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Early metformin minimizes antipsychotic-induced weight gain
MAR DEL PLATA, ARGENTINA – , according to a new evidence-based Irish guideline for the management of this common complication in adults with psychoses who are taking medications.
The document was discussed during one of the sessions of the XXXV Argentine Congress of Psychiatry of the Association of Argentine Psychiatrists. The document also was presented by one of its authors at the European Congress on Obesity 2022.
The guideline encourages psychiatrists not to underestimate the adverse metabolic effects of their treatments and encourages them to contemplate and carry out this prevention and management strategy, commented María Delia Michat, PhD, professor of clinical psychiatry and psychopharmacology at the APSA Postgraduate Training Institute, Buenos Aires.
“Although it is always good to work as a team, it is usually we psychiatrists who coordinate the pharmacological treatment of our patients, and we have to know how to manage drugs that can prevent cardiovascular disease,” Dr. Michat said in an interview.
“The new guideline is helpful because it protocolizes the use of metformin, which is the cheapest drug and has the most evidence for antipsychotic-induced weight gain,” she added.
Avoiding metabolic syndrome
In patients with schizophrenia, obesity rates are 40% higher than in the general population, and 80% of patients develop weight gain after their first treatment, noted Dr. Michat. “Right away, weight gain is seen in the first month. And it is a serious problem, because patients with schizophrenia, major depression, or bipolar disorder already have an increased risk of premature mortality, especially from cardiovascular diseases, and they have an increased risk of metabolic syndrome. And we sometimes give drugs that further increase that risk,” she said.
Being overweight is a major criterion for defining metabolic syndrome. Dr. Michat noted that, among the antipsychotic drugs that increase weight the most are clozapine, olanzapine, chlorpromazine, quetiapine, and risperidone, in addition to other psychoactive drugs, such as valproic acid, lithium, mirtazapine, and tricyclic antidepressants.
Several clinical trials, such as a pioneering Chinese study from 2008, have shown the potential of metformin to mitigate the weight gain induced by this type of drug.
However, Dr. Michat noted that so far the major guidelines (for example, the Canadian Network for Mood and Anxiety Treatments [CANMAT]/International Society for Bipolar Disorders [ISBD] for bipolar disorder and the American Psychiatric Association [APA] for schizophrenia) “say very little” on how to address this complication. They propose what she defined as a “problematic” order of action in which the initial emphasis is on promoting lifestyle changes, which are difficult for these patients to carry out, as well as general proposals for changing medication (which is not simple to implement when the patient’s condition is stabilized) and eventual consultation with a clinician to start therapy with metformin or other drugs, such as liraglutide, semaglutide, and topiramate.
The new clinical practice guideline, which was published in Evidence-Based Mental Health (of the BMJ journal group), was written by a multidisciplinary team of pharmacists, psychiatrists, and mental health nurses from Ireland. It aims to fill that gap. The investigators reviewed 1,270 scientific articles and analyzed 26 of them in depth, including seven randomized clinical trials and a 2016 systematic review and meta-analysis. The authors made a “strong” recommendation, for which there was moderate-quality evidence, that for patients for whom a lifestyle intervention is unacceptable or inappropriate the use of metformin is an “alternative first-line intervention” for antipsychotic drug–induced weight gain.
Likewise, as a strong recommendation with moderate-quality evidence, the guidance encourages the use of metformin when nonpharmacologic intervention does not seem to be effective.
The guideline also says it is preferable to start metformin early for patients who gain more than 7% of their baseline weight within the first month of antipsychotic treatment. It also endorses metformin when weight gain is established.
Other recommendations include evaluating baseline kidney function before starting metformin treatment and suggest a dose adjustment when the estimated glomerular filtration rate (eGFR) is < 60 mL/min/1.73 m2. The guidance says the use of metformin is contraindicated for patients in whom eGFR is <30 mL/min per 1.73 m2. The proposed starting dosage is 500 mg twice per day with meals, with increments of 500 mg every 1-2 weeks until reaching a target dose of 2,000 mg/day. The guidance recommends that consideration always be given to individual tolerability and efficacy.
Treatment goals should be personalized and agreed upon with patients. In the case of early intervention, the guideline proposes initially stabilizing the weight gained or, if possible, reverse excess weight. When weight gain is established, the goal would be to lose at least 5% of the weight within the next 6 months.
The authors also recommend monitoring kidney function annually, as well as vitamin B12 levels and individual tolerability and compliance. Gastrointestinal adverse effects can be managed by dose reduction or slower dose titration. The risk of lactic acidosis, which affects 4.3 per 100,000 person-years among those taking metformin, can be attenuated by adjusting the dose according to kidney function or avoiding prescribing it to patients who have a history of alcohol abuse or who are receiving treatment that may interact with the drug.
Validating pharmacologic management
The lead author of the new guideline, Ita Fitzgerald, a teacher in clinical pharmacy and senior pharmacist at St. Patrick’s Mental Health Services in Dublin, pointed out that there is a bias toward not using drugs for weight management and shifting the responsibility onto the patients themselves, something that is very often out of their control.
“The purpose of the guideline was to decide on a range of criteria to maximize the use of metformin, to recognize that for many people, pharmacological management is a valid and important option that could and should be more widely used and to provide precise and practical guidance to physicians to facilitate a more widespread use,” Ms. Fitzgerald said in an interview.
According to Fitzgerald, who is pursuing her doctorate at University College Cork (Ireland), one of the most outstanding results of the work is that it highlights that the main benefit of metformin is to flatten rather than reverse antipsychotic-induced weight gain and that indicating it late can nullify that effect.
“In all the recommendations, we try very hard to shift the focus from metformin’s role as a weight reversal agent to one as a weight management agent that should be used early in treatment, which is when most weight gain occurs. If metformin succeeds in flattening that increase, that’s a huge potential benefit for an inexpensive and easily accessible drug. When people have already established weight gain, metformin may not be enough and alternative treatments should be used,” she said.
In addition to its effects on weight, metformin has many other potential health benefits. Of particular importance is that it reduces hyperphagia-mediated antipsychotic-induced weight gain, Ms. Fitzgerald pointed out.
“This is subjectively very important for patients and provides a more positive experience when taking antipsychotics. Antipsychotic-induced weight gain is one of the main reasons for premature discontinuation or incomplete adherence to these drugs and therefore needs to be addressed proactively,” she concluded.
Ms. Fitzgerald and Dr. Michat have disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com. This article was translated from the Medscape Spanish edition.
MAR DEL PLATA, ARGENTINA – , according to a new evidence-based Irish guideline for the management of this common complication in adults with psychoses who are taking medications.
The document was discussed during one of the sessions of the XXXV Argentine Congress of Psychiatry of the Association of Argentine Psychiatrists. The document also was presented by one of its authors at the European Congress on Obesity 2022.
The guideline encourages psychiatrists not to underestimate the adverse metabolic effects of their treatments and encourages them to contemplate and carry out this prevention and management strategy, commented María Delia Michat, PhD, professor of clinical psychiatry and psychopharmacology at the APSA Postgraduate Training Institute, Buenos Aires.
“Although it is always good to work as a team, it is usually we psychiatrists who coordinate the pharmacological treatment of our patients, and we have to know how to manage drugs that can prevent cardiovascular disease,” Dr. Michat said in an interview.
“The new guideline is helpful because it protocolizes the use of metformin, which is the cheapest drug and has the most evidence for antipsychotic-induced weight gain,” she added.
Avoiding metabolic syndrome
In patients with schizophrenia, obesity rates are 40% higher than in the general population, and 80% of patients develop weight gain after their first treatment, noted Dr. Michat. “Right away, weight gain is seen in the first month. And it is a serious problem, because patients with schizophrenia, major depression, or bipolar disorder already have an increased risk of premature mortality, especially from cardiovascular diseases, and they have an increased risk of metabolic syndrome. And we sometimes give drugs that further increase that risk,” she said.
Being overweight is a major criterion for defining metabolic syndrome. Dr. Michat noted that, among the antipsychotic drugs that increase weight the most are clozapine, olanzapine, chlorpromazine, quetiapine, and risperidone, in addition to other psychoactive drugs, such as valproic acid, lithium, mirtazapine, and tricyclic antidepressants.
Several clinical trials, such as a pioneering Chinese study from 2008, have shown the potential of metformin to mitigate the weight gain induced by this type of drug.
However, Dr. Michat noted that so far the major guidelines (for example, the Canadian Network for Mood and Anxiety Treatments [CANMAT]/International Society for Bipolar Disorders [ISBD] for bipolar disorder and the American Psychiatric Association [APA] for schizophrenia) “say very little” on how to address this complication. They propose what she defined as a “problematic” order of action in which the initial emphasis is on promoting lifestyle changes, which are difficult for these patients to carry out, as well as general proposals for changing medication (which is not simple to implement when the patient’s condition is stabilized) and eventual consultation with a clinician to start therapy with metformin or other drugs, such as liraglutide, semaglutide, and topiramate.
The new clinical practice guideline, which was published in Evidence-Based Mental Health (of the BMJ journal group), was written by a multidisciplinary team of pharmacists, psychiatrists, and mental health nurses from Ireland. It aims to fill that gap. The investigators reviewed 1,270 scientific articles and analyzed 26 of them in depth, including seven randomized clinical trials and a 2016 systematic review and meta-analysis. The authors made a “strong” recommendation, for which there was moderate-quality evidence, that for patients for whom a lifestyle intervention is unacceptable or inappropriate the use of metformin is an “alternative first-line intervention” for antipsychotic drug–induced weight gain.
Likewise, as a strong recommendation with moderate-quality evidence, the guidance encourages the use of metformin when nonpharmacologic intervention does not seem to be effective.
The guideline also says it is preferable to start metformin early for patients who gain more than 7% of their baseline weight within the first month of antipsychotic treatment. It also endorses metformin when weight gain is established.
Other recommendations include evaluating baseline kidney function before starting metformin treatment and suggest a dose adjustment when the estimated glomerular filtration rate (eGFR) is < 60 mL/min/1.73 m2. The guidance says the use of metformin is contraindicated for patients in whom eGFR is <30 mL/min per 1.73 m2. The proposed starting dosage is 500 mg twice per day with meals, with increments of 500 mg every 1-2 weeks until reaching a target dose of 2,000 mg/day. The guidance recommends that consideration always be given to individual tolerability and efficacy.
Treatment goals should be personalized and agreed upon with patients. In the case of early intervention, the guideline proposes initially stabilizing the weight gained or, if possible, reverse excess weight. When weight gain is established, the goal would be to lose at least 5% of the weight within the next 6 months.
The authors also recommend monitoring kidney function annually, as well as vitamin B12 levels and individual tolerability and compliance. Gastrointestinal adverse effects can be managed by dose reduction or slower dose titration. The risk of lactic acidosis, which affects 4.3 per 100,000 person-years among those taking metformin, can be attenuated by adjusting the dose according to kidney function or avoiding prescribing it to patients who have a history of alcohol abuse or who are receiving treatment that may interact with the drug.
Validating pharmacologic management
The lead author of the new guideline, Ita Fitzgerald, a teacher in clinical pharmacy and senior pharmacist at St. Patrick’s Mental Health Services in Dublin, pointed out that there is a bias toward not using drugs for weight management and shifting the responsibility onto the patients themselves, something that is very often out of their control.
“The purpose of the guideline was to decide on a range of criteria to maximize the use of metformin, to recognize that for many people, pharmacological management is a valid and important option that could and should be more widely used and to provide precise and practical guidance to physicians to facilitate a more widespread use,” Ms. Fitzgerald said in an interview.
According to Fitzgerald, who is pursuing her doctorate at University College Cork (Ireland), one of the most outstanding results of the work is that it highlights that the main benefit of metformin is to flatten rather than reverse antipsychotic-induced weight gain and that indicating it late can nullify that effect.
“In all the recommendations, we try very hard to shift the focus from metformin’s role as a weight reversal agent to one as a weight management agent that should be used early in treatment, which is when most weight gain occurs. If metformin succeeds in flattening that increase, that’s a huge potential benefit for an inexpensive and easily accessible drug. When people have already established weight gain, metformin may not be enough and alternative treatments should be used,” she said.
In addition to its effects on weight, metformin has many other potential health benefits. Of particular importance is that it reduces hyperphagia-mediated antipsychotic-induced weight gain, Ms. Fitzgerald pointed out.
“This is subjectively very important for patients and provides a more positive experience when taking antipsychotics. Antipsychotic-induced weight gain is one of the main reasons for premature discontinuation or incomplete adherence to these drugs and therefore needs to be addressed proactively,” she concluded.
Ms. Fitzgerald and Dr. Michat have disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com. This article was translated from the Medscape Spanish edition.
MAR DEL PLATA, ARGENTINA – , according to a new evidence-based Irish guideline for the management of this common complication in adults with psychoses who are taking medications.
The document was discussed during one of the sessions of the XXXV Argentine Congress of Psychiatry of the Association of Argentine Psychiatrists. The document also was presented by one of its authors at the European Congress on Obesity 2022.
The guideline encourages psychiatrists not to underestimate the adverse metabolic effects of their treatments and encourages them to contemplate and carry out this prevention and management strategy, commented María Delia Michat, PhD, professor of clinical psychiatry and psychopharmacology at the APSA Postgraduate Training Institute, Buenos Aires.
“Although it is always good to work as a team, it is usually we psychiatrists who coordinate the pharmacological treatment of our patients, and we have to know how to manage drugs that can prevent cardiovascular disease,” Dr. Michat said in an interview.
“The new guideline is helpful because it protocolizes the use of metformin, which is the cheapest drug and has the most evidence for antipsychotic-induced weight gain,” she added.
Avoiding metabolic syndrome
In patients with schizophrenia, obesity rates are 40% higher than in the general population, and 80% of patients develop weight gain after their first treatment, noted Dr. Michat. “Right away, weight gain is seen in the first month. And it is a serious problem, because patients with schizophrenia, major depression, or bipolar disorder already have an increased risk of premature mortality, especially from cardiovascular diseases, and they have an increased risk of metabolic syndrome. And we sometimes give drugs that further increase that risk,” she said.
Being overweight is a major criterion for defining metabolic syndrome. Dr. Michat noted that, among the antipsychotic drugs that increase weight the most are clozapine, olanzapine, chlorpromazine, quetiapine, and risperidone, in addition to other psychoactive drugs, such as valproic acid, lithium, mirtazapine, and tricyclic antidepressants.
Several clinical trials, such as a pioneering Chinese study from 2008, have shown the potential of metformin to mitigate the weight gain induced by this type of drug.
However, Dr. Michat noted that so far the major guidelines (for example, the Canadian Network for Mood and Anxiety Treatments [CANMAT]/International Society for Bipolar Disorders [ISBD] for bipolar disorder and the American Psychiatric Association [APA] for schizophrenia) “say very little” on how to address this complication. They propose what she defined as a “problematic” order of action in which the initial emphasis is on promoting lifestyle changes, which are difficult for these patients to carry out, as well as general proposals for changing medication (which is not simple to implement when the patient’s condition is stabilized) and eventual consultation with a clinician to start therapy with metformin or other drugs, such as liraglutide, semaglutide, and topiramate.
The new clinical practice guideline, which was published in Evidence-Based Mental Health (of the BMJ journal group), was written by a multidisciplinary team of pharmacists, psychiatrists, and mental health nurses from Ireland. It aims to fill that gap. The investigators reviewed 1,270 scientific articles and analyzed 26 of them in depth, including seven randomized clinical trials and a 2016 systematic review and meta-analysis. The authors made a “strong” recommendation, for which there was moderate-quality evidence, that for patients for whom a lifestyle intervention is unacceptable or inappropriate the use of metformin is an “alternative first-line intervention” for antipsychotic drug–induced weight gain.
Likewise, as a strong recommendation with moderate-quality evidence, the guidance encourages the use of metformin when nonpharmacologic intervention does not seem to be effective.
The guideline also says it is preferable to start metformin early for patients who gain more than 7% of their baseline weight within the first month of antipsychotic treatment. It also endorses metformin when weight gain is established.
Other recommendations include evaluating baseline kidney function before starting metformin treatment and suggest a dose adjustment when the estimated glomerular filtration rate (eGFR) is < 60 mL/min/1.73 m2. The guidance says the use of metformin is contraindicated for patients in whom eGFR is <30 mL/min per 1.73 m2. The proposed starting dosage is 500 mg twice per day with meals, with increments of 500 mg every 1-2 weeks until reaching a target dose of 2,000 mg/day. The guidance recommends that consideration always be given to individual tolerability and efficacy.
Treatment goals should be personalized and agreed upon with patients. In the case of early intervention, the guideline proposes initially stabilizing the weight gained or, if possible, reverse excess weight. When weight gain is established, the goal would be to lose at least 5% of the weight within the next 6 months.
The authors also recommend monitoring kidney function annually, as well as vitamin B12 levels and individual tolerability and compliance. Gastrointestinal adverse effects can be managed by dose reduction or slower dose titration. The risk of lactic acidosis, which affects 4.3 per 100,000 person-years among those taking metformin, can be attenuated by adjusting the dose according to kidney function or avoiding prescribing it to patients who have a history of alcohol abuse or who are receiving treatment that may interact with the drug.
Validating pharmacologic management
The lead author of the new guideline, Ita Fitzgerald, a teacher in clinical pharmacy and senior pharmacist at St. Patrick’s Mental Health Services in Dublin, pointed out that there is a bias toward not using drugs for weight management and shifting the responsibility onto the patients themselves, something that is very often out of their control.
“The purpose of the guideline was to decide on a range of criteria to maximize the use of metformin, to recognize that for many people, pharmacological management is a valid and important option that could and should be more widely used and to provide precise and practical guidance to physicians to facilitate a more widespread use,” Ms. Fitzgerald said in an interview.
According to Fitzgerald, who is pursuing her doctorate at University College Cork (Ireland), one of the most outstanding results of the work is that it highlights that the main benefit of metformin is to flatten rather than reverse antipsychotic-induced weight gain and that indicating it late can nullify that effect.
“In all the recommendations, we try very hard to shift the focus from metformin’s role as a weight reversal agent to one as a weight management agent that should be used early in treatment, which is when most weight gain occurs. If metformin succeeds in flattening that increase, that’s a huge potential benefit for an inexpensive and easily accessible drug. When people have already established weight gain, metformin may not be enough and alternative treatments should be used,” she said.
In addition to its effects on weight, metformin has many other potential health benefits. Of particular importance is that it reduces hyperphagia-mediated antipsychotic-induced weight gain, Ms. Fitzgerald pointed out.
“This is subjectively very important for patients and provides a more positive experience when taking antipsychotics. Antipsychotic-induced weight gain is one of the main reasons for premature discontinuation or incomplete adherence to these drugs and therefore needs to be addressed proactively,” she concluded.
Ms. Fitzgerald and Dr. Michat have disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com. This article was translated from the Medscape Spanish edition.
Refugees have a high burden of chronic pain associated with mental illness
The study covered in this summary was published in researchsquare.com and has not yet been peer reviewed.
Key takeaways
- Anxiety, , and PTSD are associated with higher levels of chronic pain in the refugee population studied.
- Being a male refugee is associated more strongly with anxiety and depression leading to functional impairment than being a woman. Being a woman is associated with higher odds of chronic pain. Gender acted as an effect modifier between mental illness and functional impairment.
- Future research aimed toward harmonizing and standardizing pain measurement to measure its effect on health burden is needed. Pain should be understood under an ethnocultural construct to enhance transcultural validity.
Why this matters
- The present cross-sectional survey of adult refugees from Syria resettled in Norway is only one of a few studies investigating the burden of chronic pain and how it relates to mental ill health in a general refugee population. Elevated rates of PTSD, depression, and anxiety have been repeatedly found in refugee populations, and high levels of pain have also been documented.
- Attention to the association between chronic pain and mental health should be made by personnel working with refugees. Because of the gender-specific associations between mental illness and functional impairment, initiatives addressing mental health, chronic pain, or functional impairment in refugee populations should consider gender when tailoring their content and outreach.
Study design
- The study involved a cross-sectional, postal survey questionnaire of participants randomly drawn from full population registries in Norway. There was an initial low response. Invitations were sent out in November 2018 and did not close until September 2019. Several efforts were made to boost participation, including one postal or telephone reminder to all nonresponders.
- Participants were refugee adults from Syria aged 18 and older who arrived in Norway between 2015 and 2017. Gender was tested as an effect modifier.
- Chronic pain was measured with 10 items on the questionnaire and was defined as pain for 3 or more consecutive months in the last year. It included both musculoskeletal pain and pain in five other body regions (stomach, head, genital area, chest, other).
- Anxiety, depression, and PTSD symptoms were measured with the 25-item Hopkins Symptom Checklist, the Harvard Trauma Questionnaire, and the Refugee Trauma History Checklist.
- Questionnaires on perceived general health regarding refugee perceptions of their own health, and functional impairment affecting daily activities because of illness, disability, and mental health were adapted from the European Social Survey 2010.
Key results
- A total of 902 participants who responded to the questionnaire were included in the study from roughly 10,000 invitations, giving a participation rate of about 10%, with no differences in gender distribution.
- The overall prevalence of severe chronic pain was 43.1%, and overall perception of poor general health was 39.9%.
- There was a strong association of chronic pain with all mental illness measured, poor perceived general health, and functional impairment (P < .001). All mental health variables were associated with increased odds of chronic pain (anxiety odds ratio), 2.42; depression, OR, 2.28; PTSD, OR, 1.97; all OR fully adjusted).
- Chronic pain was associated with poor perceived general health and functional impairment with no difference across gender. Mental health showed weaker association with poor perceived general health than chronic pain.
- Syrian men with mental health had three times higher odds of functional impairment. For women, there was no evidence of association between any of the mental ill health variables and functional impairment. Being a woman was associated with chronic pain and poor perceived general health but not functional impairment.
- Being a woman was associated with 50% higher odds of chronic pain in both unadjusted and adjusted models.
Limitations
- With a 10% response rate, selection bias in this cross-sectional study may have been present.
- The cross-sectional design of the study limits causality.
- The validity of the survey is questionable because of transcultural construct regarding pain and mental illness.
- Regression models were built with data at hand. Without preregistered plans for data handling, the findings should be viewed as exploratory with a risk for false-positive findings.
Disclosures
- No external funding was received. The study was funded by the Norwegian Center for Violence and Traumatic Stress Studies.
- None of the authors disclosed relevant financial relationships.
This is a summary of a preprint research study, “Chronic pain, mental health and functional impairment in adult refugees from Syria resettled in Norway: a cross-sectional study,” written by researchers at the Norwegian Centre for Violence and Traumatic Stress Studies in Oslo, the Norwegian Institute of Public Health in Oslo, and the Weill Cornell Medicine in New York City on Research Square. This study has not yet been peer reviewed. The full text of the study can be found on researchsquare.com. A version of this article first appeared on Medscape.com.
The study covered in this summary was published in researchsquare.com and has not yet been peer reviewed.
Key takeaways
- Anxiety, , and PTSD are associated with higher levels of chronic pain in the refugee population studied.
- Being a male refugee is associated more strongly with anxiety and depression leading to functional impairment than being a woman. Being a woman is associated with higher odds of chronic pain. Gender acted as an effect modifier between mental illness and functional impairment.
- Future research aimed toward harmonizing and standardizing pain measurement to measure its effect on health burden is needed. Pain should be understood under an ethnocultural construct to enhance transcultural validity.
Why this matters
- The present cross-sectional survey of adult refugees from Syria resettled in Norway is only one of a few studies investigating the burden of chronic pain and how it relates to mental ill health in a general refugee population. Elevated rates of PTSD, depression, and anxiety have been repeatedly found in refugee populations, and high levels of pain have also been documented.
- Attention to the association between chronic pain and mental health should be made by personnel working with refugees. Because of the gender-specific associations between mental illness and functional impairment, initiatives addressing mental health, chronic pain, or functional impairment in refugee populations should consider gender when tailoring their content and outreach.
Study design
- The study involved a cross-sectional, postal survey questionnaire of participants randomly drawn from full population registries in Norway. There was an initial low response. Invitations were sent out in November 2018 and did not close until September 2019. Several efforts were made to boost participation, including one postal or telephone reminder to all nonresponders.
- Participants were refugee adults from Syria aged 18 and older who arrived in Norway between 2015 and 2017. Gender was tested as an effect modifier.
- Chronic pain was measured with 10 items on the questionnaire and was defined as pain for 3 or more consecutive months in the last year. It included both musculoskeletal pain and pain in five other body regions (stomach, head, genital area, chest, other).
- Anxiety, depression, and PTSD symptoms were measured with the 25-item Hopkins Symptom Checklist, the Harvard Trauma Questionnaire, and the Refugee Trauma History Checklist.
- Questionnaires on perceived general health regarding refugee perceptions of their own health, and functional impairment affecting daily activities because of illness, disability, and mental health were adapted from the European Social Survey 2010.
Key results
- A total of 902 participants who responded to the questionnaire were included in the study from roughly 10,000 invitations, giving a participation rate of about 10%, with no differences in gender distribution.
- The overall prevalence of severe chronic pain was 43.1%, and overall perception of poor general health was 39.9%.
- There was a strong association of chronic pain with all mental illness measured, poor perceived general health, and functional impairment (P < .001). All mental health variables were associated with increased odds of chronic pain (anxiety odds ratio), 2.42; depression, OR, 2.28; PTSD, OR, 1.97; all OR fully adjusted).
- Chronic pain was associated with poor perceived general health and functional impairment with no difference across gender. Mental health showed weaker association with poor perceived general health than chronic pain.
- Syrian men with mental health had three times higher odds of functional impairment. For women, there was no evidence of association between any of the mental ill health variables and functional impairment. Being a woman was associated with chronic pain and poor perceived general health but not functional impairment.
- Being a woman was associated with 50% higher odds of chronic pain in both unadjusted and adjusted models.
Limitations
- With a 10% response rate, selection bias in this cross-sectional study may have been present.
- The cross-sectional design of the study limits causality.
- The validity of the survey is questionable because of transcultural construct regarding pain and mental illness.
- Regression models were built with data at hand. Without preregistered plans for data handling, the findings should be viewed as exploratory with a risk for false-positive findings.
Disclosures
- No external funding was received. The study was funded by the Norwegian Center for Violence and Traumatic Stress Studies.
- None of the authors disclosed relevant financial relationships.
This is a summary of a preprint research study, “Chronic pain, mental health and functional impairment in adult refugees from Syria resettled in Norway: a cross-sectional study,” written by researchers at the Norwegian Centre for Violence and Traumatic Stress Studies in Oslo, the Norwegian Institute of Public Health in Oslo, and the Weill Cornell Medicine in New York City on Research Square. This study has not yet been peer reviewed. The full text of the study can be found on researchsquare.com. A version of this article first appeared on Medscape.com.
The study covered in this summary was published in researchsquare.com and has not yet been peer reviewed.
Key takeaways
- Anxiety, , and PTSD are associated with higher levels of chronic pain in the refugee population studied.
- Being a male refugee is associated more strongly with anxiety and depression leading to functional impairment than being a woman. Being a woman is associated with higher odds of chronic pain. Gender acted as an effect modifier between mental illness and functional impairment.
- Future research aimed toward harmonizing and standardizing pain measurement to measure its effect on health burden is needed. Pain should be understood under an ethnocultural construct to enhance transcultural validity.
Why this matters
- The present cross-sectional survey of adult refugees from Syria resettled in Norway is only one of a few studies investigating the burden of chronic pain and how it relates to mental ill health in a general refugee population. Elevated rates of PTSD, depression, and anxiety have been repeatedly found in refugee populations, and high levels of pain have also been documented.
- Attention to the association between chronic pain and mental health should be made by personnel working with refugees. Because of the gender-specific associations between mental illness and functional impairment, initiatives addressing mental health, chronic pain, or functional impairment in refugee populations should consider gender when tailoring their content and outreach.
Study design
- The study involved a cross-sectional, postal survey questionnaire of participants randomly drawn from full population registries in Norway. There was an initial low response. Invitations were sent out in November 2018 and did not close until September 2019. Several efforts were made to boost participation, including one postal or telephone reminder to all nonresponders.
- Participants were refugee adults from Syria aged 18 and older who arrived in Norway between 2015 and 2017. Gender was tested as an effect modifier.
- Chronic pain was measured with 10 items on the questionnaire and was defined as pain for 3 or more consecutive months in the last year. It included both musculoskeletal pain and pain in five other body regions (stomach, head, genital area, chest, other).
- Anxiety, depression, and PTSD symptoms were measured with the 25-item Hopkins Symptom Checklist, the Harvard Trauma Questionnaire, and the Refugee Trauma History Checklist.
- Questionnaires on perceived general health regarding refugee perceptions of their own health, and functional impairment affecting daily activities because of illness, disability, and mental health were adapted from the European Social Survey 2010.
Key results
- A total of 902 participants who responded to the questionnaire were included in the study from roughly 10,000 invitations, giving a participation rate of about 10%, with no differences in gender distribution.
- The overall prevalence of severe chronic pain was 43.1%, and overall perception of poor general health was 39.9%.
- There was a strong association of chronic pain with all mental illness measured, poor perceived general health, and functional impairment (P < .001). All mental health variables were associated with increased odds of chronic pain (anxiety odds ratio), 2.42; depression, OR, 2.28; PTSD, OR, 1.97; all OR fully adjusted).
- Chronic pain was associated with poor perceived general health and functional impairment with no difference across gender. Mental health showed weaker association with poor perceived general health than chronic pain.
- Syrian men with mental health had three times higher odds of functional impairment. For women, there was no evidence of association between any of the mental ill health variables and functional impairment. Being a woman was associated with chronic pain and poor perceived general health but not functional impairment.
- Being a woman was associated with 50% higher odds of chronic pain in both unadjusted and adjusted models.
Limitations
- With a 10% response rate, selection bias in this cross-sectional study may have been present.
- The cross-sectional design of the study limits causality.
- The validity of the survey is questionable because of transcultural construct regarding pain and mental illness.
- Regression models were built with data at hand. Without preregistered plans for data handling, the findings should be viewed as exploratory with a risk for false-positive findings.
Disclosures
- No external funding was received. The study was funded by the Norwegian Center for Violence and Traumatic Stress Studies.
- None of the authors disclosed relevant financial relationships.
This is a summary of a preprint research study, “Chronic pain, mental health and functional impairment in adult refugees from Syria resettled in Norway: a cross-sectional study,” written by researchers at the Norwegian Centre for Violence and Traumatic Stress Studies in Oslo, the Norwegian Institute of Public Health in Oslo, and the Weill Cornell Medicine in New York City on Research Square. This study has not yet been peer reviewed. The full text of the study can be found on researchsquare.com. A version of this article first appeared on Medscape.com.
Psilocybin benefits in severe depression observed up to 12 weeks
NEW ORLEANS –
“This is easily the largest study of a psychedelic drug employing modern randomized controlled trial methodology [with] 22 sites and 10 countries, so it’s not your typical phase 2 trial,” the study’s lead author, Guy M. Goodwin, MD, emeritus professor of psychiatry at the University of Oxford, England, said in an interview.
“Importantly, 94% of the patients in the study were psilocybin naive, which is very important for generalizability,” Dr. Goodwin noted.
Long used as psychedelic ‘magic mushrooms,’ psilocybin has gained increased interest in psychiatry in recent years as a potential treatment for severe depression after showing benefits in patients with life-threatening cancers and others with major depressive disorder (MDD).
To put the therapy to test in a more rigorous, randomized trial, Dr. Goodwin and colleagues conducted the phase 2b study of a proprietary synthetic formulation of psilocybin, COMP360 (COMPASS Pathways), recruiting 233 patients with treatment-resistant depression at 22 centers.
The study was presented at the annual meeting of the American Psychiatric Association.
After a 2-week washout period following the discontinuation of antidepressants, the patients were randomized to one of three groups: A single dose of 25 mg (n = 79), 10 mg (n = 75), or a subtherapeutic comparison of 1 mg (n = 79).
The psilocybin was administered in the presence of specially trained therapists who provided psychological support before, during, and after the 6- to 8-hour session.
Patients were then asked to refrain from antidepressant use for at least 3 weeks following the session, and had periodic follow-up for 12 weeks.
For the primary endpoint, those in the 25-mg group, but not the 10-mg dose, showed a significantly greater reduction in depression from baseline versus the 1-mg group on the Montgomery-Åsberg Depression Rating Scale at week 3 (MADRS; -6.6; P < .001).
The benefit was observed at day 2 and week 1 following administration, “confirming the rapid-acting character of the effect,” the investigators reported.
Sustained responses, defined as at least a 50% change from baseline in MADRS total score, were further observed up to week 12 among 20.3% in the 25-mg group and among 5.3% in the 10-mg groups versus 10.1% in the 1-mg group.
On the day of psilocybin treatment, the treatment-emergent side effects that were reported were headache, nausea, and dizziness, with event rates of 83.5% in the 25-mg group, 74.7% in the 10-mg group, and 72.2% in the 1-mg group.
One participant in the 25-mg group experienced acute anxiety and was treated with lorazepam.
The incidence of treatment-emergent serious adverse events from day 2 to week 3 was 6.3% (five patients) in the 25-mg group, 8.0% (six patients) in the 10-mg group, and 1.3% (one patient) in the 1-mg group.
Serious AEs included suicidal ideation and intentional self-injury among two patients each in the 25-mg group, while in the 10-mg group, two had suicidal ideation and one had hospitalization for severe depression.
There were no significant differences between the groups in terms of vital signs or clinical laboratory tests.
Of note, two patients in the 25-mg group had a change from baseline in QTcF >60 msec on day 2. For one patient, the increase was within normal range, and the other had a QTcF interval duration >500 msec on day 2, but levels returned to normal by day 9.
Improvements in context
Dr. Goodwin noted that the improvements were swift and impressive when compared with those of the STAR*D trial, which is the largest prospective study of treatment outcomes in patients with MDD.
“In the STAR*D trial, third- and fourth-step treatments showed low response rates of under 15% and high relapse rates,” Dr. Goodwin said. “By comparison, our response rates at 12 weeks were 20%-25%, so almost double that seen for probably equivalent treatment steps in STAR*D, with a single treatment with 25 mg, and no additional antidepressant, so no side effect burden.
“We hope to follow up enough of these patients [in the new study] to get some idea of relapse rates,” Dr. Goodwin added. “These have been low in comparable studies with MDD patients: We will see.”
Commenting on the research, Balwinder Singh, MD, of the department of psychiatry and psychology, Mayo Clinic, Rochester, Minn., said the study represents a valuable addition to needed evidence on psilocybin – with some caveats.
“This study adds to the emerging evidence base of psilocybin for treatment-resistant depression, at least in the short term,” he said in an interview. “I think the challenge in the real world would be to have access to 6-8 hours of therapy with psilocybin when patients struggle to find good therapists who could provide even weekly therapy for an hour.”
In addition, Dr. Singh questioned the durability of a single dose of psilocybin in the long term, noting a recent study (N Engl J Med. 2021 Apr 15. doi: 10.1056/NEJMoa2032994) that evaluated two doses of psilocybin (25 mg) 3 weeks apart, and failed to show any significant difference compared with the serotonergic antidepressant escitalopram at 6 weeks.
He further expressed concern about the emergence of suicidal behaviors in some patients, as well as the prolongation of QTc > 60 msec reported in the two patients.
“This is something to be carefully assessed in future studies, due to the risk of arrhythmias,” Dr. Singh said.
The study was sponsored by COMPASS Pathfinder Limited. Dr. Goodwin is chief medical officer for COMPASS Pathways. Dr. Singh had no disclosures to report.
NEW ORLEANS –
“This is easily the largest study of a psychedelic drug employing modern randomized controlled trial methodology [with] 22 sites and 10 countries, so it’s not your typical phase 2 trial,” the study’s lead author, Guy M. Goodwin, MD, emeritus professor of psychiatry at the University of Oxford, England, said in an interview.
“Importantly, 94% of the patients in the study were psilocybin naive, which is very important for generalizability,” Dr. Goodwin noted.
Long used as psychedelic ‘magic mushrooms,’ psilocybin has gained increased interest in psychiatry in recent years as a potential treatment for severe depression after showing benefits in patients with life-threatening cancers and others with major depressive disorder (MDD).
To put the therapy to test in a more rigorous, randomized trial, Dr. Goodwin and colleagues conducted the phase 2b study of a proprietary synthetic formulation of psilocybin, COMP360 (COMPASS Pathways), recruiting 233 patients with treatment-resistant depression at 22 centers.
The study was presented at the annual meeting of the American Psychiatric Association.
After a 2-week washout period following the discontinuation of antidepressants, the patients were randomized to one of three groups: A single dose of 25 mg (n = 79), 10 mg (n = 75), or a subtherapeutic comparison of 1 mg (n = 79).
The psilocybin was administered in the presence of specially trained therapists who provided psychological support before, during, and after the 6- to 8-hour session.
Patients were then asked to refrain from antidepressant use for at least 3 weeks following the session, and had periodic follow-up for 12 weeks.
For the primary endpoint, those in the 25-mg group, but not the 10-mg dose, showed a significantly greater reduction in depression from baseline versus the 1-mg group on the Montgomery-Åsberg Depression Rating Scale at week 3 (MADRS; -6.6; P < .001).
The benefit was observed at day 2 and week 1 following administration, “confirming the rapid-acting character of the effect,” the investigators reported.
Sustained responses, defined as at least a 50% change from baseline in MADRS total score, were further observed up to week 12 among 20.3% in the 25-mg group and among 5.3% in the 10-mg groups versus 10.1% in the 1-mg group.
On the day of psilocybin treatment, the treatment-emergent side effects that were reported were headache, nausea, and dizziness, with event rates of 83.5% in the 25-mg group, 74.7% in the 10-mg group, and 72.2% in the 1-mg group.
One participant in the 25-mg group experienced acute anxiety and was treated with lorazepam.
The incidence of treatment-emergent serious adverse events from day 2 to week 3 was 6.3% (five patients) in the 25-mg group, 8.0% (six patients) in the 10-mg group, and 1.3% (one patient) in the 1-mg group.
Serious AEs included suicidal ideation and intentional self-injury among two patients each in the 25-mg group, while in the 10-mg group, two had suicidal ideation and one had hospitalization for severe depression.
There were no significant differences between the groups in terms of vital signs or clinical laboratory tests.
Of note, two patients in the 25-mg group had a change from baseline in QTcF >60 msec on day 2. For one patient, the increase was within normal range, and the other had a QTcF interval duration >500 msec on day 2, but levels returned to normal by day 9.
Improvements in context
Dr. Goodwin noted that the improvements were swift and impressive when compared with those of the STAR*D trial, which is the largest prospective study of treatment outcomes in patients with MDD.
“In the STAR*D trial, third- and fourth-step treatments showed low response rates of under 15% and high relapse rates,” Dr. Goodwin said. “By comparison, our response rates at 12 weeks were 20%-25%, so almost double that seen for probably equivalent treatment steps in STAR*D, with a single treatment with 25 mg, and no additional antidepressant, so no side effect burden.
“We hope to follow up enough of these patients [in the new study] to get some idea of relapse rates,” Dr. Goodwin added. “These have been low in comparable studies with MDD patients: We will see.”
Commenting on the research, Balwinder Singh, MD, of the department of psychiatry and psychology, Mayo Clinic, Rochester, Minn., said the study represents a valuable addition to needed evidence on psilocybin – with some caveats.
“This study adds to the emerging evidence base of psilocybin for treatment-resistant depression, at least in the short term,” he said in an interview. “I think the challenge in the real world would be to have access to 6-8 hours of therapy with psilocybin when patients struggle to find good therapists who could provide even weekly therapy for an hour.”
In addition, Dr. Singh questioned the durability of a single dose of psilocybin in the long term, noting a recent study (N Engl J Med. 2021 Apr 15. doi: 10.1056/NEJMoa2032994) that evaluated two doses of psilocybin (25 mg) 3 weeks apart, and failed to show any significant difference compared with the serotonergic antidepressant escitalopram at 6 weeks.
He further expressed concern about the emergence of suicidal behaviors in some patients, as well as the prolongation of QTc > 60 msec reported in the two patients.
“This is something to be carefully assessed in future studies, due to the risk of arrhythmias,” Dr. Singh said.
The study was sponsored by COMPASS Pathfinder Limited. Dr. Goodwin is chief medical officer for COMPASS Pathways. Dr. Singh had no disclosures to report.
NEW ORLEANS –
“This is easily the largest study of a psychedelic drug employing modern randomized controlled trial methodology [with] 22 sites and 10 countries, so it’s not your typical phase 2 trial,” the study’s lead author, Guy M. Goodwin, MD, emeritus professor of psychiatry at the University of Oxford, England, said in an interview.
“Importantly, 94% of the patients in the study were psilocybin naive, which is very important for generalizability,” Dr. Goodwin noted.
Long used as psychedelic ‘magic mushrooms,’ psilocybin has gained increased interest in psychiatry in recent years as a potential treatment for severe depression after showing benefits in patients with life-threatening cancers and others with major depressive disorder (MDD).
To put the therapy to test in a more rigorous, randomized trial, Dr. Goodwin and colleagues conducted the phase 2b study of a proprietary synthetic formulation of psilocybin, COMP360 (COMPASS Pathways), recruiting 233 patients with treatment-resistant depression at 22 centers.
The study was presented at the annual meeting of the American Psychiatric Association.
After a 2-week washout period following the discontinuation of antidepressants, the patients were randomized to one of three groups: A single dose of 25 mg (n = 79), 10 mg (n = 75), or a subtherapeutic comparison of 1 mg (n = 79).
The psilocybin was administered in the presence of specially trained therapists who provided psychological support before, during, and after the 6- to 8-hour session.
Patients were then asked to refrain from antidepressant use for at least 3 weeks following the session, and had periodic follow-up for 12 weeks.
For the primary endpoint, those in the 25-mg group, but not the 10-mg dose, showed a significantly greater reduction in depression from baseline versus the 1-mg group on the Montgomery-Åsberg Depression Rating Scale at week 3 (MADRS; -6.6; P < .001).
The benefit was observed at day 2 and week 1 following administration, “confirming the rapid-acting character of the effect,” the investigators reported.
Sustained responses, defined as at least a 50% change from baseline in MADRS total score, were further observed up to week 12 among 20.3% in the 25-mg group and among 5.3% in the 10-mg groups versus 10.1% in the 1-mg group.
On the day of psilocybin treatment, the treatment-emergent side effects that were reported were headache, nausea, and dizziness, with event rates of 83.5% in the 25-mg group, 74.7% in the 10-mg group, and 72.2% in the 1-mg group.
One participant in the 25-mg group experienced acute anxiety and was treated with lorazepam.
The incidence of treatment-emergent serious adverse events from day 2 to week 3 was 6.3% (five patients) in the 25-mg group, 8.0% (six patients) in the 10-mg group, and 1.3% (one patient) in the 1-mg group.
Serious AEs included suicidal ideation and intentional self-injury among two patients each in the 25-mg group, while in the 10-mg group, two had suicidal ideation and one had hospitalization for severe depression.
There were no significant differences between the groups in terms of vital signs or clinical laboratory tests.
Of note, two patients in the 25-mg group had a change from baseline in QTcF >60 msec on day 2. For one patient, the increase was within normal range, and the other had a QTcF interval duration >500 msec on day 2, but levels returned to normal by day 9.
Improvements in context
Dr. Goodwin noted that the improvements were swift and impressive when compared with those of the STAR*D trial, which is the largest prospective study of treatment outcomes in patients with MDD.
“In the STAR*D trial, third- and fourth-step treatments showed low response rates of under 15% and high relapse rates,” Dr. Goodwin said. “By comparison, our response rates at 12 weeks were 20%-25%, so almost double that seen for probably equivalent treatment steps in STAR*D, with a single treatment with 25 mg, and no additional antidepressant, so no side effect burden.
“We hope to follow up enough of these patients [in the new study] to get some idea of relapse rates,” Dr. Goodwin added. “These have been low in comparable studies with MDD patients: We will see.”
Commenting on the research, Balwinder Singh, MD, of the department of psychiatry and psychology, Mayo Clinic, Rochester, Minn., said the study represents a valuable addition to needed evidence on psilocybin – with some caveats.
“This study adds to the emerging evidence base of psilocybin for treatment-resistant depression, at least in the short term,” he said in an interview. “I think the challenge in the real world would be to have access to 6-8 hours of therapy with psilocybin when patients struggle to find good therapists who could provide even weekly therapy for an hour.”
In addition, Dr. Singh questioned the durability of a single dose of psilocybin in the long term, noting a recent study (N Engl J Med. 2021 Apr 15. doi: 10.1056/NEJMoa2032994) that evaluated two doses of psilocybin (25 mg) 3 weeks apart, and failed to show any significant difference compared with the serotonergic antidepressant escitalopram at 6 weeks.
He further expressed concern about the emergence of suicidal behaviors in some patients, as well as the prolongation of QTc > 60 msec reported in the two patients.
“This is something to be carefully assessed in future studies, due to the risk of arrhythmias,” Dr. Singh said.
The study was sponsored by COMPASS Pathfinder Limited. Dr. Goodwin is chief medical officer for COMPASS Pathways. Dr. Singh had no disclosures to report.
AT APA 2022
Hearing, vision loss combo a colossal risk for cognitive decline
The combination of hearing loss and vision loss is linked to an eightfold increased risk of cognitive impairment, new research shows.
Investigators analyzed data on more than 5 million U.S. seniors. Adjusted results show that participants with hearing impairment alone had more than twice the odds of also having cognitive impairment, while those with vision impairment alone had more than triple the odds of cognitive impairment.
However, those with dual sensory impairment (DSI) had an eightfold higher risk for cognitive impairment.
In addition, half of the participants with DSI also had cognitive impairment. Of those with cognitive impairment, 16% had DSI, compared with only about 2% of their peers without cognitive impairment.
“The findings of the present study may inform interventions that can support older people with concurrent sensory impairment and cognitive impairment,” said lead author Esme Fuller-Thomson, PhD, professor, Factor-Inwentash Faculty of Social Work, University of Toronto.
“Special attention, in particular, should be given to those aged 65-74 who have serious hearing and/or vision impairment [because], if the relationship with dementia is found to be causal, such interventions can potentially mitigate the development of cognitive impairment,” said Dr. Fuller-Thomson, who is also director of the Institute for Life Course and Aging and a professor in the department of family and community medicine and faculty of nursing, all at the University of Toronto.
The findings were published online in the Journal of Alzheimer’s Disease Reports.
Sensory isolation
Hearing and vision impairment increase with age; it is estimated that one-third of U.S. adults between the ages of 65 and 74 experience hearing loss, and 4% experience vision impairment, the investigators note.
“The link between dual hearing loss and seeing loss and mental health problems such as depression and social isolation have been well researched, but we were very interested in the link between dual sensory loss and cognitive problems,” Dr. Fuller-Thomson said.
Additionally, “there have been several studies in the past decade linking hearing loss to dementia and cognitive decline, but less attention has been paid to cognitive problems among those with DSI, despite this group being particularly isolated,” she said. Existing research into DSI suggests an association with cognitive decline; the current investigators sought to expand on this previous work.
To do so, they used merged data from 10 consecutive waves from 2008 to 2017 of the American Community Survey (ACS), which was conducted by the U.S. Census Bureau. The ACS is a nationally representative sample of 3.5 million randomly selected U.S. addresses and includes community-dwelling adults and those residing in institutional settings.
Participants aged 65 or older (n = 5,405,135; 56.4% women) were asked yes/no questions regarding serious cognitive impairment, hearing impairment, and vision impairment. A proxy, such as a family member or nursing home staff member, provided answers for individuals not capable of self-report.
Potential confounding variables included age, race/ethnicity, sex, education, and household income.
Potential mechanisms
Results showed that, among those with cognitive impairment, there was a higher prevalence of hearing impairment, vision impairment, and DSI than among their peers without cognitive impairment; in addition, a lower percentage of these persons had no sensory impairment (P < .001).
The prevalence of DSI climbed with age, from 1.5% for respondents aged 65-74 years to 2.6% for those aged 75-84 and to 10.8% in those 85 years and older.
Individuals with higher levels of poverty also had higher levels of DSI. Among those who had not completed high school, the prevalence of DSI was higher, compared with high school or university graduates (6.3% vs. 3.1% and 1.85, respectively).
After controlling for age, race, education, and income, the researchers found “substantially” higher odds of cognitive impairment in those with vs. those without sensory impairments.
“The magnitude of the odds of cognitive impairment by sensory impairment was greatest for the youngest cohort (age 65-74) and lowest for the oldest cohort (age 85+),” the investigators wrote. Among participants in the youngest cohort, there was a “dose-response relationship” for those with hearing impairment only, visual impairment only, and DSI.
Because the study was observational, it “does not provide sufficient information to determine the reasons behind the observed link between sensory loss and cognitive problems,” Dr. Fuller-Thomson said. However, there are “several potential causal mechanisms [that] warrant future research.”
The “sensory deprivation hypothesis” suggests that DSI could cause cognitive deterioration because of decreased auditory and visual input. The “resource allocation hypothesis” posits that hearing- or vision-impaired older adults “may use more cognitive resources to accommodate for sensory deficits, allocating fewer cognitive resources for higher-order memory processes,” the researchers wrote. Hearing impairment “may also lead to social disengagement among older adults, hastening cognitive decline due to isolation and lack of stimulation,” they added.
Reverse causality is also possible. In the “cognitive load on perception” hypothesis, cognitive decline may lead to declines in hearing and vision because of “decreased resources for sensory processing.”
In addition, the association may be noncausal. “The ‘common cause hypothesis’ theorizes that sensory impairment and cognitive impairment may be due to shared age-related degeneration of the central nervous system ... or frailty,” Dr. Fuller-Thomson said.
Parallel findings
The results are similar to those from a study conducted by Phillip Hwang, PhD, of the department of anatomy and neurobiology, Boston University, and colleagues that was published online in JAMA Network Open.
They analyzed data on 8 years of follow-up of 2,927 participants in the Cardiovascular Health Study (mean age, 74.6 years; 58.2% women).
Compared with no sensory impairment, DSI was associated with increased risk for all-cause dementia and Alzheimer’s disease, but not with vascular dementia.
“Future work in health care guidelines could consider incorporating screening of sensory impairment in older adults as part of risk assessment for dementia,” Nicholas Reed, AuD, and Esther Oh, MD, PhD, both of Johns Hopkins University, Baltimore, wrote in an accompanying editorial.
Accurate testing
Commenting on both studies, Heather Whitson, MD, professor of medicine (geriatrics) and ophthalmology and director at the Duke University Center for the Study of Aging and Human Development, Durham, N.C., said both “add further strength to the evidence base, which has really converged in the last few years to support that there is a link between sensory health and cognitive health.”
However, “we still don’t know whether hearing/vision loss causes cognitive decline, though there are plausible ways that sensory loss could affect cognitive abilities like memory, language, and executive function,” she said
Dr. Whitson, who was not involved with the research, is also codirector of the Duke/University of North Carolina Alzheimer’s Disease Research Center at Duke University, Durham, N.C., and the Durham VA Medical Center.
“The big question is whether we can improve patients’ cognitive performance by treating or accommodating their sensory impairments,” she said. “If safe and feasible things like hearing aids or cataract surgery improve cognitive health, even a little bit, it would be a huge benefit to society, because sensory loss is very common, and there are many treatment options,” Dr. Whitson added.
Dr. Fuller-Thomson emphasized that practitioners should “consider the full impact of sensory impairment on cognitive testing methods, as both auditory and visual testing methods may fail to take hearing and vision impairment into account.”
Thus, “when performing cognitive tests on older adults with sensory impairments, practitioners should ensure they are communicating audibly and/or using visual speech cues for hearing-impaired individuals, eliminating items from cognitive tests that rely on vision for those who are visually impaired, and using physical cues for individuals with hearing or dual sensory impairment, as this can help increase the accuracy of testing and prevent confounding,” she said.
The study by Fuller-Thomson et al. was funded by a donation from Janis Rotman. Its investigators have reported no relevant financial relationships. The study by Hwang et al. was funded by contracts from the National Heart, Lung, and Blood Institute, the National Institute of Neurological Disorders and Stroke, and the National Institute on Aging. Dr. Hwang reports no relevant financial relationships. The other investigators’ disclosures are listed in the original article. Dr. Reed received grants from the National Institute on Aging during the conduct of the study and has served on the advisory board of Neosensory outside the submitted work. Dr. Oh and Dr. Whitson report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The combination of hearing loss and vision loss is linked to an eightfold increased risk of cognitive impairment, new research shows.
Investigators analyzed data on more than 5 million U.S. seniors. Adjusted results show that participants with hearing impairment alone had more than twice the odds of also having cognitive impairment, while those with vision impairment alone had more than triple the odds of cognitive impairment.
However, those with dual sensory impairment (DSI) had an eightfold higher risk for cognitive impairment.
In addition, half of the participants with DSI also had cognitive impairment. Of those with cognitive impairment, 16% had DSI, compared with only about 2% of their peers without cognitive impairment.
“The findings of the present study may inform interventions that can support older people with concurrent sensory impairment and cognitive impairment,” said lead author Esme Fuller-Thomson, PhD, professor, Factor-Inwentash Faculty of Social Work, University of Toronto.
“Special attention, in particular, should be given to those aged 65-74 who have serious hearing and/or vision impairment [because], if the relationship with dementia is found to be causal, such interventions can potentially mitigate the development of cognitive impairment,” said Dr. Fuller-Thomson, who is also director of the Institute for Life Course and Aging and a professor in the department of family and community medicine and faculty of nursing, all at the University of Toronto.
The findings were published online in the Journal of Alzheimer’s Disease Reports.
Sensory isolation
Hearing and vision impairment increase with age; it is estimated that one-third of U.S. adults between the ages of 65 and 74 experience hearing loss, and 4% experience vision impairment, the investigators note.
“The link between dual hearing loss and seeing loss and mental health problems such as depression and social isolation have been well researched, but we were very interested in the link between dual sensory loss and cognitive problems,” Dr. Fuller-Thomson said.
Additionally, “there have been several studies in the past decade linking hearing loss to dementia and cognitive decline, but less attention has been paid to cognitive problems among those with DSI, despite this group being particularly isolated,” she said. Existing research into DSI suggests an association with cognitive decline; the current investigators sought to expand on this previous work.
To do so, they used merged data from 10 consecutive waves from 2008 to 2017 of the American Community Survey (ACS), which was conducted by the U.S. Census Bureau. The ACS is a nationally representative sample of 3.5 million randomly selected U.S. addresses and includes community-dwelling adults and those residing in institutional settings.
Participants aged 65 or older (n = 5,405,135; 56.4% women) were asked yes/no questions regarding serious cognitive impairment, hearing impairment, and vision impairment. A proxy, such as a family member or nursing home staff member, provided answers for individuals not capable of self-report.
Potential confounding variables included age, race/ethnicity, sex, education, and household income.
Potential mechanisms
Results showed that, among those with cognitive impairment, there was a higher prevalence of hearing impairment, vision impairment, and DSI than among their peers without cognitive impairment; in addition, a lower percentage of these persons had no sensory impairment (P < .001).
The prevalence of DSI climbed with age, from 1.5% for respondents aged 65-74 years to 2.6% for those aged 75-84 and to 10.8% in those 85 years and older.
Individuals with higher levels of poverty also had higher levels of DSI. Among those who had not completed high school, the prevalence of DSI was higher, compared with high school or university graduates (6.3% vs. 3.1% and 1.85, respectively).
After controlling for age, race, education, and income, the researchers found “substantially” higher odds of cognitive impairment in those with vs. those without sensory impairments.
“The magnitude of the odds of cognitive impairment by sensory impairment was greatest for the youngest cohort (age 65-74) and lowest for the oldest cohort (age 85+),” the investigators wrote. Among participants in the youngest cohort, there was a “dose-response relationship” for those with hearing impairment only, visual impairment only, and DSI.
Because the study was observational, it “does not provide sufficient information to determine the reasons behind the observed link between sensory loss and cognitive problems,” Dr. Fuller-Thomson said. However, there are “several potential causal mechanisms [that] warrant future research.”
The “sensory deprivation hypothesis” suggests that DSI could cause cognitive deterioration because of decreased auditory and visual input. The “resource allocation hypothesis” posits that hearing- or vision-impaired older adults “may use more cognitive resources to accommodate for sensory deficits, allocating fewer cognitive resources for higher-order memory processes,” the researchers wrote. Hearing impairment “may also lead to social disengagement among older adults, hastening cognitive decline due to isolation and lack of stimulation,” they added.
Reverse causality is also possible. In the “cognitive load on perception” hypothesis, cognitive decline may lead to declines in hearing and vision because of “decreased resources for sensory processing.”
In addition, the association may be noncausal. “The ‘common cause hypothesis’ theorizes that sensory impairment and cognitive impairment may be due to shared age-related degeneration of the central nervous system ... or frailty,” Dr. Fuller-Thomson said.
Parallel findings
The results are similar to those from a study conducted by Phillip Hwang, PhD, of the department of anatomy and neurobiology, Boston University, and colleagues that was published online in JAMA Network Open.
They analyzed data on 8 years of follow-up of 2,927 participants in the Cardiovascular Health Study (mean age, 74.6 years; 58.2% women).
Compared with no sensory impairment, DSI was associated with increased risk for all-cause dementia and Alzheimer’s disease, but not with vascular dementia.
“Future work in health care guidelines could consider incorporating screening of sensory impairment in older adults as part of risk assessment for dementia,” Nicholas Reed, AuD, and Esther Oh, MD, PhD, both of Johns Hopkins University, Baltimore, wrote in an accompanying editorial.
Accurate testing
Commenting on both studies, Heather Whitson, MD, professor of medicine (geriatrics) and ophthalmology and director at the Duke University Center for the Study of Aging and Human Development, Durham, N.C., said both “add further strength to the evidence base, which has really converged in the last few years to support that there is a link between sensory health and cognitive health.”
However, “we still don’t know whether hearing/vision loss causes cognitive decline, though there are plausible ways that sensory loss could affect cognitive abilities like memory, language, and executive function,” she said
Dr. Whitson, who was not involved with the research, is also codirector of the Duke/University of North Carolina Alzheimer’s Disease Research Center at Duke University, Durham, N.C., and the Durham VA Medical Center.
“The big question is whether we can improve patients’ cognitive performance by treating or accommodating their sensory impairments,” she said. “If safe and feasible things like hearing aids or cataract surgery improve cognitive health, even a little bit, it would be a huge benefit to society, because sensory loss is very common, and there are many treatment options,” Dr. Whitson added.
Dr. Fuller-Thomson emphasized that practitioners should “consider the full impact of sensory impairment on cognitive testing methods, as both auditory and visual testing methods may fail to take hearing and vision impairment into account.”
Thus, “when performing cognitive tests on older adults with sensory impairments, practitioners should ensure they are communicating audibly and/or using visual speech cues for hearing-impaired individuals, eliminating items from cognitive tests that rely on vision for those who are visually impaired, and using physical cues for individuals with hearing or dual sensory impairment, as this can help increase the accuracy of testing and prevent confounding,” she said.
The study by Fuller-Thomson et al. was funded by a donation from Janis Rotman. Its investigators have reported no relevant financial relationships. The study by Hwang et al. was funded by contracts from the National Heart, Lung, and Blood Institute, the National Institute of Neurological Disorders and Stroke, and the National Institute on Aging. Dr. Hwang reports no relevant financial relationships. The other investigators’ disclosures are listed in the original article. Dr. Reed received grants from the National Institute on Aging during the conduct of the study and has served on the advisory board of Neosensory outside the submitted work. Dr. Oh and Dr. Whitson report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The combination of hearing loss and vision loss is linked to an eightfold increased risk of cognitive impairment, new research shows.
Investigators analyzed data on more than 5 million U.S. seniors. Adjusted results show that participants with hearing impairment alone had more than twice the odds of also having cognitive impairment, while those with vision impairment alone had more than triple the odds of cognitive impairment.
However, those with dual sensory impairment (DSI) had an eightfold higher risk for cognitive impairment.
In addition, half of the participants with DSI also had cognitive impairment. Of those with cognitive impairment, 16% had DSI, compared with only about 2% of their peers without cognitive impairment.
“The findings of the present study may inform interventions that can support older people with concurrent sensory impairment and cognitive impairment,” said lead author Esme Fuller-Thomson, PhD, professor, Factor-Inwentash Faculty of Social Work, University of Toronto.
“Special attention, in particular, should be given to those aged 65-74 who have serious hearing and/or vision impairment [because], if the relationship with dementia is found to be causal, such interventions can potentially mitigate the development of cognitive impairment,” said Dr. Fuller-Thomson, who is also director of the Institute for Life Course and Aging and a professor in the department of family and community medicine and faculty of nursing, all at the University of Toronto.
The findings were published online in the Journal of Alzheimer’s Disease Reports.
Sensory isolation
Hearing and vision impairment increase with age; it is estimated that one-third of U.S. adults between the ages of 65 and 74 experience hearing loss, and 4% experience vision impairment, the investigators note.
“The link between dual hearing loss and seeing loss and mental health problems such as depression and social isolation have been well researched, but we were very interested in the link between dual sensory loss and cognitive problems,” Dr. Fuller-Thomson said.
Additionally, “there have been several studies in the past decade linking hearing loss to dementia and cognitive decline, but less attention has been paid to cognitive problems among those with DSI, despite this group being particularly isolated,” she said. Existing research into DSI suggests an association with cognitive decline; the current investigators sought to expand on this previous work.
To do so, they used merged data from 10 consecutive waves from 2008 to 2017 of the American Community Survey (ACS), which was conducted by the U.S. Census Bureau. The ACS is a nationally representative sample of 3.5 million randomly selected U.S. addresses and includes community-dwelling adults and those residing in institutional settings.
Participants aged 65 or older (n = 5,405,135; 56.4% women) were asked yes/no questions regarding serious cognitive impairment, hearing impairment, and vision impairment. A proxy, such as a family member or nursing home staff member, provided answers for individuals not capable of self-report.
Potential confounding variables included age, race/ethnicity, sex, education, and household income.
Potential mechanisms
Results showed that, among those with cognitive impairment, there was a higher prevalence of hearing impairment, vision impairment, and DSI than among their peers without cognitive impairment; in addition, a lower percentage of these persons had no sensory impairment (P < .001).
The prevalence of DSI climbed with age, from 1.5% for respondents aged 65-74 years to 2.6% for those aged 75-84 and to 10.8% in those 85 years and older.
Individuals with higher levels of poverty also had higher levels of DSI. Among those who had not completed high school, the prevalence of DSI was higher, compared with high school or university graduates (6.3% vs. 3.1% and 1.85, respectively).
After controlling for age, race, education, and income, the researchers found “substantially” higher odds of cognitive impairment in those with vs. those without sensory impairments.
“The magnitude of the odds of cognitive impairment by sensory impairment was greatest for the youngest cohort (age 65-74) and lowest for the oldest cohort (age 85+),” the investigators wrote. Among participants in the youngest cohort, there was a “dose-response relationship” for those with hearing impairment only, visual impairment only, and DSI.
Because the study was observational, it “does not provide sufficient information to determine the reasons behind the observed link between sensory loss and cognitive problems,” Dr. Fuller-Thomson said. However, there are “several potential causal mechanisms [that] warrant future research.”
The “sensory deprivation hypothesis” suggests that DSI could cause cognitive deterioration because of decreased auditory and visual input. The “resource allocation hypothesis” posits that hearing- or vision-impaired older adults “may use more cognitive resources to accommodate for sensory deficits, allocating fewer cognitive resources for higher-order memory processes,” the researchers wrote. Hearing impairment “may also lead to social disengagement among older adults, hastening cognitive decline due to isolation and lack of stimulation,” they added.
Reverse causality is also possible. In the “cognitive load on perception” hypothesis, cognitive decline may lead to declines in hearing and vision because of “decreased resources for sensory processing.”
In addition, the association may be noncausal. “The ‘common cause hypothesis’ theorizes that sensory impairment and cognitive impairment may be due to shared age-related degeneration of the central nervous system ... or frailty,” Dr. Fuller-Thomson said.
Parallel findings
The results are similar to those from a study conducted by Phillip Hwang, PhD, of the department of anatomy and neurobiology, Boston University, and colleagues that was published online in JAMA Network Open.
They analyzed data on 8 years of follow-up of 2,927 participants in the Cardiovascular Health Study (mean age, 74.6 years; 58.2% women).
Compared with no sensory impairment, DSI was associated with increased risk for all-cause dementia and Alzheimer’s disease, but not with vascular dementia.
“Future work in health care guidelines could consider incorporating screening of sensory impairment in older adults as part of risk assessment for dementia,” Nicholas Reed, AuD, and Esther Oh, MD, PhD, both of Johns Hopkins University, Baltimore, wrote in an accompanying editorial.
Accurate testing
Commenting on both studies, Heather Whitson, MD, professor of medicine (geriatrics) and ophthalmology and director at the Duke University Center for the Study of Aging and Human Development, Durham, N.C., said both “add further strength to the evidence base, which has really converged in the last few years to support that there is a link between sensory health and cognitive health.”
However, “we still don’t know whether hearing/vision loss causes cognitive decline, though there are plausible ways that sensory loss could affect cognitive abilities like memory, language, and executive function,” she said
Dr. Whitson, who was not involved with the research, is also codirector of the Duke/University of North Carolina Alzheimer’s Disease Research Center at Duke University, Durham, N.C., and the Durham VA Medical Center.
“The big question is whether we can improve patients’ cognitive performance by treating or accommodating their sensory impairments,” she said. “If safe and feasible things like hearing aids or cataract surgery improve cognitive health, even a little bit, it would be a huge benefit to society, because sensory loss is very common, and there are many treatment options,” Dr. Whitson added.
Dr. Fuller-Thomson emphasized that practitioners should “consider the full impact of sensory impairment on cognitive testing methods, as both auditory and visual testing methods may fail to take hearing and vision impairment into account.”
Thus, “when performing cognitive tests on older adults with sensory impairments, practitioners should ensure they are communicating audibly and/or using visual speech cues for hearing-impaired individuals, eliminating items from cognitive tests that rely on vision for those who are visually impaired, and using physical cues for individuals with hearing or dual sensory impairment, as this can help increase the accuracy of testing and prevent confounding,” she said.
The study by Fuller-Thomson et al. was funded by a donation from Janis Rotman. Its investigators have reported no relevant financial relationships. The study by Hwang et al. was funded by contracts from the National Heart, Lung, and Blood Institute, the National Institute of Neurological Disorders and Stroke, and the National Institute on Aging. Dr. Hwang reports no relevant financial relationships. The other investigators’ disclosures are listed in the original article. Dr. Reed received grants from the National Institute on Aging during the conduct of the study and has served on the advisory board of Neosensory outside the submitted work. Dr. Oh and Dr. Whitson report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF ALZHEIMER’S DISEASE REPORTS
Long COVID neuropsychiatric deficits greater than expected
NEW ORLEANS – , adding to mounting evidence of the significant toll the chronic condition can have on mental health.
“Many clinicians have observed the symptoms we describe in this study, however this report is among the first which identify the specific deficits using neuropsychological testing to better characterize the syndrome,” Sean T. Lynch, MD, first author of a study on the issue presented at the annual meeting of the American Psychiatric Association, said in an interview.
Dr. Lynch, of the department of psychiatry, Westchester Medical Center Health System, Valhalla, N.Y., and his colleagues enrolled 60 participants who had experienced acute COVID-19 disease 6-8 months earlier and had undergone neuropsychological, psychiatric, medical, functional, and quality-of-life assessments. Results from the study were published online in the Journal of the Academy of Consultation–Liaison Psychiatry (2022 Jan 25. doi: 10.1016/j.jaclp.2022.01.003).
Among the study participants, 32 were seeking treatment for brain fog in a clinical program for survivors of COVID-19, while the remaining 28 were part of an ongoing longitudinal investigation of neuropsychological, medical, and psychiatric sequelae of COVID-19, but were not seeking care for the persistent symptoms.
Assessments for neurocognitive impairment included a battery of tests used in infectious and other diseases, including the Test of Premorbid Function, the Patient Assessment of Own Function, the Trail Making Test parts A and B, the Stroop Color and Word Test, and others.
Overall, the battery of assessments showed that 37 (62%) of participants had neuropsychological test impairment, with results below the 16th percentile in two tests, while 16 (27%) showed scores indicative of severe impairment (below the second percentile in at least one test and below the 16th percentile in one test).
Those reporting brain fog had scores that were even lower than expected on tests of attention, processing speed, memory, and executive function. And among those reporting brain fog, significantly more had scores reflecting severe impairment compared with the controls (38% vs. 14%; P < .04).
“Based on what we’ve observed in our patients and what others have previously reported, we did expect to find some impairment in this study sample,” Dr. Lynch noted.
“However, we were surprised to find that 27% of the study sample had extremely low neuropsychological test scores, meaning that they scored at least two standard deviations below the expected score on at least one neuropsychological test based on their age and level of education.”
The brain fog group also reported significantly higher levels of depression, fatigue, PTSD, and functional difficulties, and lower quality of life.
Severe impairment on the neuropsychological tests correlated with the extent of acute COVID-19 symptoms, as well as depression scores, number of medical comorbidities, and subjective cognitive complaints.
An analysis of serum levels of the inflammatory markers among 50 of the 60 participants showed that 45% of the patients had an elevated IL-6, 20% had elevated TNF-alpha, and 41% had elevated CRP, compared with reference ranges.
IL-6 levels were found to correlate with acute COVID-19 symptoms, the number of medical comorbidities, fatigue, and measures of executive function, while C-reactive protein (CRP) correlated with current COVID-19 symptoms and depression scores.
In terms of clinical factors that might predict low neuropsychological test scores, Dr. Lynch noted that the “markers that we found to be significant included severity of acute COVID-19 illness, current post-COVID-19 symptoms, measures of depression and anxiety, level of fatigue, and number of medical comorbidities.”
Dr. Lynch noted that the ongoing study will include up to 18-month follow-ups that are currently underway. “The [follow-ups] will examine if symptoms improve over time and evaluate if any intervention that took place was successful,” he said.
Survey supports findings
The detrimental effects of mental health symptoms in long COVID were further supported in another study at the APA meeting, an online survey of 787 survivors of acute COVID-19.
In the community survey, presented by Michael Van Ameringen, MD, a professor in the department of psychiatry and behavioral neurosciences at McMaster University, in Hamilton, Ont., all respondents (100%) reported having persistent symptoms of the virus, and as many as 68% indicated that they had not returned to normal functioning, despite only 15% of the respondents having been hospitalized with COVID-19.
A large proportion showed significant depression, anxiety, and posttraumatic stress disorder (PTSD), and the most commonly reported persistent symptoms were fatigue in 75.9% of respondents, brain fog in 67.9%, concentration difficulties in 61.1%, and weakness in 51.2%.
As many as 88.2% of patients said they experienced persistent neurocognitive symptoms, with poor memory and concentration; 56% reported problems with word finding; and 54.1% had slowed thinking.
The respondents showed high rates of anxiety (41.7%) as well as depression (61.4%) as determined by scores above 9 on the Generalized Anxiety Disorder–7 (GAD-7) and Patient Health Questionnaires (PHQ-9).
As many as 40.5% of respondents showed probable PTSD, with scores above 30 on the PTSD checklist (PCL-5). Their mean resilience score on the Brief Resilient Coping Scale was 13.5, suggesting low resilience.
Among the respondents, 43.3% said they had received past treatment for mental health, while 33.5% were currently receiving mental health treatment.
Dr. Van Ameringen noted the important limitation of the study being an online survey with no control group, but said the responses nevertheless raise the question of the role of prior psychiatric disorders in long COVID.
“In our sample, 40% of respondents had a past psychiatric history, so you wonder if that also makes you vulnerable to long COVID,” he said in an interview.
“About a third were getting psychiatric help, but I think the more impaired you are, the more likely you are to seek help.”
Those who were hospitalized with COVID-19 were at a higher risk of PTSD compared with those not hospitalized (P < .001), as were those under the age of 30 (P < .05) or between 31 and 50 vs. over 50 (P < .01).
Dr. Van Ameringen noted that the survey’s high rate of subjects who had not returned to normal functioning was especially striking.
“This is not a minor issue – these are people who are no longer functioning in society,” he said.
In pandemics, the brain tends to be ‘overlooked’
Further addressing the neurological effects of COVID-19 at the APA meeting, Avindra Nath, MD, clinical director of the National Institutes of Neurologic Disorders and Stroke in Bethesda, Md., noted that the persisting cognitive and psychiatric symptoms after illness, such as brain fog and depression and anxiety, are not necessarily unique to COVID-19.
“We have seen this before,” he said. “There have been at least seven or eight human coronaviruses, and the interesting thing is each one affects the brain and causes neurological complications.”
The effects are classified differently and have slightly different receptors, “but the consequences are the same.”
Of note, however, research published in The Lancet Psychiatry (2021 May. doi: 10.1016/S2215-0366[21]00084-5) revealed that symptoms such as dementia, mood, and anxiety are significantly higher after COVID-19 compared with other respiratory infections, with the differences increasing at 180 days since the index event.
Dr. Nath noted that, over the decades, he has observed that in pandemics “the brain tends to get overlooked.” He explained that “what can be most important in the end is what happened in the brain, because those are the things that really cause the long-term consequences.”
“These patients are depressed; they have dementia, they have brain fog, and even now that we recognize these issues, we haven’t done a very good job of studying them,” he said. “There’s so much we still don’t know, and a lot of patients are left with these symptoms and nowhere to go.”
Dr. Lynch, Dr. Van Ameringen, and Dr. Nath had no disclosures to report.
NEW ORLEANS – , adding to mounting evidence of the significant toll the chronic condition can have on mental health.
“Many clinicians have observed the symptoms we describe in this study, however this report is among the first which identify the specific deficits using neuropsychological testing to better characterize the syndrome,” Sean T. Lynch, MD, first author of a study on the issue presented at the annual meeting of the American Psychiatric Association, said in an interview.
Dr. Lynch, of the department of psychiatry, Westchester Medical Center Health System, Valhalla, N.Y., and his colleagues enrolled 60 participants who had experienced acute COVID-19 disease 6-8 months earlier and had undergone neuropsychological, psychiatric, medical, functional, and quality-of-life assessments. Results from the study were published online in the Journal of the Academy of Consultation–Liaison Psychiatry (2022 Jan 25. doi: 10.1016/j.jaclp.2022.01.003).
Among the study participants, 32 were seeking treatment for brain fog in a clinical program for survivors of COVID-19, while the remaining 28 were part of an ongoing longitudinal investigation of neuropsychological, medical, and psychiatric sequelae of COVID-19, but were not seeking care for the persistent symptoms.
Assessments for neurocognitive impairment included a battery of tests used in infectious and other diseases, including the Test of Premorbid Function, the Patient Assessment of Own Function, the Trail Making Test parts A and B, the Stroop Color and Word Test, and others.
Overall, the battery of assessments showed that 37 (62%) of participants had neuropsychological test impairment, with results below the 16th percentile in two tests, while 16 (27%) showed scores indicative of severe impairment (below the second percentile in at least one test and below the 16th percentile in one test).
Those reporting brain fog had scores that were even lower than expected on tests of attention, processing speed, memory, and executive function. And among those reporting brain fog, significantly more had scores reflecting severe impairment compared with the controls (38% vs. 14%; P < .04).
“Based on what we’ve observed in our patients and what others have previously reported, we did expect to find some impairment in this study sample,” Dr. Lynch noted.
“However, we were surprised to find that 27% of the study sample had extremely low neuropsychological test scores, meaning that they scored at least two standard deviations below the expected score on at least one neuropsychological test based on their age and level of education.”
The brain fog group also reported significantly higher levels of depression, fatigue, PTSD, and functional difficulties, and lower quality of life.
Severe impairment on the neuropsychological tests correlated with the extent of acute COVID-19 symptoms, as well as depression scores, number of medical comorbidities, and subjective cognitive complaints.
An analysis of serum levels of the inflammatory markers among 50 of the 60 participants showed that 45% of the patients had an elevated IL-6, 20% had elevated TNF-alpha, and 41% had elevated CRP, compared with reference ranges.
IL-6 levels were found to correlate with acute COVID-19 symptoms, the number of medical comorbidities, fatigue, and measures of executive function, while C-reactive protein (CRP) correlated with current COVID-19 symptoms and depression scores.
In terms of clinical factors that might predict low neuropsychological test scores, Dr. Lynch noted that the “markers that we found to be significant included severity of acute COVID-19 illness, current post-COVID-19 symptoms, measures of depression and anxiety, level of fatigue, and number of medical comorbidities.”
Dr. Lynch noted that the ongoing study will include up to 18-month follow-ups that are currently underway. “The [follow-ups] will examine if symptoms improve over time and evaluate if any intervention that took place was successful,” he said.
Survey supports findings
The detrimental effects of mental health symptoms in long COVID were further supported in another study at the APA meeting, an online survey of 787 survivors of acute COVID-19.
In the community survey, presented by Michael Van Ameringen, MD, a professor in the department of psychiatry and behavioral neurosciences at McMaster University, in Hamilton, Ont., all respondents (100%) reported having persistent symptoms of the virus, and as many as 68% indicated that they had not returned to normal functioning, despite only 15% of the respondents having been hospitalized with COVID-19.
A large proportion showed significant depression, anxiety, and posttraumatic stress disorder (PTSD), and the most commonly reported persistent symptoms were fatigue in 75.9% of respondents, brain fog in 67.9%, concentration difficulties in 61.1%, and weakness in 51.2%.
As many as 88.2% of patients said they experienced persistent neurocognitive symptoms, with poor memory and concentration; 56% reported problems with word finding; and 54.1% had slowed thinking.
The respondents showed high rates of anxiety (41.7%) as well as depression (61.4%) as determined by scores above 9 on the Generalized Anxiety Disorder–7 (GAD-7) and Patient Health Questionnaires (PHQ-9).
As many as 40.5% of respondents showed probable PTSD, with scores above 30 on the PTSD checklist (PCL-5). Their mean resilience score on the Brief Resilient Coping Scale was 13.5, suggesting low resilience.
Among the respondents, 43.3% said they had received past treatment for mental health, while 33.5% were currently receiving mental health treatment.
Dr. Van Ameringen noted the important limitation of the study being an online survey with no control group, but said the responses nevertheless raise the question of the role of prior psychiatric disorders in long COVID.
“In our sample, 40% of respondents had a past psychiatric history, so you wonder if that also makes you vulnerable to long COVID,” he said in an interview.
“About a third were getting psychiatric help, but I think the more impaired you are, the more likely you are to seek help.”
Those who were hospitalized with COVID-19 were at a higher risk of PTSD compared with those not hospitalized (P < .001), as were those under the age of 30 (P < .05) or between 31 and 50 vs. over 50 (P < .01).
Dr. Van Ameringen noted that the survey’s high rate of subjects who had not returned to normal functioning was especially striking.
“This is not a minor issue – these are people who are no longer functioning in society,” he said.
In pandemics, the brain tends to be ‘overlooked’
Further addressing the neurological effects of COVID-19 at the APA meeting, Avindra Nath, MD, clinical director of the National Institutes of Neurologic Disorders and Stroke in Bethesda, Md., noted that the persisting cognitive and psychiatric symptoms after illness, such as brain fog and depression and anxiety, are not necessarily unique to COVID-19.
“We have seen this before,” he said. “There have been at least seven or eight human coronaviruses, and the interesting thing is each one affects the brain and causes neurological complications.”
The effects are classified differently and have slightly different receptors, “but the consequences are the same.”
Of note, however, research published in The Lancet Psychiatry (2021 May. doi: 10.1016/S2215-0366[21]00084-5) revealed that symptoms such as dementia, mood, and anxiety are significantly higher after COVID-19 compared with other respiratory infections, with the differences increasing at 180 days since the index event.
Dr. Nath noted that, over the decades, he has observed that in pandemics “the brain tends to get overlooked.” He explained that “what can be most important in the end is what happened in the brain, because those are the things that really cause the long-term consequences.”
“These patients are depressed; they have dementia, they have brain fog, and even now that we recognize these issues, we haven’t done a very good job of studying them,” he said. “There’s so much we still don’t know, and a lot of patients are left with these symptoms and nowhere to go.”
Dr. Lynch, Dr. Van Ameringen, and Dr. Nath had no disclosures to report.
NEW ORLEANS – , adding to mounting evidence of the significant toll the chronic condition can have on mental health.
“Many clinicians have observed the symptoms we describe in this study, however this report is among the first which identify the specific deficits using neuropsychological testing to better characterize the syndrome,” Sean T. Lynch, MD, first author of a study on the issue presented at the annual meeting of the American Psychiatric Association, said in an interview.
Dr. Lynch, of the department of psychiatry, Westchester Medical Center Health System, Valhalla, N.Y., and his colleagues enrolled 60 participants who had experienced acute COVID-19 disease 6-8 months earlier and had undergone neuropsychological, psychiatric, medical, functional, and quality-of-life assessments. Results from the study were published online in the Journal of the Academy of Consultation–Liaison Psychiatry (2022 Jan 25. doi: 10.1016/j.jaclp.2022.01.003).
Among the study participants, 32 were seeking treatment for brain fog in a clinical program for survivors of COVID-19, while the remaining 28 were part of an ongoing longitudinal investigation of neuropsychological, medical, and psychiatric sequelae of COVID-19, but were not seeking care for the persistent symptoms.
Assessments for neurocognitive impairment included a battery of tests used in infectious and other diseases, including the Test of Premorbid Function, the Patient Assessment of Own Function, the Trail Making Test parts A and B, the Stroop Color and Word Test, and others.
Overall, the battery of assessments showed that 37 (62%) of participants had neuropsychological test impairment, with results below the 16th percentile in two tests, while 16 (27%) showed scores indicative of severe impairment (below the second percentile in at least one test and below the 16th percentile in one test).
Those reporting brain fog had scores that were even lower than expected on tests of attention, processing speed, memory, and executive function. And among those reporting brain fog, significantly more had scores reflecting severe impairment compared with the controls (38% vs. 14%; P < .04).
“Based on what we’ve observed in our patients and what others have previously reported, we did expect to find some impairment in this study sample,” Dr. Lynch noted.
“However, we were surprised to find that 27% of the study sample had extremely low neuropsychological test scores, meaning that they scored at least two standard deviations below the expected score on at least one neuropsychological test based on their age and level of education.”
The brain fog group also reported significantly higher levels of depression, fatigue, PTSD, and functional difficulties, and lower quality of life.
Severe impairment on the neuropsychological tests correlated with the extent of acute COVID-19 symptoms, as well as depression scores, number of medical comorbidities, and subjective cognitive complaints.
An analysis of serum levels of the inflammatory markers among 50 of the 60 participants showed that 45% of the patients had an elevated IL-6, 20% had elevated TNF-alpha, and 41% had elevated CRP, compared with reference ranges.
IL-6 levels were found to correlate with acute COVID-19 symptoms, the number of medical comorbidities, fatigue, and measures of executive function, while C-reactive protein (CRP) correlated with current COVID-19 symptoms and depression scores.
In terms of clinical factors that might predict low neuropsychological test scores, Dr. Lynch noted that the “markers that we found to be significant included severity of acute COVID-19 illness, current post-COVID-19 symptoms, measures of depression and anxiety, level of fatigue, and number of medical comorbidities.”
Dr. Lynch noted that the ongoing study will include up to 18-month follow-ups that are currently underway. “The [follow-ups] will examine if symptoms improve over time and evaluate if any intervention that took place was successful,” he said.
Survey supports findings
The detrimental effects of mental health symptoms in long COVID were further supported in another study at the APA meeting, an online survey of 787 survivors of acute COVID-19.
In the community survey, presented by Michael Van Ameringen, MD, a professor in the department of psychiatry and behavioral neurosciences at McMaster University, in Hamilton, Ont., all respondents (100%) reported having persistent symptoms of the virus, and as many as 68% indicated that they had not returned to normal functioning, despite only 15% of the respondents having been hospitalized with COVID-19.
A large proportion showed significant depression, anxiety, and posttraumatic stress disorder (PTSD), and the most commonly reported persistent symptoms were fatigue in 75.9% of respondents, brain fog in 67.9%, concentration difficulties in 61.1%, and weakness in 51.2%.
As many as 88.2% of patients said they experienced persistent neurocognitive symptoms, with poor memory and concentration; 56% reported problems with word finding; and 54.1% had slowed thinking.
The respondents showed high rates of anxiety (41.7%) as well as depression (61.4%) as determined by scores above 9 on the Generalized Anxiety Disorder–7 (GAD-7) and Patient Health Questionnaires (PHQ-9).
As many as 40.5% of respondents showed probable PTSD, with scores above 30 on the PTSD checklist (PCL-5). Their mean resilience score on the Brief Resilient Coping Scale was 13.5, suggesting low resilience.
Among the respondents, 43.3% said they had received past treatment for mental health, while 33.5% were currently receiving mental health treatment.
Dr. Van Ameringen noted the important limitation of the study being an online survey with no control group, but said the responses nevertheless raise the question of the role of prior psychiatric disorders in long COVID.
“In our sample, 40% of respondents had a past psychiatric history, so you wonder if that also makes you vulnerable to long COVID,” he said in an interview.
“About a third were getting psychiatric help, but I think the more impaired you are, the more likely you are to seek help.”
Those who were hospitalized with COVID-19 were at a higher risk of PTSD compared with those not hospitalized (P < .001), as were those under the age of 30 (P < .05) or between 31 and 50 vs. over 50 (P < .01).
Dr. Van Ameringen noted that the survey’s high rate of subjects who had not returned to normal functioning was especially striking.
“This is not a minor issue – these are people who are no longer functioning in society,” he said.
In pandemics, the brain tends to be ‘overlooked’
Further addressing the neurological effects of COVID-19 at the APA meeting, Avindra Nath, MD, clinical director of the National Institutes of Neurologic Disorders and Stroke in Bethesda, Md., noted that the persisting cognitive and psychiatric symptoms after illness, such as brain fog and depression and anxiety, are not necessarily unique to COVID-19.
“We have seen this before,” he said. “There have been at least seven or eight human coronaviruses, and the interesting thing is each one affects the brain and causes neurological complications.”
The effects are classified differently and have slightly different receptors, “but the consequences are the same.”
Of note, however, research published in The Lancet Psychiatry (2021 May. doi: 10.1016/S2215-0366[21]00084-5) revealed that symptoms such as dementia, mood, and anxiety are significantly higher after COVID-19 compared with other respiratory infections, with the differences increasing at 180 days since the index event.
Dr. Nath noted that, over the decades, he has observed that in pandemics “the brain tends to get overlooked.” He explained that “what can be most important in the end is what happened in the brain, because those are the things that really cause the long-term consequences.”
“These patients are depressed; they have dementia, they have brain fog, and even now that we recognize these issues, we haven’t done a very good job of studying them,” he said. “There’s so much we still don’t know, and a lot of patients are left with these symptoms and nowhere to go.”
Dr. Lynch, Dr. Van Ameringen, and Dr. Nath had no disclosures to report.
AT APA 2022
Don’t equate mass shootings with mental illness
Here we go again, and again, and again.
There just aren’t enough tears, and before the bodies of 19 small children are identified, the political noise starts up. Mass shootings are a part of the American landscape, but when they happen at schools, we all feel a distinct sense of violation and gaping grief. Those children are so innocent, so deserving of a right to live their lives, hold their place with their families, create their own legacies, and die of natural causes at a ripe old age. And those children could have been our children. There was nothing special about them; they were just sent to school that day like every child who is sent to school every day.
Here is how the politics goes: The Republicans will blame the Democrats and the Democrats will blame the Republicans. Is Rachel Maddow at fault, or is it Tucker Carlson? Social media accounts blamed both of them for the racially motivated mass murder in a Buffalo grocery store on May 14.
Mass murders were previously defined as a shooting where four or more victims are killed, excluding the shooter, in a public place that is not related to the commission of another crime. In 2012, the definition was changed to include events with three victims. This definition excludes gang violence and the murder of family members.
When it comes to explaining mass murder, the camps divide: They are the result of some combination of mental illness, easy access to firearms, and terrorism and hate. For psychiatry, there is a unique place in the argument – half of all mass shooters have exhibited signs or symptoms of psychiatric illness, and for those who want to deflect the issue away from issues related to the regulation of firearms, it becomes easy to blame “mental illness,” as though that explains it all. Either the gunman “snapped” in such a way that no one could have predicted, or the mental health system is at fault for not preventing it.
There are many ways to be emotionally disturbed; mental illness is only one of them, and there is no psychiatric diagnosis that includes the symptom of shooting strangers, or shooting children. The vast majority of people, including nearly all psychiatrists, will never know someone who perpetrates a mass shooting.
Take John Hinckley Jr., who shot President Ronald Reagan as a means to impress actress Jodie Foster. Sometimes these killings are motivated by delusional beliefs. But the planning and preparation that goes into most mass shootings involves a degree of organization and forethought that we don’t typically see in those with severe psychotic disorders.
The other psychological explanation that satisfies some of a nonmedical population is that these killers “just snap.” This, too, is a term that is not included in our diagnostic vocabulary, but it remains a way for some to explain that which can’t be explained. If mental illness, however, is the cause of mass murders, then more stringent gun control is unnecessary. Every state already has a mechanism to prevent those with criminal and specified psychiatric histories from buying legal firearms, and it may be inevitable that these screens are not perfect.
The next line of political thinking moves to the psychiatric “if only.” If only there were more state hospital beds and if only it were easier to compel people with psychiatric disorders to get treatment against their will, then we could eliminate these crimes. The Virginia tech shooter was mandated to get outpatient psychiatric treatment after a brief hospitalization, yet he never went and there was no mechanism in place to track him.
In cases where a person with a psychotic illness has a history of repeated violent episodes after stopping medications, it does make sense to mandate treatment, not because they are likely to shoot strangers, but because some people do become violent when they are ill and mental illness is believed to play a role in 10% of murders.
Mass murders remain rare, and while advocates for legislation that would make it easier to mandate involuntary care have cited violence prevention as a reason, it is hard to imagine that we would force people to get care because they “might” commit such a crime – unless there was convincing evidence that someone was at risk of committing such a heinous act.
For those who oppose stronger gun control laws, the “what if” may circulate around the need for even more firearms. What if teachers carried guns? What if schools were more heavily policed? What if the criminals were made to be afraid?
We are left with the fact that other countries do not see these numbers of mass shooting events, yet mental illness is ubiquitous. While the presence of psychiatric disorders does little to explain school shootings, we still have no understanding of what motivated the Sandy Hook killer, and it remains to be seen what we will come to understand about the gunman in Uvalde, Texas.
Mental illness is not unique to the United States; however, the number of available firearms is. In a country of 323 million people (including children and people who live in institutions where they have no access to firearms), there are estimated to be over 400 million guns in the United States, 98% of which are owned by civilians.
Hate crimes and terrorism are another explanation for mass murders. In these instances, the gunman makes his motive obvious: There are social media announcements, or the site of the shooting is a synagogue, a mosque, or a location where the victims are of a specific race or religion. But hate may come out of a psychotic illness, and easy access to firearms allows for these crimes to continue.
Firearms are now the No. 1 cause of mortality in children. Very few of these deaths are the result of mass murders. Many more are from accidental deaths, targeted crime, or suicide. Still, school shootings rip at our hearts. Neither the victims nor their grieving families have any role in the act, and suffering leaves its mark on families, communities, and all of us.
Are there answers?
In many states, physicians can now request emergency removal of firearms from the home of someone who is both mentally ill and threatening either suicide or homicide. During the era when high-capacity firearms were banned, from 1994 to 2004, mass murders decreased in our country. While most gunmen use legal firearms they have purchased, I would contend that “smart guns” – firearms that allow only the legal owner to operate them based on biometrics – would prevent some mass shootings and many accidents, crimes, and suicides. Universal background checks and tracking gun purchases in the way we monitor controlled medications, or even Sudafed, might allow authorities to predict who might be at risk of committing these heinous acts.
In his newly released book, Trigger Points: Inside the Mission to Stop Mass Murders in America, journalist Mark Follman argues for a proactive community approach using threat assessment methods and providing wraparound services to those who are deemed to be at risk for violent acts. Mr. Follman’s voice is one of the few out there saying that these events are not random and are, in fact, preventable.
In psychiatry, we struggle with school shootings such as the one we just saw in Uvalde. Our own hearts ache as we hold our children close and empathize with the loss of strangers who have been through the unthinkable. We help our patients as they process their emotions. And we wonder whether any of our patients might ever do anything so horrific. The feelings get complicated, the sadness and anger intermingle while the frustration builds, and we are left with our fears and the hope that if that very rare person were to walk through our office door, we would know what to do.
Dr. Miller is a coauthor of Committed: The Battle Over Involuntary Psychiatric Care (Johns Hopkins University Press, 2016). She has a private practice and is assistant professor of psychiatry and behavioral sciences at Johns Hopkins in Baltimore. A version of this article first appeared on Medscape.com.
Here we go again, and again, and again.
There just aren’t enough tears, and before the bodies of 19 small children are identified, the political noise starts up. Mass shootings are a part of the American landscape, but when they happen at schools, we all feel a distinct sense of violation and gaping grief. Those children are so innocent, so deserving of a right to live their lives, hold their place with their families, create their own legacies, and die of natural causes at a ripe old age. And those children could have been our children. There was nothing special about them; they were just sent to school that day like every child who is sent to school every day.
Here is how the politics goes: The Republicans will blame the Democrats and the Democrats will blame the Republicans. Is Rachel Maddow at fault, or is it Tucker Carlson? Social media accounts blamed both of them for the racially motivated mass murder in a Buffalo grocery store on May 14.
Mass murders were previously defined as a shooting where four or more victims are killed, excluding the shooter, in a public place that is not related to the commission of another crime. In 2012, the definition was changed to include events with three victims. This definition excludes gang violence and the murder of family members.
When it comes to explaining mass murder, the camps divide: They are the result of some combination of mental illness, easy access to firearms, and terrorism and hate. For psychiatry, there is a unique place in the argument – half of all mass shooters have exhibited signs or symptoms of psychiatric illness, and for those who want to deflect the issue away from issues related to the regulation of firearms, it becomes easy to blame “mental illness,” as though that explains it all. Either the gunman “snapped” in such a way that no one could have predicted, or the mental health system is at fault for not preventing it.
There are many ways to be emotionally disturbed; mental illness is only one of them, and there is no psychiatric diagnosis that includes the symptom of shooting strangers, or shooting children. The vast majority of people, including nearly all psychiatrists, will never know someone who perpetrates a mass shooting.
Take John Hinckley Jr., who shot President Ronald Reagan as a means to impress actress Jodie Foster. Sometimes these killings are motivated by delusional beliefs. But the planning and preparation that goes into most mass shootings involves a degree of organization and forethought that we don’t typically see in those with severe psychotic disorders.
The other psychological explanation that satisfies some of a nonmedical population is that these killers “just snap.” This, too, is a term that is not included in our diagnostic vocabulary, but it remains a way for some to explain that which can’t be explained. If mental illness, however, is the cause of mass murders, then more stringent gun control is unnecessary. Every state already has a mechanism to prevent those with criminal and specified psychiatric histories from buying legal firearms, and it may be inevitable that these screens are not perfect.
The next line of political thinking moves to the psychiatric “if only.” If only there were more state hospital beds and if only it were easier to compel people with psychiatric disorders to get treatment against their will, then we could eliminate these crimes. The Virginia tech shooter was mandated to get outpatient psychiatric treatment after a brief hospitalization, yet he never went and there was no mechanism in place to track him.
In cases where a person with a psychotic illness has a history of repeated violent episodes after stopping medications, it does make sense to mandate treatment, not because they are likely to shoot strangers, but because some people do become violent when they are ill and mental illness is believed to play a role in 10% of murders.
Mass murders remain rare, and while advocates for legislation that would make it easier to mandate involuntary care have cited violence prevention as a reason, it is hard to imagine that we would force people to get care because they “might” commit such a crime – unless there was convincing evidence that someone was at risk of committing such a heinous act.
For those who oppose stronger gun control laws, the “what if” may circulate around the need for even more firearms. What if teachers carried guns? What if schools were more heavily policed? What if the criminals were made to be afraid?
We are left with the fact that other countries do not see these numbers of mass shooting events, yet mental illness is ubiquitous. While the presence of psychiatric disorders does little to explain school shootings, we still have no understanding of what motivated the Sandy Hook killer, and it remains to be seen what we will come to understand about the gunman in Uvalde, Texas.
Mental illness is not unique to the United States; however, the number of available firearms is. In a country of 323 million people (including children and people who live in institutions where they have no access to firearms), there are estimated to be over 400 million guns in the United States, 98% of which are owned by civilians.
Hate crimes and terrorism are another explanation for mass murders. In these instances, the gunman makes his motive obvious: There are social media announcements, or the site of the shooting is a synagogue, a mosque, or a location where the victims are of a specific race or religion. But hate may come out of a psychotic illness, and easy access to firearms allows for these crimes to continue.
Firearms are now the No. 1 cause of mortality in children. Very few of these deaths are the result of mass murders. Many more are from accidental deaths, targeted crime, or suicide. Still, school shootings rip at our hearts. Neither the victims nor their grieving families have any role in the act, and suffering leaves its mark on families, communities, and all of us.
Are there answers?
In many states, physicians can now request emergency removal of firearms from the home of someone who is both mentally ill and threatening either suicide or homicide. During the era when high-capacity firearms were banned, from 1994 to 2004, mass murders decreased in our country. While most gunmen use legal firearms they have purchased, I would contend that “smart guns” – firearms that allow only the legal owner to operate them based on biometrics – would prevent some mass shootings and many accidents, crimes, and suicides. Universal background checks and tracking gun purchases in the way we monitor controlled medications, or even Sudafed, might allow authorities to predict who might be at risk of committing these heinous acts.
In his newly released book, Trigger Points: Inside the Mission to Stop Mass Murders in America, journalist Mark Follman argues for a proactive community approach using threat assessment methods and providing wraparound services to those who are deemed to be at risk for violent acts. Mr. Follman’s voice is one of the few out there saying that these events are not random and are, in fact, preventable.
In psychiatry, we struggle with school shootings such as the one we just saw in Uvalde. Our own hearts ache as we hold our children close and empathize with the loss of strangers who have been through the unthinkable. We help our patients as they process their emotions. And we wonder whether any of our patients might ever do anything so horrific. The feelings get complicated, the sadness and anger intermingle while the frustration builds, and we are left with our fears and the hope that if that very rare person were to walk through our office door, we would know what to do.
Dr. Miller is a coauthor of Committed: The Battle Over Involuntary Psychiatric Care (Johns Hopkins University Press, 2016). She has a private practice and is assistant professor of psychiatry and behavioral sciences at Johns Hopkins in Baltimore. A version of this article first appeared on Medscape.com.
Here we go again, and again, and again.
There just aren’t enough tears, and before the bodies of 19 small children are identified, the political noise starts up. Mass shootings are a part of the American landscape, but when they happen at schools, we all feel a distinct sense of violation and gaping grief. Those children are so innocent, so deserving of a right to live their lives, hold their place with their families, create their own legacies, and die of natural causes at a ripe old age. And those children could have been our children. There was nothing special about them; they were just sent to school that day like every child who is sent to school every day.
Here is how the politics goes: The Republicans will blame the Democrats and the Democrats will blame the Republicans. Is Rachel Maddow at fault, or is it Tucker Carlson? Social media accounts blamed both of them for the racially motivated mass murder in a Buffalo grocery store on May 14.
Mass murders were previously defined as a shooting where four or more victims are killed, excluding the shooter, in a public place that is not related to the commission of another crime. In 2012, the definition was changed to include events with three victims. This definition excludes gang violence and the murder of family members.
When it comes to explaining mass murder, the camps divide: They are the result of some combination of mental illness, easy access to firearms, and terrorism and hate. For psychiatry, there is a unique place in the argument – half of all mass shooters have exhibited signs or symptoms of psychiatric illness, and for those who want to deflect the issue away from issues related to the regulation of firearms, it becomes easy to blame “mental illness,” as though that explains it all. Either the gunman “snapped” in such a way that no one could have predicted, or the mental health system is at fault for not preventing it.
There are many ways to be emotionally disturbed; mental illness is only one of them, and there is no psychiatric diagnosis that includes the symptom of shooting strangers, or shooting children. The vast majority of people, including nearly all psychiatrists, will never know someone who perpetrates a mass shooting.
Take John Hinckley Jr., who shot President Ronald Reagan as a means to impress actress Jodie Foster. Sometimes these killings are motivated by delusional beliefs. But the planning and preparation that goes into most mass shootings involves a degree of organization and forethought that we don’t typically see in those with severe psychotic disorders.
The other psychological explanation that satisfies some of a nonmedical population is that these killers “just snap.” This, too, is a term that is not included in our diagnostic vocabulary, but it remains a way for some to explain that which can’t be explained. If mental illness, however, is the cause of mass murders, then more stringent gun control is unnecessary. Every state already has a mechanism to prevent those with criminal and specified psychiatric histories from buying legal firearms, and it may be inevitable that these screens are not perfect.
The next line of political thinking moves to the psychiatric “if only.” If only there were more state hospital beds and if only it were easier to compel people with psychiatric disorders to get treatment against their will, then we could eliminate these crimes. The Virginia tech shooter was mandated to get outpatient psychiatric treatment after a brief hospitalization, yet he never went and there was no mechanism in place to track him.
In cases where a person with a psychotic illness has a history of repeated violent episodes after stopping medications, it does make sense to mandate treatment, not because they are likely to shoot strangers, but because some people do become violent when they are ill and mental illness is believed to play a role in 10% of murders.
Mass murders remain rare, and while advocates for legislation that would make it easier to mandate involuntary care have cited violence prevention as a reason, it is hard to imagine that we would force people to get care because they “might” commit such a crime – unless there was convincing evidence that someone was at risk of committing such a heinous act.
For those who oppose stronger gun control laws, the “what if” may circulate around the need for even more firearms. What if teachers carried guns? What if schools were more heavily policed? What if the criminals were made to be afraid?
We are left with the fact that other countries do not see these numbers of mass shooting events, yet mental illness is ubiquitous. While the presence of psychiatric disorders does little to explain school shootings, we still have no understanding of what motivated the Sandy Hook killer, and it remains to be seen what we will come to understand about the gunman in Uvalde, Texas.
Mental illness is not unique to the United States; however, the number of available firearms is. In a country of 323 million people (including children and people who live in institutions where they have no access to firearms), there are estimated to be over 400 million guns in the United States, 98% of which are owned by civilians.
Hate crimes and terrorism are another explanation for mass murders. In these instances, the gunman makes his motive obvious: There are social media announcements, or the site of the shooting is a synagogue, a mosque, or a location where the victims are of a specific race or religion. But hate may come out of a psychotic illness, and easy access to firearms allows for these crimes to continue.
Firearms are now the No. 1 cause of mortality in children. Very few of these deaths are the result of mass murders. Many more are from accidental deaths, targeted crime, or suicide. Still, school shootings rip at our hearts. Neither the victims nor their grieving families have any role in the act, and suffering leaves its mark on families, communities, and all of us.
Are there answers?
In many states, physicians can now request emergency removal of firearms from the home of someone who is both mentally ill and threatening either suicide or homicide. During the era when high-capacity firearms were banned, from 1994 to 2004, mass murders decreased in our country. While most gunmen use legal firearms they have purchased, I would contend that “smart guns” – firearms that allow only the legal owner to operate them based on biometrics – would prevent some mass shootings and many accidents, crimes, and suicides. Universal background checks and tracking gun purchases in the way we monitor controlled medications, or even Sudafed, might allow authorities to predict who might be at risk of committing these heinous acts.
In his newly released book, Trigger Points: Inside the Mission to Stop Mass Murders in America, journalist Mark Follman argues for a proactive community approach using threat assessment methods and providing wraparound services to those who are deemed to be at risk for violent acts. Mr. Follman’s voice is one of the few out there saying that these events are not random and are, in fact, preventable.
In psychiatry, we struggle with school shootings such as the one we just saw in Uvalde. Our own hearts ache as we hold our children close and empathize with the loss of strangers who have been through the unthinkable. We help our patients as they process their emotions. And we wonder whether any of our patients might ever do anything so horrific. The feelings get complicated, the sadness and anger intermingle while the frustration builds, and we are left with our fears and the hope that if that very rare person were to walk through our office door, we would know what to do.
Dr. Miller is a coauthor of Committed: The Battle Over Involuntary Psychiatric Care (Johns Hopkins University Press, 2016). She has a private practice and is assistant professor of psychiatry and behavioral sciences at Johns Hopkins in Baltimore. A version of this article first appeared on Medscape.com.
What can we do about mass shootings?
“It must be mental illness. My mind cannot possibly conceive of an alternative. A rational healthy mind cannot be capable of this, Doc.”
These were the opening words of one of many discussions that I had with patients in the wake of yet another gut-wrenching tragedy where we saw innocent children and their teachers murdered in school.
This narrative is appealing, regardless of whether or not it is true, because we find some measure of solace in it. We are now at a point in our nation where we are not ashamed to say that we live in a mental health crisis. It is inconceivable to us that a “healthy” brain could plot and premeditate the cold-blooded execution of children.
But just because something feels true does not mean that it actually is.
I personally felt this after a shooter walked into my hospital and shot my coworkers, murdering one and injuring several others. How can this be? It didn’t make a whole lot of sense then. I don’t know if it makes any more sense now. But he had no mental illness that we knew of.
Do any mass shooters have untreated mental illness?
Could we have diagnosed those cases earlier? Intervened sooner? Offered more effective treatment? Certainly. Would that have explain away the rest of the cases? Unfortunately, no.
What is it, then?
The scary answer is that the people who are capable of doing this are not so far away. They are not the folks that we would image locking up in a “psych ward” and throwing away the key. They are, rather, people who are lonely, neglected, rejected, bullied, and broken down by life. Anger, hatred, racism, and evil may be ailments of the soul, but they are not mental illnesses. The carnage they produce is just as tangible. As a psychiatrist, I must admit to you that I do not have a good medication to treat these manifestations of the human condition.
What do we do as a society?
Gun reform is the first obvious and essential answer, without which little else is truly as impactful. We must advocate for it and fight tirelessly.
But at the time you will read this article, your disgruntled coworker will be able to walk into a local store in a moment of despair, anguish, and hopelessness and purchase a semiautomatic weapon of war.
What if we were to start seeing, as a society, that our lives are interwoven? What if we saw that our health is truly interdependent? The COVID-19 pandemic shattered many things in our lives, but one element in particular is our radical individualism. We saw that the choices you make certainly affect me and vice versa. We saw that public health is just that – a public matter, not a private one. We saw that there are some areas of our lives that force us to come together for our own survival.
Perhaps politicians will not save us here. Perhaps kindness will. Empathy can be as potent as legislation, and compassion as impactful as a Twitter hashtag. We each know a lonely coworker, an isolated neighbor, a bullied student, or someone beaten down by life.
What if some of the prevention is in fact in our hands? Together.
“Darkness cannot drive out darkness. Only light can do that. Hate cannot drive out hate; only love can do that.” – Reverend Dr. Martin Luther King, Jr.
Mena Mirhom, MD, is an assistant professor of psychiatry at Columbia University and teaches writing to public psychiatry fellows. He is a board-certified psychiatrist and a consultant for the National Basketball Players Association, treating NBA players and staff.
A version of this article first appeared on Medscape.com.
“It must be mental illness. My mind cannot possibly conceive of an alternative. A rational healthy mind cannot be capable of this, Doc.”
These were the opening words of one of many discussions that I had with patients in the wake of yet another gut-wrenching tragedy where we saw innocent children and their teachers murdered in school.
This narrative is appealing, regardless of whether or not it is true, because we find some measure of solace in it. We are now at a point in our nation where we are not ashamed to say that we live in a mental health crisis. It is inconceivable to us that a “healthy” brain could plot and premeditate the cold-blooded execution of children.
But just because something feels true does not mean that it actually is.
I personally felt this after a shooter walked into my hospital and shot my coworkers, murdering one and injuring several others. How can this be? It didn’t make a whole lot of sense then. I don’t know if it makes any more sense now. But he had no mental illness that we knew of.
Do any mass shooters have untreated mental illness?
Could we have diagnosed those cases earlier? Intervened sooner? Offered more effective treatment? Certainly. Would that have explain away the rest of the cases? Unfortunately, no.
What is it, then?
The scary answer is that the people who are capable of doing this are not so far away. They are not the folks that we would image locking up in a “psych ward” and throwing away the key. They are, rather, people who are lonely, neglected, rejected, bullied, and broken down by life. Anger, hatred, racism, and evil may be ailments of the soul, but they are not mental illnesses. The carnage they produce is just as tangible. As a psychiatrist, I must admit to you that I do not have a good medication to treat these manifestations of the human condition.
What do we do as a society?
Gun reform is the first obvious and essential answer, without which little else is truly as impactful. We must advocate for it and fight tirelessly.
But at the time you will read this article, your disgruntled coworker will be able to walk into a local store in a moment of despair, anguish, and hopelessness and purchase a semiautomatic weapon of war.
What if we were to start seeing, as a society, that our lives are interwoven? What if we saw that our health is truly interdependent? The COVID-19 pandemic shattered many things in our lives, but one element in particular is our radical individualism. We saw that the choices you make certainly affect me and vice versa. We saw that public health is just that – a public matter, not a private one. We saw that there are some areas of our lives that force us to come together for our own survival.
Perhaps politicians will not save us here. Perhaps kindness will. Empathy can be as potent as legislation, and compassion as impactful as a Twitter hashtag. We each know a lonely coworker, an isolated neighbor, a bullied student, or someone beaten down by life.
What if some of the prevention is in fact in our hands? Together.
“Darkness cannot drive out darkness. Only light can do that. Hate cannot drive out hate; only love can do that.” – Reverend Dr. Martin Luther King, Jr.
Mena Mirhom, MD, is an assistant professor of psychiatry at Columbia University and teaches writing to public psychiatry fellows. He is a board-certified psychiatrist and a consultant for the National Basketball Players Association, treating NBA players and staff.
A version of this article first appeared on Medscape.com.
“It must be mental illness. My mind cannot possibly conceive of an alternative. A rational healthy mind cannot be capable of this, Doc.”
These were the opening words of one of many discussions that I had with patients in the wake of yet another gut-wrenching tragedy where we saw innocent children and their teachers murdered in school.
This narrative is appealing, regardless of whether or not it is true, because we find some measure of solace in it. We are now at a point in our nation where we are not ashamed to say that we live in a mental health crisis. It is inconceivable to us that a “healthy” brain could plot and premeditate the cold-blooded execution of children.
But just because something feels true does not mean that it actually is.
I personally felt this after a shooter walked into my hospital and shot my coworkers, murdering one and injuring several others. How can this be? It didn’t make a whole lot of sense then. I don’t know if it makes any more sense now. But he had no mental illness that we knew of.
Do any mass shooters have untreated mental illness?
Could we have diagnosed those cases earlier? Intervened sooner? Offered more effective treatment? Certainly. Would that have explain away the rest of the cases? Unfortunately, no.
What is it, then?
The scary answer is that the people who are capable of doing this are not so far away. They are not the folks that we would image locking up in a “psych ward” and throwing away the key. They are, rather, people who are lonely, neglected, rejected, bullied, and broken down by life. Anger, hatred, racism, and evil may be ailments of the soul, but they are not mental illnesses. The carnage they produce is just as tangible. As a psychiatrist, I must admit to you that I do not have a good medication to treat these manifestations of the human condition.
What do we do as a society?
Gun reform is the first obvious and essential answer, without which little else is truly as impactful. We must advocate for it and fight tirelessly.
But at the time you will read this article, your disgruntled coworker will be able to walk into a local store in a moment of despair, anguish, and hopelessness and purchase a semiautomatic weapon of war.
What if we were to start seeing, as a society, that our lives are interwoven? What if we saw that our health is truly interdependent? The COVID-19 pandemic shattered many things in our lives, but one element in particular is our radical individualism. We saw that the choices you make certainly affect me and vice versa. We saw that public health is just that – a public matter, not a private one. We saw that there are some areas of our lives that force us to come together for our own survival.
Perhaps politicians will not save us here. Perhaps kindness will. Empathy can be as potent as legislation, and compassion as impactful as a Twitter hashtag. We each know a lonely coworker, an isolated neighbor, a bullied student, or someone beaten down by life.
What if some of the prevention is in fact in our hands? Together.
“Darkness cannot drive out darkness. Only light can do that. Hate cannot drive out hate; only love can do that.” – Reverend Dr. Martin Luther King, Jr.
Mena Mirhom, MD, is an assistant professor of psychiatry at Columbia University and teaches writing to public psychiatry fellows. He is a board-certified psychiatrist and a consultant for the National Basketball Players Association, treating NBA players and staff.
A version of this article first appeared on Medscape.com.
The whitest specialty: Bias
As Usha Lee McFarling has pointed out, the orthopedic surgeon specialty suffers from a gross underrepresentation of minorities and women, more severe than in other medical specialties. There are various reasons for this and a variety of possible paths toward improvement, but the “critical first step,” as American Academy of Orthopedic Surgeons former president Kristy Weber, MD, told Ms. McFarling, “is changing the culture.”
“Changing the culture” is a large, diffuse aspiration. The AAOS has taken a number of steps toward that end, but they have not had much success. The two of us have identified others, which may help to move the needle.
Viewed from this perspective, the cultural barriers to inclusivity are similar to those that perpetuate inequitable health care. Both are driven by ingroup/outgroup prejudices that operate below the level of consciousness and are largely unseen.In our book Seeing Patients, we examined health disparities in six “non-mainstream” groups: African Americans, Hispanic Americans, women, gays and lesbians, and the elderly. We based our work initially on the Institute of Medicine’s breakthrough 2003 compendium, Unequal Treatment, which brought together a large number of studies on health care inequities that had appeared in a variety of journals over many years, but had never generated the critical mass necessary to create a call for action or even attract serious attention.
Unequal Treatment allowed us to understand that each medical specialty, right down the line – orthopedics, cardiology, gynecology, oncology, psychiatry, to name just a few – has its own grim history of discrimination. Our sense of the medical community in the 21st century led us away from the idea that overt bias is a significant cause of these still ongoing inequities. Most physicians, we believed, consider themselves to be, and strive to be, humane, compassionate, and egalitarian caregivers. The answer then seemed to be in subconscious rather than conscious bias.
As we reviewed the literature and strove to understand the primary drivers of the discrimination that systematically affects medical care, our attention was drawn to two critical and complementary mechanisms hard-wired into our systems for parsing and responding to our environment. The first was “stereotyping,” so often used as a pejorative, but which is, in fact, a primary and essential mental function.
“We all make stereotypic judgments,” says Rice University emeritus professor of psychology David Schneider in The Psychology of Stereotyping (page 419). “It happens with race. It happens with disability. It happens ... with gender, age, and physical appearance. ... That’s just the way it is: Our mental apparatus was designed to facilitate quick decisions based on category membership.”
Differentiation – social stereotyping in our case – is a given, then; it’s innate. The content of stereotyping – of Blacks, gays, women, and others – is not innate, but it is deeply ingrained by living in a given milieu and just as impossible to ignore.
The second mechanism we focused on was the neurobiology that underlies the impact of hidden emotion on rational thought. In his seminal book Descartes’ Error, neuroscientist Antonio Damasio spells out how the mind with its cognitive functions has evolved from the body and its emotional systems, and how they function together through neuro-networks that connect the mechanisms of feeling with the brain’s decision-making centers.
“Feelings,” Dr. Damasio tells us, “come first in [brain] development and retain a primacy that pervades our mental life.” The limbic system, the part of the brain that controls our emotional responses, constitutes a “frame of reference and has “a say on how the rest of the brain and cognition go about their business. [Its] influence is immense.” (Page 185)
Dr. Damasio was not focusing on medical decisions, but his insights, we felt, had great relevance for the question of unconscious bias in health care. Various studies by physicians and medical scientists do speak directly to the issue of how affective bias influences diagnosis and treatment. Pat Croskerry, director of Dalhousie University’s Clinical Research Center, argues that “cognitive and affective biases are known to compromise the decision-making” and that commonly “these are largely unconscious mistakes.”
Harvard’s Jerome Groopman, in his book How Doctors Think (page 40), writes that most incorrect diagnoses and treatments are “mistakes in thinking. And part of what causes these cognitive errors is our inner feelings, feelings we ... often don’t even recognize.” Cognition and emotion, Dr. Groopman insists, are inseparable. The emotional landscape sets the ground for decision-making.
The underlying mechanisms that enable health care prejudice are the same that enable interpersonal prejudice generally. Unseen and largely unrecognized, they affect ingroup/outgroup relations in every field of interaction, from bias in policing, to bias in housing, to bias in employment – “powerful and universal,” in Dr. Croskerry’s words, “affecting all walks of life.”
Decision-making about acceptance into orthopedic residencies is no exception. As Prof. Schneider says, “That’s just the way it is.”
What conclusions can be drawn from understanding the deep origins of subconscious bias that might improve the inclusion of minorities and women in orthopedics? A growing interest in “debiasing” in both the medical and cognitive psychology literature has identified or suggested methods of counteracting the prejudices we all harbor. (See Bhatti’s “Cognitive Bias in Clinical Practice,” Wilson and Brekke’s “Mental Contamination and Mental Correction: Unwanted Influences on Judgments and Evaluations,” and De Neys and colleagues’ “Feeling We’re Biased: Autonomic Arousal and Reasoning Conflict.”)
Many of these debiasing techniques have to do with education regarding cognitive functions, from training in decision-making processes to “time outs,” to checklists à la Atul Gawande, to other methods of metacognition.
But the two key prerequisites to all of these approaches are more or less self-evident. “For biases to be successfully addressed,” says Dr. Croskerry, “there needs to be ... awareness as well as the motivation for change.”
In a previous article we discussed the need to heighten awareness over and above current levels, and we have suggested steps toward that end. But awareness is only the first prerequisite; the second is motivation, and the depth of motivation necessary to create change in the business of orthopedic inclusion is, for all the AAOS’s efforts, simply inadequate – the result being that the culture does not change, or it changes so glacially as to be hardly noticeable.
Ms. McFarling noted in her interviews with orthopedic leaders, clinicians, residents, and medical students simmering feelings of frustration and perplexity. We would suggest that the frustration is because of the fact that, while there is a general awareness of the problem, there has simply not been the sufficiently determined motivation to fix it. “It is not neglected truths,” as religious scholar Gregory Dix put it, “but those that are at once fully acknowledged and frustrated of their proper expression, which take the most drastic psychological revenge.”
All of this leads back to the original problem posed by Prof. Weber, the former AAOS president: changing the orthopedic culture. The question of how cultures undergo transformation has been addressed by scholars across widely diverse fields (see, for example, Thomas Kuhn’s The Structure of Scientific Revolutions, Francis Fukuyama›s The End of History and the Last Man, and many others). But we are addressing here a narrow, well-defined slice of that problem. And our own explorations have led to the conclusion that the answer here lies in the issue of motivation – namely, how can a community that is aware of a problem be sufficiently motivated to fix it?
In Seeing Patients we argued that doctoring is the paradigmatic humanitarian profession, that physicians’ whole business is to care for and alleviate the suffering of other human beings. In this sense, doctors are the carriers of the humane ideal, which is congruent also with the noblest egalitarian principles of our life as a nation. We argued also that humanitarian medicine with its egalitarian mandate is a win-win-win proposition. The patient wins, the doctor wins, the society wins.
We think arguments like these should provide plenty of motivation for change. But in reality they are not sufficient. Our arguments and those of others along the same lines (see Louis Sullivan’s Breaking Ground and David McBride’s Caring for Equality) are directed for the most part at the better angels of our nature. They appeal to personal and political values: compassion, fairness, equality – powerful yet set against custom, habituation, and the daily pressures of practice, such arguments can and do easily come up short.
But when looked at straight on, with unblinking eyes, health care disparities should provoke other more forceful emotions: anger, to begin with; chagrin, consternation. Women receive fewer heart catheterizations and reperfusions than men. (See R. Di Cecco and colleagues’ “Is There a Clinically Significant Gender Bias in Post-Myocardial Infarction Pharmacological Management in the Older Population of a Primary Care Practice?” and Jneid and coworkers’ “Sex Difference in Medical Care and Early Death after Acute Myocardial Infarction.”) Because of this, more women die.
Blacks and Hispanics receive fewer analgesics for the excruciating pain of broken bones, and they are amputated more frequently than whites for identical peripheral arterial disease. (See Knox and colleagues’ “Ethnicity as a Risk Factor for Inadequate Emergency Department Analgesia,” Bonham’s “Race, Ethnicity and Pain Treatments: Striving to Understand the Causes and Solutions to the Disparities in Pain Treatments,” and Feinglass and coworkers’ “Racial Differences in Primary and Repeat Lower Extremity Amputation: Results From a Multihospital Study.”) They suffer accordingly.
The statistical accounting of these disparities masks the faces of pain and desperation – of disabilities, often of mortality. These are hard visceral truths that derive in part from the underrepresentation of minorities in various specialties, most pronounced in orthopedics. These are the truths that, when actually absorbed rather than just registered, have the capacity to transform awareness into motivation and in so doing can begin reshaping a culture that restricts minorities and women and makes orthopedics, as Ms. McFarling calls it, “the whitest specialty.”
A version of this article first appeared on Medscape.com.
As Usha Lee McFarling has pointed out, the orthopedic surgeon specialty suffers from a gross underrepresentation of minorities and women, more severe than in other medical specialties. There are various reasons for this and a variety of possible paths toward improvement, but the “critical first step,” as American Academy of Orthopedic Surgeons former president Kristy Weber, MD, told Ms. McFarling, “is changing the culture.”
“Changing the culture” is a large, diffuse aspiration. The AAOS has taken a number of steps toward that end, but they have not had much success. The two of us have identified others, which may help to move the needle.
Viewed from this perspective, the cultural barriers to inclusivity are similar to those that perpetuate inequitable health care. Both are driven by ingroup/outgroup prejudices that operate below the level of consciousness and are largely unseen.In our book Seeing Patients, we examined health disparities in six “non-mainstream” groups: African Americans, Hispanic Americans, women, gays and lesbians, and the elderly. We based our work initially on the Institute of Medicine’s breakthrough 2003 compendium, Unequal Treatment, which brought together a large number of studies on health care inequities that had appeared in a variety of journals over many years, but had never generated the critical mass necessary to create a call for action or even attract serious attention.
Unequal Treatment allowed us to understand that each medical specialty, right down the line – orthopedics, cardiology, gynecology, oncology, psychiatry, to name just a few – has its own grim history of discrimination. Our sense of the medical community in the 21st century led us away from the idea that overt bias is a significant cause of these still ongoing inequities. Most physicians, we believed, consider themselves to be, and strive to be, humane, compassionate, and egalitarian caregivers. The answer then seemed to be in subconscious rather than conscious bias.
As we reviewed the literature and strove to understand the primary drivers of the discrimination that systematically affects medical care, our attention was drawn to two critical and complementary mechanisms hard-wired into our systems for parsing and responding to our environment. The first was “stereotyping,” so often used as a pejorative, but which is, in fact, a primary and essential mental function.
“We all make stereotypic judgments,” says Rice University emeritus professor of psychology David Schneider in The Psychology of Stereotyping (page 419). “It happens with race. It happens with disability. It happens ... with gender, age, and physical appearance. ... That’s just the way it is: Our mental apparatus was designed to facilitate quick decisions based on category membership.”
Differentiation – social stereotyping in our case – is a given, then; it’s innate. The content of stereotyping – of Blacks, gays, women, and others – is not innate, but it is deeply ingrained by living in a given milieu and just as impossible to ignore.
The second mechanism we focused on was the neurobiology that underlies the impact of hidden emotion on rational thought. In his seminal book Descartes’ Error, neuroscientist Antonio Damasio spells out how the mind with its cognitive functions has evolved from the body and its emotional systems, and how they function together through neuro-networks that connect the mechanisms of feeling with the brain’s decision-making centers.
“Feelings,” Dr. Damasio tells us, “come first in [brain] development and retain a primacy that pervades our mental life.” The limbic system, the part of the brain that controls our emotional responses, constitutes a “frame of reference and has “a say on how the rest of the brain and cognition go about their business. [Its] influence is immense.” (Page 185)
Dr. Damasio was not focusing on medical decisions, but his insights, we felt, had great relevance for the question of unconscious bias in health care. Various studies by physicians and medical scientists do speak directly to the issue of how affective bias influences diagnosis and treatment. Pat Croskerry, director of Dalhousie University’s Clinical Research Center, argues that “cognitive and affective biases are known to compromise the decision-making” and that commonly “these are largely unconscious mistakes.”
Harvard’s Jerome Groopman, in his book How Doctors Think (page 40), writes that most incorrect diagnoses and treatments are “mistakes in thinking. And part of what causes these cognitive errors is our inner feelings, feelings we ... often don’t even recognize.” Cognition and emotion, Dr. Groopman insists, are inseparable. The emotional landscape sets the ground for decision-making.
The underlying mechanisms that enable health care prejudice are the same that enable interpersonal prejudice generally. Unseen and largely unrecognized, they affect ingroup/outgroup relations in every field of interaction, from bias in policing, to bias in housing, to bias in employment – “powerful and universal,” in Dr. Croskerry’s words, “affecting all walks of life.”
Decision-making about acceptance into orthopedic residencies is no exception. As Prof. Schneider says, “That’s just the way it is.”
What conclusions can be drawn from understanding the deep origins of subconscious bias that might improve the inclusion of minorities and women in orthopedics? A growing interest in “debiasing” in both the medical and cognitive psychology literature has identified or suggested methods of counteracting the prejudices we all harbor. (See Bhatti’s “Cognitive Bias in Clinical Practice,” Wilson and Brekke’s “Mental Contamination and Mental Correction: Unwanted Influences on Judgments and Evaluations,” and De Neys and colleagues’ “Feeling We’re Biased: Autonomic Arousal and Reasoning Conflict.”)
Many of these debiasing techniques have to do with education regarding cognitive functions, from training in decision-making processes to “time outs,” to checklists à la Atul Gawande, to other methods of metacognition.
But the two key prerequisites to all of these approaches are more or less self-evident. “For biases to be successfully addressed,” says Dr. Croskerry, “there needs to be ... awareness as well as the motivation for change.”
In a previous article we discussed the need to heighten awareness over and above current levels, and we have suggested steps toward that end. But awareness is only the first prerequisite; the second is motivation, and the depth of motivation necessary to create change in the business of orthopedic inclusion is, for all the AAOS’s efforts, simply inadequate – the result being that the culture does not change, or it changes so glacially as to be hardly noticeable.
Ms. McFarling noted in her interviews with orthopedic leaders, clinicians, residents, and medical students simmering feelings of frustration and perplexity. We would suggest that the frustration is because of the fact that, while there is a general awareness of the problem, there has simply not been the sufficiently determined motivation to fix it. “It is not neglected truths,” as religious scholar Gregory Dix put it, “but those that are at once fully acknowledged and frustrated of their proper expression, which take the most drastic psychological revenge.”
All of this leads back to the original problem posed by Prof. Weber, the former AAOS president: changing the orthopedic culture. The question of how cultures undergo transformation has been addressed by scholars across widely diverse fields (see, for example, Thomas Kuhn’s The Structure of Scientific Revolutions, Francis Fukuyama›s The End of History and the Last Man, and many others). But we are addressing here a narrow, well-defined slice of that problem. And our own explorations have led to the conclusion that the answer here lies in the issue of motivation – namely, how can a community that is aware of a problem be sufficiently motivated to fix it?
In Seeing Patients we argued that doctoring is the paradigmatic humanitarian profession, that physicians’ whole business is to care for and alleviate the suffering of other human beings. In this sense, doctors are the carriers of the humane ideal, which is congruent also with the noblest egalitarian principles of our life as a nation. We argued also that humanitarian medicine with its egalitarian mandate is a win-win-win proposition. The patient wins, the doctor wins, the society wins.
We think arguments like these should provide plenty of motivation for change. But in reality they are not sufficient. Our arguments and those of others along the same lines (see Louis Sullivan’s Breaking Ground and David McBride’s Caring for Equality) are directed for the most part at the better angels of our nature. They appeal to personal and political values: compassion, fairness, equality – powerful yet set against custom, habituation, and the daily pressures of practice, such arguments can and do easily come up short.
But when looked at straight on, with unblinking eyes, health care disparities should provoke other more forceful emotions: anger, to begin with; chagrin, consternation. Women receive fewer heart catheterizations and reperfusions than men. (See R. Di Cecco and colleagues’ “Is There a Clinically Significant Gender Bias in Post-Myocardial Infarction Pharmacological Management in the Older Population of a Primary Care Practice?” and Jneid and coworkers’ “Sex Difference in Medical Care and Early Death after Acute Myocardial Infarction.”) Because of this, more women die.
Blacks and Hispanics receive fewer analgesics for the excruciating pain of broken bones, and they are amputated more frequently than whites for identical peripheral arterial disease. (See Knox and colleagues’ “Ethnicity as a Risk Factor for Inadequate Emergency Department Analgesia,” Bonham’s “Race, Ethnicity and Pain Treatments: Striving to Understand the Causes and Solutions to the Disparities in Pain Treatments,” and Feinglass and coworkers’ “Racial Differences in Primary and Repeat Lower Extremity Amputation: Results From a Multihospital Study.”) They suffer accordingly.
The statistical accounting of these disparities masks the faces of pain and desperation – of disabilities, often of mortality. These are hard visceral truths that derive in part from the underrepresentation of minorities in various specialties, most pronounced in orthopedics. These are the truths that, when actually absorbed rather than just registered, have the capacity to transform awareness into motivation and in so doing can begin reshaping a culture that restricts minorities and women and makes orthopedics, as Ms. McFarling calls it, “the whitest specialty.”
A version of this article first appeared on Medscape.com.
As Usha Lee McFarling has pointed out, the orthopedic surgeon specialty suffers from a gross underrepresentation of minorities and women, more severe than in other medical specialties. There are various reasons for this and a variety of possible paths toward improvement, but the “critical first step,” as American Academy of Orthopedic Surgeons former president Kristy Weber, MD, told Ms. McFarling, “is changing the culture.”
“Changing the culture” is a large, diffuse aspiration. The AAOS has taken a number of steps toward that end, but they have not had much success. The two of us have identified others, which may help to move the needle.
Viewed from this perspective, the cultural barriers to inclusivity are similar to those that perpetuate inequitable health care. Both are driven by ingroup/outgroup prejudices that operate below the level of consciousness and are largely unseen.In our book Seeing Patients, we examined health disparities in six “non-mainstream” groups: African Americans, Hispanic Americans, women, gays and lesbians, and the elderly. We based our work initially on the Institute of Medicine’s breakthrough 2003 compendium, Unequal Treatment, which brought together a large number of studies on health care inequities that had appeared in a variety of journals over many years, but had never generated the critical mass necessary to create a call for action or even attract serious attention.
Unequal Treatment allowed us to understand that each medical specialty, right down the line – orthopedics, cardiology, gynecology, oncology, psychiatry, to name just a few – has its own grim history of discrimination. Our sense of the medical community in the 21st century led us away from the idea that overt bias is a significant cause of these still ongoing inequities. Most physicians, we believed, consider themselves to be, and strive to be, humane, compassionate, and egalitarian caregivers. The answer then seemed to be in subconscious rather than conscious bias.
As we reviewed the literature and strove to understand the primary drivers of the discrimination that systematically affects medical care, our attention was drawn to two critical and complementary mechanisms hard-wired into our systems for parsing and responding to our environment. The first was “stereotyping,” so often used as a pejorative, but which is, in fact, a primary and essential mental function.
“We all make stereotypic judgments,” says Rice University emeritus professor of psychology David Schneider in The Psychology of Stereotyping (page 419). “It happens with race. It happens with disability. It happens ... with gender, age, and physical appearance. ... That’s just the way it is: Our mental apparatus was designed to facilitate quick decisions based on category membership.”
Differentiation – social stereotyping in our case – is a given, then; it’s innate. The content of stereotyping – of Blacks, gays, women, and others – is not innate, but it is deeply ingrained by living in a given milieu and just as impossible to ignore.
The second mechanism we focused on was the neurobiology that underlies the impact of hidden emotion on rational thought. In his seminal book Descartes’ Error, neuroscientist Antonio Damasio spells out how the mind with its cognitive functions has evolved from the body and its emotional systems, and how they function together through neuro-networks that connect the mechanisms of feeling with the brain’s decision-making centers.
“Feelings,” Dr. Damasio tells us, “come first in [brain] development and retain a primacy that pervades our mental life.” The limbic system, the part of the brain that controls our emotional responses, constitutes a “frame of reference and has “a say on how the rest of the brain and cognition go about their business. [Its] influence is immense.” (Page 185)
Dr. Damasio was not focusing on medical decisions, but his insights, we felt, had great relevance for the question of unconscious bias in health care. Various studies by physicians and medical scientists do speak directly to the issue of how affective bias influences diagnosis and treatment. Pat Croskerry, director of Dalhousie University’s Clinical Research Center, argues that “cognitive and affective biases are known to compromise the decision-making” and that commonly “these are largely unconscious mistakes.”
Harvard’s Jerome Groopman, in his book How Doctors Think (page 40), writes that most incorrect diagnoses and treatments are “mistakes in thinking. And part of what causes these cognitive errors is our inner feelings, feelings we ... often don’t even recognize.” Cognition and emotion, Dr. Groopman insists, are inseparable. The emotional landscape sets the ground for decision-making.
The underlying mechanisms that enable health care prejudice are the same that enable interpersonal prejudice generally. Unseen and largely unrecognized, they affect ingroup/outgroup relations in every field of interaction, from bias in policing, to bias in housing, to bias in employment – “powerful and universal,” in Dr. Croskerry’s words, “affecting all walks of life.”
Decision-making about acceptance into orthopedic residencies is no exception. As Prof. Schneider says, “That’s just the way it is.”
What conclusions can be drawn from understanding the deep origins of subconscious bias that might improve the inclusion of minorities and women in orthopedics? A growing interest in “debiasing” in both the medical and cognitive psychology literature has identified or suggested methods of counteracting the prejudices we all harbor. (See Bhatti’s “Cognitive Bias in Clinical Practice,” Wilson and Brekke’s “Mental Contamination and Mental Correction: Unwanted Influences on Judgments and Evaluations,” and De Neys and colleagues’ “Feeling We’re Biased: Autonomic Arousal and Reasoning Conflict.”)
Many of these debiasing techniques have to do with education regarding cognitive functions, from training in decision-making processes to “time outs,” to checklists à la Atul Gawande, to other methods of metacognition.
But the two key prerequisites to all of these approaches are more or less self-evident. “For biases to be successfully addressed,” says Dr. Croskerry, “there needs to be ... awareness as well as the motivation for change.”
In a previous article we discussed the need to heighten awareness over and above current levels, and we have suggested steps toward that end. But awareness is only the first prerequisite; the second is motivation, and the depth of motivation necessary to create change in the business of orthopedic inclusion is, for all the AAOS’s efforts, simply inadequate – the result being that the culture does not change, or it changes so glacially as to be hardly noticeable.
Ms. McFarling noted in her interviews with orthopedic leaders, clinicians, residents, and medical students simmering feelings of frustration and perplexity. We would suggest that the frustration is because of the fact that, while there is a general awareness of the problem, there has simply not been the sufficiently determined motivation to fix it. “It is not neglected truths,” as religious scholar Gregory Dix put it, “but those that are at once fully acknowledged and frustrated of their proper expression, which take the most drastic psychological revenge.”
All of this leads back to the original problem posed by Prof. Weber, the former AAOS president: changing the orthopedic culture. The question of how cultures undergo transformation has been addressed by scholars across widely diverse fields (see, for example, Thomas Kuhn’s The Structure of Scientific Revolutions, Francis Fukuyama›s The End of History and the Last Man, and many others). But we are addressing here a narrow, well-defined slice of that problem. And our own explorations have led to the conclusion that the answer here lies in the issue of motivation – namely, how can a community that is aware of a problem be sufficiently motivated to fix it?
In Seeing Patients we argued that doctoring is the paradigmatic humanitarian profession, that physicians’ whole business is to care for and alleviate the suffering of other human beings. In this sense, doctors are the carriers of the humane ideal, which is congruent also with the noblest egalitarian principles of our life as a nation. We argued also that humanitarian medicine with its egalitarian mandate is a win-win-win proposition. The patient wins, the doctor wins, the society wins.
We think arguments like these should provide plenty of motivation for change. But in reality they are not sufficient. Our arguments and those of others along the same lines (see Louis Sullivan’s Breaking Ground and David McBride’s Caring for Equality) are directed for the most part at the better angels of our nature. They appeal to personal and political values: compassion, fairness, equality – powerful yet set against custom, habituation, and the daily pressures of practice, such arguments can and do easily come up short.
But when looked at straight on, with unblinking eyes, health care disparities should provoke other more forceful emotions: anger, to begin with; chagrin, consternation. Women receive fewer heart catheterizations and reperfusions than men. (See R. Di Cecco and colleagues’ “Is There a Clinically Significant Gender Bias in Post-Myocardial Infarction Pharmacological Management in the Older Population of a Primary Care Practice?” and Jneid and coworkers’ “Sex Difference in Medical Care and Early Death after Acute Myocardial Infarction.”) Because of this, more women die.
Blacks and Hispanics receive fewer analgesics for the excruciating pain of broken bones, and they are amputated more frequently than whites for identical peripheral arterial disease. (See Knox and colleagues’ “Ethnicity as a Risk Factor for Inadequate Emergency Department Analgesia,” Bonham’s “Race, Ethnicity and Pain Treatments: Striving to Understand the Causes and Solutions to the Disparities in Pain Treatments,” and Feinglass and coworkers’ “Racial Differences in Primary and Repeat Lower Extremity Amputation: Results From a Multihospital Study.”) They suffer accordingly.
The statistical accounting of these disparities masks the faces of pain and desperation – of disabilities, often of mortality. These are hard visceral truths that derive in part from the underrepresentation of minorities in various specialties, most pronounced in orthopedics. These are the truths that, when actually absorbed rather than just registered, have the capacity to transform awareness into motivation and in so doing can begin reshaping a culture that restricts minorities and women and makes orthopedics, as Ms. McFarling calls it, “the whitest specialty.”
A version of this article first appeared on Medscape.com.
Medical trauma an under-recognized trigger for PTSD
NEW ORLEANS – Recent studies have confirmed that posttraumatic stress disorder can be triggered by health-related stress such as stints in the ICU and life-threatening medical emergencies, but most psychiatrists may not be aware of the latest research, according to an expert in mental trauma.
“This is true among children as well as adults, but it is not generally appreciated by psychiatrists and not at all by non-physicians,” said Charles B. Nemeroff, MD, PhD, professor and chair of the department of psychiatry and behavioral sciences at the University of Texas at Austin’s Dell Medical School, in a presentation at the annual meeting of the American Psychiatric Association. “It’s something that we all need to educate our colleagues about.”
As Dr. Nemeroff noted in a wide-ranging discussion about the latest trends in PTSD diagnosis and treatment, the DSM-5 doesn’t yet mention medical trauma in its definition of PTSD but refers more vaguely to triggering events that involve “actual or threatened death, serious injury, or sexual violence.”
However, multiple recent studies have linked medical trauma to PTSD. A 2019 study in Intensive Care Medicine found that 25% of 99 patients who were treated for emergency respiratory or cardiovascular crises showed PTSD symptoms at 6 months, and the percentage of childhood cancer survivors with PTSD was estimated at as high as 22%, according to research published in Frontiers in Psychology.In 2013, a meta-analysis suggested that 23% of stroke survivors have PTSD symptoms within 1 year, and 11% after 1 year.
PTSD is unique
Dr. Nemeroff noted that PTSD is the only diagnosis in the DSM-5 that’s directly linked to an environmental event. Specifically, he said, PTSD is caused by “very unexpected traumatic events that occur outside the normal repertoire of human behavior.”
In response, “most people that have an acute stress disorder response will fundamentally extinguish it and end up returning to the baseline level of functioning,” he said. But those with PTSD do not recover.
Dr. Nemeroff recommends the use of the 20-question self-report tool known as PCL-5. “It’s your friend,” he said. “It takes a few minutes for the patients to fill out while in the front office, and it doesn’t cost anything. Most patients who have PTSD will have a score of 50-55, maybe 60. You’re going to try to get them down to below 30, and you’re going to give this to them every time they come to your office to follow their progress. It works like a charm.”
As for treatment, psychotherapy and medications remain standard, he said, although “PTSD is a tough disorder to treat.”
According to him, brief cognitive behavioral therapy (CBT) – 4-5 sessions – has shown the greatest benefit and highest level of evidence in support when initiated within 4-30 days of trauma. Group therapy may be helpful, while it’s not clear if spiritual support and “psychological first aid” are useful during this time period.
There’s no evidence that medications such as SSRIs and atypical antipsychotics will prevent PTSD from developing; typical antipsychotics are not recommended. Individual or group “debriefing” is highly not recommended, Dr. Nemeroff said, because the experience can re-traumatize patients, as researchers learned after 9/11 when encouraging people to relive their experiences triggered PTSD and heartbreak.
Also not recommended: Benzodiazepines and formal psychotherapy in people without symptoms.
Exposure-based CBT has been proven to be successful, Dr. Nemeroff said, but it must be provided by a trained professional. “Going for a weekend course isn’t sufficient,” he said, and research suggests that group CBT is not as helpfulas individual CBT.
As for medication over the longer term, research supports SNRIs and SSRIs such as sertaline (Zoloft) and paroxetine (Paxil). Dr. Nemeroff is a fan of venlafaxine (Effexor): “It has a wide dose range. I can go from 75 to 150 milligrams at the low end and 450 and even 600 milligrams at the high end. I’ve had some amazing successes.”
In addition, atypical antipsychotics can be helpful in non-responders or psychotic PTSD patients, he said.
Dr. Nemeroff said he’s skeptical of ketamine as a treatment for PTSD, but he’s most hopeful about MDMA-assisted therapy due to “impressive data” regarding PTSD that was released last year. A bid for FDA approval is in the works, he said.
He added that data is promising from trials examining transcranial magnetic stimulationand (in work by his own team) electroconvulsive therapy. Both therapies are worth considering, he said.
Dr. Nemeroff reported multiple disclosures including research/grant support, stock holdings, scientific advisory board service, consulting relationships, board of director service, and patents.
NEW ORLEANS – Recent studies have confirmed that posttraumatic stress disorder can be triggered by health-related stress such as stints in the ICU and life-threatening medical emergencies, but most psychiatrists may not be aware of the latest research, according to an expert in mental trauma.
“This is true among children as well as adults, but it is not generally appreciated by psychiatrists and not at all by non-physicians,” said Charles B. Nemeroff, MD, PhD, professor and chair of the department of psychiatry and behavioral sciences at the University of Texas at Austin’s Dell Medical School, in a presentation at the annual meeting of the American Psychiatric Association. “It’s something that we all need to educate our colleagues about.”
As Dr. Nemeroff noted in a wide-ranging discussion about the latest trends in PTSD diagnosis and treatment, the DSM-5 doesn’t yet mention medical trauma in its definition of PTSD but refers more vaguely to triggering events that involve “actual or threatened death, serious injury, or sexual violence.”
However, multiple recent studies have linked medical trauma to PTSD. A 2019 study in Intensive Care Medicine found that 25% of 99 patients who were treated for emergency respiratory or cardiovascular crises showed PTSD symptoms at 6 months, and the percentage of childhood cancer survivors with PTSD was estimated at as high as 22%, according to research published in Frontiers in Psychology.In 2013, a meta-analysis suggested that 23% of stroke survivors have PTSD symptoms within 1 year, and 11% after 1 year.
PTSD is unique
Dr. Nemeroff noted that PTSD is the only diagnosis in the DSM-5 that’s directly linked to an environmental event. Specifically, he said, PTSD is caused by “very unexpected traumatic events that occur outside the normal repertoire of human behavior.”
In response, “most people that have an acute stress disorder response will fundamentally extinguish it and end up returning to the baseline level of functioning,” he said. But those with PTSD do not recover.
Dr. Nemeroff recommends the use of the 20-question self-report tool known as PCL-5. “It’s your friend,” he said. “It takes a few minutes for the patients to fill out while in the front office, and it doesn’t cost anything. Most patients who have PTSD will have a score of 50-55, maybe 60. You’re going to try to get them down to below 30, and you’re going to give this to them every time they come to your office to follow their progress. It works like a charm.”
As for treatment, psychotherapy and medications remain standard, he said, although “PTSD is a tough disorder to treat.”
According to him, brief cognitive behavioral therapy (CBT) – 4-5 sessions – has shown the greatest benefit and highest level of evidence in support when initiated within 4-30 days of trauma. Group therapy may be helpful, while it’s not clear if spiritual support and “psychological first aid” are useful during this time period.
There’s no evidence that medications such as SSRIs and atypical antipsychotics will prevent PTSD from developing; typical antipsychotics are not recommended. Individual or group “debriefing” is highly not recommended, Dr. Nemeroff said, because the experience can re-traumatize patients, as researchers learned after 9/11 when encouraging people to relive their experiences triggered PTSD and heartbreak.
Also not recommended: Benzodiazepines and formal psychotherapy in people without symptoms.
Exposure-based CBT has been proven to be successful, Dr. Nemeroff said, but it must be provided by a trained professional. “Going for a weekend course isn’t sufficient,” he said, and research suggests that group CBT is not as helpfulas individual CBT.
As for medication over the longer term, research supports SNRIs and SSRIs such as sertaline (Zoloft) and paroxetine (Paxil). Dr. Nemeroff is a fan of venlafaxine (Effexor): “It has a wide dose range. I can go from 75 to 150 milligrams at the low end and 450 and even 600 milligrams at the high end. I’ve had some amazing successes.”
In addition, atypical antipsychotics can be helpful in non-responders or psychotic PTSD patients, he said.
Dr. Nemeroff said he’s skeptical of ketamine as a treatment for PTSD, but he’s most hopeful about MDMA-assisted therapy due to “impressive data” regarding PTSD that was released last year. A bid for FDA approval is in the works, he said.
He added that data is promising from trials examining transcranial magnetic stimulationand (in work by his own team) electroconvulsive therapy. Both therapies are worth considering, he said.
Dr. Nemeroff reported multiple disclosures including research/grant support, stock holdings, scientific advisory board service, consulting relationships, board of director service, and patents.
NEW ORLEANS – Recent studies have confirmed that posttraumatic stress disorder can be triggered by health-related stress such as stints in the ICU and life-threatening medical emergencies, but most psychiatrists may not be aware of the latest research, according to an expert in mental trauma.
“This is true among children as well as adults, but it is not generally appreciated by psychiatrists and not at all by non-physicians,” said Charles B. Nemeroff, MD, PhD, professor and chair of the department of psychiatry and behavioral sciences at the University of Texas at Austin’s Dell Medical School, in a presentation at the annual meeting of the American Psychiatric Association. “It’s something that we all need to educate our colleagues about.”
As Dr. Nemeroff noted in a wide-ranging discussion about the latest trends in PTSD diagnosis and treatment, the DSM-5 doesn’t yet mention medical trauma in its definition of PTSD but refers more vaguely to triggering events that involve “actual or threatened death, serious injury, or sexual violence.”
However, multiple recent studies have linked medical trauma to PTSD. A 2019 study in Intensive Care Medicine found that 25% of 99 patients who were treated for emergency respiratory or cardiovascular crises showed PTSD symptoms at 6 months, and the percentage of childhood cancer survivors with PTSD was estimated at as high as 22%, according to research published in Frontiers in Psychology.In 2013, a meta-analysis suggested that 23% of stroke survivors have PTSD symptoms within 1 year, and 11% after 1 year.
PTSD is unique
Dr. Nemeroff noted that PTSD is the only diagnosis in the DSM-5 that’s directly linked to an environmental event. Specifically, he said, PTSD is caused by “very unexpected traumatic events that occur outside the normal repertoire of human behavior.”
In response, “most people that have an acute stress disorder response will fundamentally extinguish it and end up returning to the baseline level of functioning,” he said. But those with PTSD do not recover.
Dr. Nemeroff recommends the use of the 20-question self-report tool known as PCL-5. “It’s your friend,” he said. “It takes a few minutes for the patients to fill out while in the front office, and it doesn’t cost anything. Most patients who have PTSD will have a score of 50-55, maybe 60. You’re going to try to get them down to below 30, and you’re going to give this to them every time they come to your office to follow their progress. It works like a charm.”
As for treatment, psychotherapy and medications remain standard, he said, although “PTSD is a tough disorder to treat.”
According to him, brief cognitive behavioral therapy (CBT) – 4-5 sessions – has shown the greatest benefit and highest level of evidence in support when initiated within 4-30 days of trauma. Group therapy may be helpful, while it’s not clear if spiritual support and “psychological first aid” are useful during this time period.
There’s no evidence that medications such as SSRIs and atypical antipsychotics will prevent PTSD from developing; typical antipsychotics are not recommended. Individual or group “debriefing” is highly not recommended, Dr. Nemeroff said, because the experience can re-traumatize patients, as researchers learned after 9/11 when encouraging people to relive their experiences triggered PTSD and heartbreak.
Also not recommended: Benzodiazepines and formal psychotherapy in people without symptoms.
Exposure-based CBT has been proven to be successful, Dr. Nemeroff said, but it must be provided by a trained professional. “Going for a weekend course isn’t sufficient,” he said, and research suggests that group CBT is not as helpfulas individual CBT.
As for medication over the longer term, research supports SNRIs and SSRIs such as sertaline (Zoloft) and paroxetine (Paxil). Dr. Nemeroff is a fan of venlafaxine (Effexor): “It has a wide dose range. I can go from 75 to 150 milligrams at the low end and 450 and even 600 milligrams at the high end. I’ve had some amazing successes.”
In addition, atypical antipsychotics can be helpful in non-responders or psychotic PTSD patients, he said.
Dr. Nemeroff said he’s skeptical of ketamine as a treatment for PTSD, but he’s most hopeful about MDMA-assisted therapy due to “impressive data” regarding PTSD that was released last year. A bid for FDA approval is in the works, he said.
He added that data is promising from trials examining transcranial magnetic stimulationand (in work by his own team) electroconvulsive therapy. Both therapies are worth considering, he said.
Dr. Nemeroff reported multiple disclosures including research/grant support, stock holdings, scientific advisory board service, consulting relationships, board of director service, and patents.
at APA 2022
Telepsychiatry helped maintain standard of schizophrenia care during COVID
, new survey data show.
“Mental health centers rose to the challenge and did what they needed to do for their patients,” study investigator Dawn Velligan, PhD, University of Texas Health Science Center at San Antonio, told this news organization.
“Some decided to put patients on longer-acting injectable formulations. Some centers gave injections outside to make people feel safer,” Dr. Velligan said.
She added that other patients who might not have had transportation, or were too afraid to come in, were switched to oral medications. However, “switching to orals isn’t something that should be done lightly. I would only want patients to switch to orals as a last resort, but you do what you have to do,” Dr. Velligan said.
The findings were presented at the annual meeting of the American Psychiatric Association.
No going back?
When COVID hit, many mental health clinics closed for in-person visits. “This was unprecedented and we wanted to understand how clinics adapted their services and clinical management of patients with schizophrenia” on LAIs, Dr. Velligan said.
She and her colleagues surveyed 35 mental health clinics, with one respondent at each clinic, between October and November 2020.
All 35 clinics reported using telepsychiatry; 15 had been using telepsychiatry before the pandemic, while 20 (57%) began using it after COVID hit.
Across outpatient visit types, telepsychiatry use for noninjection visits rose from 12%-15% before the pandemic to 45%-69% after the pandemic.
In addition, patients were more apt to keep their telehealth visit. The frequency of appointment “no shows” and/or cancellations for telepsychiatry visits decreased by roughly one-third after the pandemic, compared with before the pandemic.
For patients with schizophrenia treated with LAIs, the frequency of telepsychiatry visits increased in 46% of the clinics during the pandemic.
For these patients, management options included switching patients from LAIs to oral antipsychotics in 34% of clinics and switching patients to LAIs with longer injection intervals in 31% of clinics.
Chief barriers to telepsychiatry visits were low reimbursement rate and lack of access to technology/reliable Internet.
Nearly all respondents reported being satisfied with the use of telepsychiatry to support patients with schizophrenia, whether treated with LAIs (94%) or with oral antipsychotics (97%).
Sixty percent of respondents reported no change in medication adherence for patients treated with LAIs since the start of the pandemic, while less than half (43%) reported no change in adherence to oral antipsychotics.
Most respondents (69%) felt that telepsychiatry visits would very likely continue to be used in combination with in-person office visits after the pandemic.
“Telemedicine is here to stay,” Dr. Velligan said.
Moving to a ‘hybrid universe’
Hector Colon-Rivera, MD, University of Pittsburgh Medical Center and president of the APA’s Hispanic Caucus, agrees.
Commenting on the findings, he noted that, because of shifts in care brought on by COVID, psychiatrists had to adopt telemedicine practices. As a result, many “now feel more comfortable” with telehealth visits for medication management and psychotherapy, said Dr. Colon-Rivera, who was not involved with the research.
He added this study is important because it shows that even patients with severe mental illness can be successfully managed with telepsychiatry, and with good adherence.
“Especially for patients with schizophrenia who have access issues, telepsychiatry is really helpful,” Dr. Colon-Rivera said.
“Telepsychiatry is becoming standard. Most clinics are moving to the hybrid universe now by having a telemedicine component and also seeing patients in person. Even places like emergency rooms and psychiatrists who do consults on medical floors are using telepsychiatry as an option,” he added.
Study funding was provided by Alkermes. Dr. Velligan has reported financial relationships with Alkermes, Otsuka, Janssen, and Lyndra. Dr. Colon-Rivera has reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, new survey data show.
“Mental health centers rose to the challenge and did what they needed to do for their patients,” study investigator Dawn Velligan, PhD, University of Texas Health Science Center at San Antonio, told this news organization.
“Some decided to put patients on longer-acting injectable formulations. Some centers gave injections outside to make people feel safer,” Dr. Velligan said.
She added that other patients who might not have had transportation, or were too afraid to come in, were switched to oral medications. However, “switching to orals isn’t something that should be done lightly. I would only want patients to switch to orals as a last resort, but you do what you have to do,” Dr. Velligan said.
The findings were presented at the annual meeting of the American Psychiatric Association.
No going back?
When COVID hit, many mental health clinics closed for in-person visits. “This was unprecedented and we wanted to understand how clinics adapted their services and clinical management of patients with schizophrenia” on LAIs, Dr. Velligan said.
She and her colleagues surveyed 35 mental health clinics, with one respondent at each clinic, between October and November 2020.
All 35 clinics reported using telepsychiatry; 15 had been using telepsychiatry before the pandemic, while 20 (57%) began using it after COVID hit.
Across outpatient visit types, telepsychiatry use for noninjection visits rose from 12%-15% before the pandemic to 45%-69% after the pandemic.
In addition, patients were more apt to keep their telehealth visit. The frequency of appointment “no shows” and/or cancellations for telepsychiatry visits decreased by roughly one-third after the pandemic, compared with before the pandemic.
For patients with schizophrenia treated with LAIs, the frequency of telepsychiatry visits increased in 46% of the clinics during the pandemic.
For these patients, management options included switching patients from LAIs to oral antipsychotics in 34% of clinics and switching patients to LAIs with longer injection intervals in 31% of clinics.
Chief barriers to telepsychiatry visits were low reimbursement rate and lack of access to technology/reliable Internet.
Nearly all respondents reported being satisfied with the use of telepsychiatry to support patients with schizophrenia, whether treated with LAIs (94%) or with oral antipsychotics (97%).
Sixty percent of respondents reported no change in medication adherence for patients treated with LAIs since the start of the pandemic, while less than half (43%) reported no change in adherence to oral antipsychotics.
Most respondents (69%) felt that telepsychiatry visits would very likely continue to be used in combination with in-person office visits after the pandemic.
“Telemedicine is here to stay,” Dr. Velligan said.
Moving to a ‘hybrid universe’
Hector Colon-Rivera, MD, University of Pittsburgh Medical Center and president of the APA’s Hispanic Caucus, agrees.
Commenting on the findings, he noted that, because of shifts in care brought on by COVID, psychiatrists had to adopt telemedicine practices. As a result, many “now feel more comfortable” with telehealth visits for medication management and psychotherapy, said Dr. Colon-Rivera, who was not involved with the research.
He added this study is important because it shows that even patients with severe mental illness can be successfully managed with telepsychiatry, and with good adherence.
“Especially for patients with schizophrenia who have access issues, telepsychiatry is really helpful,” Dr. Colon-Rivera said.
“Telepsychiatry is becoming standard. Most clinics are moving to the hybrid universe now by having a telemedicine component and also seeing patients in person. Even places like emergency rooms and psychiatrists who do consults on medical floors are using telepsychiatry as an option,” he added.
Study funding was provided by Alkermes. Dr. Velligan has reported financial relationships with Alkermes, Otsuka, Janssen, and Lyndra. Dr. Colon-Rivera has reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, new survey data show.
“Mental health centers rose to the challenge and did what they needed to do for their patients,” study investigator Dawn Velligan, PhD, University of Texas Health Science Center at San Antonio, told this news organization.
“Some decided to put patients on longer-acting injectable formulations. Some centers gave injections outside to make people feel safer,” Dr. Velligan said.
She added that other patients who might not have had transportation, or were too afraid to come in, were switched to oral medications. However, “switching to orals isn’t something that should be done lightly. I would only want patients to switch to orals as a last resort, but you do what you have to do,” Dr. Velligan said.
The findings were presented at the annual meeting of the American Psychiatric Association.
No going back?
When COVID hit, many mental health clinics closed for in-person visits. “This was unprecedented and we wanted to understand how clinics adapted their services and clinical management of patients with schizophrenia” on LAIs, Dr. Velligan said.
She and her colleagues surveyed 35 mental health clinics, with one respondent at each clinic, between October and November 2020.
All 35 clinics reported using telepsychiatry; 15 had been using telepsychiatry before the pandemic, while 20 (57%) began using it after COVID hit.
Across outpatient visit types, telepsychiatry use for noninjection visits rose from 12%-15% before the pandemic to 45%-69% after the pandemic.
In addition, patients were more apt to keep their telehealth visit. The frequency of appointment “no shows” and/or cancellations for telepsychiatry visits decreased by roughly one-third after the pandemic, compared with before the pandemic.
For patients with schizophrenia treated with LAIs, the frequency of telepsychiatry visits increased in 46% of the clinics during the pandemic.
For these patients, management options included switching patients from LAIs to oral antipsychotics in 34% of clinics and switching patients to LAIs with longer injection intervals in 31% of clinics.
Chief barriers to telepsychiatry visits were low reimbursement rate and lack of access to technology/reliable Internet.
Nearly all respondents reported being satisfied with the use of telepsychiatry to support patients with schizophrenia, whether treated with LAIs (94%) or with oral antipsychotics (97%).
Sixty percent of respondents reported no change in medication adherence for patients treated with LAIs since the start of the pandemic, while less than half (43%) reported no change in adherence to oral antipsychotics.
Most respondents (69%) felt that telepsychiatry visits would very likely continue to be used in combination with in-person office visits after the pandemic.
“Telemedicine is here to stay,” Dr. Velligan said.
Moving to a ‘hybrid universe’
Hector Colon-Rivera, MD, University of Pittsburgh Medical Center and president of the APA’s Hispanic Caucus, agrees.
Commenting on the findings, he noted that, because of shifts in care brought on by COVID, psychiatrists had to adopt telemedicine practices. As a result, many “now feel more comfortable” with telehealth visits for medication management and psychotherapy, said Dr. Colon-Rivera, who was not involved with the research.
He added this study is important because it shows that even patients with severe mental illness can be successfully managed with telepsychiatry, and with good adherence.
“Especially for patients with schizophrenia who have access issues, telepsychiatry is really helpful,” Dr. Colon-Rivera said.
“Telepsychiatry is becoming standard. Most clinics are moving to the hybrid universe now by having a telemedicine component and also seeing patients in person. Even places like emergency rooms and psychiatrists who do consults on medical floors are using telepsychiatry as an option,” he added.
Study funding was provided by Alkermes. Dr. Velligan has reported financial relationships with Alkermes, Otsuka, Janssen, and Lyndra. Dr. Colon-Rivera has reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM APA 2022