked which guidelines were most used. It was a very interesting set of responses. The three dominant guidelines – this will surprise no one – are the NCCN (National Comprehensive Cancer Network) guidelines, the ESMO guidelines, and the ASCO (American Society of Clinical Oncology) guidelines.

Rather than selecting one and one being completely dominant, what seemed to be the case is that our colleagues around the world dipped in and used all three. They may prefer NCCN for some particular tumor type or some particular aspect of how they’re structured, but at the same time, we would dip into the ESMO guidelines for specific bits of help, as well as the ASCO guidelines.

I find this fascinating. I assume that in different regions, depending on how they were affiliated in terms of additional training or links to Europe or links to the United States, that one or other of these guideline groups would predominate, but no. In each country, in each region, given the large data bank that we have of guidelines now, it’s a sort of pick-and-mix situation.

I was initially surprised but then took comfort from it. There’s nothing I hate more than the wasted energy of reduplication and saying, well come on, if there is one guideline set that does truly command the attention of the world, then the other should stop. It’s wasted energy, which is something that none of us can afford.

The fact that each of these trusted, evidence-based, beautifully presented guidelines is used in different ways was important. A message to the guideline groups from me is: “Thank you for your professionalism, for the hard work of hundreds of cancer specialists from all different specialties, and for their contribution to developing these guidelines.”

It’s worth it, it’s working, people are using them, and they’re making a difference. It’s all about leveling up the quality of cancer care that we deliver.

Specifically, have a look at the ESMO immune guidelines. They are great. I hope you find them helpful. Generically, thanks to all of you who are contributing and working so hard to make these data available to improve the quality of cancer care around the world.

Thanks for listening, as always. I’m interested in any comments that you might have, but for the time being, Medscapers, ahoy.

David J. Kerr, CBE, MD, DSc, is a professor of cancer medicine at the University of Oxford. He reported conflicts of interest with Celleron Therapeutics, Oxford Cancer Biomarkers, Afrox, GlaxoSmithKline, Bayer, Genomic Health, and Merck Serono.

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

This transcript has been edited for clarity.

I’m David Kerr, professor of cancer medicine at the University of Oxford. I’d like to talk to you today about something specific and generic around guidelines.

Annals of Oncology, my old journal, has just published an outstanding set of guidelines delivered by the ESMO (European Society for Medical Oncology) guidelines group. It’s around the management of toxicities from immunotherapy, and it’s the ESMO Clinical Practice Guideline for diagnosis, treatment, and follow-up, delivered by Dr. Haanen and, of course, a number of colleagues on behalf of the wider committee.

Have a look at it. I’m not going to talk about the details of it. It’s very well written. It’s very clear and evidence based, of course. There are many helpful hints and a very clear blueprint as to how we should better manage the myriad of potential side effects from immunotherapy.

It tells us a little about the basis of the science, some of the mechanistic work that’s going on in allowing us to understand why some people react in such different ways, almost as if the immune systems are primed to overreact. It gives a very helpful, stepwise look at how we best diagnose, manage, and, in the longer term, follow up patients who have problems with these very important drugs.

All of us recognize the extraordinary impact they’ve made across a wide range of different tumor types, and therefore, as practicing oncologists and health care professionals in the field, all of us need to understand better the details as to how we better care for our patients on these drugs.

Have a look at it. It’s well written and useful, and I think it’s a document that I’ll turn to when I’m looking for a refresher or advice in the future.

The generic focus is about guidelines. Many years ago, I was one of the architects of the British National Cancer Plan, and for me, there were four simple principles at that stage in our development of how we would improve the delivery of cancer control in the United Kingdom. It was around site specialization, particularly of our surgical colleagues who embraced this with vigor. God bless them.

It was using guidelines to help level up the quality of treatment that we were giving, of course underpinned by research, and using – one would hope – modern IT and telecommunications to improve the networking that we use to deliver multidisciplinary cancer care, one of the key elements. Guidelines were embedded in that.

A couple of years ago, we did a survey of cancer physicians around the world. Almost 30 different countries were represented, and we asked which guidelines were most used. It was a very interesting set of responses. The three dominant guidelines – this will surprise no one – are the NCCN (National Comprehensive Cancer Network) guidelines, the ESMO guidelines, and the ASCO (American Society of Clinical Oncology) guidelines.

Rather than selecting one and one being completely dominant, what seemed to be the case is that our colleagues around the world dipped in and used all three. They may prefer NCCN for some particular tumor type or some particular aspect of how they’re structured, but at the same time, we would dip into the ESMO guidelines for specific bits of help, as well as the ASCO guidelines.

I find this fascinating. I assume that in different regions, depending on how they were affiliated in terms of additional training or links to Europe or links to the United States, that one or other of these guideline groups would predominate, but no. In each country, in each region, given the large data bank that we have of guidelines now, it’s a sort of pick-and-mix situation.

I was initially surprised but then took comfort from it. There’s nothing I hate more than the wasted energy of reduplication and saying, well come on, if there is one guideline set that does truly command the attention of the world, then the other should stop. It’s wasted energy, which is something that none of us can afford.

The fact that each of these trusted, evidence-based, beautifully presented guidelines is used in different ways was important. A message to the guideline groups from me is: “Thank you for your professionalism, for the hard work of hundreds of cancer specialists from all different specialties, and for their contribution to developing these guidelines.”

It’s worth it, it’s working, people are using them, and they’re making a difference. It’s all about leveling up the quality of cancer care that we deliver.

Specifically, have a look at the ESMO immune guidelines. They are great. I hope you find them helpful. Generically, thanks to all of you who are contributing and working so hard to make these data available to improve the quality of cancer care around the world.

Thanks for listening, as always. I’m interested in any comments that you might have, but for the time being, Medscapers, ahoy.

David J. Kerr, CBE, MD, DSc, is a professor of cancer medicine at the University of Oxford. He reported conflicts of interest with Celleron Therapeutics, Oxford Cancer Biomarkers, Afrox, GlaxoSmithKline, Bayer, Genomic Health, and Merck Serono.

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

This transcript has been edited for clarity.

I’m David Kerr, professor of cancer medicine at the University of Oxford. I’d like to talk to you today about something specific and generic around guidelines.

Annals of Oncology, my old journal, has just published an outstanding set of guidelines delivered by the ESMO (European Society for Medical Oncology) guidelines group. It’s around the management of toxicities from immunotherapy, and it’s the ESMO Clinical Practice Guideline for diagnosis, treatment, and follow-up, delivered by Dr. Haanen and, of course, a number of colleagues on behalf of the wider committee.

Have a look at it. I’m not going to talk about the details of it. It’s very well written. It’s very clear and evidence based, of course. There are many helpful hints and a very clear blueprint as to how we should better manage the myriad of potential side effects from immunotherapy.

It tells us a little about the basis of the science, some of the mechanistic work that’s going on in allowing us to understand why some people react in such different ways, almost as if the immune systems are primed to overreact. It gives a very helpful, stepwise look at how we best diagnose, manage, and, in the longer term, follow up patients who have problems with these very important drugs.

All of us recognize the extraordinary impact they’ve made across a wide range of different tumor types, and therefore, as practicing oncologists and health care professionals in the field, all of us need to understand better the details as to how we better care for our patients on these drugs.

Have a look at it. It’s well written and useful, and I think it’s a document that I’ll turn to when I’m looking for a refresher or advice in the future.

The generic focus is about guidelines. Many years ago, I was one of the architects of the British National Cancer Plan, and for me, there were four simple principles at that stage in our development of how we would improve the delivery of cancer control in the United Kingdom. It was around site specialization, particularly of our surgical colleagues who embraced this with vigor. God bless them.

It was using guidelines to help level up the quality of treatment that we were giving, of course underpinned by research, and using – one would hope – modern IT and telecommunications to improve the networking that we use to deliver multidisciplinary cancer care, one of the key elements. Guidelines were embedded in that.

A couple of years ago, we did a survey of cancer physicians around the world. Almost 30 different countries were represented, and we asked which guidelines were most used. It was a very interesting set of responses. The three dominant guidelines – this will surprise no one – are the NCCN (National Comprehensive Cancer Network) guidelines, the ESMO guidelines, and the ASCO (American Society of Clinical Oncology) guidelines.

Rather than selecting one and one being completely dominant, what seemed to be the case is that our colleagues around the world dipped in and used all three. They may prefer NCCN for some particular tumor type or some particular aspect of how they’re structured, but at the same time, we would dip into the ESMO guidelines for specific bits of help, as well as the ASCO guidelines.

I find this fascinating. I assume that in different regions, depending on how they were affiliated in terms of additional training or links to Europe or links to the United States, that one or other of these guideline groups would predominate, but no. In each country, in each region, given the large data bank that we have of guidelines now, it’s a sort of pick-and-mix situation.

I was initially surprised but then took comfort from it. There’s nothing I hate more than the wasted energy of reduplication and saying, well come on, if there is one guideline set that does truly command the attention of the world, then the other should stop. It’s wasted energy, which is something that none of us can afford.

The fact that each of these trusted, evidence-based, beautifully presented guidelines is used in different ways was important. A message to the guideline groups from me is: “Thank you for your professionalism, for the hard work of hundreds of cancer specialists from all different specialties, and for their contribution to developing these guidelines.”

It’s worth it, it’s working, people are using them, and they’re making a difference. It’s all about leveling up the quality of cancer care that we deliver.

Specifically, have a look at the ESMO immune guidelines. They are great. I hope you find them helpful. Generically, thanks to all of you who are contributing and working so hard to make these data available to improve the quality of cancer care around the world.

Thanks for listening, as always. I’m interested in any comments that you might have, but for the time being, Medscapers, ahoy.

David J. Kerr, CBE, MD, DSc, is a professor of cancer medicine at the University of Oxford. He reported conflicts of interest with Celleron Therapeutics, Oxford Cancer Biomarkers, Afrox, GlaxoSmithKline, Bayer, Genomic Health, and Merck Serono.

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

Cognition represents the most important function of the human brain and the essence of the mind. Cognitive functions such as memory, learning, comprehension, processing speed, attention, planning, and problem-solving are the best indicators of the status of brain health.

Many psychiatric brain disorders are associated with cognitive impairments. Decades of extensive research have documented that the most severe cognitive deficits occur in schizophrenia. No wonder Emil Kraepelin coined the term “dementia praecox,” which means premature dementia (in youth)¹ for this neuropsychiatric brain disorder. This condition was later renamed schizophrenia by Eugen Bleuler,² who regarded it primarily as a thought disorder, with splitting of associations (not split personality, as misinterpreted by many in the public). Interestingly, a century ago both of those early masters of psychiatry de-emphasized psychotic symptoms (delusions and hallucinations), regarding them as “supplemental symptoms.”³ Yet for the next 100 years, clinicians overemphasized psychotic symptoms in schizophrenia and overlooked the more disabling cognitive impairment and negative symptoms, referred to as Bleuler’s 4 A’s—Associations disruption, Ambivalence, Affect pathology, and Avolition—symptoms that persist even after the psychotic symptoms are successfully treated.³

Most contemporary researchers regard cognitive impairment as the “core” feature of schizophrenia.⁴ The justification of this view is that cognitive deficits are detected in childhood and early adolescence (by age 13),⁵ long before the appearance of psychotic symptoms, and many studies have confirmed that cognitive deficits are the primary cause of functional disability and unemployment of patients with schizophrenia. Cognitive dysfunction is also found in milder forms in the parents and siblings of patients with schizophrenia,⁶ and is thus considered an “endophenotype” of the illness.

Because of its centrality, cognition has emerged as a major focus of schizophrenia research over the past 20 years. Multiple stakeholders (academic investigators, the National Institute of Mental Health, and the FDA) have collaborated to develop a standard measurement for cognition in schizophrenia. The project culminated in what was labeled MATRICS (Measurement and Treatment Research to Improve Cognition in Schizophrenia).⁷ The MATRICS settled on a battery of 7 major cognitive functions that are often impaired in individuals with schizophrenia (Table 1⁸). Most contemporary researchers have adopted MATRICS in their studies, which facilitates replication to confirm research findings.

Measuring cognition in patients with schizophrenia is extremely important, as critical as measuring fasting glucose in patients with diabetes or blood pressure in patients with hypertension. Measuring the extent of impairment or nonimpairment across various cognitive tests can help with vocational rehabilitation, to place a patient in a job consistent with their level of cognitive functioning. In addition, once medications are developed and approved for cognitive impairments in schizophrenia, measuring cognition will be necessary to gauge the degree of improvement.

Currently, few psychiatric practitioners measure cognition in their patients. This is perplexing because cognitive measurement is important for confirming the diagnosis of schizophrenia in first-episode psychosis, or distinguishing it from other psychotic disorders (such as drug-induced psychosis, brief reactive psychosis, or delusional disorders) that do not have severe cognitive deficits.

The scores of various cognitive functions in individuals with schizophrenia range from .75 to 2.0 SD below the performance of the general population (matched for age and gender).⁹ This translates to dismally low percentiles of 2% and 24%. It is essential that all clinicians measure cognition in every patient with psychotic symptoms. It can be argued that cognition should even be measured in other psychiatric patients because cognitive deficits have been well documented in bipolar disorder, major depressive disorder, attention-deficit/hyperactivity disorder, and other disorders, albeit not as severe as in schizophrenia, and these deficits usually correlate with the patient’s vocational and social functioning.

Continue to: So how is cognition measured...

So how is cognition measured, and can clinicians incorporate cognitive batteries in their practices? The most logical answer is to refer the patient to a board-certified neuropsychologist. These specialists are well-trained in assessing cognitive functions, and their evaluations generally are covered by health insurance. They use various validated cognitive batteries. Table 2^10-18 lists the currently recognized cognitive assessments and how much time they require. Psychiatrists can have nurses or medical assistants administer a brief cognitive test.

C-SARS: A self-rated cognition scale

Patient self-rating can provide psychiatric clinicians with valuable information, and is a time-saver. The widely used Patient Health Questionaire-9 (PHQ-9)¹⁹ is an excellent example of a self-rating scale for depression that enables patients to recognize and rate their depressive symptoms. It immediately informs the clinician how depressed their patient is and whether the severity of the depression has improved from the previous visit, which can indicate whether the prescribed medication is working. Based on the PHQ-9, which I regularly use—and recognizing that there is no cognition counterpart and that almost all clinicians could use a practical method of measuring their patients’ cognitive function—I developed an instrument called the Cognition Self-Assessment Rating Scale (C-SARS) (Table 3). The C-SARS can be completed online at https://curesz.org/csars/ and patients will be emailed the results within a minute. The C-SARS can be completed by the patient (with the help of their family or caregiver, if necessary, who observe the patient’s daily functioning, which corresponds to their cognition). The main purpose of the C-SARS is to inform the clinician about serious cognitive dysfunction in their patients, which should instigate a referral for formal neurocognitive assessment by a neuropsychology expert.

The items on the C-SARS reflect how well the patient is performing routine daily functions, each of which correlates with one of the cognitive domains of the MATRICS battery. Table 3 shows the 12 items in the C-SARS, their scoring, and their clinical implications (ie, when the results require referral for formal neurocognitive testing). In the future, when the FDA approves medications for addressing cognitive impairment (and several molecules are currently undergoing clinical trials), clinicians will be able to gauge a patient’s response to such treatments using the C-SARS and formal testing as needed. It may take several weeks to detect a significant reversal of cognitive deficits, but doing so would address a major unmet need in schizophrenia and may speed up vocational rehabilitation. The C-SARS also contains 2 items related to social cognition (items 11 and 12), which is also impaired in schizophrenia.²⁰ Future medications that improve social cognition in addition to neurocognition may also lead to improved social functioning among patients with schizophrenia.

In conclusion, the C-SARS, which needs to be validated in controlled studies, is the first cognition self-rating scale for schizophrenia and may be useful for other major psychiatric disorders. It will be a substantial time-saver for clinicians and will facilitate the routine incorporation of the cognitive assessment of patients with psychotic symptoms to help with the differential diagnosis of schizophrenia vs other psychotic disorders. Measuring cognitive functions is a vital step towards the valid diagnosis and treatment of this major clinical challenge in schizophrenia and improving patient outcomes in this serious psychiatric brain syndrome, in which up to 98% of patients have cognitive impairment across several domains.²¹

Cognition represents the most important function of the human brain and the essence of the mind. Cognitive functions such as memory, learning, comprehension, processing speed, attention, planning, and problem-solving are the best indicators of the status of brain health.

Many psychiatric brain disorders are associated with cognitive impairments. Decades of extensive research have documented that the most severe cognitive deficits occur in schizophrenia. No wonder Emil Kraepelin coined the term “dementia praecox,” which means premature dementia (in youth)¹ for this neuropsychiatric brain disorder. This condition was later renamed schizophrenia by Eugen Bleuler,² who regarded it primarily as a thought disorder, with splitting of associations (not split personality, as misinterpreted by many in the public). Interestingly, a century ago both of those early masters of psychiatry de-emphasized psychotic symptoms (delusions and hallucinations), regarding them as “supplemental symptoms.”³ Yet for the next 100 years, clinicians overemphasized psychotic symptoms in schizophrenia and overlooked the more disabling cognitive impairment and negative symptoms, referred to as Bleuler’s 4 A’s—Associations disruption, Ambivalence, Affect pathology, and Avolition—symptoms that persist even after the psychotic symptoms are successfully treated.³

Most contemporary researchers regard cognitive impairment as the “core” feature of schizophrenia.⁴ The justification of this view is that cognitive deficits are detected in childhood and early adolescence (by age 13),⁵ long before the appearance of psychotic symptoms, and many studies have confirmed that cognitive deficits are the primary cause of functional disability and unemployment of patients with schizophrenia. Cognitive dysfunction is also found in milder forms in the parents and siblings of patients with schizophrenia,⁶ and is thus considered an “endophenotype” of the illness.

Because of its centrality, cognition has emerged as a major focus of schizophrenia research over the past 20 years. Multiple stakeholders (academic investigators, the National Institute of Mental Health, and the FDA) have collaborated to develop a standard measurement for cognition in schizophrenia. The project culminated in what was labeled MATRICS (Measurement and Treatment Research to Improve Cognition in Schizophrenia).⁷ The MATRICS settled on a battery of 7 major cognitive functions that are often impaired in individuals with schizophrenia (Table 1⁸). Most contemporary researchers have adopted MATRICS in their studies, which facilitates replication to confirm research findings.

Measuring cognition in patients with schizophrenia is extremely important, as critical as measuring fasting glucose in patients with diabetes or blood pressure in patients with hypertension. Measuring the extent of impairment or nonimpairment across various cognitive tests can help with vocational rehabilitation, to place a patient in a job consistent with their level of cognitive functioning. In addition, once medications are developed and approved for cognitive impairments in schizophrenia, measuring cognition will be necessary to gauge the degree of improvement.

Currently, few psychiatric practitioners measure cognition in their patients. This is perplexing because cognitive measurement is important for confirming the diagnosis of schizophrenia in first-episode psychosis, or distinguishing it from other psychotic disorders (such as drug-induced psychosis, brief reactive psychosis, or delusional disorders) that do not have severe cognitive deficits.

The scores of various cognitive functions in individuals with schizophrenia range from .75 to 2.0 SD below the performance of the general population (matched for age and gender).⁹ This translates to dismally low percentiles of 2% and 24%. It is essential that all clinicians measure cognition in every patient with psychotic symptoms. It can be argued that cognition should even be measured in other psychiatric patients because cognitive deficits have been well documented in bipolar disorder, major depressive disorder, attention-deficit/hyperactivity disorder, and other disorders, albeit not as severe as in schizophrenia, and these deficits usually correlate with the patient’s vocational and social functioning.

Continue to: So how is cognition measured...

So how is cognition measured, and can clinicians incorporate cognitive batteries in their practices? The most logical answer is to refer the patient to a board-certified neuropsychologist. These specialists are well-trained in assessing cognitive functions, and their evaluations generally are covered by health insurance. They use various validated cognitive batteries. Table 2^10-18 lists the currently recognized cognitive assessments and how much time they require. Psychiatrists can have nurses or medical assistants administer a brief cognitive test.

C-SARS: A self-rated cognition scale

Patient self-rating can provide psychiatric clinicians with valuable information, and is a time-saver. The widely used Patient Health Questionaire-9 (PHQ-9)¹⁹ is an excellent example of a self-rating scale for depression that enables patients to recognize and rate their depressive symptoms. It immediately informs the clinician how depressed their patient is and whether the severity of the depression has improved from the previous visit, which can indicate whether the prescribed medication is working. Based on the PHQ-9, which I regularly use—and recognizing that there is no cognition counterpart and that almost all clinicians could use a practical method of measuring their patients’ cognitive function—I developed an instrument called the Cognition Self-Assessment Rating Scale (C-SARS) (Table 3). The C-SARS can be completed online at https://curesz.org/csars/ and patients will be emailed the results within a minute. The C-SARS can be completed by the patient (with the help of their family or caregiver, if necessary, who observe the patient’s daily functioning, which corresponds to their cognition). The main purpose of the C-SARS is to inform the clinician about serious cognitive dysfunction in their patients, which should instigate a referral for formal neurocognitive assessment by a neuropsychology expert.

The items on the C-SARS reflect how well the patient is performing routine daily functions, each of which correlates with one of the cognitive domains of the MATRICS battery. Table 3 shows the 12 items in the C-SARS, their scoring, and their clinical implications (ie, when the results require referral for formal neurocognitive testing). In the future, when the FDA approves medications for addressing cognitive impairment (and several molecules are currently undergoing clinical trials), clinicians will be able to gauge a patient’s response to such treatments using the C-SARS and formal testing as needed. It may take several weeks to detect a significant reversal of cognitive deficits, but doing so would address a major unmet need in schizophrenia and may speed up vocational rehabilitation. The C-SARS also contains 2 items related to social cognition (items 11 and 12), which is also impaired in schizophrenia.²⁰ Future medications that improve social cognition in addition to neurocognition may also lead to improved social functioning among patients with schizophrenia.

In conclusion, the C-SARS, which needs to be validated in controlled studies, is the first cognition self-rating scale for schizophrenia and may be useful for other major psychiatric disorders. It will be a substantial time-saver for clinicians and will facilitate the routine incorporation of the cognitive assessment of patients with psychotic symptoms to help with the differential diagnosis of schizophrenia vs other psychotic disorders. Measuring cognitive functions is a vital step towards the valid diagnosis and treatment of this major clinical challenge in schizophrenia and improving patient outcomes in this serious psychiatric brain syndrome, in which up to 98% of patients have cognitive impairment across several domains.²¹

Cognition represents the most important function of the human brain and the essence of the mind. Cognitive functions such as memory, learning, comprehension, processing speed, attention, planning, and problem-solving are the best indicators of the status of brain health.

Many psychiatric brain disorders are associated with cognitive impairments. Decades of extensive research have documented that the most severe cognitive deficits occur in schizophrenia. No wonder Emil Kraepelin coined the term “dementia praecox,” which means premature dementia (in youth)¹ for this neuropsychiatric brain disorder. This condition was later renamed schizophrenia by Eugen Bleuler,² who regarded it primarily as a thought disorder, with splitting of associations (not split personality, as misinterpreted by many in the public). Interestingly, a century ago both of those early masters of psychiatry de-emphasized psychotic symptoms (delusions and hallucinations), regarding them as “supplemental symptoms.”³ Yet for the next 100 years, clinicians overemphasized psychotic symptoms in schizophrenia and overlooked the more disabling cognitive impairment and negative symptoms, referred to as Bleuler’s 4 A’s—Associations disruption, Ambivalence, Affect pathology, and Avolition—symptoms that persist even after the psychotic symptoms are successfully treated.³

Most contemporary researchers regard cognitive impairment as the “core” feature of schizophrenia.⁴ The justification of this view is that cognitive deficits are detected in childhood and early adolescence (by age 13),⁵ long before the appearance of psychotic symptoms, and many studies have confirmed that cognitive deficits are the primary cause of functional disability and unemployment of patients with schizophrenia. Cognitive dysfunction is also found in milder forms in the parents and siblings of patients with schizophrenia,⁶ and is thus considered an “endophenotype” of the illness.

Because of its centrality, cognition has emerged as a major focus of schizophrenia research over the past 20 years. Multiple stakeholders (academic investigators, the National Institute of Mental Health, and the FDA) have collaborated to develop a standard measurement for cognition in schizophrenia. The project culminated in what was labeled MATRICS (Measurement and Treatment Research to Improve Cognition in Schizophrenia).⁷ The MATRICS settled on a battery of 7 major cognitive functions that are often impaired in individuals with schizophrenia (Table 1⁸). Most contemporary researchers have adopted MATRICS in their studies, which facilitates replication to confirm research findings.

Measuring cognition in patients with schizophrenia is extremely important, as critical as measuring fasting glucose in patients with diabetes or blood pressure in patients with hypertension. Measuring the extent of impairment or nonimpairment across various cognitive tests can help with vocational rehabilitation, to place a patient in a job consistent with their level of cognitive functioning. In addition, once medications are developed and approved for cognitive impairments in schizophrenia, measuring cognition will be necessary to gauge the degree of improvement.

Currently, few psychiatric practitioners measure cognition in their patients. This is perplexing because cognitive measurement is important for confirming the diagnosis of schizophrenia in first-episode psychosis, or distinguishing it from other psychotic disorders (such as drug-induced psychosis, brief reactive psychosis, or delusional disorders) that do not have severe cognitive deficits.

The scores of various cognitive functions in individuals with schizophrenia range from .75 to 2.0 SD below the performance of the general population (matched for age and gender).⁹ This translates to dismally low percentiles of 2% and 24%. It is essential that all clinicians measure cognition in every patient with psychotic symptoms. It can be argued that cognition should even be measured in other psychiatric patients because cognitive deficits have been well documented in bipolar disorder, major depressive disorder, attention-deficit/hyperactivity disorder, and other disorders, albeit not as severe as in schizophrenia, and these deficits usually correlate with the patient’s vocational and social functioning.

Continue to: So how is cognition measured...

So how is cognition measured, and can clinicians incorporate cognitive batteries in their practices? The most logical answer is to refer the patient to a board-certified neuropsychologist. These specialists are well-trained in assessing cognitive functions, and their evaluations generally are covered by health insurance. They use various validated cognitive batteries. Table 2^10-18 lists the currently recognized cognitive assessments and how much time they require. Psychiatrists can have nurses or medical assistants administer a brief cognitive test.

C-SARS: A self-rated cognition scale

Patient self-rating can provide psychiatric clinicians with valuable information, and is a time-saver. The widely used Patient Health Questionaire-9 (PHQ-9)¹⁹ is an excellent example of a self-rating scale for depression that enables patients to recognize and rate their depressive symptoms. It immediately informs the clinician how depressed their patient is and whether the severity of the depression has improved from the previous visit, which can indicate whether the prescribed medication is working. Based on the PHQ-9, which I regularly use—and recognizing that there is no cognition counterpart and that almost all clinicians could use a practical method of measuring their patients’ cognitive function—I developed an instrument called the Cognition Self-Assessment Rating Scale (C-SARS) (Table 3). The C-SARS can be completed online at https://curesz.org/csars/ and patients will be emailed the results within a minute. The C-SARS can be completed by the patient (with the help of their family or caregiver, if necessary, who observe the patient’s daily functioning, which corresponds to their cognition). The main purpose of the C-SARS is to inform the clinician about serious cognitive dysfunction in their patients, which should instigate a referral for formal neurocognitive assessment by a neuropsychology expert.

The items on the C-SARS reflect how well the patient is performing routine daily functions, each of which correlates with one of the cognitive domains of the MATRICS battery. Table 3 shows the 12 items in the C-SARS, their scoring, and their clinical implications (ie, when the results require referral for formal neurocognitive testing). In the future, when the FDA approves medications for addressing cognitive impairment (and several molecules are currently undergoing clinical trials), clinicians will be able to gauge a patient’s response to such treatments using the C-SARS and formal testing as needed. It may take several weeks to detect a significant reversal of cognitive deficits, but doing so would address a major unmet need in schizophrenia and may speed up vocational rehabilitation. The C-SARS also contains 2 items related to social cognition (items 11 and 12), which is also impaired in schizophrenia.²⁰ Future medications that improve social cognition in addition to neurocognition may also lead to improved social functioning among patients with schizophrenia.

In conclusion, the C-SARS, which needs to be validated in controlled studies, is the first cognition self-rating scale for schizophrenia and may be useful for other major psychiatric disorders. It will be a substantial time-saver for clinicians and will facilitate the routine incorporation of the cognitive assessment of patients with psychotic symptoms to help with the differential diagnosis of schizophrenia vs other psychotic disorders. Measuring cognitive functions is a vital step towards the valid diagnosis and treatment of this major clinical challenge in schizophrenia and improving patient outcomes in this serious psychiatric brain syndrome, in which up to 98% of patients have cognitive impairment across several domains.²¹

Psychogenic nonepileptic seizures (PNES) are a physical manifestation of a psychological disturbance. They are characterized by episodes of altered subjective experience and movements that can resemble epilepsy, syncope, or other paroxysmal disorders, but are not caused by neuronal hypersynchronization or other epileptic semiology.¹ Asynchronous movements, closed eyes, crying, stuttering, side-to-side head movement, and pelvic thrusting may be observed, all of which are atypical of epileptic seizures.¹ PNES, a syndrome of “pseudo-seizures,” is recognized in 11% of convulsive seizure cases presenting to the emergency department (ED).² PNES can co-occur with epilepsy; in 2 population-based studies, the pooled rate of EEG-confirmed comorbid epilepsy in PNES was 14%.³

Patients with PNES may present to multiple clinicians and hospitals for assessment. Access to outside hospital records can be limited, which can lead to redundant testing and increased health care costs and burden. Additionally, repeat presentations can increase stigmatization of the patient and delay or prevent appropriate therapeutic management, which might exacerbate a patient’s underlying psychiatric condition and could be dangerous in a patient with a co-occurring true seizure disorder. Though obtaining and reviewing external medical records can be cumbersome, doing so may prevent unnecessary testing, guide medical treatment, and strengthen the patient-doctor therapeutic alliance.

In this article, I discuss our treatment team’s management of a patient with PNES who, based on our careful review of records from previous hospitalizations, may have had a co-occurring true seizure disorder.

Case report

Ms. M, age 31, has a medical history of anxiety, depression, first-degree atrioventricular block, type 2 diabetes, and PNES. She presented to the ED with witnessed seizure activity at home.

According to collateral information, earlier that day Ms. M said she felt like she was seizing and began mumbling, but returned to baseline within a few minutes. Later, she demonstrated intermittent upper and lower extremity shaking for more than 1 hour. At one point, Ms. M appeared to be not breathing. However, upon initiation of chest compressions, she began gasping for air and immediately returned to baseline.

In the ED, Ms. M demonstrated multiple seizure-like episodes every 5 minutes, each lasting 5 to 10 seconds. These episodes were described as thrashing of the bilateral limbs and head crossing midline with eyes closed. No urinary incontinence or tongue biting was observed. Following each episode, Ms. M was unresponsive to verbal or tactile stimuli but intermittently opened her eyes. Laboratory test results were notable for an elevated serum lactate and positive for cannabinoids on urine drug screen.

Ms. M expressed frustration when told that her seizures were psychogenic. She was adamant that she had a true seizure disorder, demanded testing, and threatened to leave against medical advice without it. She said her brother had epilepsy, and thus she knew how seizures present. The interview was complicated by Ms. M’s mistrust and Cluster B personality disorder traits, such as splitting staff into “good and bad.” Ultimately, she was able to be reassured and did not leave the hospital.

Continue to: The treatment team...

The treatment team reviewed external records from 2 hospitals, Hospital A and Hospital B. These records showed well-documented inpatient and outpatient Psychiatry and Neurology diagnoses of PNES and other conversion disorders. Her medications included 2 anticonvulsants—topiramate 200 mg every 12 hours and oxcarbazepine 300 mg every 12 hours—as well as clonazepam 0.5 mg as needed for seizures and anxiety.

Ms. M’s first lifetime documented seizure occurred in May 2020, when she woke up with tongue biting, extremity shaking (laterality was unclear), and urinary incontinence followed by fatigue. She did not go to the hospital after this first episode. In June 2020, she presented and was admitted to Hospital A after similar seizure-like activity. While admitted and monitored on continuous EEG (cEEG), she had numerous events consistent with a nonepileptic etiology without a postictal state. A brain MRI was unremarkable, and Ms. M was diagnosed with PNES.

She presented to Hospital B in October 2020 reporting seizure-like activity. Hospital B reviewed Hospital A’s brain MRI and found right temporal lobe cortical dysplasia that was not noted in Hospital A’s MRI read. Ms. M again underwent cEEG while at Hospital B and had 2 recorded nonepileptic events. Interestingly, the cEEG demonstrated right temporal spikes that were consistent with the dysplasia location on the MRI. Ms. M was discharged and instructed to keep a seizure journal until outpatient follow-up.

Ms. M documented 3 seizure-like events between October and December 2020. She documented activity with and without full-body convulsions, some with laterality, some with loss of consciousness, and some preceded by an aura of impending doom. Ms. M was referred to psychotherapy and instructed to continue topiramate 100 mg every 12 hours for seizure prophylaxis.

Ms. M presented to Hospital B again in March 2022 reporting seizure-like activity. A brain MRI found cortical dysplasia in the right temporal lobe, consistent with the MRI at Hospital A in June 2020. cEEG was also repeated at Hospital B and was unremarkable. Oxcarbazepine 300 mg every 12 hours was added to Ms. M’s medications.

Ultimately, based on an external record review, our team (at Hospital C) concluded Ms. M had a possible true seizure co-occurrence with PNES. To avoid redundant testing, we did not repeat imaging or cEEG. Instead, we increased the patient’s oxcarbazepine to 450 mg every 12 hours, for both its effectiveness in temporal seizures and its mood-stabilizing properties. Moreover, in collecting our own data to draw a conclusion by a thorough record review, we gained Ms. M’s trust and strengthened the therapeutic alliance. She was agreeable to forgo more testing and continue outpatient follow-up with our hospital’s Neurology team.

Take-home points

Although PNES and true seizure disorder may not frequently co-occur, this case highlights the importance of clinician due diligence when evaluating a potential psychogenic illness, both for patient safety and clinician liability. By trusting our patients and drawing our own data-based conclusions, we can cultivate a safer and more satisfactory patient-clinician experience in the context of psychosomatic disorders.

Psychogenic nonepileptic seizures (PNES) are a physical manifestation of a psychological disturbance. They are characterized by episodes of altered subjective experience and movements that can resemble epilepsy, syncope, or other paroxysmal disorders, but are not caused by neuronal hypersynchronization or other epileptic semiology.¹ Asynchronous movements, closed eyes, crying, stuttering, side-to-side head movement, and pelvic thrusting may be observed, all of which are atypical of epileptic seizures.¹ PNES, a syndrome of “pseudo-seizures,” is recognized in 11% of convulsive seizure cases presenting to the emergency department (ED).² PNES can co-occur with epilepsy; in 2 population-based studies, the pooled rate of EEG-confirmed comorbid epilepsy in PNES was 14%.³

Patients with PNES may present to multiple clinicians and hospitals for assessment. Access to outside hospital records can be limited, which can lead to redundant testing and increased health care costs and burden. Additionally, repeat presentations can increase stigmatization of the patient and delay or prevent appropriate therapeutic management, which might exacerbate a patient’s underlying psychiatric condition and could be dangerous in a patient with a co-occurring true seizure disorder. Though obtaining and reviewing external medical records can be cumbersome, doing so may prevent unnecessary testing, guide medical treatment, and strengthen the patient-doctor therapeutic alliance.

In this article, I discuss our treatment team’s management of a patient with PNES who, based on our careful review of records from previous hospitalizations, may have had a co-occurring true seizure disorder.

Case report

Ms. M, age 31, has a medical history of anxiety, depression, first-degree atrioventricular block, type 2 diabetes, and PNES. She presented to the ED with witnessed seizure activity at home.

According to collateral information, earlier that day Ms. M said she felt like she was seizing and began mumbling, but returned to baseline within a few minutes. Later, she demonstrated intermittent upper and lower extremity shaking for more than 1 hour. At one point, Ms. M appeared to be not breathing. However, upon initiation of chest compressions, she began gasping for air and immediately returned to baseline.

In the ED, Ms. M demonstrated multiple seizure-like episodes every 5 minutes, each lasting 5 to 10 seconds. These episodes were described as thrashing of the bilateral limbs and head crossing midline with eyes closed. No urinary incontinence or tongue biting was observed. Following each episode, Ms. M was unresponsive to verbal or tactile stimuli but intermittently opened her eyes. Laboratory test results were notable for an elevated serum lactate and positive for cannabinoids on urine drug screen.

Ms. M expressed frustration when told that her seizures were psychogenic. She was adamant that she had a true seizure disorder, demanded testing, and threatened to leave against medical advice without it. She said her brother had epilepsy, and thus she knew how seizures present. The interview was complicated by Ms. M’s mistrust and Cluster B personality disorder traits, such as splitting staff into “good and bad.” Ultimately, she was able to be reassured and did not leave the hospital.

Continue to: The treatment team...

The treatment team reviewed external records from 2 hospitals, Hospital A and Hospital B. These records showed well-documented inpatient and outpatient Psychiatry and Neurology diagnoses of PNES and other conversion disorders. Her medications included 2 anticonvulsants—topiramate 200 mg every 12 hours and oxcarbazepine 300 mg every 12 hours—as well as clonazepam 0.5 mg as needed for seizures and anxiety.

Ms. M’s first lifetime documented seizure occurred in May 2020, when she woke up with tongue biting, extremity shaking (laterality was unclear), and urinary incontinence followed by fatigue. She did not go to the hospital after this first episode. In June 2020, she presented and was admitted to Hospital A after similar seizure-like activity. While admitted and monitored on continuous EEG (cEEG), she had numerous events consistent with a nonepileptic etiology without a postictal state. A brain MRI was unremarkable, and Ms. M was diagnosed with PNES.

She presented to Hospital B in October 2020 reporting seizure-like activity. Hospital B reviewed Hospital A’s brain MRI and found right temporal lobe cortical dysplasia that was not noted in Hospital A’s MRI read. Ms. M again underwent cEEG while at Hospital B and had 2 recorded nonepileptic events. Interestingly, the cEEG demonstrated right temporal spikes that were consistent with the dysplasia location on the MRI. Ms. M was discharged and instructed to keep a seizure journal until outpatient follow-up.

Ms. M documented 3 seizure-like events between October and December 2020. She documented activity with and without full-body convulsions, some with laterality, some with loss of consciousness, and some preceded by an aura of impending doom. Ms. M was referred to psychotherapy and instructed to continue topiramate 100 mg every 12 hours for seizure prophylaxis.

Ms. M presented to Hospital B again in March 2022 reporting seizure-like activity. A brain MRI found cortical dysplasia in the right temporal lobe, consistent with the MRI at Hospital A in June 2020. cEEG was also repeated at Hospital B and was unremarkable. Oxcarbazepine 300 mg every 12 hours was added to Ms. M’s medications.

Ultimately, based on an external record review, our team (at Hospital C) concluded Ms. M had a possible true seizure co-occurrence with PNES. To avoid redundant testing, we did not repeat imaging or cEEG. Instead, we increased the patient’s oxcarbazepine to 450 mg every 12 hours, for both its effectiveness in temporal seizures and its mood-stabilizing properties. Moreover, in collecting our own data to draw a conclusion by a thorough record review, we gained Ms. M’s trust and strengthened the therapeutic alliance. She was agreeable to forgo more testing and continue outpatient follow-up with our hospital’s Neurology team.

Take-home points

Although PNES and true seizure disorder may not frequently co-occur, this case highlights the importance of clinician due diligence when evaluating a potential psychogenic illness, both for patient safety and clinician liability. By trusting our patients and drawing our own data-based conclusions, we can cultivate a safer and more satisfactory patient-clinician experience in the context of psychosomatic disorders.

Psychogenic nonepileptic seizures (PNES) are a physical manifestation of a psychological disturbance. They are characterized by episodes of altered subjective experience and movements that can resemble epilepsy, syncope, or other paroxysmal disorders, but are not caused by neuronal hypersynchronization or other epileptic semiology.¹ Asynchronous movements, closed eyes, crying, stuttering, side-to-side head movement, and pelvic thrusting may be observed, all of which are atypical of epileptic seizures.¹ PNES, a syndrome of “pseudo-seizures,” is recognized in 11% of convulsive seizure cases presenting to the emergency department (ED).² PNES can co-occur with epilepsy; in 2 population-based studies, the pooled rate of EEG-confirmed comorbid epilepsy in PNES was 14%.³

Patients with PNES may present to multiple clinicians and hospitals for assessment. Access to outside hospital records can be limited, which can lead to redundant testing and increased health care costs and burden. Additionally, repeat presentations can increase stigmatization of the patient and delay or prevent appropriate therapeutic management, which might exacerbate a patient’s underlying psychiatric condition and could be dangerous in a patient with a co-occurring true seizure disorder. Though obtaining and reviewing external medical records can be cumbersome, doing so may prevent unnecessary testing, guide medical treatment, and strengthen the patient-doctor therapeutic alliance.

In this article, I discuss our treatment team’s management of a patient with PNES who, based on our careful review of records from previous hospitalizations, may have had a co-occurring true seizure disorder.

Case report

Ms. M, age 31, has a medical history of anxiety, depression, first-degree atrioventricular block, type 2 diabetes, and PNES. She presented to the ED with witnessed seizure activity at home.

According to collateral information, earlier that day Ms. M said she felt like she was seizing and began mumbling, but returned to baseline within a few minutes. Later, she demonstrated intermittent upper and lower extremity shaking for more than 1 hour. At one point, Ms. M appeared to be not breathing. However, upon initiation of chest compressions, she began gasping for air and immediately returned to baseline.

In the ED, Ms. M demonstrated multiple seizure-like episodes every 5 minutes, each lasting 5 to 10 seconds. These episodes were described as thrashing of the bilateral limbs and head crossing midline with eyes closed. No urinary incontinence or tongue biting was observed. Following each episode, Ms. M was unresponsive to verbal or tactile stimuli but intermittently opened her eyes. Laboratory test results were notable for an elevated serum lactate and positive for cannabinoids on urine drug screen.

Ms. M expressed frustration when told that her seizures were psychogenic. She was adamant that she had a true seizure disorder, demanded testing, and threatened to leave against medical advice without it. She said her brother had epilepsy, and thus she knew how seizures present. The interview was complicated by Ms. M’s mistrust and Cluster B personality disorder traits, such as splitting staff into “good and bad.” Ultimately, she was able to be reassured and did not leave the hospital.

Continue to: The treatment team...

The treatment team reviewed external records from 2 hospitals, Hospital A and Hospital B. These records showed well-documented inpatient and outpatient Psychiatry and Neurology diagnoses of PNES and other conversion disorders. Her medications included 2 anticonvulsants—topiramate 200 mg every 12 hours and oxcarbazepine 300 mg every 12 hours—as well as clonazepam 0.5 mg as needed for seizures and anxiety.

Ms. M’s first lifetime documented seizure occurred in May 2020, when she woke up with tongue biting, extremity shaking (laterality was unclear), and urinary incontinence followed by fatigue. She did not go to the hospital after this first episode. In June 2020, she presented and was admitted to Hospital A after similar seizure-like activity. While admitted and monitored on continuous EEG (cEEG), she had numerous events consistent with a nonepileptic etiology without a postictal state. A brain MRI was unremarkable, and Ms. M was diagnosed with PNES.

She presented to Hospital B in October 2020 reporting seizure-like activity. Hospital B reviewed Hospital A’s brain MRI and found right temporal lobe cortical dysplasia that was not noted in Hospital A’s MRI read. Ms. M again underwent cEEG while at Hospital B and had 2 recorded nonepileptic events. Interestingly, the cEEG demonstrated right temporal spikes that were consistent with the dysplasia location on the MRI. Ms. M was discharged and instructed to keep a seizure journal until outpatient follow-up.

Ms. M documented 3 seizure-like events between October and December 2020. She documented activity with and without full-body convulsions, some with laterality, some with loss of consciousness, and some preceded by an aura of impending doom. Ms. M was referred to psychotherapy and instructed to continue topiramate 100 mg every 12 hours for seizure prophylaxis.

Ms. M presented to Hospital B again in March 2022 reporting seizure-like activity. A brain MRI found cortical dysplasia in the right temporal lobe, consistent with the MRI at Hospital A in June 2020. cEEG was also repeated at Hospital B and was unremarkable. Oxcarbazepine 300 mg every 12 hours was added to Ms. M’s medications.

Ultimately, based on an external record review, our team (at Hospital C) concluded Ms. M had a possible true seizure co-occurrence with PNES. To avoid redundant testing, we did not repeat imaging or cEEG. Instead, we increased the patient’s oxcarbazepine to 450 mg every 12 hours, for both its effectiveness in temporal seizures and its mood-stabilizing properties. Moreover, in collecting our own data to draw a conclusion by a thorough record review, we gained Ms. M’s trust and strengthened the therapeutic alliance. She was agreeable to forgo more testing and continue outpatient follow-up with our hospital’s Neurology team.

Take-home points

Although PNES and true seizure disorder may not frequently co-occur, this case highlights the importance of clinician due diligence when evaluating a potential psychogenic illness, both for patient safety and clinician liability. By trusting our patients and drawing our own data-based conclusions, we can cultivate a safer and more satisfactory patient-clinician experience in the context of psychosomatic disorders.

Many psychiatric physicians lament the dearth of procedures in psychiatry compared to other medical specialties such as surgery, cardiology, gastroenterology, or radiology. The few procedures in psychiatry include electroconvulsive therapy (ECT), repetitive transcranial magnetic stimulation, and vagus nerve stimulation, which are restricted to a small number of sites and not available for most psychiatric practitioners. This lack of tangible/physical procedures should not be surprising because psychiatry deals with disorders of the mind, which are invisible.

However, when one closely examines what psychiatrists do in daily practice to heal our patients, most of what we do actually qualifies as “procedures” although no hardware, machines, or gadgets are involved. Treating psychiatric brain disorders (aka mental illness) requires exquisite skills and expertise, just like medical specialties that use machines to measure or treat various body organs.

It’s time to relabel psychiatric interventions as procedures designed to improve anomalous thoughts, affect, emotions, cognition, and behavior. After giving it some thought (and with a bit of tongue in cheek), I came up with the following list of “psychiatric procedures”:

• Psychosocial exploratory laparotomy: The comprehensive psychiatric assessment and mental status exam.
• Chemotherapy: Oral or injective pharmacotherapeutic intervention.
• Psychoplastic repair: Neuroplasticity, including neurogenesis, synaptogenesis, and dendritic spine regeneration, have been shown to be associated with both psychotherapy and psychotropic medications.^1,2
• Suicidectomy: Extracting the lethal urge to die by suicide.
• Anger debridement: Removing the irritability and destructive anger outbursts frequently associated with various psychopathologies.
• Anxiety ablation: Eliminating the noxious emotional state of anxiety and frightening panic attacks.
• Empathy infusion: Enabling patients to become more understanding of other people and bolstering their impaired “theory of mind.”
• Personality transplant: Replacing a maladaptive personality with a healthier one (eg, using dialectical behavior therapy for borderline personality disorder).
• Cognitive LASIK: To improve insight, analogous to how ophthalmologic LASIK improves sight.
• Mental embolectomy: Removing a blockage to repair rigid attitudes and develop “open-mindedness.”
• Behavioral dilation and curettage (D&C): To rid patients of negative attributes such as impulsivity or reckless behavior.
• Psychotherapeutic anesthesia: Numbing emotional pain or severe grief reaction.
• Social anastomosis: Helping patients who are schizoid or isolative via group therapy, an effective interpersonal and social procedure.
• Psychotherapeutic stent: To open the vessels of narrow-mindedness.
• Cortico-psychological resuscitation (CPR): For patients experiencing stress-induced behavioral arrhythmias or emotional infarction.
• Immunotherapy: Using various neuroprotective psychotropic medications with anti-inflammatory properties or employing evidence-based psychotherapy such as cognitive-behavior therapy (aka neuropsychotherapy), which have been shown to reduce inflammatory biomarkers such as C-reactive protein and cytokines.³
• Psychotherapy: A neuromodulation procedure for a variety of psychiatric disorders.⁴
• Neurobiological facelift: It is well established that neurogenesis, synaptogenesis, and dendritic spine sprouting are significantly increased with both neuroprotective psychotropic medications (antidepressants, lithium, valproate, and second-generationantipsychotics⁵) as well as with psych­otherapy. There is growing evidence of “premature brain aging” in schizophrenia, bipolar disorder, and depression, with shrinkage in the volume of the cortex and subcortical regions, especially the hippocampus. Psychiatric biopsychosocial interven­tion rebuilds those brain regions by stimulating and replenishing the neuropil and neuro­genic regions (dentate gyrus and subventricular zone). This is like performing virtual plastic surgery on a wrinkled brain and its sagging mind. MRI scans before and after ECT show a remarkable ≥10% increase in the volume of the hippocampus and amygdala, which translates to billions of new neurons, glia, and synapses.⁶

Reinventing psychiatric therapies as procedures may elicit sarcasm from skeptics, but when you think about it, it is justified. Excising depression is like excising a tumor, not with a scalpel, but virtually. Stabilizing the broken brain and mind after a psychotic episode (aka brain attack) is like stabilizing the heart after a myocardial infarction (aka heart attack). Just because the mind is virtual doesn’t mean it is not “real and tangible.” A desktop computer is visible, but the software that brings it to life is invisible. Healing the human mind requires multiple medical interventions by psychiatrists in hospitals and clinics, just like surgeons and endoscopists or cardiologists. Mental health care is as much procedural as other medical and surgical specialties.

One more thing: the validated clinical rating scales for various psychiatric brain disorders (eg, the Positive and Negative Syndrome Scale for schizophrenia, Montgomery-Åsberg Depression Rating Scale for depression, Young Mania Rating Scale for bipolar mania, Hamilton Anxiety Rating Scale for anxiety, Yale-Brown Obsessive Compulsive Scale for obsessive-compulsive disorder) are actual measurement procedures for the severity of the illness, just as a sphygmomanometer measures blood pressure and its improvement with treatment. There are also multiple cognitive test batteries to measure cognitive impairment.⁷

Finally, unlike psychiatric reimbursement, which is tethered to time, procedures are compensated more generously, irrespective of the time involved. The complexities of diagnosing and treating psychiatric brain disorders that dangerously disrupt thoughts, feelings, behavior, and cognition are just as intricate and demanding as the diagnosis and treatment of general medical and surgical conditions. They should all be equally appreciated as vital life-saving procedures for the human body, brain, and mind.

Many psychiatric physicians lament the dearth of procedures in psychiatry compared to other medical specialties such as surgery, cardiology, gastroenterology, or radiology. The few procedures in psychiatry include electroconvulsive therapy (ECT), repetitive transcranial magnetic stimulation, and vagus nerve stimulation, which are restricted to a small number of sites and not available for most psychiatric practitioners. This lack of tangible/physical procedures should not be surprising because psychiatry deals with disorders of the mind, which are invisible.

However, when one closely examines what psychiatrists do in daily practice to heal our patients, most of what we do actually qualifies as “procedures” although no hardware, machines, or gadgets are involved. Treating psychiatric brain disorders (aka mental illness) requires exquisite skills and expertise, just like medical specialties that use machines to measure or treat various body organs.

It’s time to relabel psychiatric interventions as procedures designed to improve anomalous thoughts, affect, emotions, cognition, and behavior. After giving it some thought (and with a bit of tongue in cheek), I came up with the following list of “psychiatric procedures”:

• Psychosocial exploratory laparotomy: The comprehensive psychiatric assessment and mental status exam.
• Chemotherapy: Oral or injective pharmacotherapeutic intervention.
• Psychoplastic repair: Neuroplasticity, including neurogenesis, synaptogenesis, and dendritic spine regeneration, have been shown to be associated with both psychotherapy and psychotropic medications.^1,2
• Suicidectomy: Extracting the lethal urge to die by suicide.
• Anger debridement: Removing the irritability and destructive anger outbursts frequently associated with various psychopathologies.
• Anxiety ablation: Eliminating the noxious emotional state of anxiety and frightening panic attacks.
• Empathy infusion: Enabling patients to become more understanding of other people and bolstering their impaired “theory of mind.”
• Personality transplant: Replacing a maladaptive personality with a healthier one (eg, using dialectical behavior therapy for borderline personality disorder).
• Cognitive LASIK: To improve insight, analogous to how ophthalmologic LASIK improves sight.
• Mental embolectomy: Removing a blockage to repair rigid attitudes and develop “open-mindedness.”
• Behavioral dilation and curettage (D&C): To rid patients of negative attributes such as impulsivity or reckless behavior.
• Psychotherapeutic anesthesia: Numbing emotional pain or severe grief reaction.
• Social anastomosis: Helping patients who are schizoid or isolative via group therapy, an effective interpersonal and social procedure.
• Psychotherapeutic stent: To open the vessels of narrow-mindedness.
• Cortico-psychological resuscitation (CPR): For patients experiencing stress-induced behavioral arrhythmias or emotional infarction.
• Immunotherapy: Using various neuroprotective psychotropic medications with anti-inflammatory properties or employing evidence-based psychotherapy such as cognitive-behavior therapy (aka neuropsychotherapy), which have been shown to reduce inflammatory biomarkers such as C-reactive protein and cytokines.³
• Psychotherapy: A neuromodulation procedure for a variety of psychiatric disorders.⁴
• Neurobiological facelift: It is well established that neurogenesis, synaptogenesis, and dendritic spine sprouting are significantly increased with both neuroprotective psychotropic medications (antidepressants, lithium, valproate, and second-generationantipsychotics⁵) as well as with psych­otherapy. There is growing evidence of “premature brain aging” in schizophrenia, bipolar disorder, and depression, with shrinkage in the volume of the cortex and subcortical regions, especially the hippocampus. Psychiatric biopsychosocial interven­tion rebuilds those brain regions by stimulating and replenishing the neuropil and neuro­genic regions (dentate gyrus and subventricular zone). This is like performing virtual plastic surgery on a wrinkled brain and its sagging mind. MRI scans before and after ECT show a remarkable ≥10% increase in the volume of the hippocampus and amygdala, which translates to billions of new neurons, glia, and synapses.⁶

Reinventing psychiatric therapies as procedures may elicit sarcasm from skeptics, but when you think about it, it is justified. Excising depression is like excising a tumor, not with a scalpel, but virtually. Stabilizing the broken brain and mind after a psychotic episode (aka brain attack) is like stabilizing the heart after a myocardial infarction (aka heart attack). Just because the mind is virtual doesn’t mean it is not “real and tangible.” A desktop computer is visible, but the software that brings it to life is invisible. Healing the human mind requires multiple medical interventions by psychiatrists in hospitals and clinics, just like surgeons and endoscopists or cardiologists. Mental health care is as much procedural as other medical and surgical specialties.

One more thing: the validated clinical rating scales for various psychiatric brain disorders (eg, the Positive and Negative Syndrome Scale for schizophrenia, Montgomery-Åsberg Depression Rating Scale for depression, Young Mania Rating Scale for bipolar mania, Hamilton Anxiety Rating Scale for anxiety, Yale-Brown Obsessive Compulsive Scale for obsessive-compulsive disorder) are actual measurement procedures for the severity of the illness, just as a sphygmomanometer measures blood pressure and its improvement with treatment. There are also multiple cognitive test batteries to measure cognitive impairment.⁷

Finally, unlike psychiatric reimbursement, which is tethered to time, procedures are compensated more generously, irrespective of the time involved. The complexities of diagnosing and treating psychiatric brain disorders that dangerously disrupt thoughts, feelings, behavior, and cognition are just as intricate and demanding as the diagnosis and treatment of general medical and surgical conditions. They should all be equally appreciated as vital life-saving procedures for the human body, brain, and mind.

Many psychiatric physicians lament the dearth of procedures in psychiatry compared to other medical specialties such as surgery, cardiology, gastroenterology, or radiology. The few procedures in psychiatry include electroconvulsive therapy (ECT), repetitive transcranial magnetic stimulation, and vagus nerve stimulation, which are restricted to a small number of sites and not available for most psychiatric practitioners. This lack of tangible/physical procedures should not be surprising because psychiatry deals with disorders of the mind, which are invisible.

However, when one closely examines what psychiatrists do in daily practice to heal our patients, most of what we do actually qualifies as “procedures” although no hardware, machines, or gadgets are involved. Treating psychiatric brain disorders (aka mental illness) requires exquisite skills and expertise, just like medical specialties that use machines to measure or treat various body organs.

It’s time to relabel psychiatric interventions as procedures designed to improve anomalous thoughts, affect, emotions, cognition, and behavior. After giving it some thought (and with a bit of tongue in cheek), I came up with the following list of “psychiatric procedures”:

• Psychosocial exploratory laparotomy: The comprehensive psychiatric assessment and mental status exam.
• Chemotherapy: Oral or injective pharmacotherapeutic intervention.
• Psychoplastic repair: Neuroplasticity, including neurogenesis, synaptogenesis, and dendritic spine regeneration, have been shown to be associated with both psychotherapy and psychotropic medications.^1,2
• Suicidectomy: Extracting the lethal urge to die by suicide.
• Anger debridement: Removing the irritability and destructive anger outbursts frequently associated with various psychopathologies.
• Anxiety ablation: Eliminating the noxious emotional state of anxiety and frightening panic attacks.
• Empathy infusion: Enabling patients to become more understanding of other people and bolstering their impaired “theory of mind.”
• Personality transplant: Replacing a maladaptive personality with a healthier one (eg, using dialectical behavior therapy for borderline personality disorder).
• Cognitive LASIK: To improve insight, analogous to how ophthalmologic LASIK improves sight.
• Mental embolectomy: Removing a blockage to repair rigid attitudes and develop “open-mindedness.”
• Behavioral dilation and curettage (D&C): To rid patients of negative attributes such as impulsivity or reckless behavior.
• Psychotherapeutic anesthesia: Numbing emotional pain or severe grief reaction.
• Social anastomosis: Helping patients who are schizoid or isolative via group therapy, an effective interpersonal and social procedure.
• Psychotherapeutic stent: To open the vessels of narrow-mindedness.
• Cortico-psychological resuscitation (CPR): For patients experiencing stress-induced behavioral arrhythmias or emotional infarction.
• Immunotherapy: Using various neuroprotective psychotropic medications with anti-inflammatory properties or employing evidence-based psychotherapy such as cognitive-behavior therapy (aka neuropsychotherapy), which have been shown to reduce inflammatory biomarkers such as C-reactive protein and cytokines.³
• Psychotherapy: A neuromodulation procedure for a variety of psychiatric disorders.⁴
• Neurobiological facelift: It is well established that neurogenesis, synaptogenesis, and dendritic spine sprouting are significantly increased with both neuroprotective psychotropic medications (antidepressants, lithium, valproate, and second-generationantipsychotics⁵) as well as with psych­otherapy. There is growing evidence of “premature brain aging” in schizophrenia, bipolar disorder, and depression, with shrinkage in the volume of the cortex and subcortical regions, especially the hippocampus. Psychiatric biopsychosocial interven­tion rebuilds those brain regions by stimulating and replenishing the neuropil and neuro­genic regions (dentate gyrus and subventricular zone). This is like performing virtual plastic surgery on a wrinkled brain and its sagging mind. MRI scans before and after ECT show a remarkable ≥10% increase in the volume of the hippocampus and amygdala, which translates to billions of new neurons, glia, and synapses.⁶

Reinventing psychiatric therapies as procedures may elicit sarcasm from skeptics, but when you think about it, it is justified. Excising depression is like excising a tumor, not with a scalpel, but virtually. Stabilizing the broken brain and mind after a psychotic episode (aka brain attack) is like stabilizing the heart after a myocardial infarction (aka heart attack). Just because the mind is virtual doesn’t mean it is not “real and tangible.” A desktop computer is visible, but the software that brings it to life is invisible. Healing the human mind requires multiple medical interventions by psychiatrists in hospitals and clinics, just like surgeons and endoscopists or cardiologists. Mental health care is as much procedural as other medical and surgical specialties.

One more thing: the validated clinical rating scales for various psychiatric brain disorders (eg, the Positive and Negative Syndrome Scale for schizophrenia, Montgomery-Åsberg Depression Rating Scale for depression, Young Mania Rating Scale for bipolar mania, Hamilton Anxiety Rating Scale for anxiety, Yale-Brown Obsessive Compulsive Scale for obsessive-compulsive disorder) are actual measurement procedures for the severity of the illness, just as a sphygmomanometer measures blood pressure and its improvement with treatment. There are also multiple cognitive test batteries to measure cognitive impairment.⁷

Finally, unlike psychiatric reimbursement, which is tethered to time, procedures are compensated more generously, irrespective of the time involved. The complexities of diagnosing and treating psychiatric brain disorders that dangerously disrupt thoughts, feelings, behavior, and cognition are just as intricate and demanding as the diagnosis and treatment of general medical and surgical conditions. They should all be equally appreciated as vital life-saving procedures for the human body, brain, and mind.

Editor’s note: Readers’ Forum is a department for correspondence from readers that is not in response to articles published in Current Psychiatry. All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact letters@currentpsychiatry.com.

I (MZP) just completed my first semester of medical school. An important lesson imparted in my coursework so far has been to remain a staunch advocate for patients. Yet compared to the rigors of medical school, over the past year it has been far more difficult to help patients locate generic Adderall. Physicians were already overburdened with administrative responsibilities stretching into burnout territory well before the shortage, and now this! Unlike paper prescriptions of old, which patients could take to any pharmacy, e-prescribing apps require selection of a specific pharmacy, and controlled substances such as stimulants require 2-factor authentication. But if the designated pharmacy does not have the medication in stock, the entire process must be repeated with an alternative pharmacy, long after the visit has concluded.

To add insult to injury, the generic stimulant shortage has grown even worse. As of February 2023, generic Adderall remained hard to find and generic Concerta was also in short supply. How did this happen? In 1985, Bulow et al¹ coined the game theory concept of “strategic substitutes,” where (for example) as beef becomes less readily accessible, consumers may switch to eating chicken as their protein. Unable to locate generic Adderall, many patients have turned to generic Concerta as a substitute psychostimulant to continue management of their attention-deficit/hyperactivity disorder.

In addition to the increase in demand, compounding the shortage is that one of the manufacturers of generic Concerta has discontinued production.² Branded methylphenidates and amphetamines, which are much more expensive than their generic counterparts, have remained in ample supply, but many insurers require trials of generics before considering coverage for more expensive brands.

Our approach to this situation

Each morning we call our local and chain pharmacies to take a census of their supply of generic stimulants. Some pharmacies refuse to release this information. Despite these census reports, we have found cases where patients have been turned away from pharmacies when they are not “regular customers,” while patients whom the pharmacies know retain access as “members.” Hence, a patient is unlikely to obtain these medications if their regular pharmacy is out of stock.

We want to share a workaround that has been effective. After unsuccessfully searching for generic stimulants at the patient’s regular pharmacy, I (RLP) write “dispense as written” for the closest branded version and file a prior authorization with the patient’s insurance company, noting “patient unable to trial any generic amphetamines or methylphenidates due to current nationwide shortage.” Even with the most difficult insurers, the response has been “a temporary 3-month authorization has been granted,” which is at least a small victory for our desperate patients and busy prescribers who are both struggling to negotiate a fragmented health care system.

Editor’s note: Readers’ Forum is a department for correspondence from readers that is not in response to articles published in Current Psychiatry. All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact letters@currentpsychiatry.com.

I (MZP) just completed my first semester of medical school. An important lesson imparted in my coursework so far has been to remain a staunch advocate for patients. Yet compared to the rigors of medical school, over the past year it has been far more difficult to help patients locate generic Adderall. Physicians were already overburdened with administrative responsibilities stretching into burnout territory well before the shortage, and now this! Unlike paper prescriptions of old, which patients could take to any pharmacy, e-prescribing apps require selection of a specific pharmacy, and controlled substances such as stimulants require 2-factor authentication. But if the designated pharmacy does not have the medication in stock, the entire process must be repeated with an alternative pharmacy, long after the visit has concluded.

To add insult to injury, the generic stimulant shortage has grown even worse. As of February 2023, generic Adderall remained hard to find and generic Concerta was also in short supply. How did this happen? In 1985, Bulow et al¹ coined the game theory concept of “strategic substitutes,” where (for example) as beef becomes less readily accessible, consumers may switch to eating chicken as their protein. Unable to locate generic Adderall, many patients have turned to generic Concerta as a substitute psychostimulant to continue management of their attention-deficit/hyperactivity disorder.

In addition to the increase in demand, compounding the shortage is that one of the manufacturers of generic Concerta has discontinued production.² Branded methylphenidates and amphetamines, which are much more expensive than their generic counterparts, have remained in ample supply, but many insurers require trials of generics before considering coverage for more expensive brands.

Our approach to this situation

Each morning we call our local and chain pharmacies to take a census of their supply of generic stimulants. Some pharmacies refuse to release this information. Despite these census reports, we have found cases where patients have been turned away from pharmacies when they are not “regular customers,” while patients whom the pharmacies know retain access as “members.” Hence, a patient is unlikely to obtain these medications if their regular pharmacy is out of stock.

We want to share a workaround that has been effective. After unsuccessfully searching for generic stimulants at the patient’s regular pharmacy, I (RLP) write “dispense as written” for the closest branded version and file a prior authorization with the patient’s insurance company, noting “patient unable to trial any generic amphetamines or methylphenidates due to current nationwide shortage.” Even with the most difficult insurers, the response has been “a temporary 3-month authorization has been granted,” which is at least a small victory for our desperate patients and busy prescribers who are both struggling to negotiate a fragmented health care system.

Editor’s note: Readers’ Forum is a department for correspondence from readers that is not in response to articles published in Current Psychiatry. All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact letters@currentpsychiatry.com.

I (MZP) just completed my first semester of medical school. An important lesson imparted in my coursework so far has been to remain a staunch advocate for patients. Yet compared to the rigors of medical school, over the past year it has been far more difficult to help patients locate generic Adderall. Physicians were already overburdened with administrative responsibilities stretching into burnout territory well before the shortage, and now this! Unlike paper prescriptions of old, which patients could take to any pharmacy, e-prescribing apps require selection of a specific pharmacy, and controlled substances such as stimulants require 2-factor authentication. But if the designated pharmacy does not have the medication in stock, the entire process must be repeated with an alternative pharmacy, long after the visit has concluded.

To add insult to injury, the generic stimulant shortage has grown even worse. As of February 2023, generic Adderall remained hard to find and generic Concerta was also in short supply. How did this happen? In 1985, Bulow et al¹ coined the game theory concept of “strategic substitutes,” where (for example) as beef becomes less readily accessible, consumers may switch to eating chicken as their protein. Unable to locate generic Adderall, many patients have turned to generic Concerta as a substitute psychostimulant to continue management of their attention-deficit/hyperactivity disorder.

In addition to the increase in demand, compounding the shortage is that one of the manufacturers of generic Concerta has discontinued production.² Branded methylphenidates and amphetamines, which are much more expensive than their generic counterparts, have remained in ample supply, but many insurers require trials of generics before considering coverage for more expensive brands.

Our approach to this situation

Each morning we call our local and chain pharmacies to take a census of their supply of generic stimulants. Some pharmacies refuse to release this information. Despite these census reports, we have found cases where patients have been turned away from pharmacies when they are not “regular customers,” while patients whom the pharmacies know retain access as “members.” Hence, a patient is unlikely to obtain these medications if their regular pharmacy is out of stock.

We want to share a workaround that has been effective. After unsuccessfully searching for generic stimulants at the patient’s regular pharmacy, I (RLP) write “dispense as written” for the closest branded version and file a prior authorization with the patient’s insurance company, noting “patient unable to trial any generic amphetamines or methylphenidates due to current nationwide shortage.” Even with the most difficult insurers, the response has been “a temporary 3-month authorization has been granted,” which is at least a small victory for our desperate patients and busy prescribers who are both struggling to negotiate a fragmented health care system.

Each March, we celebrate National Colorectal Cancer Awareness Month to raise awareness of this common, deadly, and preventable form of cancer and advocate for increased screening uptake and investment in related research. Enhancing awareness is particularly important for those estimated 20 million average-risk individuals between the ages of 45 and 49 who became newly eligible for screening under the revised 2021 U.S. Preventive Services Task Force CRC screening guidelines, given alarming increases in early-onset CRC incidence. But as we know, awareness of CRC and screening eligibility alone is not enough to improve outcomes without addressing the many other patient, provider, and system-level barriers to screening uptake. Indeed, even before health care delivery disruptions related to the COVID-19 pandemic, CRC screening was underutilized, and inequities in screening uptake and downstream outcomes existed.

While there is not space here for a full discussion of these important topics, I refer you to our Gastroenterology Data Trends 2022 supplement (https://cdn.mdedge.com/files/s3fs-public/aga_data_trends_2022_web.pdf), which includes two excellent articles by Dr. Rachel Issaka of the University of Washington (“The Impact of COVID-19 on Colorectal Cancer Screening Programs”) and Dr. Aasma Shaukat of NYU (“Early Onset Colorectal Cancer: Trends in Incidence and Screening”).

In our March issue, we highlight the AGA’s decade-long advocacy efforts to close the “colonoscopy loophole” and reduce financial barriers to colorectal cancer screening. From AGA’s flagship journals, we report on the first Delphi-based consensus recommendations on early-onset colorectal cancer and highlight a study out of Italy comparing two computer-aided optical diagnosis systems for detection of small, leave-in-situ colon polyps. In our March Member Spotlight, we introduce you to gastroenterologist Christina Tennyson, MD, who shares the rewards and challenges of practicing gastroenterology in a rural area and explains how she incorporates “lifestyle medicine” into her clinical practice. Finally, GIHN Associate Editor Dr. Avi Ketwaroo introduces our quarterly Perspectives column on endoscopic innovation in management of GI perforation and acute cholecystitis.

We hope you enjoy these stories and all the exciting content featured in our March issue!

Megan A. Adams, MD, JD, MSc

Editor-in-Chief

Each March, we celebrate National Colorectal Cancer Awareness Month to raise awareness of this common, deadly, and preventable form of cancer and advocate for increased screening uptake and investment in related research. Enhancing awareness is particularly important for those estimated 20 million average-risk individuals between the ages of 45 and 49 who became newly eligible for screening under the revised 2021 U.S. Preventive Services Task Force CRC screening guidelines, given alarming increases in early-onset CRC incidence. But as we know, awareness of CRC and screening eligibility alone is not enough to improve outcomes without addressing the many other patient, provider, and system-level barriers to screening uptake. Indeed, even before health care delivery disruptions related to the COVID-19 pandemic, CRC screening was underutilized, and inequities in screening uptake and downstream outcomes existed.

While there is not space here for a full discussion of these important topics, I refer you to our Gastroenterology Data Trends 2022 supplement (https://cdn.mdedge.com/files/s3fs-public/aga_data_trends_2022_web.pdf), which includes two excellent articles by Dr. Rachel Issaka of the University of Washington (“The Impact of COVID-19 on Colorectal Cancer Screening Programs”) and Dr. Aasma Shaukat of NYU (“Early Onset Colorectal Cancer: Trends in Incidence and Screening”).

In our March issue, we highlight the AGA’s decade-long advocacy efforts to close the “colonoscopy loophole” and reduce financial barriers to colorectal cancer screening. From AGA’s flagship journals, we report on the first Delphi-based consensus recommendations on early-onset colorectal cancer and highlight a study out of Italy comparing two computer-aided optical diagnosis systems for detection of small, leave-in-situ colon polyps. In our March Member Spotlight, we introduce you to gastroenterologist Christina Tennyson, MD, who shares the rewards and challenges of practicing gastroenterology in a rural area and explains how she incorporates “lifestyle medicine” into her clinical practice. Finally, GIHN Associate Editor Dr. Avi Ketwaroo introduces our quarterly Perspectives column on endoscopic innovation in management of GI perforation and acute cholecystitis.

We hope you enjoy these stories and all the exciting content featured in our March issue!

Megan A. Adams, MD, JD, MSc

Editor-in-Chief

Each March, we celebrate National Colorectal Cancer Awareness Month to raise awareness of this common, deadly, and preventable form of cancer and advocate for increased screening uptake and investment in related research. Enhancing awareness is particularly important for those estimated 20 million average-risk individuals between the ages of 45 and 49 who became newly eligible for screening under the revised 2021 U.S. Preventive Services Task Force CRC screening guidelines, given alarming increases in early-onset CRC incidence. But as we know, awareness of CRC and screening eligibility alone is not enough to improve outcomes without addressing the many other patient, provider, and system-level barriers to screening uptake. Indeed, even before health care delivery disruptions related to the COVID-19 pandemic, CRC screening was underutilized, and inequities in screening uptake and downstream outcomes existed.

While there is not space here for a full discussion of these important topics, I refer you to our Gastroenterology Data Trends 2022 supplement (https://cdn.mdedge.com/files/s3fs-public/aga_data_trends_2022_web.pdf), which includes two excellent articles by Dr. Rachel Issaka of the University of Washington (“The Impact of COVID-19 on Colorectal Cancer Screening Programs”) and Dr. Aasma Shaukat of NYU (“Early Onset Colorectal Cancer: Trends in Incidence and Screening”).

In our March issue, we highlight the AGA’s decade-long advocacy efforts to close the “colonoscopy loophole” and reduce financial barriers to colorectal cancer screening. From AGA’s flagship journals, we report on the first Delphi-based consensus recommendations on early-onset colorectal cancer and highlight a study out of Italy comparing two computer-aided optical diagnosis systems for detection of small, leave-in-situ colon polyps. In our March Member Spotlight, we introduce you to gastroenterologist Christina Tennyson, MD, who shares the rewards and challenges of practicing gastroenterology in a rural area and explains how she incorporates “lifestyle medicine” into her clinical practice. Finally, GIHN Associate Editor Dr. Avi Ketwaroo introduces our quarterly Perspectives column on endoscopic innovation in management of GI perforation and acute cholecystitis.

We hope you enjoy these stories and all the exciting content featured in our March issue!

Megan A. Adams, MD, JD, MSc

Editor-in-Chief

Introduction: The preoperative evaluation for endometriosis – more than meets the eye

It is well known that it often takes 6-10 years for endometriosis to be diagnosed in patients who have the disease, depending on where the patient lives. I certainly am not surprised. During my residency at Parkland Memorial Hospital, if a patient had chronic pelvic pain and no fibroids, her diagnosis was usually pelvic inflammatory disease. Later, during my fellowship in reproductive endocrinology at the University of Pennsylvania, the diagnosis became endometriosis.

As I gained more interest and expertise in the treatment of endometriosis, I became aware of several articles concluding that if a woman sought treatment for chronic pelvic pain with an internist, the diagnosis would be irritable bowel syndrome (IBS); with a urologist, it would be interstitial cystitis; and with a gynecologist, endometriosis. Moreover, there is an increased propensity for IBS and IC in patients with endometriosis. There also is an increased risk of small intestine bacterial overgrowth (SIBO), as noted by our guest author for this latest installment of the Master Class in Gynecologic Surgery, Iris Orbuch, MD.

Like our guest author, I have also noted increased risk of pelvic floor myalgia. Dr. Orbuch clearly outlines why this occurs. In fact, we can now understand why many patients have multiple pelvic pain–inducing issues compounding their pain secondary to endometriosis and leading to remodeling of the central nervous system. Therefore, it certainly makes sense to follow Dr. Orbuch’s recommendation for a multidisciplinary pre- and postsurgical approach “to downregulate the pain generators.”

Dr. Orbuch is a minimally invasive gynecologic surgeon in Los Angeles who specializes in the treatment of patients diagnosed with endometriosis. Dr. Orbuch serves on the Board of Directors of the Foundation of the American Association of Gynecologic Laparoscopists and has served as the chair of the AAGL’s Special Interest Group on Endometriosis and Reproductive Surgery. She is the coauthor of the book “Beating Endo – How to Reclaim Your Life From Endometriosis” (New York: HarperCollins; 2019). The book is written for patients but addresses many issues discussed in this installment of the Master Class in Gynecologic Surgery.

Dr. Miller, MD, FACOG, is professor of obstetrics and gynecology, department of clinical sciences, Rosalind Franklin University of Medicine and Science, North Chicago. He has no conflicts of interest to report.

For optimal surgical outcomes, and to help our patients recover from years of this inflammatory, systemic disease, we must treat our patients holistically and work to downregulate their pain as much as possible before excision surgery. I work with patients a few months prior to surgery, often for 4-5 months, during which time they not only see me for informative follow-ups, but also pelvic floor physical therapists, gastroenterologists, mental health professionals, integrative nutritionists, and physiatrists or pain specialists, depending on their needs.¹

By identifying coexisting conditions in an initial consult and employing a presurgical multidisciplinary approach to downregulate the pain generators, my patients recover well from excision surgery, with greater and faster relief from pain, compared with those using standard approaches, and with little to no use of opioids.

At a minimum, given the unfortunate time constraints and productivity demands of working within health systems – and considering that surgeries are often scheduled a couple of months out – the surgeon could ensure that patients are engaged in at least 6-8 weeks of pelvic floor physical therapy before surgery to sufficiently lengthen the pelvic muscles and loosen surrounding fascia.

Short, tight pelvic floor muscles are almost universal in patients with delayed diagnosis of endometriosis and are significant generators of pain.
 

Appreciating sequelae of diagnostic delay

After my fellowship in advanced laparoscopic and pelvic surgery with Harry Reich, MD, and C. Y. Liu, MD, pioneers of endometriosis excision surgery, and as I did my residency in the early 2000s, I noticed puzzlement in the literature about why some patients still had lasting pain after thorough excision.

I didn’t doubt the efficacy of excision. It is the cornerstone of treatment, and at least one randomized double-blind trial² and a systematic review and meta-analysis³ have demonstrated its superior efficacy over ablation in symptom reduction. What I did doubt was any presumption that surgery alone was enough. I knew there was more to healing when a disease process wreaks havoc on the body for more than a decade and that there were other generators of pain in addition to the endometriosis implants themselves.

As I began to focus on endometriosis in my own surgical practice, I strove to detect and treat endometriosis in teens. But in those patients with longstanding disease, I recognized patterns and began to more fully appreciate the systemic sequelae of endometriosis.

To cope with dysmenorrhea, patients curl up and assume a fetal position, tensing the abdominal muscles, inner thigh muscles, and pelvic floor muscles. Over time, these muscles come to maintain a short, tight, and painful state. (Hence the need for physical therapy to undo this decade-long pattern.)

Endometriosis implants on or near the gastrointestinal tract tug on fascia and muscles and commonly cause constipation, leading women to further overwork the pelvic floor muscles. In the case of diarrhea-predominant dysfunction, our patients squeeze pelvic floor muscles to prevent leakage. And in the case of urinary urgency, they squeeze muscles to release urine that isn’t really there.

As the chronic inflammation of the disease grows, and as pain worsens, the patient is increasingly in sympathetic overdrive (also known as ”fight or flight”), as opposed to a parasympathetic state (also known as “rest and digest”). The bowel’s motility slows, allowing the bacteria of the small intestine to grow beyond what is normal, leading to SIBO, a condition increasingly recognized by gastroenterologists and others that can impede nutrient absorption and cause bloat and pain and exacerbate constipation and diarrhea.

Key to my conceptualization of pain was a review published in 2011 by Pam Stratton, MD, of the National Institutes of Health, and Karen J. Berkley, PhD, then of Florida State University, on chronic pain and endometriosis.⁴ They detailed how endometriotic lesions can develop their own nerve supply that interacts directly and in a two-way fashion with the CNS – and how the lesions can engage the nervous system in ways that create comorbid conditions and pain that becomes “independent of the disease itself.”

Sensitized peripheral nerve fibers innervating a deeply infiltrating lesion on the left uterosacral ligament, for instance, can sensitize neurons in the spinal sacral segment. Branches of these nerve fibers can extend to other segments of the spinal cord, and, once sensitized themselves, turn on neurons in these other segments. There is a resultant remodeling of the central nervous system, in essence, and what is called “remote central sensitization.” The CNS becomes independent from peripheral neural processes.

I now explain to both patients and physicians that those who have had endometriosis for years have had an enduring “hand on the stove,” with a persistent signal to the CNS. Tight muscles are a hand on the stove, painful bladder syndrome is another hand on the stove, and SIBO is yet another. So are anxiety and depression.

The CNS becomes so upregulated and overloaded that messages branch out through the spinal cord to other available pathways and to other organs, muscles, and nerves. The CNS also starts firing on its own – and once it becomes its own pain generator, taking one hand off the stove (for instance, excising implants) while leaving multiple other hands on the hot stove won’t remove all pain. We must downregulate the CNS more broadly.

As I began addressing pain generators and instigators of CNS sensitization – and waiting for excision surgery until the CNS had sufficiently cooled – I saw that my patients had a better chance of more significant and lasting pain relief.
 

Pearls for a multimodal approach

My initial physical exam includes an assessment of the pelvic floor for overly tight musculature. An abdominal exam will usually reveal whether there is asymmetry of the abdominal wall muscles, which typically informs me of the likelihood of tightness and pulling on either side of the pelvic anatomy. On the internal exam, then, the pelvic floor muscles can be palpated and assessed. These findings will guide my referrals and my discussions with patients about the value of pelvic floor physical therapy. The cervix should be in the midline of the vagina – equidistant from the left and right vaginal fornices. If the cervix is pulled away from this midline, and a palpation of a thickened uterosacral ligament reproduces pain, endometriosis is 90% likely.

Patients who report significant “burning” pain that’s suggestive of neuropathic pain should be referred to a physical medicine rehabilitation physician or a pain specialist who can help downregulate their CNS. And patients who have symptoms of depression, anxiety disorders (including obsessive-compulsive disorder), or posttraumatic stress disorder should be referred to pain therapists, psychologists, or other mental health professionals, preferably well before surgery. I will also often discuss mindfulness practices and give my patients “meditation challenges” to achieve during the presurgical phase.

Additional points of emphasis about a multidisciplinary, multimodal approach include:

Advanced pelvic floor therapy: Therapists with specialized training in pelvic health and manual therapy utilize a range of techniques and modalities to release tension in affected muscles, fascia, nerves, and bone, and in doing so, they help to downregulate the CNS. Myofascial release, myofascial trigger point release, neural mobilization, and visceral mobilization are among these techniques. In addition to using manual therapy, many of these therapists may also employ neuromuscular reeducation and other techniques that will be helpful for the longer term.

It is important to identify physical therapists who have training in this approach; women with endometriosis often have a history of treatment by physical therapists whose focus is on incontinence and muscle strengthening (that is, Kegel exercises), which is the opposite of what endometriosis patients need.

Treating SIBO: Symptoms commonly associated with SIBO often overlap with symptoms of irritable bowel syndrome (IBS) – namely constipation, diarrhea (or both), and bloating. Indeed, many patients with undiagnosed endometriosis have been diagnosed with IBS. I send every patient who has one of these symptoms for SIBO breath testing, which utilizes carbohydrate substrates (glucose or lactulose) and measures hydrogen and/or methane in the breath.

SIBO is typically treated with rifampin, which stays in the small bowel and will not negatively affect beneficial bacteria, with or without neomycin. Gastroenterologists with more integrative practices also consider the use of herbals in addition to – or instead of – antibiotics. It can sometimes take months or a couple of years to correct SIBO, depending on how long the patient has been affected, but with presurgical diagnosis and a start on treatment, we can remove or at least tone down another instigator of CNS sensitization.

I estimate that 80% of my patients have tested positive for SIBO. Notably, in a testament to the systemic nature of endometriosis, a study published in 2009 of 355 women undergoing operative laparoscopy for suspected endometriosis found that 90% had gastrointestinal symptoms, but only 7.6% of the vast majority whose endometriosis was confirmed were found to have endometrial implants on the bowel itself.⁵

Addressing bladder issues: I routinely administer the PUF (Pain, Urgency, Frequency) questionnaire as part of my intake package and follow it up with conversation. For just about every patient with painful bladder syndrome, pelvic floor physical therapy in combination with a low-acid, low-potassium diet will work effectively together to reduce symptoms and pain. The IC Network offers a helpful food list, and patients can be counseled to choose foods that are also anti-inflammatory. When referrals to a urologist for bladder instillations are possible, these can be helpful as well.

Our communication with patients

Our patients need to have their symptoms and pain validated and to understand why we’re recommending these measures before surgery. Some education is necessary. Few patients will go to an integrative nutritionist, for example, if we just write a referral without explaining how years of inflammation and disruption in the gut can affect the whole body – including mental health – and that it can be corrected over time.

Also necessary is an appreciation of the fact that patients with delayed diagnoses have lived with gastrointestinal and other symptoms and patterns for so long – and often have mothers whose endometriosis caused similar symptoms – that some of their own experiences can seem almost “normal.” A patient whose mother had bowel movements every 7 days may think that 4-5 day intervals are acceptable, for instance. This means we have to carefully consider how we ask our questions.

I always ask my patients as we’re going into surgery, what percentage better are you? I’ve long aimed for at least 30% improvement, but most of the time, with pelvic floor therapy and as many other pain-generator–focused measures as possible, we’re getting them 70% better.

Excision surgery will remove the inflammation that has helped fuel the SIBO and other coconditions. Then, everything done to prepare the body must continue for some time. Certain practices, such as eating an anti-inflammatory diet, should be lifelong.

One day, it is hoped, a pediatrician or other physician will suspect endometriosis early on. The patient will see the surgeon within several months of the onset of pain, and we won’t need to unravel layers of pain generation and CNS upregulation before operating. But until this happens and we shorten the diagnostic delay, we must consider the benefits of presurgical preparation.
 

References

1. Orbuch I, Stein A. Beating Endo: How to Reclaim Your Life From Endometriosis. (New York: HarperCollins, 2019).

2. Healey M et al. J Minim Invasive Gynecol. 2014;21(6):999-1004.

3. Pundir J et al. J Minim Invasive Gynecol. 2017;24(5):747-56.

4. Stratton P, Berkley KJ. Hum Repro Update. 2011;17(3):327-46.

5. Maroun P et al. Aust N Z J Obstet Gynaecol. 2009;49(4):411-4.

Dr. Orbuch is a minimally invasive gynecologic surgeon in Los Angeles who specializes in endometriosis. She has no conflicts of interest to report.

Introduction: The preoperative evaluation for endometriosis – more than meets the eye

It is well known that it often takes 6-10 years for endometriosis to be diagnosed in patients who have the disease, depending on where the patient lives. I certainly am not surprised. During my residency at Parkland Memorial Hospital, if a patient had chronic pelvic pain and no fibroids, her diagnosis was usually pelvic inflammatory disease. Later, during my fellowship in reproductive endocrinology at the University of Pennsylvania, the diagnosis became endometriosis.

As I gained more interest and expertise in the treatment of endometriosis, I became aware of several articles concluding that if a woman sought treatment for chronic pelvic pain with an internist, the diagnosis would be irritable bowel syndrome (IBS); with a urologist, it would be interstitial cystitis; and with a gynecologist, endometriosis. Moreover, there is an increased propensity for IBS and IC in patients with endometriosis. There also is an increased risk of small intestine bacterial overgrowth (SIBO), as noted by our guest author for this latest installment of the Master Class in Gynecologic Surgery, Iris Orbuch, MD.

Like our guest author, I have also noted increased risk of pelvic floor myalgia. Dr. Orbuch clearly outlines why this occurs. In fact, we can now understand why many patients have multiple pelvic pain–inducing issues compounding their pain secondary to endometriosis and leading to remodeling of the central nervous system. Therefore, it certainly makes sense to follow Dr. Orbuch’s recommendation for a multidisciplinary pre- and postsurgical approach “to downregulate the pain generators.”

Dr. Orbuch is a minimally invasive gynecologic surgeon in Los Angeles who specializes in the treatment of patients diagnosed with endometriosis. Dr. Orbuch serves on the Board of Directors of the Foundation of the American Association of Gynecologic Laparoscopists and has served as the chair of the AAGL’s Special Interest Group on Endometriosis and Reproductive Surgery. She is the coauthor of the book “Beating Endo – How to Reclaim Your Life From Endometriosis” (New York: HarperCollins; 2019). The book is written for patients but addresses many issues discussed in this installment of the Master Class in Gynecologic Surgery.

Dr. Miller, MD, FACOG, is professor of obstetrics and gynecology, department of clinical sciences, Rosalind Franklin University of Medicine and Science, North Chicago. He has no conflicts of interest to report.

For optimal surgical outcomes, and to help our patients recover from years of this inflammatory, systemic disease, we must treat our patients holistically and work to downregulate their pain as much as possible before excision surgery. I work with patients a few months prior to surgery, often for 4-5 months, during which time they not only see me for informative follow-ups, but also pelvic floor physical therapists, gastroenterologists, mental health professionals, integrative nutritionists, and physiatrists or pain specialists, depending on their needs.¹

By identifying coexisting conditions in an initial consult and employing a presurgical multidisciplinary approach to downregulate the pain generators, my patients recover well from excision surgery, with greater and faster relief from pain, compared with those using standard approaches, and with little to no use of opioids.

At a minimum, given the unfortunate time constraints and productivity demands of working within health systems – and considering that surgeries are often scheduled a couple of months out – the surgeon could ensure that patients are engaged in at least 6-8 weeks of pelvic floor physical therapy before surgery to sufficiently lengthen the pelvic muscles and loosen surrounding fascia.

Short, tight pelvic floor muscles are almost universal in patients with delayed diagnosis of endometriosis and are significant generators of pain.
 

Appreciating sequelae of diagnostic delay

After my fellowship in advanced laparoscopic and pelvic surgery with Harry Reich, MD, and C. Y. Liu, MD, pioneers of endometriosis excision surgery, and as I did my residency in the early 2000s, I noticed puzzlement in the literature about why some patients still had lasting pain after thorough excision.

I didn’t doubt the efficacy of excision. It is the cornerstone of treatment, and at least one randomized double-blind trial² and a systematic review and meta-analysis³ have demonstrated its superior efficacy over ablation in symptom reduction. What I did doubt was any presumption that surgery alone was enough. I knew there was more to healing when a disease process wreaks havoc on the body for more than a decade and that there were other generators of pain in addition to the endometriosis implants themselves.

As I began to focus on endometriosis in my own surgical practice, I strove to detect and treat endometriosis in teens. But in those patients with longstanding disease, I recognized patterns and began to more fully appreciate the systemic sequelae of endometriosis.

To cope with dysmenorrhea, patients curl up and assume a fetal position, tensing the abdominal muscles, inner thigh muscles, and pelvic floor muscles. Over time, these muscles come to maintain a short, tight, and painful state. (Hence the need for physical therapy to undo this decade-long pattern.)

Endometriosis implants on or near the gastrointestinal tract tug on fascia and muscles and commonly cause constipation, leading women to further overwork the pelvic floor muscles. In the case of diarrhea-predominant dysfunction, our patients squeeze pelvic floor muscles to prevent leakage. And in the case of urinary urgency, they squeeze muscles to release urine that isn’t really there.

As the chronic inflammation of the disease grows, and as pain worsens, the patient is increasingly in sympathetic overdrive (also known as ”fight or flight”), as opposed to a parasympathetic state (also known as “rest and digest”). The bowel’s motility slows, allowing the bacteria of the small intestine to grow beyond what is normal, leading to SIBO, a condition increasingly recognized by gastroenterologists and others that can impede nutrient absorption and cause bloat and pain and exacerbate constipation and diarrhea.

Key to my conceptualization of pain was a review published in 2011 by Pam Stratton, MD, of the National Institutes of Health, and Karen J. Berkley, PhD, then of Florida State University, on chronic pain and endometriosis.⁴ They detailed how endometriotic lesions can develop their own nerve supply that interacts directly and in a two-way fashion with the CNS – and how the lesions can engage the nervous system in ways that create comorbid conditions and pain that becomes “independent of the disease itself.”

Sensitized peripheral nerve fibers innervating a deeply infiltrating lesion on the left uterosacral ligament, for instance, can sensitize neurons in the spinal sacral segment. Branches of these nerve fibers can extend to other segments of the spinal cord, and, once sensitized themselves, turn on neurons in these other segments. There is a resultant remodeling of the central nervous system, in essence, and what is called “remote central sensitization.” The CNS becomes independent from peripheral neural processes.

I now explain to both patients and physicians that those who have had endometriosis for years have had an enduring “hand on the stove,” with a persistent signal to the CNS. Tight muscles are a hand on the stove, painful bladder syndrome is another hand on the stove, and SIBO is yet another. So are anxiety and depression.

The CNS becomes so upregulated and overloaded that messages branch out through the spinal cord to other available pathways and to other organs, muscles, and nerves. The CNS also starts firing on its own – and once it becomes its own pain generator, taking one hand off the stove (for instance, excising implants) while leaving multiple other hands on the hot stove won’t remove all pain. We must downregulate the CNS more broadly.

As I began addressing pain generators and instigators of CNS sensitization – and waiting for excision surgery until the CNS had sufficiently cooled – I saw that my patients had a better chance of more significant and lasting pain relief.
 

Pearls for a multimodal approach

My initial physical exam includes an assessment of the pelvic floor for overly tight musculature. An abdominal exam will usually reveal whether there is asymmetry of the abdominal wall muscles, which typically informs me of the likelihood of tightness and pulling on either side of the pelvic anatomy. On the internal exam, then, the pelvic floor muscles can be palpated and assessed. These findings will guide my referrals and my discussions with patients about the value of pelvic floor physical therapy. The cervix should be in the midline of the vagina – equidistant from the left and right vaginal fornices. If the cervix is pulled away from this midline, and a palpation of a thickened uterosacral ligament reproduces pain, endometriosis is 90% likely.

Patients who report significant “burning” pain that’s suggestive of neuropathic pain should be referred to a physical medicine rehabilitation physician or a pain specialist who can help downregulate their CNS. And patients who have symptoms of depression, anxiety disorders (including obsessive-compulsive disorder), or posttraumatic stress disorder should be referred to pain therapists, psychologists, or other mental health professionals, preferably well before surgery. I will also often discuss mindfulness practices and give my patients “meditation challenges” to achieve during the presurgical phase.

Additional points of emphasis about a multidisciplinary, multimodal approach include:

Advanced pelvic floor therapy: Therapists with specialized training in pelvic health and manual therapy utilize a range of techniques and modalities to release tension in affected muscles, fascia, nerves, and bone, and in doing so, they help to downregulate the CNS. Myofascial release, myofascial trigger point release, neural mobilization, and visceral mobilization are among these techniques. In addition to using manual therapy, many of these therapists may also employ neuromuscular reeducation and other techniques that will be helpful for the longer term.

It is important to identify physical therapists who have training in this approach; women with endometriosis often have a history of treatment by physical therapists whose focus is on incontinence and muscle strengthening (that is, Kegel exercises), which is the opposite of what endometriosis patients need.

Treating SIBO: Symptoms commonly associated with SIBO often overlap with symptoms of irritable bowel syndrome (IBS) – namely constipation, diarrhea (or both), and bloating. Indeed, many patients with undiagnosed endometriosis have been diagnosed with IBS. I send every patient who has one of these symptoms for SIBO breath testing, which utilizes carbohydrate substrates (glucose or lactulose) and measures hydrogen and/or methane in the breath.

SIBO is typically treated with rifampin, which stays in the small bowel and will not negatively affect beneficial bacteria, with or without neomycin. Gastroenterologists with more integrative practices also consider the use of herbals in addition to – or instead of – antibiotics. It can sometimes take months or a couple of years to correct SIBO, depending on how long the patient has been affected, but with presurgical diagnosis and a start on treatment, we can remove or at least tone down another instigator of CNS sensitization.

I estimate that 80% of my patients have tested positive for SIBO. Notably, in a testament to the systemic nature of endometriosis, a study published in 2009 of 355 women undergoing operative laparoscopy for suspected endometriosis found that 90% had gastrointestinal symptoms, but only 7.6% of the vast majority whose endometriosis was confirmed were found to have endometrial implants on the bowel itself.⁵

Addressing bladder issues: I routinely administer the PUF (Pain, Urgency, Frequency) questionnaire as part of my intake package and follow it up with conversation. For just about every patient with painful bladder syndrome, pelvic floor physical therapy in combination with a low-acid, low-potassium diet will work effectively together to reduce symptoms and pain. The IC Network offers a helpful food list, and patients can be counseled to choose foods that are also anti-inflammatory. When referrals to a urologist for bladder instillations are possible, these can be helpful as well.

Our communication with patients

Our patients need to have their symptoms and pain validated and to understand why we’re recommending these measures before surgery. Some education is necessary. Few patients will go to an integrative nutritionist, for example, if we just write a referral without explaining how years of inflammation and disruption in the gut can affect the whole body – including mental health – and that it can be corrected over time.

Also necessary is an appreciation of the fact that patients with delayed diagnoses have lived with gastrointestinal and other symptoms and patterns for so long – and often have mothers whose endometriosis caused similar symptoms – that some of their own experiences can seem almost “normal.” A patient whose mother had bowel movements every 7 days may think that 4-5 day intervals are acceptable, for instance. This means we have to carefully consider how we ask our questions.

I always ask my patients as we’re going into surgery, what percentage better are you? I’ve long aimed for at least 30% improvement, but most of the time, with pelvic floor therapy and as many other pain-generator–focused measures as possible, we’re getting them 70% better.

Excision surgery will remove the inflammation that has helped fuel the SIBO and other coconditions. Then, everything done to prepare the body must continue for some time. Certain practices, such as eating an anti-inflammatory diet, should be lifelong.

One day, it is hoped, a pediatrician or other physician will suspect endometriosis early on. The patient will see the surgeon within several months of the onset of pain, and we won’t need to unravel layers of pain generation and CNS upregulation before operating. But until this happens and we shorten the diagnostic delay, we must consider the benefits of presurgical preparation.
 

References

1. Orbuch I, Stein A. Beating Endo: How to Reclaim Your Life From Endometriosis. (New York: HarperCollins, 2019).

2. Healey M et al. J Minim Invasive Gynecol. 2014;21(6):999-1004.

3. Pundir J et al. J Minim Invasive Gynecol. 2017;24(5):747-56.

4. Stratton P, Berkley KJ. Hum Repro Update. 2011;17(3):327-46.

5. Maroun P et al. Aust N Z J Obstet Gynaecol. 2009;49(4):411-4.

Dr. Orbuch is a minimally invasive gynecologic surgeon in Los Angeles who specializes in endometriosis. She has no conflicts of interest to report.

Introduction: The preoperative evaluation for endometriosis – more than meets the eye

It is well known that it often takes 6-10 years for endometriosis to be diagnosed in patients who have the disease, depending on where the patient lives. I certainly am not surprised. During my residency at Parkland Memorial Hospital, if a patient had chronic pelvic pain and no fibroids, her diagnosis was usually pelvic inflammatory disease. Later, during my fellowship in reproductive endocrinology at the University of Pennsylvania, the diagnosis became endometriosis.

As I gained more interest and expertise in the treatment of endometriosis, I became aware of several articles concluding that if a woman sought treatment for chronic pelvic pain with an internist, the diagnosis would be irritable bowel syndrome (IBS); with a urologist, it would be interstitial cystitis; and with a gynecologist, endometriosis. Moreover, there is an increased propensity for IBS and IC in patients with endometriosis. There also is an increased risk of small intestine bacterial overgrowth (SIBO), as noted by our guest author for this latest installment of the Master Class in Gynecologic Surgery, Iris Orbuch, MD.

Like our guest author, I have also noted increased risk of pelvic floor myalgia. Dr. Orbuch clearly outlines why this occurs. In fact, we can now understand why many patients have multiple pelvic pain–inducing issues compounding their pain secondary to endometriosis and leading to remodeling of the central nervous system. Therefore, it certainly makes sense to follow Dr. Orbuch’s recommendation for a multidisciplinary pre- and postsurgical approach “to downregulate the pain generators.”

Dr. Orbuch is a minimally invasive gynecologic surgeon in Los Angeles who specializes in the treatment of patients diagnosed with endometriosis. Dr. Orbuch serves on the Board of Directors of the Foundation of the American Association of Gynecologic Laparoscopists and has served as the chair of the AAGL’s Special Interest Group on Endometriosis and Reproductive Surgery. She is the coauthor of the book “Beating Endo – How to Reclaim Your Life From Endometriosis” (New York: HarperCollins; 2019). The book is written for patients but addresses many issues discussed in this installment of the Master Class in Gynecologic Surgery.

Dr. Miller, MD, FACOG, is professor of obstetrics and gynecology, department of clinical sciences, Rosalind Franklin University of Medicine and Science, North Chicago. He has no conflicts of interest to report.

For optimal surgical outcomes, and to help our patients recover from years of this inflammatory, systemic disease, we must treat our patients holistically and work to downregulate their pain as much as possible before excision surgery. I work with patients a few months prior to surgery, often for 4-5 months, during which time they not only see me for informative follow-ups, but also pelvic floor physical therapists, gastroenterologists, mental health professionals, integrative nutritionists, and physiatrists or pain specialists, depending on their needs.¹

By identifying coexisting conditions in an initial consult and employing a presurgical multidisciplinary approach to downregulate the pain generators, my patients recover well from excision surgery, with greater and faster relief from pain, compared with those using standard approaches, and with little to no use of opioids.

At a minimum, given the unfortunate time constraints and productivity demands of working within health systems – and considering that surgeries are often scheduled a couple of months out – the surgeon could ensure that patients are engaged in at least 6-8 weeks of pelvic floor physical therapy before surgery to sufficiently lengthen the pelvic muscles and loosen surrounding fascia.

Short, tight pelvic floor muscles are almost universal in patients with delayed diagnosis of endometriosis and are significant generators of pain.
 

Appreciating sequelae of diagnostic delay

After my fellowship in advanced laparoscopic and pelvic surgery with Harry Reich, MD, and C. Y. Liu, MD, pioneers of endometriosis excision surgery, and as I did my residency in the early 2000s, I noticed puzzlement in the literature about why some patients still had lasting pain after thorough excision.

I didn’t doubt the efficacy of excision. It is the cornerstone of treatment, and at least one randomized double-blind trial² and a systematic review and meta-analysis³ have demonstrated its superior efficacy over ablation in symptom reduction. What I did doubt was any presumption that surgery alone was enough. I knew there was more to healing when a disease process wreaks havoc on the body for more than a decade and that there were other generators of pain in addition to the endometriosis implants themselves.

As I began to focus on endometriosis in my own surgical practice, I strove to detect and treat endometriosis in teens. But in those patients with longstanding disease, I recognized patterns and began to more fully appreciate the systemic sequelae of endometriosis.

To cope with dysmenorrhea, patients curl up and assume a fetal position, tensing the abdominal muscles, inner thigh muscles, and pelvic floor muscles. Over time, these muscles come to maintain a short, tight, and painful state. (Hence the need for physical therapy to undo this decade-long pattern.)

Endometriosis implants on or near the gastrointestinal tract tug on fascia and muscles and commonly cause constipation, leading women to further overwork the pelvic floor muscles. In the case of diarrhea-predominant dysfunction, our patients squeeze pelvic floor muscles to prevent leakage. And in the case of urinary urgency, they squeeze muscles to release urine that isn’t really there.

As the chronic inflammation of the disease grows, and as pain worsens, the patient is increasingly in sympathetic overdrive (also known as ”fight or flight”), as opposed to a parasympathetic state (also known as “rest and digest”). The bowel’s motility slows, allowing the bacteria of the small intestine to grow beyond what is normal, leading to SIBO, a condition increasingly recognized by gastroenterologists and others that can impede nutrient absorption and cause bloat and pain and exacerbate constipation and diarrhea.

Key to my conceptualization of pain was a review published in 2011 by Pam Stratton, MD, of the National Institutes of Health, and Karen J. Berkley, PhD, then of Florida State University, on chronic pain and endometriosis.⁴ They detailed how endometriotic lesions can develop their own nerve supply that interacts directly and in a two-way fashion with the CNS – and how the lesions can engage the nervous system in ways that create comorbid conditions and pain that becomes “independent of the disease itself.”

Sensitized peripheral nerve fibers innervating a deeply infiltrating lesion on the left uterosacral ligament, for instance, can sensitize neurons in the spinal sacral segment. Branches of these nerve fibers can extend to other segments of the spinal cord, and, once sensitized themselves, turn on neurons in these other segments. There is a resultant remodeling of the central nervous system, in essence, and what is called “remote central sensitization.” The CNS becomes independent from peripheral neural processes.

I now explain to both patients and physicians that those who have had endometriosis for years have had an enduring “hand on the stove,” with a persistent signal to the CNS. Tight muscles are a hand on the stove, painful bladder syndrome is another hand on the stove, and SIBO is yet another. So are anxiety and depression.

The CNS becomes so upregulated and overloaded that messages branch out through the spinal cord to other available pathways and to other organs, muscles, and nerves. The CNS also starts firing on its own – and once it becomes its own pain generator, taking one hand off the stove (for instance, excising implants) while leaving multiple other hands on the hot stove won’t remove all pain. We must downregulate the CNS more broadly.

As I began addressing pain generators and instigators of CNS sensitization – and waiting for excision surgery until the CNS had sufficiently cooled – I saw that my patients had a better chance of more significant and lasting pain relief.
 

Pearls for a multimodal approach

My initial physical exam includes an assessment of the pelvic floor for overly tight musculature. An abdominal exam will usually reveal whether there is asymmetry of the abdominal wall muscles, which typically informs me of the likelihood of tightness and pulling on either side of the pelvic anatomy. On the internal exam, then, the pelvic floor muscles can be palpated and assessed. These findings will guide my referrals and my discussions with patients about the value of pelvic floor physical therapy. The cervix should be in the midline of the vagina – equidistant from the left and right vaginal fornices. If the cervix is pulled away from this midline, and a palpation of a thickened uterosacral ligament reproduces pain, endometriosis is 90% likely.

Patients who report significant “burning” pain that’s suggestive of neuropathic pain should be referred to a physical medicine rehabilitation physician or a pain specialist who can help downregulate their CNS. And patients who have symptoms of depression, anxiety disorders (including obsessive-compulsive disorder), or posttraumatic stress disorder should be referred to pain therapists, psychologists, or other mental health professionals, preferably well before surgery. I will also often discuss mindfulness practices and give my patients “meditation challenges” to achieve during the presurgical phase.

Additional points of emphasis about a multidisciplinary, multimodal approach include:

Advanced pelvic floor therapy: Therapists with specialized training in pelvic health and manual therapy utilize a range of techniques and modalities to release tension in affected muscles, fascia, nerves, and bone, and in doing so, they help to downregulate the CNS. Myofascial release, myofascial trigger point release, neural mobilization, and visceral mobilization are among these techniques. In addition to using manual therapy, many of these therapists may also employ neuromuscular reeducation and other techniques that will be helpful for the longer term.

It is important to identify physical therapists who have training in this approach; women with endometriosis often have a history of treatment by physical therapists whose focus is on incontinence and muscle strengthening (that is, Kegel exercises), which is the opposite of what endometriosis patients need.

Treating SIBO: Symptoms commonly associated with SIBO often overlap with symptoms of irritable bowel syndrome (IBS) – namely constipation, diarrhea (or both), and bloating. Indeed, many patients with undiagnosed endometriosis have been diagnosed with IBS. I send every patient who has one of these symptoms for SIBO breath testing, which utilizes carbohydrate substrates (glucose or lactulose) and measures hydrogen and/or methane in the breath.

SIBO is typically treated with rifampin, which stays in the small bowel and will not negatively affect beneficial bacteria, with or without neomycin. Gastroenterologists with more integrative practices also consider the use of herbals in addition to – or instead of – antibiotics. It can sometimes take months or a couple of years to correct SIBO, depending on how long the patient has been affected, but with presurgical diagnosis and a start on treatment, we can remove or at least tone down another instigator of CNS sensitization.

I estimate that 80% of my patients have tested positive for SIBO. Notably, in a testament to the systemic nature of endometriosis, a study published in 2009 of 355 women undergoing operative laparoscopy for suspected endometriosis found that 90% had gastrointestinal symptoms, but only 7.6% of the vast majority whose endometriosis was confirmed were found to have endometrial implants on the bowel itself.⁵

Addressing bladder issues: I routinely administer the PUF (Pain, Urgency, Frequency) questionnaire as part of my intake package and follow it up with conversation. For just about every patient with painful bladder syndrome, pelvic floor physical therapy in combination with a low-acid, low-potassium diet will work effectively together to reduce symptoms and pain. The IC Network offers a helpful food list, and patients can be counseled to choose foods that are also anti-inflammatory. When referrals to a urologist for bladder instillations are possible, these can be helpful as well.

Our communication with patients

Our patients need to have their symptoms and pain validated and to understand why we’re recommending these measures before surgery. Some education is necessary. Few patients will go to an integrative nutritionist, for example, if we just write a referral without explaining how years of inflammation and disruption in the gut can affect the whole body – including mental health – and that it can be corrected over time.

Also necessary is an appreciation of the fact that patients with delayed diagnoses have lived with gastrointestinal and other symptoms and patterns for so long – and often have mothers whose endometriosis caused similar symptoms – that some of their own experiences can seem almost “normal.” A patient whose mother had bowel movements every 7 days may think that 4-5 day intervals are acceptable, for instance. This means we have to carefully consider how we ask our questions.

I always ask my patients as we’re going into surgery, what percentage better are you? I’ve long aimed for at least 30% improvement, but most of the time, with pelvic floor therapy and as many other pain-generator–focused measures as possible, we’re getting them 70% better.

Excision surgery will remove the inflammation that has helped fuel the SIBO and other coconditions. Then, everything done to prepare the body must continue for some time. Certain practices, such as eating an anti-inflammatory diet, should be lifelong.

One day, it is hoped, a pediatrician or other physician will suspect endometriosis early on. The patient will see the surgeon within several months of the onset of pain, and we won’t need to unravel layers of pain generation and CNS upregulation before operating. But until this happens and we shorten the diagnostic delay, we must consider the benefits of presurgical preparation.
 

References

1. Orbuch I, Stein A. Beating Endo: How to Reclaim Your Life From Endometriosis. (New York: HarperCollins, 2019).

2. Healey M et al. J Minim Invasive Gynecol. 2014;21(6):999-1004.

3. Pundir J et al. J Minim Invasive Gynecol. 2017;24(5):747-56.

4. Stratton P, Berkley KJ. Hum Repro Update. 2011;17(3):327-46.

5. Maroun P et al. Aust N Z J Obstet Gynaecol. 2009;49(4):411-4.

Dr. Orbuch is a minimally invasive gynecologic surgeon in Los Angeles who specializes in endometriosis. She has no conflicts of interest to report.

In recent weeks, you may have noticed some familiar headlines about red wine and cardiovascular health. Why the sudden return of these stories? Because of an article recently published in the American Journal of Clinical Nutrition.

Funded in part by a grant from the São Paulo Research Foundation (FAPESP), the “Wine Flora Study” was carried out by prominent researchers from institutions in South America, Europe, and the United States: University of São Paulo; State University of Campinas, São Paulo; University of Brasília; University of Verona (Italy); Austrian Institute of Technology, Tulln; and Harvard Medical School, Boston. The team looked into the effects of red wine on gut flora and plasma levels of trimethylamine-N-oxide (TMAO). And what they found was quite interesting.
 

The study

Previous results have pointed to the beneficial effect that red wine has on the gut microbiome.

The Wine Flora Study involved 42 men (average age, 60 years) with documented coronary artery disease. The trial encompassed two 3-week interventions. In one, the participants consumed 250 mL of red wine per day; the red wine sample had an alcohol content (% v) of 12.75. The Brazilian Wine Institute produced and supplied the red wine: a 2014 Merlot bottled in August 2016 and customized for the study. The second intervention involved alcohol abstention.

Each intervention was preceded by a 2-week washout period. Because certain foods and drinks could interfere with the results, the participants were instructed not to consume alcoholic beverages, fermented foods (yogurt, kombucha, soy lecithin, kefir, sauerkraut, and other fermented vegetables), synthetic prebiotics (insulin, fructooligosaccharides), fiber, dairy, food polyphenols (grapes, grape juice, cranberries, strawberries), and probiotics.

At each intervention, the gut microbiota was analyzed via 16S ribosomal RNA highthroughput sequencing. This method makes it possible to identify bacterial species. The plasma metabolome of 20 randomly selected participants was evaluated by ultra–high-performance liquid chromatography with tandem mass spectrometry. In this method, liquid chromatography separates the compounds, and a mass spectrometer is used to analyze them.

One of the metabolites of interest was TMAO, which is produced from the trimethylamine released when gut bacteria process protein-rich foods. TMAO has been identified as playing a role in the development of atherosclerosis.
 

Results

After red wine consumption, there was significant remodeling of the gut microbiota, with a difference in beta diversity and predominance of Parasutterella, Ruminococcaceae, several Bacteroides species, and Prevotella.

Plasma metabolomic analysis revealed significant changes in metabolites after red wine consumption, consistent with improved redox homeostasis, which is involved in the oxidative stress that promotes atherosclerosis.

Plasma TMAO, however, did not differ between red wine intervention and alcohol abstention.
 

Implications

The researchers concluded that modulation of the gut microbiota may contribute to the putative cardiovascular benefits of moderate red wine consumption. But, as they were careful to point out in the very title of the study, a red wine intervention does not modify plasma TMAO. They also mentioned that the 3-week period may have been too short for the findings to serve as the basis for promoting any meaningful modification. In addition, the team emphasized that these data remain hypothesisgenerating and pave the way for future research.

In an interview with FAPESP, the study’s corresponding author, Protásio Lemos da Luz, MD, PhD, warned about the risks associated with drinking too much alcohol (> 8.5 oz., or 250 mL, of wine daily).

It should be kept in mind that, in Brazil, people do not drink nearly as much wine as they do beer or liquor. Furthermore, the evidence that is available does not provide confirmation of the existence or the extent of the protective health effects associated with light or moderate alcohol intake.

This article was translated from the Medscape Portuguese edition. A version appeared on Medscape.com.

In recent weeks, you may have noticed some familiar headlines about red wine and cardiovascular health. Why the sudden return of these stories? Because of an article recently published in the American Journal of Clinical Nutrition.

Funded in part by a grant from the São Paulo Research Foundation (FAPESP), the “Wine Flora Study” was carried out by prominent researchers from institutions in South America, Europe, and the United States: University of São Paulo; State University of Campinas, São Paulo; University of Brasília; University of Verona (Italy); Austrian Institute of Technology, Tulln; and Harvard Medical School, Boston. The team looked into the effects of red wine on gut flora and plasma levels of trimethylamine-N-oxide (TMAO). And what they found was quite interesting.
 

The study

Previous results have pointed to the beneficial effect that red wine has on the gut microbiome.

The Wine Flora Study involved 42 men (average age, 60 years) with documented coronary artery disease. The trial encompassed two 3-week interventions. In one, the participants consumed 250 mL of red wine per day; the red wine sample had an alcohol content (% v) of 12.75. The Brazilian Wine Institute produced and supplied the red wine: a 2014 Merlot bottled in August 2016 and customized for the study. The second intervention involved alcohol abstention.

Each intervention was preceded by a 2-week washout period. Because certain foods and drinks could interfere with the results, the participants were instructed not to consume alcoholic beverages, fermented foods (yogurt, kombucha, soy lecithin, kefir, sauerkraut, and other fermented vegetables), synthetic prebiotics (insulin, fructooligosaccharides), fiber, dairy, food polyphenols (grapes, grape juice, cranberries, strawberries), and probiotics.

At each intervention, the gut microbiota was analyzed via 16S ribosomal RNA highthroughput sequencing. This method makes it possible to identify bacterial species. The plasma metabolome of 20 randomly selected participants was evaluated by ultra–high-performance liquid chromatography with tandem mass spectrometry. In this method, liquid chromatography separates the compounds, and a mass spectrometer is used to analyze them.

One of the metabolites of interest was TMAO, which is produced from the trimethylamine released when gut bacteria process protein-rich foods. TMAO has been identified as playing a role in the development of atherosclerosis.
 

Results

After red wine consumption, there was significant remodeling of the gut microbiota, with a difference in beta diversity and predominance of Parasutterella, Ruminococcaceae, several Bacteroides species, and Prevotella.

Plasma metabolomic analysis revealed significant changes in metabolites after red wine consumption, consistent with improved redox homeostasis, which is involved in the oxidative stress that promotes atherosclerosis.

Plasma TMAO, however, did not differ between red wine intervention and alcohol abstention.
 

Implications

The researchers concluded that modulation of the gut microbiota may contribute to the putative cardiovascular benefits of moderate red wine consumption. But, as they were careful to point out in the very title of the study, a red wine intervention does not modify plasma TMAO. They also mentioned that the 3-week period may have been too short for the findings to serve as the basis for promoting any meaningful modification. In addition, the team emphasized that these data remain hypothesisgenerating and pave the way for future research.

In an interview with FAPESP, the study’s corresponding author, Protásio Lemos da Luz, MD, PhD, warned about the risks associated with drinking too much alcohol (> 8.5 oz., or 250 mL, of wine daily).

It should be kept in mind that, in Brazil, people do not drink nearly as much wine as they do beer or liquor. Furthermore, the evidence that is available does not provide confirmation of the existence or the extent of the protective health effects associated with light or moderate alcohol intake.

This article was translated from the Medscape Portuguese edition. A version appeared on Medscape.com.

In recent weeks, you may have noticed some familiar headlines about red wine and cardiovascular health. Why the sudden return of these stories? Because of an article recently published in the American Journal of Clinical Nutrition.

Funded in part by a grant from the São Paulo Research Foundation (FAPESP), the “Wine Flora Study” was carried out by prominent researchers from institutions in South America, Europe, and the United States: University of São Paulo; State University of Campinas, São Paulo; University of Brasília; University of Verona (Italy); Austrian Institute of Technology, Tulln; and Harvard Medical School, Boston. The team looked into the effects of red wine on gut flora and plasma levels of trimethylamine-N-oxide (TMAO). And what they found was quite interesting.
 

The study

Previous results have pointed to the beneficial effect that red wine has on the gut microbiome.

The Wine Flora Study involved 42 men (average age, 60 years) with documented coronary artery disease. The trial encompassed two 3-week interventions. In one, the participants consumed 250 mL of red wine per day; the red wine sample had an alcohol content (% v) of 12.75. The Brazilian Wine Institute produced and supplied the red wine: a 2014 Merlot bottled in August 2016 and customized for the study. The second intervention involved alcohol abstention.

Each intervention was preceded by a 2-week washout period. Because certain foods and drinks could interfere with the results, the participants were instructed not to consume alcoholic beverages, fermented foods (yogurt, kombucha, soy lecithin, kefir, sauerkraut, and other fermented vegetables), synthetic prebiotics (insulin, fructooligosaccharides), fiber, dairy, food polyphenols (grapes, grape juice, cranberries, strawberries), and probiotics.

At each intervention, the gut microbiota was analyzed via 16S ribosomal RNA highthroughput sequencing. This method makes it possible to identify bacterial species. The plasma metabolome of 20 randomly selected participants was evaluated by ultra–high-performance liquid chromatography with tandem mass spectrometry. In this method, liquid chromatography separates the compounds, and a mass spectrometer is used to analyze them.

One of the metabolites of interest was TMAO, which is produced from the trimethylamine released when gut bacteria process protein-rich foods. TMAO has been identified as playing a role in the development of atherosclerosis.
 

Results

After red wine consumption, there was significant remodeling of the gut microbiota, with a difference in beta diversity and predominance of Parasutterella, Ruminococcaceae, several Bacteroides species, and Prevotella.

Plasma metabolomic analysis revealed significant changes in metabolites after red wine consumption, consistent with improved redox homeostasis, which is involved in the oxidative stress that promotes atherosclerosis.

Plasma TMAO, however, did not differ between red wine intervention and alcohol abstention.
 

Implications

The researchers concluded that modulation of the gut microbiota may contribute to the putative cardiovascular benefits of moderate red wine consumption. But, as they were careful to point out in the very title of the study, a red wine intervention does not modify plasma TMAO. They also mentioned that the 3-week period may have been too short for the findings to serve as the basis for promoting any meaningful modification. In addition, the team emphasized that these data remain hypothesisgenerating and pave the way for future research.

In an interview with FAPESP, the study’s corresponding author, Protásio Lemos da Luz, MD, PhD, warned about the risks associated with drinking too much alcohol (> 8.5 oz., or 250 mL, of wine daily).

It should be kept in mind that, in Brazil, people do not drink nearly as much wine as they do beer or liquor. Furthermore, the evidence that is available does not provide confirmation of the existence or the extent of the protective health effects associated with light or moderate alcohol intake.

This article was translated from the Medscape Portuguese edition. A version appeared on Medscape.com.