MDedge Psychiatry

Symptom timelines surrounding COVID infection tend to center on either the immediate 5-day quarantine protocols for acute infection or the long-COVID symptoms that can last a month or potentially far longer.

But some patients report a “middle-range” COVID that will resolve before it becomes long COVID, yet still lasts longer than is typical for viral infections. People may return to work or daily routines, but something is off: What had been simple exercise regimens become onerous. Everyday tasks take more effort.

Does this ill-defined subset point to a “medium COVID?”

Farha Ikramuddin, MD, MHA, a physiatrist and rehabilitation specialist at the University of Minnesota and M Health Fairview in Minneapolis, points out there is no definition or diagnostic code or shared official understanding of a middle category for COVID.

“But am I seeing that? Absolutely,” she said in an interview.

“I have seen patients who are younger, healthier, [and] with not so many comorbidities have either persistence of symptoms or reappearance after the initial infection is done,” she said.

Some patients report they had very low infection or were nonsymptomatic and returned to their normal health fairly quickly after infection. Then a week later they began experiencing fatigue, lost appetite, loss of smell, and feeling full after a few bites, Dr. Ikramuddin said.

Part of the trouble in categorizing the space between returning to normal after a week and having symptoms for months is that organizations can’t agree on a timeline for when symptoms warrant a “long-COVID” label.

For instance, the Centers for Disease Control and Prevention defines it as 4 or more weeks after infection. The World Health Organization defines it as starting 3 months after COVID-19 symptom onset.

“I’m seeing ‘medium COVID’ – as one would call it – in younger and healthier patients. I’m also noticing that these symptoms are not severe enough to warrant stopping their job or changing their job schedules,” Dr. Ikramuddin said.

They go back to work, she said, but start noticing something is off.

“I am seeing that.”

“I discharge at least two patients a week from my clinic because they have moved on and no longer have symptoms,” Dr. Ikramuddin said.

In a story from Kaiser Health News published last month, WHYY health reporter Nina Feldman writes: “What I’ve come to think of as my ‘medium COVID’ affected my life. I couldn’t socialize much, drink, or stay up past 9:30 p.m. It took me 10 weeks to go for my first run – I’d been too afraid to try.”

She described a dinner with a friend after ending initial isolation protocols: “One glass of wine left me feeling like I’d had a whole bottle. I was bone-achingly exhausted but couldn’t sleep.”
 

Medical mystery

Dr. Ikramuddin notes the mechanism behind prolonged COVID-19 symptoms is still a medical mystery.

“In one scenario,” she said, “the question is being asked about whether the virus is staying dormant, similar to herpes zoster or HIV.”

“Right now, instead of getting more answers, we’re getting more questions,” Dr. Ikramuddin  said.

Mouhib Naddour, MD, a pulmonary specialist with Sharp HealthCare in San Diego, said he’s seeing that it’s taking some patients who have had COVID longer to recover than it would for other viral infections.

Some patients fall between those recovering within 2-3 weeks and patients having long COVID. Those patients in the gap could be lumped into a middle-range COVID, he told this news organization.

“We try to put things into tables and boxes but it is hard with this disease,” Dr. Naddour said.

He agrees there’s no medical definition for “medium” COVID, but he said the idea should bring hope for patients to know that, if their symptoms are persisting they don’t necessarily have long COVID – and their symptoms may still disappear.

“This is an illness that may take longer to completely recover from,” he said. “The majority of patients we’re seeing in this group could be healthy young patients who get COVID, then 2-3 weeks after they test negative, still have lingering symptoms.”
 

Common symptoms

Some commonly reported symptoms of those with enduring illness, which often overlap with other stages of COVID, are difficulty breathing, chest tightness, dry cough, chest pain, muscle and joint pain, fatigue, difficulty sleeping, and mood swings, Dr. Naddour said. 

“We need to do an extensive assessment to make sure there’s no other problem causing these symptoms,” he said.

Still, there is no set timeline for the medium-COVID range, he noted, so checking in with a primary care physician is important for people experiencing symptoms.
 

It’s a continuum, not a category

Fernando Carnavali, MD, coordinator for Mount Sinai’s Center for Post-COVID Care in New York, said he is not ready to recognize a separate category for a “medium” COVID.

He noted that science can’t even agree on a name for lasting post-COVID symptoms, whether it’s “long COVID” or “long-haul COVID,” “post-COVID syndrome” or “post-acute sequelae of COVID-19 (PASC ).” There’s no agreed-upon pathophysiology or biomarker.

“That creates these gaps of understanding on where we are,” Dr. Carnavali said in an interview.

He said he understands people’s need to categorize symptoms, but rather than a middle ground he sees a continuum.

It doesn’t mean what others may call COVID’s middle ground doesn’t exist, Dr. Carnavali said: “We are in the infancy of defining this. Trying to classify them may create more anxiety.”

The clinicians interviewed for this story report no relevant financial relationships.

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

Symptom timelines surrounding COVID infection tend to center on either the immediate 5-day quarantine protocols for acute infection or the long-COVID symptoms that can last a month or potentially far longer.

But some patients report a “middle-range” COVID that will resolve before it becomes long COVID, yet still lasts longer than is typical for viral infections. People may return to work or daily routines, but something is off: What had been simple exercise regimens become onerous. Everyday tasks take more effort.

Does this ill-defined subset point to a “medium COVID?”

Farha Ikramuddin, MD, MHA, a physiatrist and rehabilitation specialist at the University of Minnesota and M Health Fairview in Minneapolis, points out there is no definition or diagnostic code or shared official understanding of a middle category for COVID.

“But am I seeing that? Absolutely,” she said in an interview.

“I have seen patients who are younger, healthier, [and] with not so many comorbidities have either persistence of symptoms or reappearance after the initial infection is done,” she said.

Some patients report they had very low infection or were nonsymptomatic and returned to their normal health fairly quickly after infection. Then a week later they began experiencing fatigue, lost appetite, loss of smell, and feeling full after a few bites, Dr. Ikramuddin said.

Part of the trouble in categorizing the space between returning to normal after a week and having symptoms for months is that organizations can’t agree on a timeline for when symptoms warrant a “long-COVID” label.

For instance, the Centers for Disease Control and Prevention defines it as 4 or more weeks after infection. The World Health Organization defines it as starting 3 months after COVID-19 symptom onset.

“I’m seeing ‘medium COVID’ – as one would call it – in younger and healthier patients. I’m also noticing that these symptoms are not severe enough to warrant stopping their job or changing their job schedules,” Dr. Ikramuddin said.

They go back to work, she said, but start noticing something is off.

“I am seeing that.”

“I discharge at least two patients a week from my clinic because they have moved on and no longer have symptoms,” Dr. Ikramuddin said.

In a story from Kaiser Health News published last month, WHYY health reporter Nina Feldman writes: “What I’ve come to think of as my ‘medium COVID’ affected my life. I couldn’t socialize much, drink, or stay up past 9:30 p.m. It took me 10 weeks to go for my first run – I’d been too afraid to try.”

She described a dinner with a friend after ending initial isolation protocols: “One glass of wine left me feeling like I’d had a whole bottle. I was bone-achingly exhausted but couldn’t sleep.”
 

Medical mystery

Dr. Ikramuddin notes the mechanism behind prolonged COVID-19 symptoms is still a medical mystery.

“In one scenario,” she said, “the question is being asked about whether the virus is staying dormant, similar to herpes zoster or HIV.”

“Right now, instead of getting more answers, we’re getting more questions,” Dr. Ikramuddin  said.

Mouhib Naddour, MD, a pulmonary specialist with Sharp HealthCare in San Diego, said he’s seeing that it’s taking some patients who have had COVID longer to recover than it would for other viral infections.

Some patients fall between those recovering within 2-3 weeks and patients having long COVID. Those patients in the gap could be lumped into a middle-range COVID, he told this news organization.

“We try to put things into tables and boxes but it is hard with this disease,” Dr. Naddour said.

He agrees there’s no medical definition for “medium” COVID, but he said the idea should bring hope for patients to know that, if their symptoms are persisting they don’t necessarily have long COVID – and their symptoms may still disappear.

“This is an illness that may take longer to completely recover from,” he said. “The majority of patients we’re seeing in this group could be healthy young patients who get COVID, then 2-3 weeks after they test negative, still have lingering symptoms.”
 

Common symptoms

Some commonly reported symptoms of those with enduring illness, which often overlap with other stages of COVID, are difficulty breathing, chest tightness, dry cough, chest pain, muscle and joint pain, fatigue, difficulty sleeping, and mood swings, Dr. Naddour said. 

“We need to do an extensive assessment to make sure there’s no other problem causing these symptoms,” he said.

Still, there is no set timeline for the medium-COVID range, he noted, so checking in with a primary care physician is important for people experiencing symptoms.
 

It’s a continuum, not a category

Fernando Carnavali, MD, coordinator for Mount Sinai’s Center for Post-COVID Care in New York, said he is not ready to recognize a separate category for a “medium” COVID.

He noted that science can’t even agree on a name for lasting post-COVID symptoms, whether it’s “long COVID” or “long-haul COVID,” “post-COVID syndrome” or “post-acute sequelae of COVID-19 (PASC ).” There’s no agreed-upon pathophysiology or biomarker.

“That creates these gaps of understanding on where we are,” Dr. Carnavali said in an interview.

He said he understands people’s need to categorize symptoms, but rather than a middle ground he sees a continuum.

It doesn’t mean what others may call COVID’s middle ground doesn’t exist, Dr. Carnavali said: “We are in the infancy of defining this. Trying to classify them may create more anxiety.”

The clinicians interviewed for this story report no relevant financial relationships.

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

Symptom timelines surrounding COVID infection tend to center on either the immediate 5-day quarantine protocols for acute infection or the long-COVID symptoms that can last a month or potentially far longer.

But some patients report a “middle-range” COVID that will resolve before it becomes long COVID, yet still lasts longer than is typical for viral infections. People may return to work or daily routines, but something is off: What had been simple exercise regimens become onerous. Everyday tasks take more effort.

Does this ill-defined subset point to a “medium COVID?”

Farha Ikramuddin, MD, MHA, a physiatrist and rehabilitation specialist at the University of Minnesota and M Health Fairview in Minneapolis, points out there is no definition or diagnostic code or shared official understanding of a middle category for COVID.

“But am I seeing that? Absolutely,” she said in an interview.

“I have seen patients who are younger, healthier, [and] with not so many comorbidities have either persistence of symptoms or reappearance after the initial infection is done,” she said.

Some patients report they had very low infection or were nonsymptomatic and returned to their normal health fairly quickly after infection. Then a week later they began experiencing fatigue, lost appetite, loss of smell, and feeling full after a few bites, Dr. Ikramuddin said.

Part of the trouble in categorizing the space between returning to normal after a week and having symptoms for months is that organizations can’t agree on a timeline for when symptoms warrant a “long-COVID” label.

For instance, the Centers for Disease Control and Prevention defines it as 4 or more weeks after infection. The World Health Organization defines it as starting 3 months after COVID-19 symptom onset.

“I’m seeing ‘medium COVID’ – as one would call it – in younger and healthier patients. I’m also noticing that these symptoms are not severe enough to warrant stopping their job or changing their job schedules,” Dr. Ikramuddin said.

They go back to work, she said, but start noticing something is off.

“I am seeing that.”

“I discharge at least two patients a week from my clinic because they have moved on and no longer have symptoms,” Dr. Ikramuddin said.

In a story from Kaiser Health News published last month, WHYY health reporter Nina Feldman writes: “What I’ve come to think of as my ‘medium COVID’ affected my life. I couldn’t socialize much, drink, or stay up past 9:30 p.m. It took me 10 weeks to go for my first run – I’d been too afraid to try.”

She described a dinner with a friend after ending initial isolation protocols: “One glass of wine left me feeling like I’d had a whole bottle. I was bone-achingly exhausted but couldn’t sleep.”
 

Medical mystery

Dr. Ikramuddin notes the mechanism behind prolonged COVID-19 symptoms is still a medical mystery.

“In one scenario,” she said, “the question is being asked about whether the virus is staying dormant, similar to herpes zoster or HIV.”

“Right now, instead of getting more answers, we’re getting more questions,” Dr. Ikramuddin  said.

Mouhib Naddour, MD, a pulmonary specialist with Sharp HealthCare in San Diego, said he’s seeing that it’s taking some patients who have had COVID longer to recover than it would for other viral infections.

Some patients fall between those recovering within 2-3 weeks and patients having long COVID. Those patients in the gap could be lumped into a middle-range COVID, he told this news organization.

“We try to put things into tables and boxes but it is hard with this disease,” Dr. Naddour said.

He agrees there’s no medical definition for “medium” COVID, but he said the idea should bring hope for patients to know that, if their symptoms are persisting they don’t necessarily have long COVID – and their symptoms may still disappear.

“This is an illness that may take longer to completely recover from,” he said. “The majority of patients we’re seeing in this group could be healthy young patients who get COVID, then 2-3 weeks after they test negative, still have lingering symptoms.”
 

Common symptoms

Some commonly reported symptoms of those with enduring illness, which often overlap with other stages of COVID, are difficulty breathing, chest tightness, dry cough, chest pain, muscle and joint pain, fatigue, difficulty sleeping, and mood swings, Dr. Naddour said. 

“We need to do an extensive assessment to make sure there’s no other problem causing these symptoms,” he said.

Still, there is no set timeline for the medium-COVID range, he noted, so checking in with a primary care physician is important for people experiencing symptoms.
 

It’s a continuum, not a category

Fernando Carnavali, MD, coordinator for Mount Sinai’s Center for Post-COVID Care in New York, said he is not ready to recognize a separate category for a “medium” COVID.

He noted that science can’t even agree on a name for lasting post-COVID symptoms, whether it’s “long COVID” or “long-haul COVID,” “post-COVID syndrome” or “post-acute sequelae of COVID-19 (PASC ).” There’s no agreed-upon pathophysiology or biomarker.

“That creates these gaps of understanding on where we are,” Dr. Carnavali said in an interview.

He said he understands people’s need to categorize symptoms, but rather than a middle ground he sees a continuum.

It doesn’t mean what others may call COVID’s middle ground doesn’t exist, Dr. Carnavali said: “We are in the infancy of defining this. Trying to classify them may create more anxiety.”

The clinicians interviewed for this story report no relevant financial relationships.

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

The risk for dementia goes up in patients with atrial fibrillation (AFib), but some evidence suggests that risk can be blunted with therapies that restore sinus rhythm. However, a new cohort study suggests that the treatment effect’s magnitude might depend on the rhythm control strategy. It hinted that AFib catheter ablation might be more effective than pharmacologic rhythm control alone at cutting the risk for dementia.

The case-matched study of more than 38,000 adults with AFib saw a 41% reduction (P < .0001) in risk for dementia among those who underwent catheter ablation after attempted rhythm control with antiarrhythmic drugs (AAD), compared with those managed with pharmacologic rhythm control therapy alone.

The observational study comprising 20 years of data comes with big limitations and can’t say for sure whether catheter ablation is better than AAD-only at cutting the dementia risk in AFib. But it and other evidence support the idea, which has yet to be explored in a randomized fashion.

In a secondary finding, the analysis showed a similar reduction in dementia risk from catheter ablation, compared with AAD, in women and in men by 40% and 45%, respectively (P < .0001 for both). The findings are particularly relevant “given the higher life-long risk of dementia among women and the lower likelihood that women will be offered ablation, which has been demonstrated repeatedly,” Emily P. Zeitler, MD, MHS, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, told this news organization. “I think this is another reason to try to be more generous in offering ablation to women.”

Management of AFib certainly evolved in important ways from 2000 to 2021, the period covered by the study. But a sensitivity analysis based on data from 2010 to 2021 showed “no meaningful differences” in the results, said Dr. Zeitler, who is slated to present the findings April 30 at the Heart Rhythm Society 2022 Scientific Sessions, conducted virtually and live in San Francisco.

Dr. Zeitler acknowledged that the observational study, even with its propensity-matched ablation and AAD cohorts, can only hint at a preference for ablation over AAD for lowering risk for AFib-associated dementia. “We know there’s unmeasured and unfixable confounding between those two groups, so we see this really as hypothesis-generating.”

It was “a well-done analysis,” and the conclusion that the dementia risk was lower with catheter ablation is “absolutely correct,” but only as far as the study and its limitations allow, agreed David Conen, MD, MPH, McMaster University, Hamilton, Ontario, who is not a coauthor.

“Even with propensity matching, you can get rid of some sorts of confounding, but you can never get rid of all selection bias issues.” That, he said when interviewed, takes randomized trials.

Dr. Conen, who is studying cognitive decline in AFib as a SWISS-AF trial principal investigator, pointed to a secondary finding of the analysis as evidence for such confounding. He said the ablation group’s nearly 50% drop (P < .0001) in competing risk for death, compared with patients managed with AAD, isn’t plausible.

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

The risk for dementia goes up in patients with atrial fibrillation (AFib), but some evidence suggests that risk can be blunted with therapies that restore sinus rhythm. However, a new cohort study suggests that the treatment effect’s magnitude might depend on the rhythm control strategy. It hinted that AFib catheter ablation might be more effective than pharmacologic rhythm control alone at cutting the risk for dementia.

The case-matched study of more than 38,000 adults with AFib saw a 41% reduction (P < .0001) in risk for dementia among those who underwent catheter ablation after attempted rhythm control with antiarrhythmic drugs (AAD), compared with those managed with pharmacologic rhythm control therapy alone.

The observational study comprising 20 years of data comes with big limitations and can’t say for sure whether catheter ablation is better than AAD-only at cutting the dementia risk in AFib. But it and other evidence support the idea, which has yet to be explored in a randomized fashion.

In a secondary finding, the analysis showed a similar reduction in dementia risk from catheter ablation, compared with AAD, in women and in men by 40% and 45%, respectively (P < .0001 for both). The findings are particularly relevant “given the higher life-long risk of dementia among women and the lower likelihood that women will be offered ablation, which has been demonstrated repeatedly,” Emily P. Zeitler, MD, MHS, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, told this news organization. “I think this is another reason to try to be more generous in offering ablation to women.”

Management of AFib certainly evolved in important ways from 2000 to 2021, the period covered by the study. But a sensitivity analysis based on data from 2010 to 2021 showed “no meaningful differences” in the results, said Dr. Zeitler, who is slated to present the findings April 30 at the Heart Rhythm Society 2022 Scientific Sessions, conducted virtually and live in San Francisco.

Dr. Zeitler acknowledged that the observational study, even with its propensity-matched ablation and AAD cohorts, can only hint at a preference for ablation over AAD for lowering risk for AFib-associated dementia. “We know there’s unmeasured and unfixable confounding between those two groups, so we see this really as hypothesis-generating.”

It was “a well-done analysis,” and the conclusion that the dementia risk was lower with catheter ablation is “absolutely correct,” but only as far as the study and its limitations allow, agreed David Conen, MD, MPH, McMaster University, Hamilton, Ontario, who is not a coauthor.

“Even with propensity matching, you can get rid of some sorts of confounding, but you can never get rid of all selection bias issues.” That, he said when interviewed, takes randomized trials.

Dr. Conen, who is studying cognitive decline in AFib as a SWISS-AF trial principal investigator, pointed to a secondary finding of the analysis as evidence for such confounding. He said the ablation group’s nearly 50% drop (P < .0001) in competing risk for death, compared with patients managed with AAD, isn’t plausible.

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

The risk for dementia goes up in patients with atrial fibrillation (AFib), but some evidence suggests that risk can be blunted with therapies that restore sinus rhythm. However, a new cohort study suggests that the treatment effect’s magnitude might depend on the rhythm control strategy. It hinted that AFib catheter ablation might be more effective than pharmacologic rhythm control alone at cutting the risk for dementia.

The case-matched study of more than 38,000 adults with AFib saw a 41% reduction (P < .0001) in risk for dementia among those who underwent catheter ablation after attempted rhythm control with antiarrhythmic drugs (AAD), compared with those managed with pharmacologic rhythm control therapy alone.

The observational study comprising 20 years of data comes with big limitations and can’t say for sure whether catheter ablation is better than AAD-only at cutting the dementia risk in AFib. But it and other evidence support the idea, which has yet to be explored in a randomized fashion.

In a secondary finding, the analysis showed a similar reduction in dementia risk from catheter ablation, compared with AAD, in women and in men by 40% and 45%, respectively (P < .0001 for both). The findings are particularly relevant “given the higher life-long risk of dementia among women and the lower likelihood that women will be offered ablation, which has been demonstrated repeatedly,” Emily P. Zeitler, MD, MHS, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, told this news organization. “I think this is another reason to try to be more generous in offering ablation to women.”

Management of AFib certainly evolved in important ways from 2000 to 2021, the period covered by the study. But a sensitivity analysis based on data from 2010 to 2021 showed “no meaningful differences” in the results, said Dr. Zeitler, who is slated to present the findings April 30 at the Heart Rhythm Society 2022 Scientific Sessions, conducted virtually and live in San Francisco.

Dr. Zeitler acknowledged that the observational study, even with its propensity-matched ablation and AAD cohorts, can only hint at a preference for ablation over AAD for lowering risk for AFib-associated dementia. “We know there’s unmeasured and unfixable confounding between those two groups, so we see this really as hypothesis-generating.”

It was “a well-done analysis,” and the conclusion that the dementia risk was lower with catheter ablation is “absolutely correct,” but only as far as the study and its limitations allow, agreed David Conen, MD, MPH, McMaster University, Hamilton, Ontario, who is not a coauthor.

“Even with propensity matching, you can get rid of some sorts of confounding, but you can never get rid of all selection bias issues.” That, he said when interviewed, takes randomized trials.

Dr. Conen, who is studying cognitive decline in AFib as a SWISS-AF trial principal investigator, pointed to a secondary finding of the analysis as evidence for such confounding. He said the ablation group’s nearly 50% drop (P < .0001) in competing risk for death, compared with patients managed with AAD, isn’t plausible.

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

The suicide of a male nurse at a Northern California hospital has inspired an outpouring of empathy on Twitter from a coworker, nurses, and others.

The Santa Clara Police Department “thoroughly investigated” a report April 27 at Kaiser Permanente Santa Clara Medical Center that a male nurse in the emergency department died from a self-inflicted gunshot wound and ruled it a suicide, according to Wahid Kazem, assistant chief of police.

“This tragic event occurred in a closed room that is not used for patient care, adjacent to the emergency department. No other staff or patients were threatened,” according to Rakesh Chaudhary, MD, physician-in-chief of the medical center.

He added that the emergency department remained open for walk-in patients during the investigation, but ambulances were temporarily diverted to nearby hospitals. “The Santa Clara Police Department and our staff immediately took precautions to isolate the affected area and avoid impact to patient care.”

In terms of the effect on those closer to the victim, Dr. Chaudhary said, “Our hearts go out to the family, friends, and coworkers affected by this terrible loss. Our teams are on site providing emotional support and resources for staff.”

Neither the police nor the hospital released the victim’s name. “Out of respect for the privacy of our colleague and their family, we cannot provide any additional details,” Dr. Chaudhary said. 

Among those who tweeted reactions to the news the past few days was someone who worked with the victim, according to the post: “My heart goes out to my coworker who thought he had no one to lean on and to my good friend who had to witness this tragedy. Love my ER fam.”

A male critical care RN tweeted: “My heart hurts for the nurse, his loved ones, and colleagues. Anyone working in ER understands the unique stress that we’ve been under. This is so tragic.”

While others cited the need for more mental health services to care for nurses, a psychiatrist on Twitter added, “Nurses are not OK and pizza and pats on the back aren’t going to fix it. This affects all of us.”

Mental health support was listed as a prime demand of striking workers recently at Stanford (Calif.) Health Care and Lucile Packard Children’s Hospital in Palo Alto, about a half hour away from Santa Clara Medical Center.

The nurses’ strike ended May 2 with an agreement between the health systems and the Committee for Recognition of Nursing Achievement union representing the nurses. The contract includes improvements to existing benefits supporting nurses’ health and well-being, according to a StanfordPackardVoice.com newsletter updating the negotiations.

Earlier this year, an intensive care unit RN from Stanford, Michael Odell, reportedly walked off his shift and was found dead 2 days later in San Francisco by the Alameda County Sheriff’s Office dive team. No foul play was suspected and the incident was believed to be a suicide.

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

The suicide of a male nurse at a Northern California hospital has inspired an outpouring of empathy on Twitter from a coworker, nurses, and others.

The Santa Clara Police Department “thoroughly investigated” a report April 27 at Kaiser Permanente Santa Clara Medical Center that a male nurse in the emergency department died from a self-inflicted gunshot wound and ruled it a suicide, according to Wahid Kazem, assistant chief of police.

“This tragic event occurred in a closed room that is not used for patient care, adjacent to the emergency department. No other staff or patients were threatened,” according to Rakesh Chaudhary, MD, physician-in-chief of the medical center.

He added that the emergency department remained open for walk-in patients during the investigation, but ambulances were temporarily diverted to nearby hospitals. “The Santa Clara Police Department and our staff immediately took precautions to isolate the affected area and avoid impact to patient care.”

In terms of the effect on those closer to the victim, Dr. Chaudhary said, “Our hearts go out to the family, friends, and coworkers affected by this terrible loss. Our teams are on site providing emotional support and resources for staff.”

Neither the police nor the hospital released the victim’s name. “Out of respect for the privacy of our colleague and their family, we cannot provide any additional details,” Dr. Chaudhary said. 

Among those who tweeted reactions to the news the past few days was someone who worked with the victim, according to the post: “My heart goes out to my coworker who thought he had no one to lean on and to my good friend who had to witness this tragedy. Love my ER fam.”

A male critical care RN tweeted: “My heart hurts for the nurse, his loved ones, and colleagues. Anyone working in ER understands the unique stress that we’ve been under. This is so tragic.”

While others cited the need for more mental health services to care for nurses, a psychiatrist on Twitter added, “Nurses are not OK and pizza and pats on the back aren’t going to fix it. This affects all of us.”

Mental health support was listed as a prime demand of striking workers recently at Stanford (Calif.) Health Care and Lucile Packard Children’s Hospital in Palo Alto, about a half hour away from Santa Clara Medical Center.

The nurses’ strike ended May 2 with an agreement between the health systems and the Committee for Recognition of Nursing Achievement union representing the nurses. The contract includes improvements to existing benefits supporting nurses’ health and well-being, according to a StanfordPackardVoice.com newsletter updating the negotiations.

Earlier this year, an intensive care unit RN from Stanford, Michael Odell, reportedly walked off his shift and was found dead 2 days later in San Francisco by the Alameda County Sheriff’s Office dive team. No foul play was suspected and the incident was believed to be a suicide.

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

The suicide of a male nurse at a Northern California hospital has inspired an outpouring of empathy on Twitter from a coworker, nurses, and others.

The Santa Clara Police Department “thoroughly investigated” a report April 27 at Kaiser Permanente Santa Clara Medical Center that a male nurse in the emergency department died from a self-inflicted gunshot wound and ruled it a suicide, according to Wahid Kazem, assistant chief of police.

“This tragic event occurred in a closed room that is not used for patient care, adjacent to the emergency department. No other staff or patients were threatened,” according to Rakesh Chaudhary, MD, physician-in-chief of the medical center.

He added that the emergency department remained open for walk-in patients during the investigation, but ambulances were temporarily diverted to nearby hospitals. “The Santa Clara Police Department and our staff immediately took precautions to isolate the affected area and avoid impact to patient care.”

In terms of the effect on those closer to the victim, Dr. Chaudhary said, “Our hearts go out to the family, friends, and coworkers affected by this terrible loss. Our teams are on site providing emotional support and resources for staff.”

Neither the police nor the hospital released the victim’s name. “Out of respect for the privacy of our colleague and their family, we cannot provide any additional details,” Dr. Chaudhary said. 

Among those who tweeted reactions to the news the past few days was someone who worked with the victim, according to the post: “My heart goes out to my coworker who thought he had no one to lean on and to my good friend who had to witness this tragedy. Love my ER fam.”

A male critical care RN tweeted: “My heart hurts for the nurse, his loved ones, and colleagues. Anyone working in ER understands the unique stress that we’ve been under. This is so tragic.”

While others cited the need for more mental health services to care for nurses, a psychiatrist on Twitter added, “Nurses are not OK and pizza and pats on the back aren’t going to fix it. This affects all of us.”

Mental health support was listed as a prime demand of striking workers recently at Stanford (Calif.) Health Care and Lucile Packard Children’s Hospital in Palo Alto, about a half hour away from Santa Clara Medical Center.

The nurses’ strike ended May 2 with an agreement between the health systems and the Committee for Recognition of Nursing Achievement union representing the nurses. The contract includes improvements to existing benefits supporting nurses’ health and well-being, according to a StanfordPackardVoice.com newsletter updating the negotiations.

Earlier this year, an intensive care unit RN from Stanford, Michael Odell, reportedly walked off his shift and was found dead 2 days later in San Francisco by the Alameda County Sheriff’s Office dive team. No foul play was suspected and the incident was believed to be a suicide.

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

Black patients presenting with psychiatric disorders to hospital emergency departments across the United States have significantly higher rates of chemical restraint than their White counterparts, new research shows.

Results of a national study showed Black patients presenting to the ED were 63% more likely to receive chemical sedation than White patients. The investigators also found White patients were more likely to receive chemical sedation at hospitals with a higher proportion of Black patients – a finding that suggests hospital demographics influence practice patterns and that structural racism may be a root cause.

“There is a large disparity in the rates at which patients who presented to EDs nationally in the United States are restrained by race. You are 63% more likely, for the same set of chief complaints, to be chemically sedated if you are Black versus if you’re White,” senior investigator Ari Friedman, MD, PhD, an assistant professor of emergency medicine, and medical ethics and health policy, University of Pennsylvania, Philadelphia, told this news organization.

University of Pennsylvania

First large-scale study

Chemical sedation, also known as chemical restraint, is used to calm and help protect patients from harming themselves or others. Previous research on racial differences in the care of ED psychiatric patients with agitation suggests that there may be treatment disparities.

“Previous research from single institutions [has] shown that Black patients are more likely than White patients to be physically restrained, and this has been shown to be true among adult patients and pediatric patients,” lead author Utsha Khatri, MD, assistant professor of emergency medicine at the Icahn School of Medicine, New York, told this news organization.

Specifically, two single-institution studies within the last year revealed similar disparities, with higher rates of physical restraint for Black and Hispanic psychiatric patients in the ED. Another recent study showed an association with race, ethnicity, and pharmacological restraint use among pediatric patients presenting to the ED for mental health concerns.

“There has been work in psychiatry on disparities in this context, although there is less work in emergency departments,” said Dr. Friedman. “We looked across all U.S. EDs as opposed to within a single health system. The major trade-offs for us were that we weren’t able to observe restraint orders, which don’t find their way into national datasets, so we had to make some inferences based on the type of medications given.”

For the study the investigators analyzed data from 2008-2018 through the National Hospital Ambulatory Medical Survey (NHAMCS) database. They examined the association of race and the administration of chemical sedation, with either an antipsychotic or ketamine, in ED visits for psychiatric disorders. These were any visit where the reason for the visit was “symptoms referable to psychological and mental disorders.”

Of the 76.2 million total ED visits evaluated, the researchers found that Black patients presenting with a psychiatric disorder were significantly more likely to receive chemical sedation with antipsychotics or ketamine than White patients presenting with the same conditions (5.3% vs. 3.0%; P < .01). This difference remained significant when accounting for admission or transfer to psychiatric facilities.
 

Combatting the forces of racism

When researchers accounted for the percent of hospital population that was Black, they found that patient race no longer affected the likelihood of chemical restraint.

“We found the key source of this racial disparity in use of chemical sedation is accounted for by the fact that hospitals that treat a higher proportion of Black patients tend to use more sedation,” said Dr. Khatri.

“Our findings suggest that patients who present to hospitals that serve a patient population that is 60% Black would have [a] roughly 1.8 times likelihood of getting chemically sedated, compared with a hospital that serves a population that is 10% Black,” she added.

“When a hospital has fewer resources, they often don’t have the staff or time to de-escalate a patient in distress and can have to resort to chemical sedation more quickly than a hospital with ample staff and resources,” said Dr. Friedman in a release.

Dr. Khatri added that the study highlights the need to combat the forces of racism by focusing not just on provider bias but by addressing the “underlying structural issues that lead to Black patients getting worse care based on where they live.”

“Hospitals have unequal distribution of resources and quality, largely patterned on the racial makeup of their patients. Dedicated training and funding for de-escalation techniques as well as sufficient staffing and availability of outpatient mental health care may help keep both patients and staff safe by reducing the use of physical restraint and chemical sedation in appropriate circumstances,” said Dr. Khatri.

Dr. Friedman noted that there will always be a need for restraint use to facilitate rapid medical evaluation and stabilization of patients, but “we want to make it as humane, thoughtful, and rare as possible, and to have a large armamentarium of alternative strategies that can be equitably applied across emergency departments.”
 

Need for widespread, systemic change

Commenting on the findings, Regina James, MD, the American Psychiatric Association’s chief of Diversity and Health Equity and deputy medical director, said the large-scale study confirms the widespread existence of racial and ethnic disparities in patients with psychiatric disorders.

Courtesy American Psychiatric Association

“This study and previous studies, not only in psychiatry but in other areas of medicine, all bring to light that there continues to be evidence of racial and ethnic disparities in health care, and this is consistent across a range of illnesses and health care services,” said Dr. James.

“It’s important that as we think about the solution, we also think about the etiology of the problem and the layers that have contributed to it – understanding, embracing, and recognizing that these differences didn’t just come up de novo. It’s policies, practices, and behaviors that got us to this point, and it’s going to be policies, practices, and behaviors that are going to move us away from this point,” noted Dr. James.

She added that future research should focus on further understanding which factors exacerbate agitation among patients and what resources directed at the hospital level, including de-escalation training, nursing staff, and waiting room crowding, may be effective at reducing the use of chemical sedation when clinically appropriate.

The authors and Dr. James report no relevant financial conflicts of interest.

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

Black patients presenting with psychiatric disorders to hospital emergency departments across the United States have significantly higher rates of chemical restraint than their White counterparts, new research shows.

Results of a national study showed Black patients presenting to the ED were 63% more likely to receive chemical sedation than White patients. The investigators also found White patients were more likely to receive chemical sedation at hospitals with a higher proportion of Black patients – a finding that suggests hospital demographics influence practice patterns and that structural racism may be a root cause.

“There is a large disparity in the rates at which patients who presented to EDs nationally in the United States are restrained by race. You are 63% more likely, for the same set of chief complaints, to be chemically sedated if you are Black versus if you’re White,” senior investigator Ari Friedman, MD, PhD, an assistant professor of emergency medicine, and medical ethics and health policy, University of Pennsylvania, Philadelphia, told this news organization.

University of Pennsylvania

First large-scale study

Chemical sedation, also known as chemical restraint, is used to calm and help protect patients from harming themselves or others. Previous research on racial differences in the care of ED psychiatric patients with agitation suggests that there may be treatment disparities.

“Previous research from single institutions [has] shown that Black patients are more likely than White patients to be physically restrained, and this has been shown to be true among adult patients and pediatric patients,” lead author Utsha Khatri, MD, assistant professor of emergency medicine at the Icahn School of Medicine, New York, told this news organization.

Specifically, two single-institution studies within the last year revealed similar disparities, with higher rates of physical restraint for Black and Hispanic psychiatric patients in the ED. Another recent study showed an association with race, ethnicity, and pharmacological restraint use among pediatric patients presenting to the ED for mental health concerns.

“There has been work in psychiatry on disparities in this context, although there is less work in emergency departments,” said Dr. Friedman. “We looked across all U.S. EDs as opposed to within a single health system. The major trade-offs for us were that we weren’t able to observe restraint orders, which don’t find their way into national datasets, so we had to make some inferences based on the type of medications given.”

For the study the investigators analyzed data from 2008-2018 through the National Hospital Ambulatory Medical Survey (NHAMCS) database. They examined the association of race and the administration of chemical sedation, with either an antipsychotic or ketamine, in ED visits for psychiatric disorders. These were any visit where the reason for the visit was “symptoms referable to psychological and mental disorders.”

Of the 76.2 million total ED visits evaluated, the researchers found that Black patients presenting with a psychiatric disorder were significantly more likely to receive chemical sedation with antipsychotics or ketamine than White patients presenting with the same conditions (5.3% vs. 3.0%; P < .01). This difference remained significant when accounting for admission or transfer to psychiatric facilities.
 

Combatting the forces of racism

When researchers accounted for the percent of hospital population that was Black, they found that patient race no longer affected the likelihood of chemical restraint.

“We found the key source of this racial disparity in use of chemical sedation is accounted for by the fact that hospitals that treat a higher proportion of Black patients tend to use more sedation,” said Dr. Khatri.

“Our findings suggest that patients who present to hospitals that serve a patient population that is 60% Black would have [a] roughly 1.8 times likelihood of getting chemically sedated, compared with a hospital that serves a population that is 10% Black,” she added.

“When a hospital has fewer resources, they often don’t have the staff or time to de-escalate a patient in distress and can have to resort to chemical sedation more quickly than a hospital with ample staff and resources,” said Dr. Friedman in a release.

Dr. Khatri added that the study highlights the need to combat the forces of racism by focusing not just on provider bias but by addressing the “underlying structural issues that lead to Black patients getting worse care based on where they live.”

“Hospitals have unequal distribution of resources and quality, largely patterned on the racial makeup of their patients. Dedicated training and funding for de-escalation techniques as well as sufficient staffing and availability of outpatient mental health care may help keep both patients and staff safe by reducing the use of physical restraint and chemical sedation in appropriate circumstances,” said Dr. Khatri.

Dr. Friedman noted that there will always be a need for restraint use to facilitate rapid medical evaluation and stabilization of patients, but “we want to make it as humane, thoughtful, and rare as possible, and to have a large armamentarium of alternative strategies that can be equitably applied across emergency departments.”
 

Need for widespread, systemic change

Commenting on the findings, Regina James, MD, the American Psychiatric Association’s chief of Diversity and Health Equity and deputy medical director, said the large-scale study confirms the widespread existence of racial and ethnic disparities in patients with psychiatric disorders.

Courtesy American Psychiatric Association

“This study and previous studies, not only in psychiatry but in other areas of medicine, all bring to light that there continues to be evidence of racial and ethnic disparities in health care, and this is consistent across a range of illnesses and health care services,” said Dr. James.

“It’s important that as we think about the solution, we also think about the etiology of the problem and the layers that have contributed to it – understanding, embracing, and recognizing that these differences didn’t just come up de novo. It’s policies, practices, and behaviors that got us to this point, and it’s going to be policies, practices, and behaviors that are going to move us away from this point,” noted Dr. James.

She added that future research should focus on further understanding which factors exacerbate agitation among patients and what resources directed at the hospital level, including de-escalation training, nursing staff, and waiting room crowding, may be effective at reducing the use of chemical sedation when clinically appropriate.

The authors and Dr. James report no relevant financial conflicts of interest.

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

Black patients presenting with psychiatric disorders to hospital emergency departments across the United States have significantly higher rates of chemical restraint than their White counterparts, new research shows.

Results of a national study showed Black patients presenting to the ED were 63% more likely to receive chemical sedation than White patients. The investigators also found White patients were more likely to receive chemical sedation at hospitals with a higher proportion of Black patients – a finding that suggests hospital demographics influence practice patterns and that structural racism may be a root cause.

“There is a large disparity in the rates at which patients who presented to EDs nationally in the United States are restrained by race. You are 63% more likely, for the same set of chief complaints, to be chemically sedated if you are Black versus if you’re White,” senior investigator Ari Friedman, MD, PhD, an assistant professor of emergency medicine, and medical ethics and health policy, University of Pennsylvania, Philadelphia, told this news organization.

University of Pennsylvania

First large-scale study

Chemical sedation, also known as chemical restraint, is used to calm and help protect patients from harming themselves or others. Previous research on racial differences in the care of ED psychiatric patients with agitation suggests that there may be treatment disparities.

“Previous research from single institutions [has] shown that Black patients are more likely than White patients to be physically restrained, and this has been shown to be true among adult patients and pediatric patients,” lead author Utsha Khatri, MD, assistant professor of emergency medicine at the Icahn School of Medicine, New York, told this news organization.

Specifically, two single-institution studies within the last year revealed similar disparities, with higher rates of physical restraint for Black and Hispanic psychiatric patients in the ED. Another recent study showed an association with race, ethnicity, and pharmacological restraint use among pediatric patients presenting to the ED for mental health concerns.

“There has been work in psychiatry on disparities in this context, although there is less work in emergency departments,” said Dr. Friedman. “We looked across all U.S. EDs as opposed to within a single health system. The major trade-offs for us were that we weren’t able to observe restraint orders, which don’t find their way into national datasets, so we had to make some inferences based on the type of medications given.”

For the study the investigators analyzed data from 2008-2018 through the National Hospital Ambulatory Medical Survey (NHAMCS) database. They examined the association of race and the administration of chemical sedation, with either an antipsychotic or ketamine, in ED visits for psychiatric disorders. These were any visit where the reason for the visit was “symptoms referable to psychological and mental disorders.”

Of the 76.2 million total ED visits evaluated, the researchers found that Black patients presenting with a psychiatric disorder were significantly more likely to receive chemical sedation with antipsychotics or ketamine than White patients presenting with the same conditions (5.3% vs. 3.0%; P < .01). This difference remained significant when accounting for admission or transfer to psychiatric facilities.
 

Combatting the forces of racism

When researchers accounted for the percent of hospital population that was Black, they found that patient race no longer affected the likelihood of chemical restraint.

“We found the key source of this racial disparity in use of chemical sedation is accounted for by the fact that hospitals that treat a higher proportion of Black patients tend to use more sedation,” said Dr. Khatri.

“Our findings suggest that patients who present to hospitals that serve a patient population that is 60% Black would have [a] roughly 1.8 times likelihood of getting chemically sedated, compared with a hospital that serves a population that is 10% Black,” she added.

“When a hospital has fewer resources, they often don’t have the staff or time to de-escalate a patient in distress and can have to resort to chemical sedation more quickly than a hospital with ample staff and resources,” said Dr. Friedman in a release.

Dr. Khatri added that the study highlights the need to combat the forces of racism by focusing not just on provider bias but by addressing the “underlying structural issues that lead to Black patients getting worse care based on where they live.”

“Hospitals have unequal distribution of resources and quality, largely patterned on the racial makeup of their patients. Dedicated training and funding for de-escalation techniques as well as sufficient staffing and availability of outpatient mental health care may help keep both patients and staff safe by reducing the use of physical restraint and chemical sedation in appropriate circumstances,” said Dr. Khatri.

Dr. Friedman noted that there will always be a need for restraint use to facilitate rapid medical evaluation and stabilization of patients, but “we want to make it as humane, thoughtful, and rare as possible, and to have a large armamentarium of alternative strategies that can be equitably applied across emergency departments.”
 

Need for widespread, systemic change

Commenting on the findings, Regina James, MD, the American Psychiatric Association’s chief of Diversity and Health Equity and deputy medical director, said the large-scale study confirms the widespread existence of racial and ethnic disparities in patients with psychiatric disorders.

Courtesy American Psychiatric Association

“This study and previous studies, not only in psychiatry but in other areas of medicine, all bring to light that there continues to be evidence of racial and ethnic disparities in health care, and this is consistent across a range of illnesses and health care services,” said Dr. James.

“It’s important that as we think about the solution, we also think about the etiology of the problem and the layers that have contributed to it – understanding, embracing, and recognizing that these differences didn’t just come up de novo. It’s policies, practices, and behaviors that got us to this point, and it’s going to be policies, practices, and behaviors that are going to move us away from this point,” noted Dr. James.

She added that future research should focus on further understanding which factors exacerbate agitation among patients and what resources directed at the hospital level, including de-escalation training, nursing staff, and waiting room crowding, may be effective at reducing the use of chemical sedation when clinically appropriate.

The authors and Dr. James report no relevant financial conflicts of interest.

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

The risk for dementia goes up in patients with atrial fibrillation (AFib), but some evidence suggests that risk can be blunted with therapies that restore sinus rhythm. But a new cohort study suggests that the treatment effect’s magnitude might depend on the rhythm control strategy. It hinted that AFib catheter ablation might be more effective than pharmacologic rhythm control alone at cutting the risk for dementia.

The case-matched study of more than 38,000 adults with AFib saw a 41% reduction (P < .0001) in risk for dementia among those who underwent catheter ablation after attempted rhythm control with antiarrhythmic drugs (AAD), compared with those managed with pharmacologic rhythm control therapy alone.

The observational study comprising 20 years of data comes with big limitations and can’t say for sure whether catheter ablation is better than AAD alone at cutting the dementia risk in AFib. But it and other evidence support the idea, which has yet to be explored in a randomized fashion.

In a secondary finding, the analysis showed a similar reduction in dementia risk from catheter ablation, compared with AAD, in women and in men by 40% and 45%, respectively (P < .0001 for both). The findings are particularly relevant “given the higher life-long risk of dementia among women and the lower likelihood that women will be offered ablation, which has been demonstrated repeatedly,” Emily P. Zeitler, MD, MHS, Dartmouth-Hitchcock Medical Center, Lebanon, N.H., said in an interview. “I think this is another reason to try to be more generous in offering ablation to women.”

Management of AFib certainly evolved in important ways from 2000 to 2021, the period covered by the study. But a sensitivity analysis based on data from 2010 to 2021 showed “no meaningful differences” in the results, said Dr. Zeitler, who is slated to present the findings at the annual scientific sessions of the Heart Rhythm Society.

Dr. Zeitler acknowledged that the observational study, even with its propensity-matched ablation and AAD cohorts, can only hint at a preference for ablation over AAD for lowering risk for AFib-associated dementia. “We know there’s unmeasured and unfixable confounding between those two groups, so we see this really as hypothesis-generating.”

It was “a well-done analysis,” and the conclusion that the dementia risk was lower with catheter ablation is “absolutely correct,” but only as far as the study and its limitations allow, agreed David Conen, MD, MPH, McMaster University, Hamilton, Ont., who is not a coauthor.

“Even with propensity matching, you can get rid of some sorts of confounding, but you can never get rid of all selection bias issues.” That, he said when interviewed, takes randomized trials.

Dr. Conen, who is studying cognitive decline in AFib as a SWISS-AF trial principal investigator, pointed to a secondary finding of the analysis as evidence for such confounding. He said the ablation group’s nearly 50% drop (P < .0001) in competing risk for death, compared with patients managed with AAD, isn’t plausible.

The finding “strongly suggests these people were healthier and that there’s some sort of selection bias. They were at lower risk of death, they were at lower risk of dementia, and they were probably also at lower risk of stroke, myocardial infarction, thrombosis, and cancer because they were just probably a little healthier than the others,” Dr. Conen said. The ablation and AAD groups “were two very different populations from the get-go.”

The analysis was based on U.S. insurance and Medicare claims data from AFib patients who either underwent catheter ablation after at least one AAD trial or filled prescriptions for at least two different antiarrhythmic agents in the year after AFib diagnosis. Patients with history of dementia, catheter or surgical AFib ablation, or a valve procedure were excluded.

The ablation and AAD-only groups each consisted of 19,066 patients after propensity matching, and the groups were balanced with respect to age, sex, type of insurance, CHA2DS2-VASc scores, and use of renin-angiotensin system inhibitors, oral anticoagulants, and antiplatelets.

The overall risk for dementia was 1.9% for the ablation group and 3.3% for AAD-only patients (hazard ratio, 0.59; 95% confidence interval, 0.52-0.67). Corresponding HRs by sex were 0.55 (95% CI, 0.46-0.66) for men and 0.60 (95% CI, 0.50-0.72) for women.

The competing risk for death was also significantly decreased in the ablation group (HR, 0.51; 95% CI, 0.46-0.55).

Dr. Zeitler pointed to a randomized trial now in the early stages called Neurocognition and Greater Maintenance of Sinus Rhythm in Atrial Fibrillation, or NOGGIN-AF, which will explore relationships between rhythm control therapy and dementia in patients with AFib, whether catheter ablation or AAD can mitigate that risk, and whether either strategy works better than the other, among other goals.

“I’m optimistic,” she said, “and I think it’s going to add to the growing motivations to get patients ablated more quickly and more broadly.”

The analysis was funded by Biosense-Webster. Dr. Zeitler disclosed consulting for Biosense-Webster and Arena Pharmaceuticals (now Pfizer); fees for speaking from Medtronic; and receiving research support from Boston Scientific, Sanofi, and Biosense-Webster. Dr. Conen has previously reported receiving speaker fees from Servier Canada.

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

The risk for dementia goes up in patients with atrial fibrillation (AFib), but some evidence suggests that risk can be blunted with therapies that restore sinus rhythm. But a new cohort study suggests that the treatment effect’s magnitude might depend on the rhythm control strategy. It hinted that AFib catheter ablation might be more effective than pharmacologic rhythm control alone at cutting the risk for dementia.

The case-matched study of more than 38,000 adults with AFib saw a 41% reduction (P < .0001) in risk for dementia among those who underwent catheter ablation after attempted rhythm control with antiarrhythmic drugs (AAD), compared with those managed with pharmacologic rhythm control therapy alone.

The observational study comprising 20 years of data comes with big limitations and can’t say for sure whether catheter ablation is better than AAD alone at cutting the dementia risk in AFib. But it and other evidence support the idea, which has yet to be explored in a randomized fashion.

In a secondary finding, the analysis showed a similar reduction in dementia risk from catheter ablation, compared with AAD, in women and in men by 40% and 45%, respectively (P < .0001 for both). The findings are particularly relevant “given the higher life-long risk of dementia among women and the lower likelihood that women will be offered ablation, which has been demonstrated repeatedly,” Emily P. Zeitler, MD, MHS, Dartmouth-Hitchcock Medical Center, Lebanon, N.H., said in an interview. “I think this is another reason to try to be more generous in offering ablation to women.”

Management of AFib certainly evolved in important ways from 2000 to 2021, the period covered by the study. But a sensitivity analysis based on data from 2010 to 2021 showed “no meaningful differences” in the results, said Dr. Zeitler, who is slated to present the findings at the annual scientific sessions of the Heart Rhythm Society.

Dr. Zeitler acknowledged that the observational study, even with its propensity-matched ablation and AAD cohorts, can only hint at a preference for ablation over AAD for lowering risk for AFib-associated dementia. “We know there’s unmeasured and unfixable confounding between those two groups, so we see this really as hypothesis-generating.”

It was “a well-done analysis,” and the conclusion that the dementia risk was lower with catheter ablation is “absolutely correct,” but only as far as the study and its limitations allow, agreed David Conen, MD, MPH, McMaster University, Hamilton, Ont., who is not a coauthor.

“Even with propensity matching, you can get rid of some sorts of confounding, but you can never get rid of all selection bias issues.” That, he said when interviewed, takes randomized trials.

Dr. Conen, who is studying cognitive decline in AFib as a SWISS-AF trial principal investigator, pointed to a secondary finding of the analysis as evidence for such confounding. He said the ablation group’s nearly 50% drop (P < .0001) in competing risk for death, compared with patients managed with AAD, isn’t plausible.

The finding “strongly suggests these people were healthier and that there’s some sort of selection bias. They were at lower risk of death, they were at lower risk of dementia, and they were probably also at lower risk of stroke, myocardial infarction, thrombosis, and cancer because they were just probably a little healthier than the others,” Dr. Conen said. The ablation and AAD groups “were two very different populations from the get-go.”

The analysis was based on U.S. insurance and Medicare claims data from AFib patients who either underwent catheter ablation after at least one AAD trial or filled prescriptions for at least two different antiarrhythmic agents in the year after AFib diagnosis. Patients with history of dementia, catheter or surgical AFib ablation, or a valve procedure were excluded.

The ablation and AAD-only groups each consisted of 19,066 patients after propensity matching, and the groups were balanced with respect to age, sex, type of insurance, CHA2DS2-VASc scores, and use of renin-angiotensin system inhibitors, oral anticoagulants, and antiplatelets.

The overall risk for dementia was 1.9% for the ablation group and 3.3% for AAD-only patients (hazard ratio, 0.59; 95% confidence interval, 0.52-0.67). Corresponding HRs by sex were 0.55 (95% CI, 0.46-0.66) for men and 0.60 (95% CI, 0.50-0.72) for women.

The competing risk for death was also significantly decreased in the ablation group (HR, 0.51; 95% CI, 0.46-0.55).

Dr. Zeitler pointed to a randomized trial now in the early stages called Neurocognition and Greater Maintenance of Sinus Rhythm in Atrial Fibrillation, or NOGGIN-AF, which will explore relationships between rhythm control therapy and dementia in patients with AFib, whether catheter ablation or AAD can mitigate that risk, and whether either strategy works better than the other, among other goals.

“I’m optimistic,” she said, “and I think it’s going to add to the growing motivations to get patients ablated more quickly and more broadly.”

The analysis was funded by Biosense-Webster. Dr. Zeitler disclosed consulting for Biosense-Webster and Arena Pharmaceuticals (now Pfizer); fees for speaking from Medtronic; and receiving research support from Boston Scientific, Sanofi, and Biosense-Webster. Dr. Conen has previously reported receiving speaker fees from Servier Canada.

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

The risk for dementia goes up in patients with atrial fibrillation (AFib), but some evidence suggests that risk can be blunted with therapies that restore sinus rhythm. But a new cohort study suggests that the treatment effect’s magnitude might depend on the rhythm control strategy. It hinted that AFib catheter ablation might be more effective than pharmacologic rhythm control alone at cutting the risk for dementia.

The case-matched study of more than 38,000 adults with AFib saw a 41% reduction (P < .0001) in risk for dementia among those who underwent catheter ablation after attempted rhythm control with antiarrhythmic drugs (AAD), compared with those managed with pharmacologic rhythm control therapy alone.

The observational study comprising 20 years of data comes with big limitations and can’t say for sure whether catheter ablation is better than AAD alone at cutting the dementia risk in AFib. But it and other evidence support the idea, which has yet to be explored in a randomized fashion.

In a secondary finding, the analysis showed a similar reduction in dementia risk from catheter ablation, compared with AAD, in women and in men by 40% and 45%, respectively (P < .0001 for both). The findings are particularly relevant “given the higher life-long risk of dementia among women and the lower likelihood that women will be offered ablation, which has been demonstrated repeatedly,” Emily P. Zeitler, MD, MHS, Dartmouth-Hitchcock Medical Center, Lebanon, N.H., said in an interview. “I think this is another reason to try to be more generous in offering ablation to women.”

Management of AFib certainly evolved in important ways from 2000 to 2021, the period covered by the study. But a sensitivity analysis based on data from 2010 to 2021 showed “no meaningful differences” in the results, said Dr. Zeitler, who is slated to present the findings at the annual scientific sessions of the Heart Rhythm Society.

Dr. Zeitler acknowledged that the observational study, even with its propensity-matched ablation and AAD cohorts, can only hint at a preference for ablation over AAD for lowering risk for AFib-associated dementia. “We know there’s unmeasured and unfixable confounding between those two groups, so we see this really as hypothesis-generating.”

It was “a well-done analysis,” and the conclusion that the dementia risk was lower with catheter ablation is “absolutely correct,” but only as far as the study and its limitations allow, agreed David Conen, MD, MPH, McMaster University, Hamilton, Ont., who is not a coauthor.

“Even with propensity matching, you can get rid of some sorts of confounding, but you can never get rid of all selection bias issues.” That, he said when interviewed, takes randomized trials.

Dr. Conen, who is studying cognitive decline in AFib as a SWISS-AF trial principal investigator, pointed to a secondary finding of the analysis as evidence for such confounding. He said the ablation group’s nearly 50% drop (P < .0001) in competing risk for death, compared with patients managed with AAD, isn’t plausible.

The finding “strongly suggests these people were healthier and that there’s some sort of selection bias. They were at lower risk of death, they were at lower risk of dementia, and they were probably also at lower risk of stroke, myocardial infarction, thrombosis, and cancer because they were just probably a little healthier than the others,” Dr. Conen said. The ablation and AAD groups “were two very different populations from the get-go.”

The analysis was based on U.S. insurance and Medicare claims data from AFib patients who either underwent catheter ablation after at least one AAD trial or filled prescriptions for at least two different antiarrhythmic agents in the year after AFib diagnosis. Patients with history of dementia, catheter or surgical AFib ablation, or a valve procedure were excluded.

The ablation and AAD-only groups each consisted of 19,066 patients after propensity matching, and the groups were balanced with respect to age, sex, type of insurance, CHA2DS2-VASc scores, and use of renin-angiotensin system inhibitors, oral anticoagulants, and antiplatelets.

The overall risk for dementia was 1.9% for the ablation group and 3.3% for AAD-only patients (hazard ratio, 0.59; 95% confidence interval, 0.52-0.67). Corresponding HRs by sex were 0.55 (95% CI, 0.46-0.66) for men and 0.60 (95% CI, 0.50-0.72) for women.

The competing risk for death was also significantly decreased in the ablation group (HR, 0.51; 95% CI, 0.46-0.55).

Dr. Zeitler pointed to a randomized trial now in the early stages called Neurocognition and Greater Maintenance of Sinus Rhythm in Atrial Fibrillation, or NOGGIN-AF, which will explore relationships between rhythm control therapy and dementia in patients with AFib, whether catheter ablation or AAD can mitigate that risk, and whether either strategy works better than the other, among other goals.

“I’m optimistic,” she said, “and I think it’s going to add to the growing motivations to get patients ablated more quickly and more broadly.”

The analysis was funded by Biosense-Webster. Dr. Zeitler disclosed consulting for Biosense-Webster and Arena Pharmaceuticals (now Pfizer); fees for speaking from Medtronic; and receiving research support from Boston Scientific, Sanofi, and Biosense-Webster. Dr. Conen has previously reported receiving speaker fees from Servier Canada.

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

Mild traumatic brain injury (TBI) is linked to a significantly increased risk for a host of subsequent cardiovascular, endocrine, neurologic, and psychiatric disorders, new research shows.

Incidence of hypertension, coronary heart disease, diabetes, stroke, depression, and dementia all began to increase soon after the brain injury and persisted over a decade in both mild and moderate to severe TBI.

Researchers found the multisystem comorbidities in all age groups, including in patients as young as 18. They also found that patients who developed multiple postinjury problems had higher mortality during the decade-long follow-up.

The findings suggest patients with TBI may require longer follow-up and proactive screening for multisystem disease, regardless of age or injury severity.

“The fact that both patients with mild and moderate to severe injuries both had long-term ongoing associations with comorbidities that continued over time and that they are cardiovascular, endocrine, neurologic, and behavioral health oriented was pretty striking,” study author Ross Zafonte, DO, PhD, president of Spaulding Rehab Hospital and professor and chair of physical medicine and rehab at Harvard Medical School, both in Boston, told this news organization.

The study was published online in JAMA Network Open.
 

Injury severity not a factor

An estimated 2.8 million individuals in the United States experience TBI every year. Worldwide, the figure may be as high as 74 million.

Studies have long suggested a link between brain injury and subsequent neurologic disorders, but research suggesting a possible link to cardiovascular and endocrine problems has recently gained attention.

Building on a 2021 study that showed increased incidence of cardiovascular issues following a concussion, the researchers examined medical records of previously healthy patients treated for TBI between 2000 and 2015 who also had at least 1 follow-up visit between 6 months and 10 years after the initial injury.

Researchers analyzed data from 13,053 individuals – 4,351 with mild injury (mTBI), 4351 with moderate to severe injury (msTBI), and 4351 with no TBI. The most common cause of injury was a fall. Patients with sports-related injuries were excluded.

Incidence of hypertension was significantly higher among patients with mTBI (hazard ratio, 2.5; 95% confidence interval, 2.1-2.9) and msTBI (HR, 2.4; 95% CI, 2.0-2.9), compared with the unaffected group. Risk for other cardiovascular problems, including hyperlipidemia, obesity, and coronary artery disease, were also higher in the affected groups.

TBI patients also reported higher incidence of endocrine diseases, including diabetes (mTBI: HR, 1.9; 95% CI, 1.4-2.7; msTBI: HR, 1.9; 95% CI, 1.4-2.6). Elevated risk for ischemic stroke or transient ischemic attack was also increased (mTBI: HR, 2.2; 95% CI, 1.4-3.3; msTBI: HR, 3.6; 95% CI, 2.4-5.3).

Regardless of injury severity, patients with TBI had a higher risk for neurologic and psychiatric diseases, particularly depression, dementia, and psychotic disorders. “This tells us that mild TBI is not clean of events,” Dr. Zafonte said.

Surprising rate of comorbidity in youth

Investigators found increased risk for posttrauma comorbidities in all age groups, but researchers were struck by the high rates in younger patients, aged 18-40. Compared with age-matched individuals with no TBI history, hypertension risk was nearly six times higher in those with mTBI (HR, 5.9; 95% CI, 3.9-9.1) and nearly four times higher in patients with msTBI (HR, 3.9; 95% CI, 2.5-6.1).

Rates of hyperlipidemia and diabetes were also higher in younger patients in the mTBI group and posttraumatic seizures and psychiatric disorders were elevated regardless of TBI severity.

Overall, patients with msTBI, but not those with mTBI, were at higher risk for mortality, compared with the unexposed group (432 deaths [9.9%] vs. 250 deaths [5.7%]; P < .001).

“It’s clear that what we may be dealing with is that it holds up even for the younger people,” Dr. Zafonte said. “We used to think brain injury risk is worse in the severe cases, which it is, and it’s worse later on among those who are older, which it is. But our younger folks don’t get away either.”

While the study offers associations between TBI and multisystem health problems, Dr. Zafonte said it’s impossible to say at this point whether the brain injury caused the increased risk for cardiovascular or endocrine problems. Other organ injuries sustained in the trauma may be a contributing factor.

“Further data is needed to elucidate the mechanism and the causative relationships, which we do not have here,” he said.

Many of the postinjury comorbidities emerged a median of 3.5 years after TBI, regardless of severity. But some of the cardiovascular and psychiatric conditions emerged far sooner than that.

That’s important because research suggests less than half of patients with TBI receive follow-up care.

“It does make sense for folks who are interacting with people who’ve had a TBI to be suspicious of medical comorbidities relatively early on, within the first couple of years,” Dr. Zafonte said.

In an invited commentary, Vijay Krishnamoorthy, MD, MPH, PhD, Duke University, Durham, N.C., and Monica S. Vavilala, MD, University of Washington, Seattle, highlight some of the study’s limitations, including a lack of information on comorbidity severity and the lack of a matched group of patients who experienced non-head trauma.

Despite those limitations, the study offers important information on how TBI may affect organs beyond the brain, they noted.

“These observations, if replicated in future studies, raise intriguing implications in the future care of patients with TBI, including heightened chronic disease-screening measures and possibly enhanced guidelines for chronic extracranial organ system care for patients who experience TBI,” Dr. Krishnamoorthy and Dr. Vavilala wrote.

The study received no specific funding. Dr. Zafonte reported having received personal fees from Springer/Demos, serving on scientific advisory boards for Myomo and OnCare and has received funding from the Football Players Health Study at Harvard, funded in part by the National Football League Players Association. Dr. Krishnamoorthy and Dr. Vavilala disclosed no relevant financial relationships.

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

Mild traumatic brain injury (TBI) is linked to a significantly increased risk for a host of subsequent cardiovascular, endocrine, neurologic, and psychiatric disorders, new research shows.

Incidence of hypertension, coronary heart disease, diabetes, stroke, depression, and dementia all began to increase soon after the brain injury and persisted over a decade in both mild and moderate to severe TBI.

Researchers found the multisystem comorbidities in all age groups, including in patients as young as 18. They also found that patients who developed multiple postinjury problems had higher mortality during the decade-long follow-up.

The findings suggest patients with TBI may require longer follow-up and proactive screening for multisystem disease, regardless of age or injury severity.

“The fact that both patients with mild and moderate to severe injuries both had long-term ongoing associations with comorbidities that continued over time and that they are cardiovascular, endocrine, neurologic, and behavioral health oriented was pretty striking,” study author Ross Zafonte, DO, PhD, president of Spaulding Rehab Hospital and professor and chair of physical medicine and rehab at Harvard Medical School, both in Boston, told this news organization.

The study was published online in JAMA Network Open.
 

Injury severity not a factor

An estimated 2.8 million individuals in the United States experience TBI every year. Worldwide, the figure may be as high as 74 million.

Studies have long suggested a link between brain injury and subsequent neurologic disorders, but research suggesting a possible link to cardiovascular and endocrine problems has recently gained attention.

Building on a 2021 study that showed increased incidence of cardiovascular issues following a concussion, the researchers examined medical records of previously healthy patients treated for TBI between 2000 and 2015 who also had at least 1 follow-up visit between 6 months and 10 years after the initial injury.

Researchers analyzed data from 13,053 individuals – 4,351 with mild injury (mTBI), 4351 with moderate to severe injury (msTBI), and 4351 with no TBI. The most common cause of injury was a fall. Patients with sports-related injuries were excluded.

Incidence of hypertension was significantly higher among patients with mTBI (hazard ratio, 2.5; 95% confidence interval, 2.1-2.9) and msTBI (HR, 2.4; 95% CI, 2.0-2.9), compared with the unaffected group. Risk for other cardiovascular problems, including hyperlipidemia, obesity, and coronary artery disease, were also higher in the affected groups.

TBI patients also reported higher incidence of endocrine diseases, including diabetes (mTBI: HR, 1.9; 95% CI, 1.4-2.7; msTBI: HR, 1.9; 95% CI, 1.4-2.6). Elevated risk for ischemic stroke or transient ischemic attack was also increased (mTBI: HR, 2.2; 95% CI, 1.4-3.3; msTBI: HR, 3.6; 95% CI, 2.4-5.3).

Regardless of injury severity, patients with TBI had a higher risk for neurologic and psychiatric diseases, particularly depression, dementia, and psychotic disorders. “This tells us that mild TBI is not clean of events,” Dr. Zafonte said.

Surprising rate of comorbidity in youth

Investigators found increased risk for posttrauma comorbidities in all age groups, but researchers were struck by the high rates in younger patients, aged 18-40. Compared with age-matched individuals with no TBI history, hypertension risk was nearly six times higher in those with mTBI (HR, 5.9; 95% CI, 3.9-9.1) and nearly four times higher in patients with msTBI (HR, 3.9; 95% CI, 2.5-6.1).

Rates of hyperlipidemia and diabetes were also higher in younger patients in the mTBI group and posttraumatic seizures and psychiatric disorders were elevated regardless of TBI severity.

Overall, patients with msTBI, but not those with mTBI, were at higher risk for mortality, compared with the unexposed group (432 deaths [9.9%] vs. 250 deaths [5.7%]; P < .001).

“It’s clear that what we may be dealing with is that it holds up even for the younger people,” Dr. Zafonte said. “We used to think brain injury risk is worse in the severe cases, which it is, and it’s worse later on among those who are older, which it is. But our younger folks don’t get away either.”

While the study offers associations between TBI and multisystem health problems, Dr. Zafonte said it’s impossible to say at this point whether the brain injury caused the increased risk for cardiovascular or endocrine problems. Other organ injuries sustained in the trauma may be a contributing factor.

“Further data is needed to elucidate the mechanism and the causative relationships, which we do not have here,” he said.

Many of the postinjury comorbidities emerged a median of 3.5 years after TBI, regardless of severity. But some of the cardiovascular and psychiatric conditions emerged far sooner than that.

That’s important because research suggests less than half of patients with TBI receive follow-up care.

“It does make sense for folks who are interacting with people who’ve had a TBI to be suspicious of medical comorbidities relatively early on, within the first couple of years,” Dr. Zafonte said.

In an invited commentary, Vijay Krishnamoorthy, MD, MPH, PhD, Duke University, Durham, N.C., and Monica S. Vavilala, MD, University of Washington, Seattle, highlight some of the study’s limitations, including a lack of information on comorbidity severity and the lack of a matched group of patients who experienced non-head trauma.

Despite those limitations, the study offers important information on how TBI may affect organs beyond the brain, they noted.

“These observations, if replicated in future studies, raise intriguing implications in the future care of patients with TBI, including heightened chronic disease-screening measures and possibly enhanced guidelines for chronic extracranial organ system care for patients who experience TBI,” Dr. Krishnamoorthy and Dr. Vavilala wrote.

The study received no specific funding. Dr. Zafonte reported having received personal fees from Springer/Demos, serving on scientific advisory boards for Myomo and OnCare and has received funding from the Football Players Health Study at Harvard, funded in part by the National Football League Players Association. Dr. Krishnamoorthy and Dr. Vavilala disclosed no relevant financial relationships.

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

Mild traumatic brain injury (TBI) is linked to a significantly increased risk for a host of subsequent cardiovascular, endocrine, neurologic, and psychiatric disorders, new research shows.

Incidence of hypertension, coronary heart disease, diabetes, stroke, depression, and dementia all began to increase soon after the brain injury and persisted over a decade in both mild and moderate to severe TBI.

Researchers found the multisystem comorbidities in all age groups, including in patients as young as 18. They also found that patients who developed multiple postinjury problems had higher mortality during the decade-long follow-up.

The findings suggest patients with TBI may require longer follow-up and proactive screening for multisystem disease, regardless of age or injury severity.

“The fact that both patients with mild and moderate to severe injuries both had long-term ongoing associations with comorbidities that continued over time and that they are cardiovascular, endocrine, neurologic, and behavioral health oriented was pretty striking,” study author Ross Zafonte, DO, PhD, president of Spaulding Rehab Hospital and professor and chair of physical medicine and rehab at Harvard Medical School, both in Boston, told this news organization.

The study was published online in JAMA Network Open.
 

Injury severity not a factor

An estimated 2.8 million individuals in the United States experience TBI every year. Worldwide, the figure may be as high as 74 million.

Studies have long suggested a link between brain injury and subsequent neurologic disorders, but research suggesting a possible link to cardiovascular and endocrine problems has recently gained attention.

Building on a 2021 study that showed increased incidence of cardiovascular issues following a concussion, the researchers examined medical records of previously healthy patients treated for TBI between 2000 and 2015 who also had at least 1 follow-up visit between 6 months and 10 years after the initial injury.

Researchers analyzed data from 13,053 individuals – 4,351 with mild injury (mTBI), 4351 with moderate to severe injury (msTBI), and 4351 with no TBI. The most common cause of injury was a fall. Patients with sports-related injuries were excluded.

Incidence of hypertension was significantly higher among patients with mTBI (hazard ratio, 2.5; 95% confidence interval, 2.1-2.9) and msTBI (HR, 2.4; 95% CI, 2.0-2.9), compared with the unaffected group. Risk for other cardiovascular problems, including hyperlipidemia, obesity, and coronary artery disease, were also higher in the affected groups.

TBI patients also reported higher incidence of endocrine diseases, including diabetes (mTBI: HR, 1.9; 95% CI, 1.4-2.7; msTBI: HR, 1.9; 95% CI, 1.4-2.6). Elevated risk for ischemic stroke or transient ischemic attack was also increased (mTBI: HR, 2.2; 95% CI, 1.4-3.3; msTBI: HR, 3.6; 95% CI, 2.4-5.3).

Regardless of injury severity, patients with TBI had a higher risk for neurologic and psychiatric diseases, particularly depression, dementia, and psychotic disorders. “This tells us that mild TBI is not clean of events,” Dr. Zafonte said.

Surprising rate of comorbidity in youth

Investigators found increased risk for posttrauma comorbidities in all age groups, but researchers were struck by the high rates in younger patients, aged 18-40. Compared with age-matched individuals with no TBI history, hypertension risk was nearly six times higher in those with mTBI (HR, 5.9; 95% CI, 3.9-9.1) and nearly four times higher in patients with msTBI (HR, 3.9; 95% CI, 2.5-6.1).

Rates of hyperlipidemia and diabetes were also higher in younger patients in the mTBI group and posttraumatic seizures and psychiatric disorders were elevated regardless of TBI severity.

Overall, patients with msTBI, but not those with mTBI, were at higher risk for mortality, compared with the unexposed group (432 deaths [9.9%] vs. 250 deaths [5.7%]; P < .001).

“It’s clear that what we may be dealing with is that it holds up even for the younger people,” Dr. Zafonte said. “We used to think brain injury risk is worse in the severe cases, which it is, and it’s worse later on among those who are older, which it is. But our younger folks don’t get away either.”

While the study offers associations between TBI and multisystem health problems, Dr. Zafonte said it’s impossible to say at this point whether the brain injury caused the increased risk for cardiovascular or endocrine problems. Other organ injuries sustained in the trauma may be a contributing factor.

“Further data is needed to elucidate the mechanism and the causative relationships, which we do not have here,” he said.

Many of the postinjury comorbidities emerged a median of 3.5 years after TBI, regardless of severity. But some of the cardiovascular and psychiatric conditions emerged far sooner than that.

That’s important because research suggests less than half of patients with TBI receive follow-up care.

“It does make sense for folks who are interacting with people who’ve had a TBI to be suspicious of medical comorbidities relatively early on, within the first couple of years,” Dr. Zafonte said.

In an invited commentary, Vijay Krishnamoorthy, MD, MPH, PhD, Duke University, Durham, N.C., and Monica S. Vavilala, MD, University of Washington, Seattle, highlight some of the study’s limitations, including a lack of information on comorbidity severity and the lack of a matched group of patients who experienced non-head trauma.

Despite those limitations, the study offers important information on how TBI may affect organs beyond the brain, they noted.

“These observations, if replicated in future studies, raise intriguing implications in the future care of patients with TBI, including heightened chronic disease-screening measures and possibly enhanced guidelines for chronic extracranial organ system care for patients who experience TBI,” Dr. Krishnamoorthy and Dr. Vavilala wrote.

The study received no specific funding. Dr. Zafonte reported having received personal fees from Springer/Demos, serving on scientific advisory boards for Myomo and OnCare and has received funding from the Football Players Health Study at Harvard, funded in part by the National Football League Players Association. Dr. Krishnamoorthy and Dr. Vavilala disclosed no relevant financial relationships.

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

It has been clearly established that most human infectious diseases are caused by infectious agents that have been transmitted from animals to humans.¹ Based on published estimates from the 2000s, 60% to 76% of emerging infectious disease events are transmitted from animals to humans.²

When we consider animals that cause human diseases, we usually think of rats and bats. We rarely think of the 90 million cats owned as pets in the United States, or the approximately 30 to 80 million feral cats. Many consider cats as family members, and three-fourths of cats owned in the United States are allowed to sleep on the beds of their owners.¹ These cats may be a substantial source of human disease. Researchers at the University of Liverpool have identified 273 infectious agents carried by cats, of which 151 are known to be shared with humans.¹ The most widely known of these agents are Lyssavirus, the virus that causes rabies; Bartonella henselae, the bacteria that causes cat scratch disease; and Toxoplasma gondii (T. gondii), the parasite that causes toxoplasmosis.

In my new open-access book Parasites, Pussycats and Psychosis (available at https://link.springer.com/book/10.1007/978-3-030-86811-6), I describe the relationship between cats, T. gondii, and toxoplasmosis, and detail the evidence linking T. gondii to some cases of schizophrenia, bipolar disorder, and other diseases.¹ Though human T. gondii infection is typically asymptomatic or produces minor, flu-like symptoms, there are a few important exceptions. This article outlines those exceptions, and investigates evidence that implicates a link between T. gondii and psychosis.

How T. gondii can be transmitted

T. gondii has been called “one of the most successful parasites on earth.”³ Globally, approximately one-third of the human population is infected with T. gondii, though this varies widely by country and is dependent on dietary habits and exposure to cats. A 2014 survey reported that 11% of Americans—approximately 40 million people—have been infected, as evidenced by the presence of antibodies in their blood.¹

T. gondii begins its life cycle when a cat becomes infected, usually as a kitten. Most infected cats are asymptomatic, but for approximately 8 days they excrete up to 50 million infectious oocysts in their feces daily. Depending on the temperature, these oocysts can live for 2 years or longer.It is thought that a single oocyst can cause human infection.¹ Since cats like loose soil for defecation, the infective oocysts commonly end up in gardens, uncovered sandboxes, or animal feed piles in barns. After 24 hours, the oocysts dry out and may become aerosolized. For this reason, cat owners are advised to change their cat’s litter daily.

The number of ways T. gondii can be transmitted to humans is extensive. Farm animals can become infected from contaminated feed; this causes T. gondii oocysts in animals’ muscles, which later may cause human infection if eaten as undercooked meat. Many such family outbreaks of toxoplasmosis have been described.¹

If infective oocysts get into the water supply, they may also cause outbreaks of disease. More than 200 such outbreaks have been described, including an instance in Victoria, British Columbia, in which 100 people became clinically infected.⁴

Continue to: Family outbreaks...

Family outbreaks have also been described that involve multiple children who played in an infected sandbox or dirt pile.⁵ Similarly, an outbreak has been reported in a riding stable that was home to infected cats. Infective oocysts were thought to have become aerosolized and breathed in by the patrons.⁶ Multiple other possible modes of transmission are being investigated, including sexual transmission among humans.⁷

Human infections are not always benign

In most human T. gondii cases, the infected individual experiences mild, flu-like symptoms, often with enlarged lymph nodes, or has no symptoms.¹ Thus, most people who have been infected with T. gondii are unaware because clinicians do not routinely test for it.

There are 3 exceptions to this otherwise benign clinical picture. The first is cerebral toxoplasmosis, which occurs in individuals who are immunosuppressed because they have AIDS or are receiving treatment for cancer or organ transplantation. Cerebral toxoplasmosis can be severe and was a common cause of death in patients with AIDS before the development of effective AIDS treatments.

The second exception is congenital toxoplasmosis, when an infection occurs in a pregnant woman. Such infections can cause severe damage to the developing fetus, including abortion, stillbirth, and brain damage. Congenital toxoplasmosis infections occur in approximately 1 of every 10,000 births in the United States, or approximately 3,800 each year.⁸ As a result, pregnant women are advised not to change their cat’s litter and to be tested for evidence of T. gondii infection.

The third exception is eye disease. Toxoplasmosis is one of the most common causes of eye disease, especially of the retina. Each year in the United States, approximately 4,800 individuals develop systematic ocular toxoplasmosis.⁹

Continue to: Toxoplasmosis and psychosis

Until recently, cerebral infections, congenital infections, and eye disease were thought to be the main clinical problems associated with toxoplasmosis. However, accumulating evidence suggests that psychosis should be added to this list. Five lines of evidence support this.

1. T. gondii can cause psychotic symptoms. It has been known for decades that T. gondii can cause delusions, auditory hallucinations, and other psychotic symptoms.¹ In one of the earliest publications (1966), Ladee¹⁰ concluded “The literature not infrequently focuses attention on psychosis with schizophrenia or schizophreniform features that accompany chronic toxoplasmosis.” Among the cases Ladee¹⁰ described was a laboratory worker who became infected with T. gondii and developed delusions and hallucinations.¹⁰

2. Patients with schizophrenia who are infected with T. gondii have more severe psychotic symptoms. This finding has been reported in at least 7 studies.¹ Holub et al¹¹ evaluated 251 patients with schizophrenia who were treated in Prague Psychiatric Centre between 2000 and 2010. Overall, 57 participants were infected with T. gondii and 194 were not infected. Compared to those who were not infected, the infected group:

• had significantly more severe symptoms (P = .032) as measured on the Positive and Negative Symptom Scale
• were prescribed higher doses of antipsychotic medications
• had been hospitalized longer.¹¹

3. Compared with controls, patients with psychosis are significantly more likely to have antibodies against T. gondii, indicating previous infection. To date there have been approximately 100 such studies, of which at least three-fourths reported a positive association. In a 2012 meta-analysis of 38 such studies, Torrey et al¹² reported an odds ratio (OR) of 2.7—compared to persons who have not been infected, those who have been infected with T. gondii were 2.7 times more likely to have schizophrenia.¹² This study replicated the findings of a previous meta-analysis of 23 antibody studies, which also found an OR of 2.7.¹³

4. Compared with controls, individuals with schizophrenia or bipolar disorder are significantly more likely as a child to have lived in a home with a cat. Since 1995, 10 such studies have been published; 7 were positive, 2 were negative, and 1 was inconclusive.¹ Torrey et al¹⁴ reviewed 2,025 individuals with schizophrenia or bipolar disorder and 4,847 controls and found that 51% of the cases and 43% of the controls had owned a cat before age 13; this difference was highly significant (P < .001). In fact, it is surprising that any study can find a statistically significant association between cat ownership and childhood psychosis. This is because a child who did not own a cat could become infected in many locations where cats have been present, including sandboxes at school, a babysitter’s or friend’s house, or a public park. And even if a child became infected at home, they would not necessarily have owned a cat, since the neighbor’s cat could have been responsible for the oocyst contamination.

Continue to: Epidemiologically...

5. Epidemiologically, there is a close temporal correlation between the rise of cats as pets and the rise of psychosis. This can be illustrated most clearly in England, where the rise of cat ownership has been documented by writers and where there is data on the rise of psychosis, especially in the 18th and 19th centuries.¹

How many cases of psychosis might be caused by T. gondii?

In 2014, using data from the antibody studies discussed above,^12,13 Smith¹⁵ sought to discover how many cases of psychosis might be caused by T. gondii. He concluded that 21% of cases of schizophrenia might have been caused by T. gondii. Based on the annual incidence of schizophrenia in the United States, this would mean an estimated >10,000 new cases of schizophrenia each year are attributable to this parasite.

Some researchers have found links between T. gondii and several nonpsychiatric diseases and conditions, including epilepsy and brain cancer (Box^1,16-19).

Box

Clinical implications: What to tell patients about cats

What do these studies of toxoplasmosis imply for psychiatric care? As mental health professionals, part of our job is to educate our patients. Anything that appears to be a risk factor for the development of psychosis is thus of interest. Consider discussing the following with your patients.

Are cats safe? Cats that are kept exclusively indoors are safe pets because they are unlikely to become infected with T. gondii. However, cats that are allowed to go outdoors may not be safe, especially for children and young adults. What is needed is an effective vaccine that could be given to newborn kittens to prevent infection, but development of this type of vaccine has never been prioritized. At the community level, programs to decrease the number of stray and feral cats would also decrease the risk of infection.

Continue to: How to decrease risk

How to decrease risk. On a personal level, we can decrease T. gondii infections by not eating undercooked meat. Pregnant women and individuals who are immunocompromised should not change cat litter. When gardening, we should wear gloves because cats favor loose soil for depositing their feces. We should also protect children by covering sandboxes when not in use and by not allowing children to play in uncovered public sandboxes.

Treatment. Toxoplasmosis typically is treated with pyrimethamine, usually in combination with a sulfa drug. However, pyrimethamine does not cross the blood brain barrier and thus is ineffective when T. gondii infects the brain. The development of a drug that will effectively treat T. gondii in the brain should be a high priority.

For additional details on the studies discussed in this article as well as more resources on the impact T. gondii can have if proper precautions are not taken, see my open-access book at https://link.springer.com/book/10.1007/978-3-030-86811-6.

Bottom Line

Some evidence suggests that infection with Toxoplasma gondii (T. gondii) may cause psychotic symptoms, may increase an individual’s risk of developing psychosis, and may result in more severe psychotic symptoms. Cats can transmit T. gondii to humans. Educate patients that they can reduce their risk by keeping their cats inside, avoiding exposure to cat feces, particularly while pregnant or if immunocompromised, and not eating undercooked meat.

Related Resources

• Torrey EF. Parasites, Pussycats, and Psychosis: The Unknown Dangers of Human Toxoplasmosis. Springer Nature; 2022. https://link.springer.com/book/10.1007/978-3-030-86811-6

Drug Brand Names

Pyrimethamine • Daraprim

It has been clearly established that most human infectious diseases are caused by infectious agents that have been transmitted from animals to humans.¹ Based on published estimates from the 2000s, 60% to 76% of emerging infectious disease events are transmitted from animals to humans.²

When we consider animals that cause human diseases, we usually think of rats and bats. We rarely think of the 90 million cats owned as pets in the United States, or the approximately 30 to 80 million feral cats. Many consider cats as family members, and three-fourths of cats owned in the United States are allowed to sleep on the beds of their owners.¹ These cats may be a substantial source of human disease. Researchers at the University of Liverpool have identified 273 infectious agents carried by cats, of which 151 are known to be shared with humans.¹ The most widely known of these agents are Lyssavirus, the virus that causes rabies; Bartonella henselae, the bacteria that causes cat scratch disease; and Toxoplasma gondii (T. gondii), the parasite that causes toxoplasmosis.

In my new open-access book Parasites, Pussycats and Psychosis (available at https://link.springer.com/book/10.1007/978-3-030-86811-6), I describe the relationship between cats, T. gondii, and toxoplasmosis, and detail the evidence linking T. gondii to some cases of schizophrenia, bipolar disorder, and other diseases.¹ Though human T. gondii infection is typically asymptomatic or produces minor, flu-like symptoms, there are a few important exceptions. This article outlines those exceptions, and investigates evidence that implicates a link between T. gondii and psychosis.

How T. gondii can be transmitted

T. gondii has been called “one of the most successful parasites on earth.”³ Globally, approximately one-third of the human population is infected with T. gondii, though this varies widely by country and is dependent on dietary habits and exposure to cats. A 2014 survey reported that 11% of Americans—approximately 40 million people—have been infected, as evidenced by the presence of antibodies in their blood.¹

T. gondii begins its life cycle when a cat becomes infected, usually as a kitten. Most infected cats are asymptomatic, but for approximately 8 days they excrete up to 50 million infectious oocysts in their feces daily. Depending on the temperature, these oocysts can live for 2 years or longer.It is thought that a single oocyst can cause human infection.¹ Since cats like loose soil for defecation, the infective oocysts commonly end up in gardens, uncovered sandboxes, or animal feed piles in barns. After 24 hours, the oocysts dry out and may become aerosolized. For this reason, cat owners are advised to change their cat’s litter daily.

The number of ways T. gondii can be transmitted to humans is extensive. Farm animals can become infected from contaminated feed; this causes T. gondii oocysts in animals’ muscles, which later may cause human infection if eaten as undercooked meat. Many such family outbreaks of toxoplasmosis have been described.¹

If infective oocysts get into the water supply, they may also cause outbreaks of disease. More than 200 such outbreaks have been described, including an instance in Victoria, British Columbia, in which 100 people became clinically infected.⁴

Continue to: Family outbreaks...

Family outbreaks have also been described that involve multiple children who played in an infected sandbox or dirt pile.⁵ Similarly, an outbreak has been reported in a riding stable that was home to infected cats. Infective oocysts were thought to have become aerosolized and breathed in by the patrons.⁶ Multiple other possible modes of transmission are being investigated, including sexual transmission among humans.⁷

Human infections are not always benign

In most human T. gondii cases, the infected individual experiences mild, flu-like symptoms, often with enlarged lymph nodes, or has no symptoms.¹ Thus, most people who have been infected with T. gondii are unaware because clinicians do not routinely test for it.

There are 3 exceptions to this otherwise benign clinical picture. The first is cerebral toxoplasmosis, which occurs in individuals who are immunosuppressed because they have AIDS or are receiving treatment for cancer or organ transplantation. Cerebral toxoplasmosis can be severe and was a common cause of death in patients with AIDS before the development of effective AIDS treatments.

The second exception is congenital toxoplasmosis, when an infection occurs in a pregnant woman. Such infections can cause severe damage to the developing fetus, including abortion, stillbirth, and brain damage. Congenital toxoplasmosis infections occur in approximately 1 of every 10,000 births in the United States, or approximately 3,800 each year.⁸ As a result, pregnant women are advised not to change their cat’s litter and to be tested for evidence of T. gondii infection.

The third exception is eye disease. Toxoplasmosis is one of the most common causes of eye disease, especially of the retina. Each year in the United States, approximately 4,800 individuals develop systematic ocular toxoplasmosis.⁹

Continue to: Toxoplasmosis and psychosis

Until recently, cerebral infections, congenital infections, and eye disease were thought to be the main clinical problems associated with toxoplasmosis. However, accumulating evidence suggests that psychosis should be added to this list. Five lines of evidence support this.

1. T. gondii can cause psychotic symptoms. It has been known for decades that T. gondii can cause delusions, auditory hallucinations, and other psychotic symptoms.¹ In one of the earliest publications (1966), Ladee¹⁰ concluded “The literature not infrequently focuses attention on psychosis with schizophrenia or schizophreniform features that accompany chronic toxoplasmosis.” Among the cases Ladee¹⁰ described was a laboratory worker who became infected with T. gondii and developed delusions and hallucinations.¹⁰

2. Patients with schizophrenia who are infected with T. gondii have more severe psychotic symptoms. This finding has been reported in at least 7 studies.¹ Holub et al¹¹ evaluated 251 patients with schizophrenia who were treated in Prague Psychiatric Centre between 2000 and 2010. Overall, 57 participants were infected with T. gondii and 194 were not infected. Compared to those who were not infected, the infected group:

• had significantly more severe symptoms (P = .032) as measured on the Positive and Negative Symptom Scale
• were prescribed higher doses of antipsychotic medications
• had been hospitalized longer.¹¹

3. Compared with controls, patients with psychosis are significantly more likely to have antibodies against T. gondii, indicating previous infection. To date there have been approximately 100 such studies, of which at least three-fourths reported a positive association. In a 2012 meta-analysis of 38 such studies, Torrey et al¹² reported an odds ratio (OR) of 2.7—compared to persons who have not been infected, those who have been infected with T. gondii were 2.7 times more likely to have schizophrenia.¹² This study replicated the findings of a previous meta-analysis of 23 antibody studies, which also found an OR of 2.7.¹³

4. Compared with controls, individuals with schizophrenia or bipolar disorder are significantly more likely as a child to have lived in a home with a cat. Since 1995, 10 such studies have been published; 7 were positive, 2 were negative, and 1 was inconclusive.¹ Torrey et al¹⁴ reviewed 2,025 individuals with schizophrenia or bipolar disorder and 4,847 controls and found that 51% of the cases and 43% of the controls had owned a cat before age 13; this difference was highly significant (P < .001). In fact, it is surprising that any study can find a statistically significant association between cat ownership and childhood psychosis. This is because a child who did not own a cat could become infected in many locations where cats have been present, including sandboxes at school, a babysitter’s or friend’s house, or a public park. And even if a child became infected at home, they would not necessarily have owned a cat, since the neighbor’s cat could have been responsible for the oocyst contamination.

Continue to: Epidemiologically...

5. Epidemiologically, there is a close temporal correlation between the rise of cats as pets and the rise of psychosis. This can be illustrated most clearly in England, where the rise of cat ownership has been documented by writers and where there is data on the rise of psychosis, especially in the 18th and 19th centuries.¹

How many cases of psychosis might be caused by T. gondii?

In 2014, using data from the antibody studies discussed above,^12,13 Smith¹⁵ sought to discover how many cases of psychosis might be caused by T. gondii. He concluded that 21% of cases of schizophrenia might have been caused by T. gondii. Based on the annual incidence of schizophrenia in the United States, this would mean an estimated >10,000 new cases of schizophrenia each year are attributable to this parasite.

Some researchers have found links between T. gondii and several nonpsychiatric diseases and conditions, including epilepsy and brain cancer (Box^1,16-19).

Box

Clinical implications: What to tell patients about cats

What do these studies of toxoplasmosis imply for psychiatric care? As mental health professionals, part of our job is to educate our patients. Anything that appears to be a risk factor for the development of psychosis is thus of interest. Consider discussing the following with your patients.

Are cats safe? Cats that are kept exclusively indoors are safe pets because they are unlikely to become infected with T. gondii. However, cats that are allowed to go outdoors may not be safe, especially for children and young adults. What is needed is an effective vaccine that could be given to newborn kittens to prevent infection, but development of this type of vaccine has never been prioritized. At the community level, programs to decrease the number of stray and feral cats would also decrease the risk of infection.

Continue to: How to decrease risk

How to decrease risk. On a personal level, we can decrease T. gondii infections by not eating undercooked meat. Pregnant women and individuals who are immunocompromised should not change cat litter. When gardening, we should wear gloves because cats favor loose soil for depositing their feces. We should also protect children by covering sandboxes when not in use and by not allowing children to play in uncovered public sandboxes.

Treatment. Toxoplasmosis typically is treated with pyrimethamine, usually in combination with a sulfa drug. However, pyrimethamine does not cross the blood brain barrier and thus is ineffective when T. gondii infects the brain. The development of a drug that will effectively treat T. gondii in the brain should be a high priority.

For additional details on the studies discussed in this article as well as more resources on the impact T. gondii can have if proper precautions are not taken, see my open-access book at https://link.springer.com/book/10.1007/978-3-030-86811-6.

Bottom Line

Some evidence suggests that infection with Toxoplasma gondii (T. gondii) may cause psychotic symptoms, may increase an individual’s risk of developing psychosis, and may result in more severe psychotic symptoms. Cats can transmit T. gondii to humans. Educate patients that they can reduce their risk by keeping their cats inside, avoiding exposure to cat feces, particularly while pregnant or if immunocompromised, and not eating undercooked meat.

Related Resources

• Torrey EF. Parasites, Pussycats, and Psychosis: The Unknown Dangers of Human Toxoplasmosis. Springer Nature; 2022. https://link.springer.com/book/10.1007/978-3-030-86811-6

Drug Brand Names

Pyrimethamine • Daraprim

It has been clearly established that most human infectious diseases are caused by infectious agents that have been transmitted from animals to humans.¹ Based on published estimates from the 2000s, 60% to 76% of emerging infectious disease events are transmitted from animals to humans.²

When we consider animals that cause human diseases, we usually think of rats and bats. We rarely think of the 90 million cats owned as pets in the United States, or the approximately 30 to 80 million feral cats. Many consider cats as family members, and three-fourths of cats owned in the United States are allowed to sleep on the beds of their owners.¹ These cats may be a substantial source of human disease. Researchers at the University of Liverpool have identified 273 infectious agents carried by cats, of which 151 are known to be shared with humans.¹ The most widely known of these agents are Lyssavirus, the virus that causes rabies; Bartonella henselae, the bacteria that causes cat scratch disease; and Toxoplasma gondii (T. gondii), the parasite that causes toxoplasmosis.

In my new open-access book Parasites, Pussycats and Psychosis (available at https://link.springer.com/book/10.1007/978-3-030-86811-6), I describe the relationship between cats, T. gondii, and toxoplasmosis, and detail the evidence linking T. gondii to some cases of schizophrenia, bipolar disorder, and other diseases.¹ Though human T. gondii infection is typically asymptomatic or produces minor, flu-like symptoms, there are a few important exceptions. This article outlines those exceptions, and investigates evidence that implicates a link between T. gondii and psychosis.

How T. gondii can be transmitted

T. gondii has been called “one of the most successful parasites on earth.”³ Globally, approximately one-third of the human population is infected with T. gondii, though this varies widely by country and is dependent on dietary habits and exposure to cats. A 2014 survey reported that 11% of Americans—approximately 40 million people—have been infected, as evidenced by the presence of antibodies in their blood.¹

T. gondii begins its life cycle when a cat becomes infected, usually as a kitten. Most infected cats are asymptomatic, but for approximately 8 days they excrete up to 50 million infectious oocysts in their feces daily. Depending on the temperature, these oocysts can live for 2 years or longer.It is thought that a single oocyst can cause human infection.¹ Since cats like loose soil for defecation, the infective oocysts commonly end up in gardens, uncovered sandboxes, or animal feed piles in barns. After 24 hours, the oocysts dry out and may become aerosolized. For this reason, cat owners are advised to change their cat’s litter daily.

The number of ways T. gondii can be transmitted to humans is extensive. Farm animals can become infected from contaminated feed; this causes T. gondii oocysts in animals’ muscles, which later may cause human infection if eaten as undercooked meat. Many such family outbreaks of toxoplasmosis have been described.¹

If infective oocysts get into the water supply, they may also cause outbreaks of disease. More than 200 such outbreaks have been described, including an instance in Victoria, British Columbia, in which 100 people became clinically infected.⁴

Continue to: Family outbreaks...

Family outbreaks have also been described that involve multiple children who played in an infected sandbox or dirt pile.⁵ Similarly, an outbreak has been reported in a riding stable that was home to infected cats. Infective oocysts were thought to have become aerosolized and breathed in by the patrons.⁶ Multiple other possible modes of transmission are being investigated, including sexual transmission among humans.⁷

Human infections are not always benign

In most human T. gondii cases, the infected individual experiences mild, flu-like symptoms, often with enlarged lymph nodes, or has no symptoms.¹ Thus, most people who have been infected with T. gondii are unaware because clinicians do not routinely test for it.

There are 3 exceptions to this otherwise benign clinical picture. The first is cerebral toxoplasmosis, which occurs in individuals who are immunosuppressed because they have AIDS or are receiving treatment for cancer or organ transplantation. Cerebral toxoplasmosis can be severe and was a common cause of death in patients with AIDS before the development of effective AIDS treatments.

The second exception is congenital toxoplasmosis, when an infection occurs in a pregnant woman. Such infections can cause severe damage to the developing fetus, including abortion, stillbirth, and brain damage. Congenital toxoplasmosis infections occur in approximately 1 of every 10,000 births in the United States, or approximately 3,800 each year.⁸ As a result, pregnant women are advised not to change their cat’s litter and to be tested for evidence of T. gondii infection.

The third exception is eye disease. Toxoplasmosis is one of the most common causes of eye disease, especially of the retina. Each year in the United States, approximately 4,800 individuals develop systematic ocular toxoplasmosis.⁹

Continue to: Toxoplasmosis and psychosis

Until recently, cerebral infections, congenital infections, and eye disease were thought to be the main clinical problems associated with toxoplasmosis. However, accumulating evidence suggests that psychosis should be added to this list. Five lines of evidence support this.

1. T. gondii can cause psychotic symptoms. It has been known for decades that T. gondii can cause delusions, auditory hallucinations, and other psychotic symptoms.¹ In one of the earliest publications (1966), Ladee¹⁰ concluded “The literature not infrequently focuses attention on psychosis with schizophrenia or schizophreniform features that accompany chronic toxoplasmosis.” Among the cases Ladee¹⁰ described was a laboratory worker who became infected with T. gondii and developed delusions and hallucinations.¹⁰

2. Patients with schizophrenia who are infected with T. gondii have more severe psychotic symptoms. This finding has been reported in at least 7 studies.¹ Holub et al¹¹ evaluated 251 patients with schizophrenia who were treated in Prague Psychiatric Centre between 2000 and 2010. Overall, 57 participants were infected with T. gondii and 194 were not infected. Compared to those who were not infected, the infected group:

• had significantly more severe symptoms (P = .032) as measured on the Positive and Negative Symptom Scale
• were prescribed higher doses of antipsychotic medications
• had been hospitalized longer.¹¹

3. Compared with controls, patients with psychosis are significantly more likely to have antibodies against T. gondii, indicating previous infection. To date there have been approximately 100 such studies, of which at least three-fourths reported a positive association. In a 2012 meta-analysis of 38 such studies, Torrey et al¹² reported an odds ratio (OR) of 2.7—compared to persons who have not been infected, those who have been infected with T. gondii were 2.7 times more likely to have schizophrenia.¹² This study replicated the findings of a previous meta-analysis of 23 antibody studies, which also found an OR of 2.7.¹³

4. Compared with controls, individuals with schizophrenia or bipolar disorder are significantly more likely as a child to have lived in a home with a cat. Since 1995, 10 such studies have been published; 7 were positive, 2 were negative, and 1 was inconclusive.¹ Torrey et al¹⁴ reviewed 2,025 individuals with schizophrenia or bipolar disorder and 4,847 controls and found that 51% of the cases and 43% of the controls had owned a cat before age 13; this difference was highly significant (P < .001). In fact, it is surprising that any study can find a statistically significant association between cat ownership and childhood psychosis. This is because a child who did not own a cat could become infected in many locations where cats have been present, including sandboxes at school, a babysitter’s or friend’s house, or a public park. And even if a child became infected at home, they would not necessarily have owned a cat, since the neighbor’s cat could have been responsible for the oocyst contamination.

Continue to: Epidemiologically...

5. Epidemiologically, there is a close temporal correlation between the rise of cats as pets and the rise of psychosis. This can be illustrated most clearly in England, where the rise of cat ownership has been documented by writers and where there is data on the rise of psychosis, especially in the 18th and 19th centuries.¹

How many cases of psychosis might be caused by T. gondii?

In 2014, using data from the antibody studies discussed above,^12,13 Smith¹⁵ sought to discover how many cases of psychosis might be caused by T. gondii. He concluded that 21% of cases of schizophrenia might have been caused by T. gondii. Based on the annual incidence of schizophrenia in the United States, this would mean an estimated >10,000 new cases of schizophrenia each year are attributable to this parasite.

Some researchers have found links between T. gondii and several nonpsychiatric diseases and conditions, including epilepsy and brain cancer (Box^1,16-19).

Box

Clinical implications: What to tell patients about cats

What do these studies of toxoplasmosis imply for psychiatric care? As mental health professionals, part of our job is to educate our patients. Anything that appears to be a risk factor for the development of psychosis is thus of interest. Consider discussing the following with your patients.

Are cats safe? Cats that are kept exclusively indoors are safe pets because they are unlikely to become infected with T. gondii. However, cats that are allowed to go outdoors may not be safe, especially for children and young adults. What is needed is an effective vaccine that could be given to newborn kittens to prevent infection, but development of this type of vaccine has never been prioritized. At the community level, programs to decrease the number of stray and feral cats would also decrease the risk of infection.

Continue to: How to decrease risk

How to decrease risk. On a personal level, we can decrease T. gondii infections by not eating undercooked meat. Pregnant women and individuals who are immunocompromised should not change cat litter. When gardening, we should wear gloves because cats favor loose soil for depositing their feces. We should also protect children by covering sandboxes when not in use and by not allowing children to play in uncovered public sandboxes.

Treatment. Toxoplasmosis typically is treated with pyrimethamine, usually in combination with a sulfa drug. However, pyrimethamine does not cross the blood brain barrier and thus is ineffective when T. gondii infects the brain. The development of a drug that will effectively treat T. gondii in the brain should be a high priority.

For additional details on the studies discussed in this article as well as more resources on the impact T. gondii can have if proper precautions are not taken, see my open-access book at https://link.springer.com/book/10.1007/978-3-030-86811-6.

Bottom Line

Some evidence suggests that infection with Toxoplasma gondii (T. gondii) may cause psychotic symptoms, may increase an individual’s risk of developing psychosis, and may result in more severe psychotic symptoms. Cats can transmit T. gondii to humans. Educate patients that they can reduce their risk by keeping their cats inside, avoiding exposure to cat feces, particularly while pregnant or if immunocompromised, and not eating undercooked meat.

Related Resources

• Torrey EF. Parasites, Pussycats, and Psychosis: The Unknown Dangers of Human Toxoplasmosis. Springer Nature; 2022. https://link.springer.com/book/10.1007/978-3-030-86811-6

Drug Brand Names

Pyrimethamine • Daraprim

Medical noncompliance and patient resistance to treatment are frequent problems in medical practice. According to an older report by the US Office of Inspector General, approximately 125,000 people die each year in the United States because they do not take their medication properly.¹ The World Health Organization reported that 10% to 25% of hospital and nursing home admissions are a result of patient noncompliance.² In addition, approximately 50% of prescriptions filled for chronic diseases in developed nations are not taken correctly, and up to 40% of patients do not adhere to their treatment regimens.² Among psychiatric patients, noncompliance with medications and other treatments ranges from 25% to 75%.³

In recent years, combining pharmacotherapy with psychodynamic psychotherapy has become a fairly common form of psychiatric practice. A main reason for combining these treatments is that a patient with severe psychiatric symptoms may be unable to engage in self-reflective insightful therapy until those symptoms are substantially relieved with pharmacotherapy. The efficacy of combined pharmacotherapy/psychotherapy may also be more than additive and result in a therapeutic alliance that is greater than the sum of the 2 individual treatments.⁴ Establishing a therapeutic alliance is critical to successful treatment, but this alliance can be distorted by the needs and expectations of both the patient and the clinician.

A psychodynamic understanding of the patient and the therapeutic alliance can facilitate combined treatment in several ways. It can lead to better communication, which in turn can lead to a realistic discussion of a patient’s fears and worries about any medications they have been prescribed. A dynamically aware clinician may better understand what the symptoms mean to the patient. Such clinicians will not only be able to explain the value of a medication, its target symptoms, and the rationale for taking it, but will also be able to discuss the psychological significance of the medication, along with its medical and biological significance.⁵

This article briefly reviews the therapeutic alliance and the influence of transference (the emotional reactions of the patient towards the clinician),⁶ countertransference (the emotional reactions of the clinician towards the patient),⁶ and patient resistance/nonadherence to treatment on the failure or success of pharmacotherapy. We provide case examples to illustrate how these psychodynamic factors can be at play in prescribing.

The therapeutic alliance

The therapeutic alliance is a rational agreement or contract between a patient and the clinician; it is a cornerstone of treatment in medicine.⁶ Its basic premise is that the patient’s rational expectation that their physician is appropriately qualified, will perform a suitable evaluation, and will prescribe relevant treatment is matched by the physician’s expectation that the patient will do their best to comply with treatment recommendations. For this to succeed, the contract needs to be straightforward, and there needs to be no covert agenda. A covert agenda may be in the form of unrealistic expectations and wishes rooted in insecure experiences in childhood by either party. A patient under stress may react to the physician with mistrust, excessive demands, and noncompliance. A physician under stress may react to a patient by becoming authoritative or indecisive, or by overmedicating or underprescribing.

Transference

Transference is a phenomenon whereby a patient’s feelings and attitudes are unconsciously transferred from a person or situation in the past to the clinician or treatment in the present.⁶ For example, a patient who is scared of a serious illness may adopt a helpless, childlike role and project an omnipotent, parentlike quality on the clinician (positive transference) that may be unrealistic. Positive transference may underlie a placebo response to medication in which a patient’s response is too quick or too complete, and it may be a way of unconsciously pleasing an authoritative parent figure from childhood. On the other hand, a patient may unconsciously view their physician as a controlling parent (negative transference) and react angrily or rebelliously. A patient’s flirtatious behavior toward their physician may be a form of transference from unresolved sexual trauma during childhood. However, not all patient reactions should be considered transference; a patient may be appropriately thankful and deferential, or irritated and questioning, depending on the clinician’s demeanor and treatment approach.

Countertransference

Countertransference is the response elicited in the physician by a patient’s appearance and behaviors, or by a patient’s transference projections.⁶ This response can be positive or negative and includes both feelings and associated thoughts related to the physician’s past experiences. For example, a physician in the emergency department may get angry with a patient with an alcohol use disorder because of the physician’s negative experiences with an alcoholic parent during childhood. On the other hand, a physician raised by a compulsive mother may order unnecessary tests on a demanding older female patient. Or, a clinician raised by a sheltering parent may react to a hapless and dependent patient by spending excessive time with them or providing additional medication samples. However, not all clinician reactions are countertransference. For example, a physician’s empathic or stoic demeanor may be an appropriate emotional response to a patient’s diagnosis such as cancer.

Continue to: Patient resistance/nonadherence

In 1920, Freud conceptualized the psychodynamic factors in patient resistance to treatment and theorized that many patients were unconsciously reluctant to give up their symptoms or were driven, for transference reasons, to resist the physician.⁷ This same concept may underlie patient resistance to pharmacotherapy. When symptoms constitute an important defense mechanism, patients are likely to resist medication effects until they have developed more mature defenses or more effective ways of coping.⁸ Even when patients do not resist symptom relief, they may still resist the physician’s choice of treatment due to negative transference. Such patients often negotiate the type of medication, dose, timing of the dose, and start date as a way of trying to “keep control” of a “doctor they don’t quite trust.”⁸ They may manage their own medication regimen by taking more or less than the prescribed dose. This resistance might lead to a “nocebo” effect in which a medication trial fails not because of its ineffectiveness but instead from the unconscious mind influencing the patient’s body to resist. Nonadherence to treatment may occur in patients who have attachment difficulties that make it difficult for them to trust anyone as a result of negative childhood experiences.⁹ Clinicians need to recognize the dynamics of power struggles, control, and trust. A warm, collaborative and cooperative stance is likely to be more beneficial than an authoritative and detached approach.¹⁰

The following 3 case examples illustrate how psychodynamic factors such as transference and countertransference can influence the therapeutic alliance, treatment decisions, and the outcomes of pharmacotherapy.

CASE 1

Mr. A, age 63, has posttraumatic stress disorder originating from his father’s death by a self-inflicted gunshot wound when Mr. A was 19, and later from the symbolic loss of his mother when she remarried. He reported vivid memories of his father sexually assaulting his mother when he was 6. This fostered a protective nature in him for his mother, as well as for his 3 younger siblings. After his father’s suicide, Mr. A had to take on a paternal role for his 3 siblings. He often feels he grew up too quickly, and resents this. He feels his mother betrayed him when she got remarried. Mr. A attempts suicide, is admitted to a local hospital, and then follows up at a university hospital outpatient psychiatry clinic.

At the clinic, Mr. A begins psychodynamic psychotherapy with a female resident physician. They establish a good rapport. Mr. A begins working through his past traumas and looks forward to his therapy sessions. The physician views this as positive transference, perhaps because her personality style and appearance are similar to that of Mr. A’s mother. She also often notes a positive counter­transference during sessions; Mr. A seemingly reminds her of her father in personality and appearance. Perhaps due to this positive transference/positive countertransference dynamic, Mr. A feels comfortable with having his medication regimen simplified after years of unsuccessful medication trials and a course of electroconvulsive therapy. His regimen soon consists of only a selective serotonin reuptake inhibitor and a glutamate modulator as an adjunct for anxiety. Psychotherapy sessions remain the mainstay of his treatment plan. Mr. A’s mood and anxiety improve significantly over a short time.

CASE 2

Ms. G, age 24, is admitted to a partial hospitalization program (PHP). Her diagnoses include seasonal affective disorder, anxiety, and attention-deficit/hyperactivity disorder (ADHD); she might have a genetic disposition to bipolar disorder. Ms. G recently had attempted suicide and was discharged from an inpatient unit. She is a middle child and was raised by emotionally and verbally abusive parents in a tumultuous household. Her father rarely kept a job for more than a few months, displayed rage, and lacked empathy. Ms. G feels unloved by her mother and says that her mother is emotionally unstable. Upon admission to the PHP, Ms. G is quick to question the credentials of every staff member she meets, and suggests the abuse and lack of trust she had experienced during her formative years have made her aggressive and paranoid.

Continue to: Since her teens...

Since her teens, Ms. G had received treatment for ADHD with various stimulant and nonstimulant medications that were prescribed by an outpatient psychiatrist. During her sophomore year of college, she was also prescribed medications for depression and anxiety. Ms. G speaks very highly of and praises the skill of her previous psychiatrist while voicing concerns about having to see new clinicians in the PHP. She had recently seen a therapist who moved out of state after a few sessions. Ms. G has abandonment fears and appears to react with anger toward new clinicians.

A negative transference towards Ms. G’s treatment team and the PHP as a whole are evident during the first week. She skips most group therapy sessions and criticizes the clinicians’ skills and training as ineffective. When her psychiatrist recommends changes in medication, she initially argues. She eventually agrees to take a new medication but soon reports intolerable adverse effects, which suggests negative transference toward the psychiatrist as an authority figure, and toward the medication as an extension of the psychiatrist. The treatment team also interprets this as nocebo effect. Ms. G engages in “splitting” by complaining about her psychiatrist to her therapist. The psychiatrist resents having been belittled. Ms. G demands to see a different psychiatrist, and when her demands are not met, she discharges herself from the PHP against medical advice. The treatment team interprets Ms. G’s resistance to treatment to have resulted from poor attachment during childhood and subsequent negative transference.

CASE 3

Ms. U, age 60, is seen at a local mental health center and diagnosed with major depressive disorder, likely resulting from grief and loss from her husband’s recent death. She was raised by her single mother and mostly absent father. Ms. U is a homemaker and had been married for more than 30 years. She participates in weekly psychotherapy with a young male psychiatrist, who prescribes an antidepressant. Ms. U is eager to please and makes every effort to be the perfect patient: she is always early for her appointments, takes her medications as prescribed, and frequently expresses her respect and appreciation for her psychiatrist. Within a few weeks, Ms. U’s depressive symptoms rapidly improve.

Ms. U is a talented and avid knit and crochet expert. At an appointment soon before Christmas, she gives her psychiatrist a pair of socks she knitted. While the gift is of little monetary value, the psychiatrist interprets this as part of transference, but the intimate nature of the gift makes him uncomfortable. He and Ms. U discuss this at length, which reveals definite transference as Ms. U says the psychiatrist perhaps reminds her of her husband, who also had brown skin. It is also apparent that Ms. U’s tendency to please perhaps comes from the lack of having a father figure, which her husband had fulfilled. The psychiatrist believes that Ms. U’s rapid response may be a placebo effect from positive transference. Upon further reflection, the psychiatrist realizes that Ms. U is a motherly figure to him, and that positive countertransference is at play in that he could not turn down the gift and had looked forward to the therapy sessions with her.

Bottom Line

Even clinicians who do not provide psychodynamic psychotherapy can use an awareness of psychodynamic factors to improve treatment. Psychodynamic factors such as transference and countertransference can influence the therapeutic alliance, treatment decisions, and patient outcomes. Patients’ experiences and difficulties with attachment during childhood should be recognized and addressed as part of pharmacotherapy.

Related Resources

• Neumann M, Silva N, Opler DJ. ARISE to supportive psychotherapy. Current Psychiatry. 2021;20(5):48-49. doi:10.12788/cp.0123
• Mintz D. Psychodynamic psychopharmacology. Psychiatric Times. 2011;28(9). https://www.psychiatrictimes.com/view/psychodynamic-psychopharmacology

Medical noncompliance and patient resistance to treatment are frequent problems in medical practice. According to an older report by the US Office of Inspector General, approximately 125,000 people die each year in the United States because they do not take their medication properly.¹ The World Health Organization reported that 10% to 25% of hospital and nursing home admissions are a result of patient noncompliance.² In addition, approximately 50% of prescriptions filled for chronic diseases in developed nations are not taken correctly, and up to 40% of patients do not adhere to their treatment regimens.² Among psychiatric patients, noncompliance with medications and other treatments ranges from 25% to 75%.³

In recent years, combining pharmacotherapy with psychodynamic psychotherapy has become a fairly common form of psychiatric practice. A main reason for combining these treatments is that a patient with severe psychiatric symptoms may be unable to engage in self-reflective insightful therapy until those symptoms are substantially relieved with pharmacotherapy. The efficacy of combined pharmacotherapy/psychotherapy may also be more than additive and result in a therapeutic alliance that is greater than the sum of the 2 individual treatments.⁴ Establishing a therapeutic alliance is critical to successful treatment, but this alliance can be distorted by the needs and expectations of both the patient and the clinician.

A psychodynamic understanding of the patient and the therapeutic alliance can facilitate combined treatment in several ways. It can lead to better communication, which in turn can lead to a realistic discussion of a patient’s fears and worries about any medications they have been prescribed. A dynamically aware clinician may better understand what the symptoms mean to the patient. Such clinicians will not only be able to explain the value of a medication, its target symptoms, and the rationale for taking it, but will also be able to discuss the psychological significance of the medication, along with its medical and biological significance.⁵

This article briefly reviews the therapeutic alliance and the influence of transference (the emotional reactions of the patient towards the clinician),⁶ countertransference (the emotional reactions of the clinician towards the patient),⁶ and patient resistance/nonadherence to treatment on the failure or success of pharmacotherapy. We provide case examples to illustrate how these psychodynamic factors can be at play in prescribing.

The therapeutic alliance

The therapeutic alliance is a rational agreement or contract between a patient and the clinician; it is a cornerstone of treatment in medicine.⁶ Its basic premise is that the patient’s rational expectation that their physician is appropriately qualified, will perform a suitable evaluation, and will prescribe relevant treatment is matched by the physician’s expectation that the patient will do their best to comply with treatment recommendations. For this to succeed, the contract needs to be straightforward, and there needs to be no covert agenda. A covert agenda may be in the form of unrealistic expectations and wishes rooted in insecure experiences in childhood by either party. A patient under stress may react to the physician with mistrust, excessive demands, and noncompliance. A physician under stress may react to a patient by becoming authoritative or indecisive, or by overmedicating or underprescribing.

Transference

Transference is a phenomenon whereby a patient’s feelings and attitudes are unconsciously transferred from a person or situation in the past to the clinician or treatment in the present.⁶ For example, a patient who is scared of a serious illness may adopt a helpless, childlike role and project an omnipotent, parentlike quality on the clinician (positive transference) that may be unrealistic. Positive transference may underlie a placebo response to medication in which a patient’s response is too quick or too complete, and it may be a way of unconsciously pleasing an authoritative parent figure from childhood. On the other hand, a patient may unconsciously view their physician as a controlling parent (negative transference) and react angrily or rebelliously. A patient’s flirtatious behavior toward their physician may be a form of transference from unresolved sexual trauma during childhood. However, not all patient reactions should be considered transference; a patient may be appropriately thankful and deferential, or irritated and questioning, depending on the clinician’s demeanor and treatment approach.

Countertransference

Countertransference is the response elicited in the physician by a patient’s appearance and behaviors, or by a patient’s transference projections.⁶ This response can be positive or negative and includes both feelings and associated thoughts related to the physician’s past experiences. For example, a physician in the emergency department may get angry with a patient with an alcohol use disorder because of the physician’s negative experiences with an alcoholic parent during childhood. On the other hand, a physician raised by a compulsive mother may order unnecessary tests on a demanding older female patient. Or, a clinician raised by a sheltering parent may react to a hapless and dependent patient by spending excessive time with them or providing additional medication samples. However, not all clinician reactions are countertransference. For example, a physician’s empathic or stoic demeanor may be an appropriate emotional response to a patient’s diagnosis such as cancer.

Continue to: Patient resistance/nonadherence

In 1920, Freud conceptualized the psychodynamic factors in patient resistance to treatment and theorized that many patients were unconsciously reluctant to give up their symptoms or were driven, for transference reasons, to resist the physician.⁷ This same concept may underlie patient resistance to pharmacotherapy. When symptoms constitute an important defense mechanism, patients are likely to resist medication effects until they have developed more mature defenses or more effective ways of coping.⁸ Even when patients do not resist symptom relief, they may still resist the physician’s choice of treatment due to negative transference. Such patients often negotiate the type of medication, dose, timing of the dose, and start date as a way of trying to “keep control” of a “doctor they don’t quite trust.”⁸ They may manage their own medication regimen by taking more or less than the prescribed dose. This resistance might lead to a “nocebo” effect in which a medication trial fails not because of its ineffectiveness but instead from the unconscious mind influencing the patient’s body to resist. Nonadherence to treatment may occur in patients who have attachment difficulties that make it difficult for them to trust anyone as a result of negative childhood experiences.⁹ Clinicians need to recognize the dynamics of power struggles, control, and trust. A warm, collaborative and cooperative stance is likely to be more beneficial than an authoritative and detached approach.¹⁰

The following 3 case examples illustrate how psychodynamic factors such as transference and countertransference can influence the therapeutic alliance, treatment decisions, and the outcomes of pharmacotherapy.

CASE 1

Mr. A, age 63, has posttraumatic stress disorder originating from his father’s death by a self-inflicted gunshot wound when Mr. A was 19, and later from the symbolic loss of his mother when she remarried. He reported vivid memories of his father sexually assaulting his mother when he was 6. This fostered a protective nature in him for his mother, as well as for his 3 younger siblings. After his father’s suicide, Mr. A had to take on a paternal role for his 3 siblings. He often feels he grew up too quickly, and resents this. He feels his mother betrayed him when she got remarried. Mr. A attempts suicide, is admitted to a local hospital, and then follows up at a university hospital outpatient psychiatry clinic.

At the clinic, Mr. A begins psychodynamic psychotherapy with a female resident physician. They establish a good rapport. Mr. A begins working through his past traumas and looks forward to his therapy sessions. The physician views this as positive transference, perhaps because her personality style and appearance are similar to that of Mr. A’s mother. She also often notes a positive counter­transference during sessions; Mr. A seemingly reminds her of her father in personality and appearance. Perhaps due to this positive transference/positive countertransference dynamic, Mr. A feels comfortable with having his medication regimen simplified after years of unsuccessful medication trials and a course of electroconvulsive therapy. His regimen soon consists of only a selective serotonin reuptake inhibitor and a glutamate modulator as an adjunct for anxiety. Psychotherapy sessions remain the mainstay of his treatment plan. Mr. A’s mood and anxiety improve significantly over a short time.

CASE 2

Ms. G, age 24, is admitted to a partial hospitalization program (PHP). Her diagnoses include seasonal affective disorder, anxiety, and attention-deficit/hyperactivity disorder (ADHD); she might have a genetic disposition to bipolar disorder. Ms. G recently had attempted suicide and was discharged from an inpatient unit. She is a middle child and was raised by emotionally and verbally abusive parents in a tumultuous household. Her father rarely kept a job for more than a few months, displayed rage, and lacked empathy. Ms. G feels unloved by her mother and says that her mother is emotionally unstable. Upon admission to the PHP, Ms. G is quick to question the credentials of every staff member she meets, and suggests the abuse and lack of trust she had experienced during her formative years have made her aggressive and paranoid.

Continue to: Since her teens...

Since her teens, Ms. G had received treatment for ADHD with various stimulant and nonstimulant medications that were prescribed by an outpatient psychiatrist. During her sophomore year of college, she was also prescribed medications for depression and anxiety. Ms. G speaks very highly of and praises the skill of her previous psychiatrist while voicing concerns about having to see new clinicians in the PHP. She had recently seen a therapist who moved out of state after a few sessions. Ms. G has abandonment fears and appears to react with anger toward new clinicians.

A negative transference towards Ms. G’s treatment team and the PHP as a whole are evident during the first week. She skips most group therapy sessions and criticizes the clinicians’ skills and training as ineffective. When her psychiatrist recommends changes in medication, she initially argues. She eventually agrees to take a new medication but soon reports intolerable adverse effects, which suggests negative transference toward the psychiatrist as an authority figure, and toward the medication as an extension of the psychiatrist. The treatment team also interprets this as nocebo effect. Ms. G engages in “splitting” by complaining about her psychiatrist to her therapist. The psychiatrist resents having been belittled. Ms. G demands to see a different psychiatrist, and when her demands are not met, she discharges herself from the PHP against medical advice. The treatment team interprets Ms. G’s resistance to treatment to have resulted from poor attachment during childhood and subsequent negative transference.

CASE 3

Ms. U, age 60, is seen at a local mental health center and diagnosed with major depressive disorder, likely resulting from grief and loss from her husband’s recent death. She was raised by her single mother and mostly absent father. Ms. U is a homemaker and had been married for more than 30 years. She participates in weekly psychotherapy with a young male psychiatrist, who prescribes an antidepressant. Ms. U is eager to please and makes every effort to be the perfect patient: she is always early for her appointments, takes her medications as prescribed, and frequently expresses her respect and appreciation for her psychiatrist. Within a few weeks, Ms. U’s depressive symptoms rapidly improve.

Ms. U is a talented and avid knit and crochet expert. At an appointment soon before Christmas, she gives her psychiatrist a pair of socks she knitted. While the gift is of little monetary value, the psychiatrist interprets this as part of transference, but the intimate nature of the gift makes him uncomfortable. He and Ms. U discuss this at length, which reveals definite transference as Ms. U says the psychiatrist perhaps reminds her of her husband, who also had brown skin. It is also apparent that Ms. U’s tendency to please perhaps comes from the lack of having a father figure, which her husband had fulfilled. The psychiatrist believes that Ms. U’s rapid response may be a placebo effect from positive transference. Upon further reflection, the psychiatrist realizes that Ms. U is a motherly figure to him, and that positive countertransference is at play in that he could not turn down the gift and had looked forward to the therapy sessions with her.

Bottom Line

Even clinicians who do not provide psychodynamic psychotherapy can use an awareness of psychodynamic factors to improve treatment. Psychodynamic factors such as transference and countertransference can influence the therapeutic alliance, treatment decisions, and patient outcomes. Patients’ experiences and difficulties with attachment during childhood should be recognized and addressed as part of pharmacotherapy.

Related Resources

• Neumann M, Silva N, Opler DJ. ARISE to supportive psychotherapy. Current Psychiatry. 2021;20(5):48-49. doi:10.12788/cp.0123
• Mintz D. Psychodynamic psychopharmacology. Psychiatric Times. 2011;28(9). https://www.psychiatrictimes.com/view/psychodynamic-psychopharmacology

Medical noncompliance and patient resistance to treatment are frequent problems in medical practice. According to an older report by the US Office of Inspector General, approximately 125,000 people die each year in the United States because they do not take their medication properly.¹ The World Health Organization reported that 10% to 25% of hospital and nursing home admissions are a result of patient noncompliance.² In addition, approximately 50% of prescriptions filled for chronic diseases in developed nations are not taken correctly, and up to 40% of patients do not adhere to their treatment regimens.² Among psychiatric patients, noncompliance with medications and other treatments ranges from 25% to 75%.³

In recent years, combining pharmacotherapy with psychodynamic psychotherapy has become a fairly common form of psychiatric practice. A main reason for combining these treatments is that a patient with severe psychiatric symptoms may be unable to engage in self-reflective insightful therapy until those symptoms are substantially relieved with pharmacotherapy. The efficacy of combined pharmacotherapy/psychotherapy may also be more than additive and result in a therapeutic alliance that is greater than the sum of the 2 individual treatments.⁴ Establishing a therapeutic alliance is critical to successful treatment, but this alliance can be distorted by the needs and expectations of both the patient and the clinician.

A psychodynamic understanding of the patient and the therapeutic alliance can facilitate combined treatment in several ways. It can lead to better communication, which in turn can lead to a realistic discussion of a patient’s fears and worries about any medications they have been prescribed. A dynamically aware clinician may better understand what the symptoms mean to the patient. Such clinicians will not only be able to explain the value of a medication, its target symptoms, and the rationale for taking it, but will also be able to discuss the psychological significance of the medication, along with its medical and biological significance.⁵

This article briefly reviews the therapeutic alliance and the influence of transference (the emotional reactions of the patient towards the clinician),⁶ countertransference (the emotional reactions of the clinician towards the patient),⁶ and patient resistance/nonadherence to treatment on the failure or success of pharmacotherapy. We provide case examples to illustrate how these psychodynamic factors can be at play in prescribing.

The therapeutic alliance

The therapeutic alliance is a rational agreement or contract between a patient and the clinician; it is a cornerstone of treatment in medicine.⁶ Its basic premise is that the patient’s rational expectation that their physician is appropriately qualified, will perform a suitable evaluation, and will prescribe relevant treatment is matched by the physician’s expectation that the patient will do their best to comply with treatment recommendations. For this to succeed, the contract needs to be straightforward, and there needs to be no covert agenda. A covert agenda may be in the form of unrealistic expectations and wishes rooted in insecure experiences in childhood by either party. A patient under stress may react to the physician with mistrust, excessive demands, and noncompliance. A physician under stress may react to a patient by becoming authoritative or indecisive, or by overmedicating or underprescribing.

Transference

Transference is a phenomenon whereby a patient’s feelings and attitudes are unconsciously transferred from a person or situation in the past to the clinician or treatment in the present.⁶ For example, a patient who is scared of a serious illness may adopt a helpless, childlike role and project an omnipotent, parentlike quality on the clinician (positive transference) that may be unrealistic. Positive transference may underlie a placebo response to medication in which a patient’s response is too quick or too complete, and it may be a way of unconsciously pleasing an authoritative parent figure from childhood. On the other hand, a patient may unconsciously view their physician as a controlling parent (negative transference) and react angrily or rebelliously. A patient’s flirtatious behavior toward their physician may be a form of transference from unresolved sexual trauma during childhood. However, not all patient reactions should be considered transference; a patient may be appropriately thankful and deferential, or irritated and questioning, depending on the clinician’s demeanor and treatment approach.

Countertransference

Countertransference is the response elicited in the physician by a patient’s appearance and behaviors, or by a patient’s transference projections.⁶ This response can be positive or negative and includes both feelings and associated thoughts related to the physician’s past experiences. For example, a physician in the emergency department may get angry with a patient with an alcohol use disorder because of the physician’s negative experiences with an alcoholic parent during childhood. On the other hand, a physician raised by a compulsive mother may order unnecessary tests on a demanding older female patient. Or, a clinician raised by a sheltering parent may react to a hapless and dependent patient by spending excessive time with them or providing additional medication samples. However, not all clinician reactions are countertransference. For example, a physician’s empathic or stoic demeanor may be an appropriate emotional response to a patient’s diagnosis such as cancer.

Continue to: Patient resistance/nonadherence

In 1920, Freud conceptualized the psychodynamic factors in patient resistance to treatment and theorized that many patients were unconsciously reluctant to give up their symptoms or were driven, for transference reasons, to resist the physician.⁷ This same concept may underlie patient resistance to pharmacotherapy. When symptoms constitute an important defense mechanism, patients are likely to resist medication effects until they have developed more mature defenses or more effective ways of coping.⁸ Even when patients do not resist symptom relief, they may still resist the physician’s choice of treatment due to negative transference. Such patients often negotiate the type of medication, dose, timing of the dose, and start date as a way of trying to “keep control” of a “doctor they don’t quite trust.”⁸ They may manage their own medication regimen by taking more or less than the prescribed dose. This resistance might lead to a “nocebo” effect in which a medication trial fails not because of its ineffectiveness but instead from the unconscious mind influencing the patient’s body to resist. Nonadherence to treatment may occur in patients who have attachment difficulties that make it difficult for them to trust anyone as a result of negative childhood experiences.⁹ Clinicians need to recognize the dynamics of power struggles, control, and trust. A warm, collaborative and cooperative stance is likely to be more beneficial than an authoritative and detached approach.¹⁰

The following 3 case examples illustrate how psychodynamic factors such as transference and countertransference can influence the therapeutic alliance, treatment decisions, and the outcomes of pharmacotherapy.

CASE 1

Mr. A, age 63, has posttraumatic stress disorder originating from his father’s death by a self-inflicted gunshot wound when Mr. A was 19, and later from the symbolic loss of his mother when she remarried. He reported vivid memories of his father sexually assaulting his mother when he was 6. This fostered a protective nature in him for his mother, as well as for his 3 younger siblings. After his father’s suicide, Mr. A had to take on a paternal role for his 3 siblings. He often feels he grew up too quickly, and resents this. He feels his mother betrayed him when she got remarried. Mr. A attempts suicide, is admitted to a local hospital, and then follows up at a university hospital outpatient psychiatry clinic.

At the clinic, Mr. A begins psychodynamic psychotherapy with a female resident physician. They establish a good rapport. Mr. A begins working through his past traumas and looks forward to his therapy sessions. The physician views this as positive transference, perhaps because her personality style and appearance are similar to that of Mr. A’s mother. She also often notes a positive counter­transference during sessions; Mr. A seemingly reminds her of her father in personality and appearance. Perhaps due to this positive transference/positive countertransference dynamic, Mr. A feels comfortable with having his medication regimen simplified after years of unsuccessful medication trials and a course of electroconvulsive therapy. His regimen soon consists of only a selective serotonin reuptake inhibitor and a glutamate modulator as an adjunct for anxiety. Psychotherapy sessions remain the mainstay of his treatment plan. Mr. A’s mood and anxiety improve significantly over a short time.

CASE 2

Ms. G, age 24, is admitted to a partial hospitalization program (PHP). Her diagnoses include seasonal affective disorder, anxiety, and attention-deficit/hyperactivity disorder (ADHD); she might have a genetic disposition to bipolar disorder. Ms. G recently had attempted suicide and was discharged from an inpatient unit. She is a middle child and was raised by emotionally and verbally abusive parents in a tumultuous household. Her father rarely kept a job for more than a few months, displayed rage, and lacked empathy. Ms. G feels unloved by her mother and says that her mother is emotionally unstable. Upon admission to the PHP, Ms. G is quick to question the credentials of every staff member she meets, and suggests the abuse and lack of trust she had experienced during her formative years have made her aggressive and paranoid.

Continue to: Since her teens...

Since her teens, Ms. G had received treatment for ADHD with various stimulant and nonstimulant medications that were prescribed by an outpatient psychiatrist. During her sophomore year of college, she was also prescribed medications for depression and anxiety. Ms. G speaks very highly of and praises the skill of her previous psychiatrist while voicing concerns about having to see new clinicians in the PHP. She had recently seen a therapist who moved out of state after a few sessions. Ms. G has abandonment fears and appears to react with anger toward new clinicians.

A negative transference towards Ms. G’s treatment team and the PHP as a whole are evident during the first week. She skips most group therapy sessions and criticizes the clinicians’ skills and training as ineffective. When her psychiatrist recommends changes in medication, she initially argues. She eventually agrees to take a new medication but soon reports intolerable adverse effects, which suggests negative transference toward the psychiatrist as an authority figure, and toward the medication as an extension of the psychiatrist. The treatment team also interprets this as nocebo effect. Ms. G engages in “splitting” by complaining about her psychiatrist to her therapist. The psychiatrist resents having been belittled. Ms. G demands to see a different psychiatrist, and when her demands are not met, she discharges herself from the PHP against medical advice. The treatment team interprets Ms. G’s resistance to treatment to have resulted from poor attachment during childhood and subsequent negative transference.

CASE 3

Ms. U, age 60, is seen at a local mental health center and diagnosed with major depressive disorder, likely resulting from grief and loss from her husband’s recent death. She was raised by her single mother and mostly absent father. Ms. U is a homemaker and had been married for more than 30 years. She participates in weekly psychotherapy with a young male psychiatrist, who prescribes an antidepressant. Ms. U is eager to please and makes every effort to be the perfect patient: she is always early for her appointments, takes her medications as prescribed, and frequently expresses her respect and appreciation for her psychiatrist. Within a few weeks, Ms. U’s depressive symptoms rapidly improve.

Ms. U is a talented and avid knit and crochet expert. At an appointment soon before Christmas, she gives her psychiatrist a pair of socks she knitted. While the gift is of little monetary value, the psychiatrist interprets this as part of transference, but the intimate nature of the gift makes him uncomfortable. He and Ms. U discuss this at length, which reveals definite transference as Ms. U says the psychiatrist perhaps reminds her of her husband, who also had brown skin. It is also apparent that Ms. U’s tendency to please perhaps comes from the lack of having a father figure, which her husband had fulfilled. The psychiatrist believes that Ms. U’s rapid response may be a placebo effect from positive transference. Upon further reflection, the psychiatrist realizes that Ms. U is a motherly figure to him, and that positive countertransference is at play in that he could not turn down the gift and had looked forward to the therapy sessions with her.

Bottom Line

Even clinicians who do not provide psychodynamic psychotherapy can use an awareness of psychodynamic factors to improve treatment. Psychodynamic factors such as transference and countertransference can influence the therapeutic alliance, treatment decisions, and patient outcomes. Patients’ experiences and difficulties with attachment during childhood should be recognized and addressed as part of pharmacotherapy.

Related Resources

• Neumann M, Silva N, Opler DJ. ARISE to supportive psychotherapy. Current Psychiatry. 2021;20(5):48-49. doi:10.12788/cp.0123
• Mintz D. Psychodynamic psychopharmacology. Psychiatric Times. 2011;28(9). https://www.psychiatrictimes.com/view/psychodynamic-psychopharmacology