User login
Routine pharmacogenetic testing in psychiatry not indicated
LAS VEGAS –
“It’s misleading to rely on results of genetic tests to drive clinical treatment,” Dr. Nurmi, a child and adolescent psychiatrist in the department of psychiatry and biobehavioral sciences at the University of California, Los Angeles, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “There’s a lot of hope and promise there. But currently, we only know the tip of the iceberg about how drugs work and the genetics influencing these effects. Current testing is probably a very poor reflection of the complexity of drug effects.”
According to Dr. Nurmi, there are at least 165 Food and Drug Administration–approved drugs with pharmacogenetic information on 64 different biomarkers – 37% with CYP p450 notations. Of these, 32 psychiatric drugs have pharmacogenetic information, and most of them are dosing recommendations based on whether a patient has the variant. However, there is wide public acceptance of genetic testing in preventing the wrong drug from being used, in selecting the best drug dose, and avoiding side effects (Pharmacogenomics 2012;12[3]:197-204). “Most people have a lot of hope [for genetic testing in psychiatry],” Dr. Nurmi said. “But is the science really there? It doesn’t matter, because these companies are doing it, and you are being shown these reports from patients. Whether or not the science supports it, we’re going to have to interpret these reports and explain them to our patients – even if we don’t order them.”
Currently, she continued, clinicians practice trial and error prescribing where they might try one treatment in a class that they think that will work based on previous literature. If nothing works, they try another one. If that’s intolerable, they try a third treatment, and so on. “When we finally find the right treatment, it can take some time to get the dosing right,” Dr. Nurmi said. “So, it can take many months to get a child on the right medication. Precision treatment, on the other hand, would start off by taking a saliva or blood sample to get a printout that lets physicians know which drugs might be used with caution because they might lack efficacy at standard doses, which ones would likely have adverse effects at standard doses, and which are the best choices and what are the dosing recommendations for those choices. If we could get all the information to guide us, that would be a useful product, but right now, we don’t know enough to be able to make these determinations.”
Current evidence-based genetic testing supports a limited role for CYP2D6 and CYP2C19 genotyping because most psychiatric drugs are metabolized by those two enzymes. Poor metabolizers have two dysfunctional copies of the enzyme-encoding gene. This results in increased drug plasma levels with a potentially increased rate of adverse effects.
“Intermediate and extensive metabolizers usually have a normal phenotype, but you can also have ultrarapid metabolizers who have duplications or other enhancing mutations of the CYP gene,” Dr. Nurmi said. “This can result in lower bioavailability and possibly efficacy. Psychiatrists treat poor metabolizers and ultrarapid metabolizers all the time, because the variants are very common.” An estimated 10% of White people are poor metabolizers at the CYP2D6 gene while about 7% are ultrarapid metabolizers. At the same time, an estimated 20% of Asians, Africans, and Whites are poor metabolizers at the CYP2C19 gene. “So, you’re seeing a lot of this in your practice, and you’re probably changing dosing based on genetic differences in metabolism,” she said.
The only FDA pharmacodynamic treatment guideline is for the risk of Stevens-Johnson syndrome (SJS) with the use of carbamazepine. In a study of 44 patients with SJS, all were positive for the HLA-B*1502 variant, compared with 3% of carbamazepine-tolerant patients (Nature 2004;428[6982]:486). The frequency of carrying this variant is an estimated 1:10,000 among Whites and 1:1,000 among Asians. In 2007, the FDA recommended that patients of Asian ancestry should be screened for HLA-B*1502 prior to starting carbamazepine.
Genetic variation also predicts clinical outcome with atomoxetine use. “Most child psychiatrists I know think atomoxetine doesn’t work as a second-line nonstimulant medication for ADHD,” Dr. Nurmi said. “I’d like to convince you that why you think it doesn’t work is because of the genetics.” In a study published in 2019, Dr. Nurmi and colleagues reviewed medical literature and provided therapeutic recommendations for atomoxetine therapy based on CYP2D6 genotype (Clin Pharmacol Ther 2019 Jul;106[1]:94-102). They observed 10- to 30-fold plasma differences in drug exposure between normal metabolizers and poor metabolizers.
“Poor metabolizers therefore get more benefit, but they are also going to get more side effects,” she said. “FDA recommended doses are inadequate for normal metabolizers, so they had to make guidelines based on poor metabolizers because there would be too much risk for them at higher doses. One-third of individuals require doses above the FDA limit to achieve a therapeutic drug level.”
Dr. Nurmi warned that the existing evidence base for using these genetic tests in children “is really poor. There is no data in adults with any diagnosis other than depression, and even those studies are plagued by concerns. When you’re implementing decision support tools in your practice, the key factors are patient presentation, history and symptoms, your clinical skills, the evidence base, FDA recommendations, and patient autonomy. Appropriate incorporation of genetic data should include avoiding a medication with high toxicity (like SJS), titration planning (dose and titration speed adjustments), and choosing between medications in the same class with an indication or evidence base for the target disorder.” She added that while the benefit of current genetic testing is limited, it may help some patients feel more comfortable tolerating a medication. “For example, being able to tell someone with anxiety that their genetics suggests that they will not have side effects could be very powerful,” she said.
In a 2018 safety communication, the FDA warned the public about its concerns with companies making claims about how to use genetic test results to manage medication treatments that are not supported by recommendations in the FDA-approved drug labeling or other scientific evidence. The American Academy of Child and Adolescent Psychiatry also published a guide for patients and families.
Dr. Nurmi disclosed that she is an unpaid advisory board member for Myriad Genetics and the Tourette Association of America, a paid adviser for Teva Pharmaceuticals, and a recipient of research support from Emalex Pharmaceuticals. She has received research funding from the National Institutes Health, the International OCD Foundation, the Tourette Association of America, and the Brain & Behavior Research Foundation.
LAS VEGAS –
“It’s misleading to rely on results of genetic tests to drive clinical treatment,” Dr. Nurmi, a child and adolescent psychiatrist in the department of psychiatry and biobehavioral sciences at the University of California, Los Angeles, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “There’s a lot of hope and promise there. But currently, we only know the tip of the iceberg about how drugs work and the genetics influencing these effects. Current testing is probably a very poor reflection of the complexity of drug effects.”
According to Dr. Nurmi, there are at least 165 Food and Drug Administration–approved drugs with pharmacogenetic information on 64 different biomarkers – 37% with CYP p450 notations. Of these, 32 psychiatric drugs have pharmacogenetic information, and most of them are dosing recommendations based on whether a patient has the variant. However, there is wide public acceptance of genetic testing in preventing the wrong drug from being used, in selecting the best drug dose, and avoiding side effects (Pharmacogenomics 2012;12[3]:197-204). “Most people have a lot of hope [for genetic testing in psychiatry],” Dr. Nurmi said. “But is the science really there? It doesn’t matter, because these companies are doing it, and you are being shown these reports from patients. Whether or not the science supports it, we’re going to have to interpret these reports and explain them to our patients – even if we don’t order them.”
Currently, she continued, clinicians practice trial and error prescribing where they might try one treatment in a class that they think that will work based on previous literature. If nothing works, they try another one. If that’s intolerable, they try a third treatment, and so on. “When we finally find the right treatment, it can take some time to get the dosing right,” Dr. Nurmi said. “So, it can take many months to get a child on the right medication. Precision treatment, on the other hand, would start off by taking a saliva or blood sample to get a printout that lets physicians know which drugs might be used with caution because they might lack efficacy at standard doses, which ones would likely have adverse effects at standard doses, and which are the best choices and what are the dosing recommendations for those choices. If we could get all the information to guide us, that would be a useful product, but right now, we don’t know enough to be able to make these determinations.”
Current evidence-based genetic testing supports a limited role for CYP2D6 and CYP2C19 genotyping because most psychiatric drugs are metabolized by those two enzymes. Poor metabolizers have two dysfunctional copies of the enzyme-encoding gene. This results in increased drug plasma levels with a potentially increased rate of adverse effects.
“Intermediate and extensive metabolizers usually have a normal phenotype, but you can also have ultrarapid metabolizers who have duplications or other enhancing mutations of the CYP gene,” Dr. Nurmi said. “This can result in lower bioavailability and possibly efficacy. Psychiatrists treat poor metabolizers and ultrarapid metabolizers all the time, because the variants are very common.” An estimated 10% of White people are poor metabolizers at the CYP2D6 gene while about 7% are ultrarapid metabolizers. At the same time, an estimated 20% of Asians, Africans, and Whites are poor metabolizers at the CYP2C19 gene. “So, you’re seeing a lot of this in your practice, and you’re probably changing dosing based on genetic differences in metabolism,” she said.
The only FDA pharmacodynamic treatment guideline is for the risk of Stevens-Johnson syndrome (SJS) with the use of carbamazepine. In a study of 44 patients with SJS, all were positive for the HLA-B*1502 variant, compared with 3% of carbamazepine-tolerant patients (Nature 2004;428[6982]:486). The frequency of carrying this variant is an estimated 1:10,000 among Whites and 1:1,000 among Asians. In 2007, the FDA recommended that patients of Asian ancestry should be screened for HLA-B*1502 prior to starting carbamazepine.
Genetic variation also predicts clinical outcome with atomoxetine use. “Most child psychiatrists I know think atomoxetine doesn’t work as a second-line nonstimulant medication for ADHD,” Dr. Nurmi said. “I’d like to convince you that why you think it doesn’t work is because of the genetics.” In a study published in 2019, Dr. Nurmi and colleagues reviewed medical literature and provided therapeutic recommendations for atomoxetine therapy based on CYP2D6 genotype (Clin Pharmacol Ther 2019 Jul;106[1]:94-102). They observed 10- to 30-fold plasma differences in drug exposure between normal metabolizers and poor metabolizers.
“Poor metabolizers therefore get more benefit, but they are also going to get more side effects,” she said. “FDA recommended doses are inadequate for normal metabolizers, so they had to make guidelines based on poor metabolizers because there would be too much risk for them at higher doses. One-third of individuals require doses above the FDA limit to achieve a therapeutic drug level.”
Dr. Nurmi warned that the existing evidence base for using these genetic tests in children “is really poor. There is no data in adults with any diagnosis other than depression, and even those studies are plagued by concerns. When you’re implementing decision support tools in your practice, the key factors are patient presentation, history and symptoms, your clinical skills, the evidence base, FDA recommendations, and patient autonomy. Appropriate incorporation of genetic data should include avoiding a medication with high toxicity (like SJS), titration planning (dose and titration speed adjustments), and choosing between medications in the same class with an indication or evidence base for the target disorder.” She added that while the benefit of current genetic testing is limited, it may help some patients feel more comfortable tolerating a medication. “For example, being able to tell someone with anxiety that their genetics suggests that they will not have side effects could be very powerful,” she said.
In a 2018 safety communication, the FDA warned the public about its concerns with companies making claims about how to use genetic test results to manage medication treatments that are not supported by recommendations in the FDA-approved drug labeling or other scientific evidence. The American Academy of Child and Adolescent Psychiatry also published a guide for patients and families.
Dr. Nurmi disclosed that she is an unpaid advisory board member for Myriad Genetics and the Tourette Association of America, a paid adviser for Teva Pharmaceuticals, and a recipient of research support from Emalex Pharmaceuticals. She has received research funding from the National Institutes Health, the International OCD Foundation, the Tourette Association of America, and the Brain & Behavior Research Foundation.
LAS VEGAS –
“It’s misleading to rely on results of genetic tests to drive clinical treatment,” Dr. Nurmi, a child and adolescent psychiatrist in the department of psychiatry and biobehavioral sciences at the University of California, Los Angeles, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “There’s a lot of hope and promise there. But currently, we only know the tip of the iceberg about how drugs work and the genetics influencing these effects. Current testing is probably a very poor reflection of the complexity of drug effects.”
According to Dr. Nurmi, there are at least 165 Food and Drug Administration–approved drugs with pharmacogenetic information on 64 different biomarkers – 37% with CYP p450 notations. Of these, 32 psychiatric drugs have pharmacogenetic information, and most of them are dosing recommendations based on whether a patient has the variant. However, there is wide public acceptance of genetic testing in preventing the wrong drug from being used, in selecting the best drug dose, and avoiding side effects (Pharmacogenomics 2012;12[3]:197-204). “Most people have a lot of hope [for genetic testing in psychiatry],” Dr. Nurmi said. “But is the science really there? It doesn’t matter, because these companies are doing it, and you are being shown these reports from patients. Whether or not the science supports it, we’re going to have to interpret these reports and explain them to our patients – even if we don’t order them.”
Currently, she continued, clinicians practice trial and error prescribing where they might try one treatment in a class that they think that will work based on previous literature. If nothing works, they try another one. If that’s intolerable, they try a third treatment, and so on. “When we finally find the right treatment, it can take some time to get the dosing right,” Dr. Nurmi said. “So, it can take many months to get a child on the right medication. Precision treatment, on the other hand, would start off by taking a saliva or blood sample to get a printout that lets physicians know which drugs might be used with caution because they might lack efficacy at standard doses, which ones would likely have adverse effects at standard doses, and which are the best choices and what are the dosing recommendations for those choices. If we could get all the information to guide us, that would be a useful product, but right now, we don’t know enough to be able to make these determinations.”
Current evidence-based genetic testing supports a limited role for CYP2D6 and CYP2C19 genotyping because most psychiatric drugs are metabolized by those two enzymes. Poor metabolizers have two dysfunctional copies of the enzyme-encoding gene. This results in increased drug plasma levels with a potentially increased rate of adverse effects.
“Intermediate and extensive metabolizers usually have a normal phenotype, but you can also have ultrarapid metabolizers who have duplications or other enhancing mutations of the CYP gene,” Dr. Nurmi said. “This can result in lower bioavailability and possibly efficacy. Psychiatrists treat poor metabolizers and ultrarapid metabolizers all the time, because the variants are very common.” An estimated 10% of White people are poor metabolizers at the CYP2D6 gene while about 7% are ultrarapid metabolizers. At the same time, an estimated 20% of Asians, Africans, and Whites are poor metabolizers at the CYP2C19 gene. “So, you’re seeing a lot of this in your practice, and you’re probably changing dosing based on genetic differences in metabolism,” she said.
The only FDA pharmacodynamic treatment guideline is for the risk of Stevens-Johnson syndrome (SJS) with the use of carbamazepine. In a study of 44 patients with SJS, all were positive for the HLA-B*1502 variant, compared with 3% of carbamazepine-tolerant patients (Nature 2004;428[6982]:486). The frequency of carrying this variant is an estimated 1:10,000 among Whites and 1:1,000 among Asians. In 2007, the FDA recommended that patients of Asian ancestry should be screened for HLA-B*1502 prior to starting carbamazepine.
Genetic variation also predicts clinical outcome with atomoxetine use. “Most child psychiatrists I know think atomoxetine doesn’t work as a second-line nonstimulant medication for ADHD,” Dr. Nurmi said. “I’d like to convince you that why you think it doesn’t work is because of the genetics.” In a study published in 2019, Dr. Nurmi and colleagues reviewed medical literature and provided therapeutic recommendations for atomoxetine therapy based on CYP2D6 genotype (Clin Pharmacol Ther 2019 Jul;106[1]:94-102). They observed 10- to 30-fold plasma differences in drug exposure between normal metabolizers and poor metabolizers.
“Poor metabolizers therefore get more benefit, but they are also going to get more side effects,” she said. “FDA recommended doses are inadequate for normal metabolizers, so they had to make guidelines based on poor metabolizers because there would be too much risk for them at higher doses. One-third of individuals require doses above the FDA limit to achieve a therapeutic drug level.”
Dr. Nurmi warned that the existing evidence base for using these genetic tests in children “is really poor. There is no data in adults with any diagnosis other than depression, and even those studies are plagued by concerns. When you’re implementing decision support tools in your practice, the key factors are patient presentation, history and symptoms, your clinical skills, the evidence base, FDA recommendations, and patient autonomy. Appropriate incorporation of genetic data should include avoiding a medication with high toxicity (like SJS), titration planning (dose and titration speed adjustments), and choosing between medications in the same class with an indication or evidence base for the target disorder.” She added that while the benefit of current genetic testing is limited, it may help some patients feel more comfortable tolerating a medication. “For example, being able to tell someone with anxiety that their genetics suggests that they will not have side effects could be very powerful,” she said.
In a 2018 safety communication, the FDA warned the public about its concerns with companies making claims about how to use genetic test results to manage medication treatments that are not supported by recommendations in the FDA-approved drug labeling or other scientific evidence. The American Academy of Child and Adolescent Psychiatry also published a guide for patients and families.
Dr. Nurmi disclosed that she is an unpaid advisory board member for Myriad Genetics and the Tourette Association of America, a paid adviser for Teva Pharmaceuticals, and a recipient of research support from Emalex Pharmaceuticals. She has received research funding from the National Institutes Health, the International OCD Foundation, the Tourette Association of America, and the Brain & Behavior Research Foundation.
REPORTING FROM NPA 2022
DSM-5 update: What’s new?
Ahead of its official release on March 18, the new Diagnostic and Statistical Manual of Mental Disorders, which is in the form of a textbook, is already drawing some criticism.
It also includes symptom codes for suicidal behavior and nonsuicidal self-injury, clarifying modifications to criteria sets for more than 70 disorders, including autism spectrum disorder; changes in terminology for gender dysphoria; and a comprehensive review of the impact of racism and discrimination on the diagnosis and manifestations of mental disorders.
The Text Revision is a compilation of iterative changes that have been made online on a rolling basis since the DSM-5 was first published in 2013.
“The goal of the Text Revision was to allow a thorough revision of the text, not the criteria,” Paul Appelbaum, MD, chair of the APA’s DSM steering committee, told this news organization.
For the Text Revision, some 200 experts across a variety of APA working groups recommended changes to the text based on a comprehensive literature review, said Appelbaum, who is the Elizabeth K. Dollard Professor of Psychiatry, Medicine and Law, and director of the division of law, ethics and psychiatry at Columbia University, New York.
However, there’s not a lot that’s new, in part, because there have been few therapeutic advances.
Money maker?
Allen Frances, MD, chair of the DSM-4 task force and professor and chair emeritus of psychiatry at Duke University, Durham, N.C., said the APA is publishing the Text Revision “just to make money. They’re very anxious to do anything that will increase sales and having a revision forces some people, especially in institutions, to buy the book, even though it may not have anything substantive to add to the original.”
Dr. Frances told this news organization that when the APA published the first DSM in the late 1970s, “it became an instantaneous best-seller, to everyone’s surprise.”
The APA would not comment on how many of the $170 (list price) volumes it sells or how much those sales contribute to its budget.
Dr. Appelbaum acknowledged, “at any point in time, the canonical version is the online version.” However, it’s clear from DSM-5 sales “that many people still value having a hard copy of the DSM available to them.”
Prolonged grief: Timely or overkill?
Persistent complex bereavement disorder (PCBD) was listed as a “condition for further study” in DSM-5. After a 2019 workshop aimed at getting consensus for diagnosis criteria, the APA board approved the new prolonged grief disorder in October 2020, and the APA assembly approved the new disorder in November 2020.
Given the 950,000 deaths from COVID-19 over the past 2 years, inclusion of prolonged grief disorder in the DSM-5 may arrive at just the right time.
The diagnostic criteria for PCBD include:
- The development of a persistent grief response (longer than a year for adults and 6 months for children and adolescents) characterized by one or both of the following symptoms, which have been present most days to a clinically significant degree, and have occurred nearly every day for at least the last month: intense yearning/longing for the deceased person; preoccupation with thoughts or memories of the deceased person.
- Since the death, at least three symptoms present most days to a clinically significant degree, and occurring nearly every day for at least the last month, including identity disruption, marked sense of disbelief about the death, avoidance of reminders that the person is dead, intense emotional pain related to the death, difficulty reintegrating into one’s relationships and activities after the death, emotional numbness, feeling that life is meaningless as a result of the death, and intense loneliness as a result of the death.
- The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
- The duration and severity of the bereavement reaction clearly exceed expected social, cultural, or religious norms for the individual’s culture and context.
- The symptoms are not better explained by another mental disorder, such as major depressive disorder (MDD) or PTSD, and are not attributable to the physiological effects of a substance or another medical condition.
Dr. Frances said he believes creating a new diagnosis pathologizes grief. In DSM-3 and DSM-4, an exception was made under the diagnosis of MDD for individuals who had recently lost a loved one. “We wanted to have at least an opportunity for people to grieve without being stigmatized, mislabeled, and overtreated with medication.”
DSM-5 removed the bereavement exclusion. After 2 weeks, people who are grieving and have particular symptoms could receive a diagnosis of MDD, said Dr. Frances. He believes the exclusion should have been broadened to cover anyone experiencing a major loss – such as a job loss or divorce. If someone is having prolonged symptoms that interfere with functioning, they should get an MDD diagnosis.
The new disorder “doesn’t solve anything, it just adds to the confusion and stigmatization, and it’s part of a kind of creeping medical imperialization of everyday life, where everything has to have a mental disorder label,” Dr. Frances said.
However, Dr. Appelbaum countered that “the criteria for prolonged grief disorder are constructed in such a way as to make every effort to exclude people who are going through a normal grieving process.”
“Part of the purpose of the data analyses was to ensure the criteria that were adopted would, in fact, effectively distinguish between what anybody goes through, say when someone close to you dies, and this unusual prolonged grieving process without end that affects a much smaller number of people but which really can be crippling for them,” he added.
The Text Revision adds new symptom codes for suicidal behavior and nonsuicidal self-injury, which appear in the chapter, “Other Conditions That May Be a Focus of Clinical Attention,” said Dr. Appelbaum.
“Both suicidal behavior and nonsuicidal self-injury seem pretty persuasively to fall into that category – something a clinician would want to know about, pay attention to, and factor into treatment planning, although they are behaviors that cross many diagnostic categories,” he added.
Codes also provide a systematic way of ascertaining the incidence and prevalence of such behaviors, said Dr. Appelbaum.
Changes to gender terminology
The Text Revision also tweaks some terminology with respect to transgender individuals. The term “desired gender” is now “experienced gender”, the term “cross-sex medical procedure” is now “gender-affirming medical procedure”, and the terms “natal male/natal female” are now “individual assigned male/female at birth”.
Dr. Frances said that the existence of gender dysphoria as a diagnosis has been a matter of controversy ever since it was first included.
“The transgender community has had mixed feelings on whether there should be anything at all in the manual,” he said. On one hand is the argument that gender dysphoria should be removed because it’s not really a psychiatric issue.
“We seriously considered eliminating it altogether in DSM-4,” said Dr. Frances.
However, an argument in favor of keeping it was that if the diagnosis was removed, it would mean that people could not receive treatment. “There’s no right argument for this dilemma,” he said.
Dr. Frances, who has been a frequent critic of DSM-5, said he believes the manual continues to miss opportunities to tighten criteria for many diagnoses, including ADHD and autism spectrum disorder.
“There’s a consistent pattern of taking behaviors and symptoms of behaviors that are on the border with normality and expanding the definition of mental disorder and reducing the realm of normality,” he said.
That has consequences, Dr. Frances added. “When someone gets a diagnosis that they need to get, it’s the beginning of a much better future. When someone gets a diagnosis that’s a mislabel that they don’t need, it has all harms and no benefits. It’s stigmatizing, leads to too much treatment, the wrong treatment, and it’s much more harmful than helpful.”
A version of this article first appeared on Medscape.com.
Ahead of its official release on March 18, the new Diagnostic and Statistical Manual of Mental Disorders, which is in the form of a textbook, is already drawing some criticism.
It also includes symptom codes for suicidal behavior and nonsuicidal self-injury, clarifying modifications to criteria sets for more than 70 disorders, including autism spectrum disorder; changes in terminology for gender dysphoria; and a comprehensive review of the impact of racism and discrimination on the diagnosis and manifestations of mental disorders.
The Text Revision is a compilation of iterative changes that have been made online on a rolling basis since the DSM-5 was first published in 2013.
“The goal of the Text Revision was to allow a thorough revision of the text, not the criteria,” Paul Appelbaum, MD, chair of the APA’s DSM steering committee, told this news organization.
For the Text Revision, some 200 experts across a variety of APA working groups recommended changes to the text based on a comprehensive literature review, said Appelbaum, who is the Elizabeth K. Dollard Professor of Psychiatry, Medicine and Law, and director of the division of law, ethics and psychiatry at Columbia University, New York.
However, there’s not a lot that’s new, in part, because there have been few therapeutic advances.
Money maker?
Allen Frances, MD, chair of the DSM-4 task force and professor and chair emeritus of psychiatry at Duke University, Durham, N.C., said the APA is publishing the Text Revision “just to make money. They’re very anxious to do anything that will increase sales and having a revision forces some people, especially in institutions, to buy the book, even though it may not have anything substantive to add to the original.”
Dr. Frances told this news organization that when the APA published the first DSM in the late 1970s, “it became an instantaneous best-seller, to everyone’s surprise.”
The APA would not comment on how many of the $170 (list price) volumes it sells or how much those sales contribute to its budget.
Dr. Appelbaum acknowledged, “at any point in time, the canonical version is the online version.” However, it’s clear from DSM-5 sales “that many people still value having a hard copy of the DSM available to them.”
Prolonged grief: Timely or overkill?
Persistent complex bereavement disorder (PCBD) was listed as a “condition for further study” in DSM-5. After a 2019 workshop aimed at getting consensus for diagnosis criteria, the APA board approved the new prolonged grief disorder in October 2020, and the APA assembly approved the new disorder in November 2020.
Given the 950,000 deaths from COVID-19 over the past 2 years, inclusion of prolonged grief disorder in the DSM-5 may arrive at just the right time.
The diagnostic criteria for PCBD include:
- The development of a persistent grief response (longer than a year for adults and 6 months for children and adolescents) characterized by one or both of the following symptoms, which have been present most days to a clinically significant degree, and have occurred nearly every day for at least the last month: intense yearning/longing for the deceased person; preoccupation with thoughts or memories of the deceased person.
- Since the death, at least three symptoms present most days to a clinically significant degree, and occurring nearly every day for at least the last month, including identity disruption, marked sense of disbelief about the death, avoidance of reminders that the person is dead, intense emotional pain related to the death, difficulty reintegrating into one’s relationships and activities after the death, emotional numbness, feeling that life is meaningless as a result of the death, and intense loneliness as a result of the death.
- The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
- The duration and severity of the bereavement reaction clearly exceed expected social, cultural, or religious norms for the individual’s culture and context.
- The symptoms are not better explained by another mental disorder, such as major depressive disorder (MDD) or PTSD, and are not attributable to the physiological effects of a substance or another medical condition.
Dr. Frances said he believes creating a new diagnosis pathologizes grief. In DSM-3 and DSM-4, an exception was made under the diagnosis of MDD for individuals who had recently lost a loved one. “We wanted to have at least an opportunity for people to grieve without being stigmatized, mislabeled, and overtreated with medication.”
DSM-5 removed the bereavement exclusion. After 2 weeks, people who are grieving and have particular symptoms could receive a diagnosis of MDD, said Dr. Frances. He believes the exclusion should have been broadened to cover anyone experiencing a major loss – such as a job loss or divorce. If someone is having prolonged symptoms that interfere with functioning, they should get an MDD diagnosis.
The new disorder “doesn’t solve anything, it just adds to the confusion and stigmatization, and it’s part of a kind of creeping medical imperialization of everyday life, where everything has to have a mental disorder label,” Dr. Frances said.
However, Dr. Appelbaum countered that “the criteria for prolonged grief disorder are constructed in such a way as to make every effort to exclude people who are going through a normal grieving process.”
“Part of the purpose of the data analyses was to ensure the criteria that were adopted would, in fact, effectively distinguish between what anybody goes through, say when someone close to you dies, and this unusual prolonged grieving process without end that affects a much smaller number of people but which really can be crippling for them,” he added.
The Text Revision adds new symptom codes for suicidal behavior and nonsuicidal self-injury, which appear in the chapter, “Other Conditions That May Be a Focus of Clinical Attention,” said Dr. Appelbaum.
“Both suicidal behavior and nonsuicidal self-injury seem pretty persuasively to fall into that category – something a clinician would want to know about, pay attention to, and factor into treatment planning, although they are behaviors that cross many diagnostic categories,” he added.
Codes also provide a systematic way of ascertaining the incidence and prevalence of such behaviors, said Dr. Appelbaum.
Changes to gender terminology
The Text Revision also tweaks some terminology with respect to transgender individuals. The term “desired gender” is now “experienced gender”, the term “cross-sex medical procedure” is now “gender-affirming medical procedure”, and the terms “natal male/natal female” are now “individual assigned male/female at birth”.
Dr. Frances said that the existence of gender dysphoria as a diagnosis has been a matter of controversy ever since it was first included.
“The transgender community has had mixed feelings on whether there should be anything at all in the manual,” he said. On one hand is the argument that gender dysphoria should be removed because it’s not really a psychiatric issue.
“We seriously considered eliminating it altogether in DSM-4,” said Dr. Frances.
However, an argument in favor of keeping it was that if the diagnosis was removed, it would mean that people could not receive treatment. “There’s no right argument for this dilemma,” he said.
Dr. Frances, who has been a frequent critic of DSM-5, said he believes the manual continues to miss opportunities to tighten criteria for many diagnoses, including ADHD and autism spectrum disorder.
“There’s a consistent pattern of taking behaviors and symptoms of behaviors that are on the border with normality and expanding the definition of mental disorder and reducing the realm of normality,” he said.
That has consequences, Dr. Frances added. “When someone gets a diagnosis that they need to get, it’s the beginning of a much better future. When someone gets a diagnosis that’s a mislabel that they don’t need, it has all harms and no benefits. It’s stigmatizing, leads to too much treatment, the wrong treatment, and it’s much more harmful than helpful.”
A version of this article first appeared on Medscape.com.
Ahead of its official release on March 18, the new Diagnostic and Statistical Manual of Mental Disorders, which is in the form of a textbook, is already drawing some criticism.
It also includes symptom codes for suicidal behavior and nonsuicidal self-injury, clarifying modifications to criteria sets for more than 70 disorders, including autism spectrum disorder; changes in terminology for gender dysphoria; and a comprehensive review of the impact of racism and discrimination on the diagnosis and manifestations of mental disorders.
The Text Revision is a compilation of iterative changes that have been made online on a rolling basis since the DSM-5 was first published in 2013.
“The goal of the Text Revision was to allow a thorough revision of the text, not the criteria,” Paul Appelbaum, MD, chair of the APA’s DSM steering committee, told this news organization.
For the Text Revision, some 200 experts across a variety of APA working groups recommended changes to the text based on a comprehensive literature review, said Appelbaum, who is the Elizabeth K. Dollard Professor of Psychiatry, Medicine and Law, and director of the division of law, ethics and psychiatry at Columbia University, New York.
However, there’s not a lot that’s new, in part, because there have been few therapeutic advances.
Money maker?
Allen Frances, MD, chair of the DSM-4 task force and professor and chair emeritus of psychiatry at Duke University, Durham, N.C., said the APA is publishing the Text Revision “just to make money. They’re very anxious to do anything that will increase sales and having a revision forces some people, especially in institutions, to buy the book, even though it may not have anything substantive to add to the original.”
Dr. Frances told this news organization that when the APA published the first DSM in the late 1970s, “it became an instantaneous best-seller, to everyone’s surprise.”
The APA would not comment on how many of the $170 (list price) volumes it sells or how much those sales contribute to its budget.
Dr. Appelbaum acknowledged, “at any point in time, the canonical version is the online version.” However, it’s clear from DSM-5 sales “that many people still value having a hard copy of the DSM available to them.”
Prolonged grief: Timely or overkill?
Persistent complex bereavement disorder (PCBD) was listed as a “condition for further study” in DSM-5. After a 2019 workshop aimed at getting consensus for diagnosis criteria, the APA board approved the new prolonged grief disorder in October 2020, and the APA assembly approved the new disorder in November 2020.
Given the 950,000 deaths from COVID-19 over the past 2 years, inclusion of prolonged grief disorder in the DSM-5 may arrive at just the right time.
The diagnostic criteria for PCBD include:
- The development of a persistent grief response (longer than a year for adults and 6 months for children and adolescents) characterized by one or both of the following symptoms, which have been present most days to a clinically significant degree, and have occurred nearly every day for at least the last month: intense yearning/longing for the deceased person; preoccupation with thoughts or memories of the deceased person.
- Since the death, at least three symptoms present most days to a clinically significant degree, and occurring nearly every day for at least the last month, including identity disruption, marked sense of disbelief about the death, avoidance of reminders that the person is dead, intense emotional pain related to the death, difficulty reintegrating into one’s relationships and activities after the death, emotional numbness, feeling that life is meaningless as a result of the death, and intense loneliness as a result of the death.
- The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
- The duration and severity of the bereavement reaction clearly exceed expected social, cultural, or religious norms for the individual’s culture and context.
- The symptoms are not better explained by another mental disorder, such as major depressive disorder (MDD) or PTSD, and are not attributable to the physiological effects of a substance or another medical condition.
Dr. Frances said he believes creating a new diagnosis pathologizes grief. In DSM-3 and DSM-4, an exception was made under the diagnosis of MDD for individuals who had recently lost a loved one. “We wanted to have at least an opportunity for people to grieve without being stigmatized, mislabeled, and overtreated with medication.”
DSM-5 removed the bereavement exclusion. After 2 weeks, people who are grieving and have particular symptoms could receive a diagnosis of MDD, said Dr. Frances. He believes the exclusion should have been broadened to cover anyone experiencing a major loss – such as a job loss or divorce. If someone is having prolonged symptoms that interfere with functioning, they should get an MDD diagnosis.
The new disorder “doesn’t solve anything, it just adds to the confusion and stigmatization, and it’s part of a kind of creeping medical imperialization of everyday life, where everything has to have a mental disorder label,” Dr. Frances said.
However, Dr. Appelbaum countered that “the criteria for prolonged grief disorder are constructed in such a way as to make every effort to exclude people who are going through a normal grieving process.”
“Part of the purpose of the data analyses was to ensure the criteria that were adopted would, in fact, effectively distinguish between what anybody goes through, say when someone close to you dies, and this unusual prolonged grieving process without end that affects a much smaller number of people but which really can be crippling for them,” he added.
The Text Revision adds new symptom codes for suicidal behavior and nonsuicidal self-injury, which appear in the chapter, “Other Conditions That May Be a Focus of Clinical Attention,” said Dr. Appelbaum.
“Both suicidal behavior and nonsuicidal self-injury seem pretty persuasively to fall into that category – something a clinician would want to know about, pay attention to, and factor into treatment planning, although they are behaviors that cross many diagnostic categories,” he added.
Codes also provide a systematic way of ascertaining the incidence and prevalence of such behaviors, said Dr. Appelbaum.
Changes to gender terminology
The Text Revision also tweaks some terminology with respect to transgender individuals. The term “desired gender” is now “experienced gender”, the term “cross-sex medical procedure” is now “gender-affirming medical procedure”, and the terms “natal male/natal female” are now “individual assigned male/female at birth”.
Dr. Frances said that the existence of gender dysphoria as a diagnosis has been a matter of controversy ever since it was first included.
“The transgender community has had mixed feelings on whether there should be anything at all in the manual,” he said. On one hand is the argument that gender dysphoria should be removed because it’s not really a psychiatric issue.
“We seriously considered eliminating it altogether in DSM-4,” said Dr. Frances.
However, an argument in favor of keeping it was that if the diagnosis was removed, it would mean that people could not receive treatment. “There’s no right argument for this dilemma,” he said.
Dr. Frances, who has been a frequent critic of DSM-5, said he believes the manual continues to miss opportunities to tighten criteria for many diagnoses, including ADHD and autism spectrum disorder.
“There’s a consistent pattern of taking behaviors and symptoms of behaviors that are on the border with normality and expanding the definition of mental disorder and reducing the realm of normality,” he said.
That has consequences, Dr. Frances added. “When someone gets a diagnosis that they need to get, it’s the beginning of a much better future. When someone gets a diagnosis that’s a mislabel that they don’t need, it has all harms and no benefits. It’s stigmatizing, leads to too much treatment, the wrong treatment, and it’s much more harmful than helpful.”
A version of this article first appeared on Medscape.com.
Self-care tips for clinicians as COVID-19 lingers
LAS VEGAS – according to Jon A. Levenson, MD.
“There are those who will need mental health treatment, so creating an easy way to reach out for help and facilitate linkage with care is critically important,” Dr. Levenson, associate professor of psychiatry at Columbia University Irving Medical Center, New York, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “The vast majority of our workforce will thrive with proper support. But what can each of us do to take care of ourselves?”
Step one is to recognize common stress reactions as well as signs of distress. He offered the oxygen mask metaphor, the idea that before we can take care of and support anyone else, we must first take care of ourselves. “When people are stressed, they don’t always think about the oxygen mask metaphor,” Dr. Levenson said. Step two is to practice and model self-care by adopting principles often discussed in acceptance and commitment therapy: to focus on what you can control, not on what you can’t control.
“We can’t control the amount of toilet paper at the grocery store, how long the pandemic will last, or how others have reacted,” Dr. Levenson said. “We also can’t control other people’s motives, predict what will happen, or the actions of others, including whether they will follow social distancing guidelines or not.”
How about what we can control? One is a positive attitude, “which can sustain people during times of intense stress,” he said. “Other things that we can do include turn off the news and find fun and enriching activities to do at home, whether it be playing a game with family or reaching out to friends through an iPad or a smartphone. You can also follow [Centers for Disease Control and Prevention] recommendations, control your own social distancing, and limit social media activity, which can be stressful. We can also control our kindness and grace.” He added that resilience does not mean “snapping back” to how you were before the pandemic, but rather “learning to integrate the adverse experiences into who you are and growing with them, which is sometimes known as posttraumatic growth.”
Dr. Levenson encouraged health care workers to use their coping resources, connect to others, and cultivate their values and purpose in life as they navigate these challenging times. “You also want to promote realistic optimism; find a way to stay positive,” he said. “We emphasize to our staff that while you won’t forget this time, focus on what you can control – your positive relationships – and remind yourself of your values and sources of gratitude. Figure out, and reflect on, what you care about, and then care about it. Remind yourself in a deliberate, purposeful way what anchors you to your job, which in the health care setting tends to be a desire to care for others, to assist those in need, and to work in teams. We also encourage staff to refrain from judgment. Guilt is a normal and near-universal response to this stressor, but there are many ways to contribute without a judgmental or guilty tone.”
Other tips for self-support are to remind yourself that it is not selfish to take breaks. “The needs of your patients are not more important than your own needs,” Dr. Levenson said. “Working nonstop can put you at higher risk for stress, exhaustion, and illness. You may need to give yourself more time to step back and recover from workplace challenges or extended coverage for peers; this is important. We remind our staff that your work may feel more emotionally draining than usual because everything is more intense overall during the COVID-19 pandemic. This reminder helps staff normalize what they already may be experiencing, and in turn, to further support each other.”
Soothing activities to relieve stress include meditation, prayer, deep and slow breathing, relaxation exercises, yoga, mindfulness, stretching, staying hydrated, eating healthfully, exercise, and getting sufficient sleep. Other stress management tips include avoiding excessive alcohol intake, reaching out to others, asking for assistance, and delegating when possible. “We want to promote psychological flexibility: the ability to stay in contact with the present moment,” he said. “We encourage our peers to be aware of unpleasant thoughts and feelings, and to try to redirect negative thought patterns to a proactive problem-solving approach; this includes choosing one’s behaviors based on the situation and personal values.”
Dr. Levenson reported having no disclosures related to his presentation.
LAS VEGAS – according to Jon A. Levenson, MD.
“There are those who will need mental health treatment, so creating an easy way to reach out for help and facilitate linkage with care is critically important,” Dr. Levenson, associate professor of psychiatry at Columbia University Irving Medical Center, New York, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “The vast majority of our workforce will thrive with proper support. But what can each of us do to take care of ourselves?”
Step one is to recognize common stress reactions as well as signs of distress. He offered the oxygen mask metaphor, the idea that before we can take care of and support anyone else, we must first take care of ourselves. “When people are stressed, they don’t always think about the oxygen mask metaphor,” Dr. Levenson said. Step two is to practice and model self-care by adopting principles often discussed in acceptance and commitment therapy: to focus on what you can control, not on what you can’t control.
“We can’t control the amount of toilet paper at the grocery store, how long the pandemic will last, or how others have reacted,” Dr. Levenson said. “We also can’t control other people’s motives, predict what will happen, or the actions of others, including whether they will follow social distancing guidelines or not.”
How about what we can control? One is a positive attitude, “which can sustain people during times of intense stress,” he said. “Other things that we can do include turn off the news and find fun and enriching activities to do at home, whether it be playing a game with family or reaching out to friends through an iPad or a smartphone. You can also follow [Centers for Disease Control and Prevention] recommendations, control your own social distancing, and limit social media activity, which can be stressful. We can also control our kindness and grace.” He added that resilience does not mean “snapping back” to how you were before the pandemic, but rather “learning to integrate the adverse experiences into who you are and growing with them, which is sometimes known as posttraumatic growth.”
Dr. Levenson encouraged health care workers to use their coping resources, connect to others, and cultivate their values and purpose in life as they navigate these challenging times. “You also want to promote realistic optimism; find a way to stay positive,” he said. “We emphasize to our staff that while you won’t forget this time, focus on what you can control – your positive relationships – and remind yourself of your values and sources of gratitude. Figure out, and reflect on, what you care about, and then care about it. Remind yourself in a deliberate, purposeful way what anchors you to your job, which in the health care setting tends to be a desire to care for others, to assist those in need, and to work in teams. We also encourage staff to refrain from judgment. Guilt is a normal and near-universal response to this stressor, but there are many ways to contribute without a judgmental or guilty tone.”
Other tips for self-support are to remind yourself that it is not selfish to take breaks. “The needs of your patients are not more important than your own needs,” Dr. Levenson said. “Working nonstop can put you at higher risk for stress, exhaustion, and illness. You may need to give yourself more time to step back and recover from workplace challenges or extended coverage for peers; this is important. We remind our staff that your work may feel more emotionally draining than usual because everything is more intense overall during the COVID-19 pandemic. This reminder helps staff normalize what they already may be experiencing, and in turn, to further support each other.”
Soothing activities to relieve stress include meditation, prayer, deep and slow breathing, relaxation exercises, yoga, mindfulness, stretching, staying hydrated, eating healthfully, exercise, and getting sufficient sleep. Other stress management tips include avoiding excessive alcohol intake, reaching out to others, asking for assistance, and delegating when possible. “We want to promote psychological flexibility: the ability to stay in contact with the present moment,” he said. “We encourage our peers to be aware of unpleasant thoughts and feelings, and to try to redirect negative thought patterns to a proactive problem-solving approach; this includes choosing one’s behaviors based on the situation and personal values.”
Dr. Levenson reported having no disclosures related to his presentation.
LAS VEGAS – according to Jon A. Levenson, MD.
“There are those who will need mental health treatment, so creating an easy way to reach out for help and facilitate linkage with care is critically important,” Dr. Levenson, associate professor of psychiatry at Columbia University Irving Medical Center, New York, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “The vast majority of our workforce will thrive with proper support. But what can each of us do to take care of ourselves?”
Step one is to recognize common stress reactions as well as signs of distress. He offered the oxygen mask metaphor, the idea that before we can take care of and support anyone else, we must first take care of ourselves. “When people are stressed, they don’t always think about the oxygen mask metaphor,” Dr. Levenson said. Step two is to practice and model self-care by adopting principles often discussed in acceptance and commitment therapy: to focus on what you can control, not on what you can’t control.
“We can’t control the amount of toilet paper at the grocery store, how long the pandemic will last, or how others have reacted,” Dr. Levenson said. “We also can’t control other people’s motives, predict what will happen, or the actions of others, including whether they will follow social distancing guidelines or not.”
How about what we can control? One is a positive attitude, “which can sustain people during times of intense stress,” he said. “Other things that we can do include turn off the news and find fun and enriching activities to do at home, whether it be playing a game with family or reaching out to friends through an iPad or a smartphone. You can also follow [Centers for Disease Control and Prevention] recommendations, control your own social distancing, and limit social media activity, which can be stressful. We can also control our kindness and grace.” He added that resilience does not mean “snapping back” to how you were before the pandemic, but rather “learning to integrate the adverse experiences into who you are and growing with them, which is sometimes known as posttraumatic growth.”
Dr. Levenson encouraged health care workers to use their coping resources, connect to others, and cultivate their values and purpose in life as they navigate these challenging times. “You also want to promote realistic optimism; find a way to stay positive,” he said. “We emphasize to our staff that while you won’t forget this time, focus on what you can control – your positive relationships – and remind yourself of your values and sources of gratitude. Figure out, and reflect on, what you care about, and then care about it. Remind yourself in a deliberate, purposeful way what anchors you to your job, which in the health care setting tends to be a desire to care for others, to assist those in need, and to work in teams. We also encourage staff to refrain from judgment. Guilt is a normal and near-universal response to this stressor, but there are many ways to contribute without a judgmental or guilty tone.”
Other tips for self-support are to remind yourself that it is not selfish to take breaks. “The needs of your patients are not more important than your own needs,” Dr. Levenson said. “Working nonstop can put you at higher risk for stress, exhaustion, and illness. You may need to give yourself more time to step back and recover from workplace challenges or extended coverage for peers; this is important. We remind our staff that your work may feel more emotionally draining than usual because everything is more intense overall during the COVID-19 pandemic. This reminder helps staff normalize what they already may be experiencing, and in turn, to further support each other.”
Soothing activities to relieve stress include meditation, prayer, deep and slow breathing, relaxation exercises, yoga, mindfulness, stretching, staying hydrated, eating healthfully, exercise, and getting sufficient sleep. Other stress management tips include avoiding excessive alcohol intake, reaching out to others, asking for assistance, and delegating when possible. “We want to promote psychological flexibility: the ability to stay in contact with the present moment,” he said. “We encourage our peers to be aware of unpleasant thoughts and feelings, and to try to redirect negative thought patterns to a proactive problem-solving approach; this includes choosing one’s behaviors based on the situation and personal values.”
Dr. Levenson reported having no disclosures related to his presentation.
AT NPA 2022
Psychoses: The 5 comorbidity-defined subtypes
How can we treat psychosis if we don’t know what we are treating? Over the years, attempts at defining psychosis subtypes have met with dead ends. However, recent research supports a new approach that offers a rational classification model organized according to 5 specific comorbid anxiety and depressive disorder diagnoses.
Anxiety and depressive symptoms are not just the result of psychotic despair. They are specific diagnoses, they precede psychosis onset, they help define psychotic syndromes, and they can point to much more effective treatment approaches. Most of the psychotic diagnoses in this schema are already recognized or posited. And, just as patients who do not have psychotic illness can have more than 1 anxiety or depressive disorder, patients with psychosis can present with a mixed picture that reflects more than 1 contributing comorbidity. Research further suggests that each of the 5 psychosis comorbidity diagnoses may involve some similar underlying factors that facilitate the formation of psychosis.
This article describes the basics of 5 psychosis subtypes, and provides initial guidelines to diagnosis, symptomatology, and treatment. Though clinical experience and existing research support the clinical presence and treatment value of this classification model, further verification will require considerably more controlled studies. An eventual validation of this approach could largely supplant ill-defined diagnoses of “schizophrenia” and other functional psychoses.
Recognizing the comorbidities in the context of their corresponding psychoses entails learning new interviewing skills and devoting more time to both initial and subsequent diagnosis and treatment. In our recently published book,1 we provide extensive details on the approach we describe in this article, including case examples, new interview tools to simplify the diagnostic journey, and novel treatment approaches.
Psychosis-proneness underlies functional psychoses
Functional (idiopathic) schizophrenia and psychotic disorders have long been difficult to separate, and many categorizations have been discarded. Despite clinical dissimilarities, today we too often casually lump psychoses together as schizophrenia.2,3 Eugen Bleuler first suggested the existence of a “group of schizophrenias.”4 It is possible that his group encompasses our 5 psychoses from 5 inbuilt emotional instincts,5 each corresponding to a specific anxiety or depressive subtype.
The 5 anxiety and depressive subtypes noted in this article are common, but psychosis is not. Considerable research suggests that certain global “psychotogenic” factors create susceptibility to all psychoses.6,7 While many genetic, neuroanatomical, experiential, and other factors have been reported, the most important may be “hypofrontality” (genetically reduced frontal lobe function, size, or neuronal activity) and dopaminergic hyperfunction (genetically increased dopamine activity).5-7
An evolutionary perspective
One evolutionary theory of psychopathology starts with the subtypes of depression and anxiety. For example, major depressive disorder and generalized anxiety disorder may encompass 5 commonplace and more specific anxiety and depressive subtypes. Consideration of the emotional, cognitive, and functional aspects of those subtypes suggests that they may have once been advantageous for primeval human herds. Those primeval altruistic instincts may have helped survival, reproduction, and preservation of kin group DNA.5
More than any other species, humans can draw upon consciousness and culture to rationally overcome the influences of unconscious instincts. But those instincts can then emerge from the deep, and painfully encourage obedience to their guidance. In nonpsychotic anxiety and depressive disorders, the specific messages are experienced as specific anxiety and depressive symptoms.5 In psychotic disorders, the messages can emerge as unreasoned and frightful fears, perceptions, beliefs, and behaviors. With newer research, clinical observation, and an evolutionary perspective, a novel and counterintuitive approach may improve our ability to help patients.8
Continue to: Five affective comorbidities evolved from primeval altruistic instincts...
Five affective comorbidities evolved from primeval altruistic instincts
Melancholic depression5
Melancholic depression is often triggered by serious illness, group exclusion, pronounced loss, or purposelessness. We hear patients talk painfully about illness, guilt, and death. Indeed, some increased risk of death, especially from infectious disease, may result from hypercortisolemia (documented by the dexamethasone suppression test). Hypercortisolemic death also occurs in salmon after spawning, and in male marsupial mice after mating. The tragic passing of an individual saves scarce resources for the remainder of the herd.
Obsessive-compulsive disorder5
Factor-analytic studies suggest 4 main obsessive-compulsive disorder (OCD) subtypes: cleanliness, hoarding, intrusive thoughts, and organizing. Obsessive-compulsive traits can help maintain a safe and efficient environment in humans and other species, but OCD is dysfunctional.
Panic anxiety5
Panic anxiety is triggered by real, symbolic, or emotional separation from home and family. In toddlers, separation anxiety can reduce the odds of getting lost and hurt.
Social anxiety5
Social anxiety includes fear of self-embarrassment, exposure as a pretender to higher social rank, and thus often a reluctant avoidance of increased social rank. While consciousness and cultural encouragement can overcome that hesitation and thus lead to greater success, social anxiety activation can still cause painful anxiety. The social hierarchies of many species include comparable biological influences, and help preserve group DNA by reducing hierarchical infighting.
Atypical depression and bipolar I mania5
Atypical depression includes increased rejection sensitivity, resulting in inoffensive behavior to avoid social rejection. This reduces risk of isolation from the group, and improves group harmony. Unlike the 4 other syndromes, atypical depression and bipolar I mania may reflect 2 separate seasonal mood phases. Atypical depression (including seasonal affective disorder) often worsens with shortened winter daylight hours, akin to hibernation. Initial bipolar I mania is more common with springtime daylight, with symptoms not unlike exaggerated hibernation awakening.9
Primeval biological altruism has great evolutionary value in many species, and even somewhat in modern humans. But it is quite different from modern rational altruism. Although we sometimes override our instincts, they respond with messages experienced as emotional pain—they still tell us to follow instructions for primeval herd survival. In an earlier book, I (JPK) provide a lengthier description of the evidence for this evolutionary psychopathology theory, including interplay of the 5 instincts with psychotogenic factors.5
Continue to: Five comorbidity psychoses from 5 primeval instincts.....
Five comorbidity psychoses from 5 primeval instincts
The 5 affective comorbidities described above contribute to the presence, subtype, and treatment approaches of 5 corresponding psychoses. Ordinary panic attacks might occur when feeling trapped or separated from home, so people want to flee to safety. Nonhuman species with limited consciousness and language are unlikely to think “time to head for safety.” Instead, instincts encourage flight from danger through internally generated perceptions of threat. Likewise, people with psychosis and panic, without sufficient conscious modulation, may experience sensory perceptions of actual danger when feeling symbolically trapped.1,10
One pilot study carefully examined the prevalence of these 5 comorbidities in an unselected group of psychotic patients.10 At least 85% met criteria for ≥1 of the 5 subtypes.10 Moreover, organic psychoses related to physical illness, substances, and iatrogenesis may also predict future episodes of functional psychoses.1
Using statistical analysis of psychosis rating scales, 2 studies took a “transdiagnostic” look at psychoses, and each found 5 psychosis subtypes and a generalized psychosis susceptibility factor.11,12 Replication of that transdiagnostic approach, newly including psychosis symptoms and our 5 specific comorbidities, might well find that the 5 subtype models resemble each other.11,12
Our proposed 5 comorbidity subtypes are1:
Delusional depression (melancholic depression). Most common in geriatric patients, this psychosis can also occur at younger ages. Prodromal melancholic depression can include guilt and hopelessness, and is acute, rather than the chronic course of our other 4 syndromes. Subsequent delusional depression includes delusions of bodily decay, illness, or death, as well as overwhelming guilt, shame, and remorse. The classic vegetative symptoms of depression continue. In addition to infectious disease issues, high suicide risk makes hospitalization imperative.
Obsessive-compulsive schizophrenia. Just as OCD has an early age of onset, obsessive-compulsive schizophrenia begins earlier than other psychoses. Despite preserved cognition, some nonpsychotic patients with OCD have diminished symptom insight. OCD may be comorbid with schizophrenia in 12% of cases, typically preceding psychosis onset. Obsessive-compulsive schizophrenia symptoms may include highly exaggerated doubt or ambivalence; contamination concerns; eccentric, ritualistic, motor stereotypy, checking, disorganized, and other behaviors; and paranoia.
Schizophrenia with voices (panic anxiety). Classic paranoid schizophrenia with voices appears to be the most similar to a “panic psychosis.” Patients with nonpsychotic panic anxiety have increased paranoid ideation and ideas of reference as measured on the Symptom Checklist-90. Schizophrenia is highly comorbid with panic anxiety, estimated at 45% in the Epidemiologic Catchment Area study.13 These are likely underestimates: cognitive impairment hinders reporting, and psychotic panic is masked as auditory hallucinations. A pilot study of schizophrenia with voices using a carbon dioxide panic induction challenge found that 100% had panic anxiety.14 That study and another found that virtually all participants reported voices concurrent with panic using our Panic and Schizophrenia Interview (PaSI) (Box 1). Panic onset precedes schizophrenia onset, and panic may reappear if antipsychotic medications sufficiently control voices: “voices without the voices,” say some.
Box 1
Let’s talk for a minute about your voices.
[IDENTIFYING PAROXYSMAL MOMENTS OF VOICE ONSET]
Do you hear voices at every single moment, or are they sometimes silent? Think about those times when you are not actually hearing any voices.
Now, there may be reasons why the voices start talking when they do, but let’s leave that aside for now.
So, whenever the voices do begin speaking—and for whatever reason they do—is it all of a sudden, or do they start very softly and then very gradually get louder?
If your voices are nearly always there, then are there times when the voices suddenly come back, get louder, get more insistent, or just get more obvious to you?
[Focus patient on sudden moment of voice onset, intensification, or awareness]
Let’s talk about that sudden moment when the voices begin (or intensify, or become obvious), even if you know the reason why they start.
I’m going to ask you about some symptoms that you might have at that same sudden moment when the voices start (or intensify, or become obvious). If you have any of these symptoms at the other times, they do not count for now.
So, when I ask about each symptom, tell me whether it comes on at the same sudden moments as the voices, and also if it used to come on with the voices in the past.
For each sudden symptom, just say “YES” or “NO” or “SOMETIMES.”
[Begin each query with: “At the same sudden moment that the voices come on”]
- Sudden anxiety, fear, or panic on the inside?
- Sudden anger or rage on the inside? [ANGER QUERY]
- Sudden heart racing? Heart pounding?
- Sudden chest pain? Chest pressure?
- Sudden sweating?
- Sudden trembling or shaking?
- Sudden shortness of breath, or like you can’t catch your breath?
- Sudden choking or a lump in your throat?
- Sudden nausea or queasiness?
- Sudden dizziness, lightheadedness, or faintness?
- Sudden feeling of detachment, sort of like you are in a glass box?
- Sudden fear of losing control? Fear of going crazy?
- Sudden fear afraid of dying? Afraid of having a heart attack?
- Sudden numbness or tingling, especially in your hands or face?
- Sudden feeling of heat, or cold?
- Sudden itching in your teeth? [VALIDITY CHECK]
- Sudden fear that people want to hurt you? [EXCESS FEAR QUERY]
- Sudden voices? [VOICES QUERY]
[PAST & PRODROMAL PANIC HISTORY]
At what age did you first see a therapist or psychiatrist?
At what age were you first hospitalized for an emotional problem?
At what age did you first start hearing voices?
At what age did you first start having strong fears of other people?
Before you ever heard voices, did you ever have any of the other sudden symptoms like the ones we just talked about?
Did those episodes back then feel sort of like your voices or sudden fears do now, except that there were no voices or sudden fears of people back then?
At what age did those sudden anxiety (or panic or rage) episodes begin?
Back then, was there MORE (M) sudden anxiety, or the SAME (S) sudden anxiety, or LESS (L) sudden anxiety than with your sudden voices now?
[PAST & PRODROMAL PANIC SYMPTOMS]
Now let’s talk about some symptoms that you might have had at those same sudden anxiety moments, in the time before you ever heard any voices. So, for each sudden symptom just say “YES” or “NO” or “SOMETIMES.”
[Begin each query with: “At the same moment the sudden anxiety came on—but only during the time before you ever heard sudden voices”]
[Ask about the same 18 panic-related symptoms listed above]
[PHOBIA-RELATED PANIC AND VOICES]
Have you ever been afraid to go into a (car, bus, plane, train, subway, elevator, mall, tunnel, bridge, heights, small place, CAT scan or MRI, being alone, crowds)?
[If yes or maybe: Ask about panic symptoms in phobic situations]
Now let’s talk about some symptoms that you might have had at some of those times you were afraid. So, for each symptom just say “YES” or “NO” or “MAYBE.”
[Ask about the same 18 panic-related symptoms listed above]
At what age did you last have sudden anxiety without voices?
Has medication ever completely stopped your voices? Somewhat?
If so, did those other sudden symptoms still happen sometimes?
Thank you for your help, and for answering all of these questions!
Persecutory delusional disorder (social anxiety). Some “schizophrenia” without voices may be misdiagnosis of persecutory (paranoid) delusional disorder (PDD). Therefore, the reported population prevalence (0.02%) may be underestimated. Social anxiety is highly comorbid with “schizophrenia” (15%).16 Case reports and clinical experience suggest that PDD is commonly preceded by social anxiety.17 Some nonpsychotic social anxiety symptoms closely resemble the PDD psychotic ideas of reference (a perception that low social rank attracts critical scrutiny by authorities). Patients with PDD may remain relatively functional, with few negative symptoms, despite pronounced paranoia. Outward manifestation of paranoia may be limited, unless quite intense. The typical age of onset (40 years) is later than that of schizophrenia, and symptoms can last a long time.18
Continue to: Bipolar 1 mania with delusions...
Bipolar I mania with delusions (atypical depression). Atypical depression is the most common depression in bipolar I disorder. Often more pronounced in winter, it may intensify at any time of year. Long ago, hypersomnia, lethargy, inactivity, inoffensiveness, and craving high-calorie food may have been conducive to hibernation.
Bipolar I mania includes delusions of special accomplishments or abilities, energetically focused on a grandiose mission to help everyone. These intense symptoms may be related to reduced frontal lobe modulation. In some milder form, bipolar I mania may once have encouraged hibernation awakening. Indeed, initial bipolar I mania episodes are more common in spring, as is the spring cleaning that helps us prepare for summer.
Recognizing affective trees in a psychotic forest
Though long observed, comorbid affective symptoms have generally been considered a hodgepodge of distress caused by painful psychotic illness. But the affective symptoms precede psychosis onset, can be masked during acute psychosis, and will revert to ordinary form if psychosis abates.11-13
Rather than affective symptoms being a consequence of psychosis, it may well be the other way around. Affective disorders could be important causal and differentiating components of psychotic disorders.11-13 Research and clinical experience suggest that adjunctive treatment of the comorbidities with correct medication can greatly enhance outcome.
Diagnostic approaches
Because interviews of patients with psychosis are often complicated by confusion, irritability, paranoid evasiveness, cognitive impairment, and medication, nuanced diagnosis is difficult. Interviews should explore psychotic syndromes and subtypes that correlate with comorbidity psychoses, including pre-psychotic anxiety and depressive diagnoses that are chronic (though unlike our 4 other diagnoses, melancholic depression is not chronic).
Establishing pre-psychotic diagnosis of chronic syndromes suggests that they are still present, even if they are difficult to assess during psychosis. Re-interview after some improvement allows for a significantly better diagnosis. Just as in nonpsychotic affective disorders, multiple comorbidities are common, and can lead to a mixed psychotic diagnosis and treatment plan.1
Structured interview tools can assist diagnosis. The PaSI (Box 1,15) elicits past, present, and detailed history of DSM panic, and has been validated in a small pilot randomized controlled trial. The PaSI focuses patient attention on paroxysmal onset voices, and then evaluates the presence of concurrent DSM panic symptoms. If voices are mostly psychotic panic, they may well be a proxy for panic. Ultimately, diagnosis of 5 comorbidities and associated psychotic symptoms may allow simpler categorization into 1 (or more) of the 5 psychosis subtypes.
Continue to: Treatment by comorbidity subtype...
Treatment by comorbidity subtype
Treatment of psychosis generally begins with antipsychotics. Nominal psychotherapy (presence of a professionally detached, compassionate clinician) improves compliance and leads to supportive therapy. Cognitive-behavioral therapy and dialectical behavior therapy may help later, with limited interpersonal approaches further on for some patients.
The suggested approaches to pharmacotherapy noted here draw on research and clinical experience.1,14,19-21 All medications used to treat comorbidities noted here are approved or generally accepted for that diagnosis. Estimated doses are similar to those for comorbidities when patients are nonpsychotic, and vary among patients. Doses, dosing schedules, and titration are extremely important for full benefit. Always consider compliance issues, suicidality, possible adverse effects, and potential drug/drug interactions. Although the medications we suggest using to treat the comorbidities may appear to also benefit psychosis, only antipsychotics are approved for psychosis per se.
Delusional depression. Antipsychotic + antidepressant. Tricyclic antidepressants are possibly most effective, but increase the risk of overdose and dangerous falls among fragile patients. Electroconvulsive therapy is sometimes used.
Obsessive-compulsive schizophrenia. Antipsychotic + selective serotonin reuptake inhibitor (SSRI). Consider aripiprazole (
Schizophrenia with voices. Antipsychotic + clonazepam. Concurrent usage may stabilize psychosis more rapidly, and with a lower antipsychotic dose.23 Titrate a fixed dose of clonazepam every 12 hours (avoid as-needed doses), starting low (ie, 0.5 mg) to limit initial drowsiness (which typically diminishes in 3 to 10 days). Titrate to full voice and panic cessation (1 to 2.5 mg every 12 hours).14 Exercise caution about excessive drowsiness, as well as outpatient compliance and abuse. Besides alprazolam, other antipanic medications have little incidental benefit for psychosis.
Persecutory delusional disorder. Antipsychotic + SSRI. Aripiprazole (consider long-acting injectable for compliance) also enhances the benefits of fluoxetine for social anxiety. Long half-life fluoxetine (20 mg/d) improves compliance and near-term outcomes.
Bipolar I mania: mania with delusions. Consider olanzapine for acute phase, then add other antimanic medication (commonly lithium or valproic acid), check blood level, and then taper olanzapine some weeks later. Importantly, lamotrigine is not effective for bipolar I mania. Consider suicide risk, medical conditions, and outpatient compliance. Comorbid panic anxiety is also common in bipolar I mania, often presenting as nonthreatening voices.
Seasonality: Following research that bipolar I mania is more common in spring and summer, studies have shown beneficial clinical augmentation from dark therapy as provided by reduced light exposure, blue-blocking glasses, and exogenous melatonin (a darkness-signaling hormone).24
Bipolar I mania atypical depression (significant current or historical symptoms). SSRI + booster medication. An SSRI (ie, escitalopram, 10 mg/d) is best started several weeks after full bipolar I mania resolution, while also continuing long-term antimanic medication. Booster medications (ie, buspirone 15 mg every 12 hours; lithium 300 mg/d; or trazodone 50 mg every 12 hours) can enhance SSRI benefits. Meta-analysis suggests SSRIs may have limited risk of inducing bipolar I mania.25 Although not yet specifically tested for atypical depression, lamotrigine may be effective, and may be safer still.25 However, lamotrigine requires very gradual dose titration to prevent a potentially dangerous rash, including after periods of outpatient noncompliance.
Seasonality: Atypical depression is often worse in winter (seasonal affective disorder). Light therapy can produce some clinically helpful benefits year-round.
To illustrate this new approach to psychosis diagnosis and treatment, our book
Box 2
Ms. B, a studious 19-year-old, has been very shy since childhood, with few friends. Meeting new people always gave her gradually increasing anxiety, thinking that she would embarrass herself in their eyes. She had that same anxiety, along with sweating and tachycardia, when she couldn’t avoid speaking in front of class. Sometimes, while walking down the street she would think that strangers were casting a disdainful eye on her, though she knew that wasn’t true. Another anxiety started when she was 16. While looking for paper in a small supply closet, she suddenly felt panicky. With a racing heart and short of breath, she desperately fled the closet. These episodes continued, sometimes for no apparent reason, and nearly always unnoticed by others.
At age 17, she began to believe that those strangers on the street were looking down on her with evil intent, and even following her around. She became afraid to walk around town. A few months later, she also started to hear angry and critical voices at sudden moments. Although the paroxysmal voices always coincided with her panicky symptoms, the threatening voices now felt more important to her than the panic itself. Nonpsychotic panics had stopped. Mostly a recluse, she saw less of her family, left her job, and stopped going to the movies.
After a family dinner, she was detached, scared, and quieter than usual. She sought help from her primary care physician, who referred her to a psychiatrist. A thorough history from Ms. B and her family revealed her disturbing fears, as well as her history of social anxiety. Interviewing for panic was prompted by her mother’s recollection of the supply closet story.
In view of Ms. B’s cooperativeness and supportive family, outpatient treatment of her recent-onset psychosis began with aripiprazole, 10 mg/d, and clonazepam, 0.5 mg every 12 hours. Clonazepam was gradually increased until voices (and panic) ceased. She was then able to describe how earlier panics had felt just like voices, but without the voices. The fears of strangers continued. Escitalopram, 20 mg/d, was added for social anxiety (aripiprazole enhances the benefits of selective serotonin reuptake inhibitors).
One month later, her fears of strangers diminished, and she felt more comfortable around people than ever before. On the same medications, and in psychotherapy over the next year, she began to increase her social network while making plans to start college.
Larger studies are needed
Current research supports the concept of a 5-diagnosis classification of psychoses, which may correlate with our comorbid anxiety and depression model. Larger diagnostic and treatment studies would invaluably examine existing research and clinical experience, and potentially encourage more clinically useful diagnoses, specific treatments, and improved outcomes.
Bottom Line
New insights from evolutionary psychopathology, clinical research and observation, psychotogenesis, genetics, and epidemiology suggest that most functional psychoses may fall into 1 of 5 comorbidity-defined subtypes, for which specific treatments can lead to much improved outcomes.
1. Veras AB, Kahn JP, eds. Psychotic Disorders: Comorbidity Detection Promotes Improved Diagnosis and Treatment. Elsevier; 2021.
2. Gaebel W, Zielasek J. Focus on psychosis. Dialogues Clin Neuroscience. 2015;17(1):9-18.
3. Guloksuz S, Van Os J. The slow death of the concept of schizophrenia and the painful birth of the psychosis spectrum. Psychological Medicine. 2018;48(2):229-244.
4. Bleuler E. Dementia Praecox or the Group of Schizophrenias. International Universities Press; 1950.
5. Kahn JP. Angst: Origins of Depression and Anxiety. Oxford University Press; 2013.
6. Howes OD, McCutcheon R, Owen MJ, et al. The role of genes, stress, and dopamine in the development of schizophrenia. Biol Psychiatry. 2017;81(1):9-20.
7. Mubarik A, Tohid H. Frontal lobe alterations in schizophrenia: a review. Trends Psychiatry Psychother. 2016;38(4):198-206.
8. Murray RM, Bhavsar V, Tripoli G, et al. 30 Years on: How the neurodevelopmental hypothesis of schizophrenia morphed into the developmental risk factor model of psychosis. Schizophr Bull. 2017;43(6):1190-1196.
9. Bauer M, Glenn T, Alda M, et al. Solar insolation in springtime influences age of onset of bipolar I disorder. Acta Psychiatr Scand. 2017;136(6):571-582.
10. Kahn JP, Bombassaro T, Veras AB. Comorbid schizophrenia and panic anxiety: panic psychosis revisited. Psychiatr Ann. 2018;48(12):561-565.
11. Bebbington P, Freeman D. Transdiagnostic extension of delusions: schizophrenia and beyond. Schizophr Bull. 2017;43(2):273-282.
12. Catalan A, Simons CJP, Bustamante S, et al. Data gathering bias: trait vulnerability to psychotic symptoms? PLoS One. 2015;10(7):e0132442. doi:10.1371/journal.pone.0132442
13. Goodwin R, Lyons JS, McNally RJ. Panic attacks in schizophrenia. Schizophr Res. 2002;58(2-3):213-220.
14. Kahn JP, Puertollano MA, Schane MD, et al. Adjunctive alprazolam for schizophrenia with panic anxiety: clinical observation and pathogenetic implications. Am J Psychiatry. 1988;145(6):742-744.
15. Kahn JP. Chapter 4: Paranoid schizophrenia with voices and panic anxiety. In: Veras AB, Kahn JP, eds. Psychotic Disorders: Comorbidity Detection Promotes Improved Diagnosis and Treatment. Elsevier; 2021.
16. Achim AM, Maziade M, Raymond E, et al. How prevalent are anxiety disorders in schizophrenia? A meta-analysis and critical review on a significant association. Schizophr Bull. 2011;37(4):811-821.
17. Veras AB, Souza TG, Ricci TG, et al. Paranoid delusional disorder follows social anxiety disorder in a long-term case series: evolutionary perspective. J Nerv Ment Dis. 2015;203(6):477-479.
18. McIntyre JC, Wickham S, Barr B, et al. Social identity and psychosis: associations and psychological mechanisms. Schizophr Bull. 2018;44(3):681-690.
19. Barbee JG, Mancuso DM, Freed CR. Alprazolam as a neuroleptic adjunct in the emergency treatment of schizophrenia. Am J Psychiatry. 1992;149(4):506-510.
20. Nardi AE, Machado S, Almada LF. Clonazepam for the treatment of panic disorder. Curr Drug Targets. 2013;14(3):353-364.
21. Poyurovsky M. Schizo-Obsessive Disorder. Cambridge University Press; 2013.
22. Reznik I, Sirota P. Obsessive and compulsive symptoms in schizophrenia: a randomized controlled trial with fluvoxamine and neuroleptics. J Clin Psychopharmacol. 2000;20(4):410-416.
23. Bodkin JA. Emerging uses for high-potency benzodiazepines in psychotic disorders. J Clin Psychiatry. 1990;51 Suppl:41-53.
24. Gottlieb JF, Benedetti F, Geoffroy PA, et al. The chronotherapeutic treatment of bipolar disorders: a systematic review and practice recommendations from the ISBD task force on chronotherapy and chronobiology. Bipolar Disord. 2019;21(8):741-773.
25. Pacchiarotti I, Bond DJ, Baldessarini RJ, et al. The International Society for Bipolar Disorders (ISBD) task force report on antidepressant use in bipolar disorders. Am J Psychiatry. 2013;170(11):1249-1262.
How can we treat psychosis if we don’t know what we are treating? Over the years, attempts at defining psychosis subtypes have met with dead ends. However, recent research supports a new approach that offers a rational classification model organized according to 5 specific comorbid anxiety and depressive disorder diagnoses.
Anxiety and depressive symptoms are not just the result of psychotic despair. They are specific diagnoses, they precede psychosis onset, they help define psychotic syndromes, and they can point to much more effective treatment approaches. Most of the psychotic diagnoses in this schema are already recognized or posited. And, just as patients who do not have psychotic illness can have more than 1 anxiety or depressive disorder, patients with psychosis can present with a mixed picture that reflects more than 1 contributing comorbidity. Research further suggests that each of the 5 psychosis comorbidity diagnoses may involve some similar underlying factors that facilitate the formation of psychosis.
This article describes the basics of 5 psychosis subtypes, and provides initial guidelines to diagnosis, symptomatology, and treatment. Though clinical experience and existing research support the clinical presence and treatment value of this classification model, further verification will require considerably more controlled studies. An eventual validation of this approach could largely supplant ill-defined diagnoses of “schizophrenia” and other functional psychoses.
Recognizing the comorbidities in the context of their corresponding psychoses entails learning new interviewing skills and devoting more time to both initial and subsequent diagnosis and treatment. In our recently published book,1 we provide extensive details on the approach we describe in this article, including case examples, new interview tools to simplify the diagnostic journey, and novel treatment approaches.
Psychosis-proneness underlies functional psychoses
Functional (idiopathic) schizophrenia and psychotic disorders have long been difficult to separate, and many categorizations have been discarded. Despite clinical dissimilarities, today we too often casually lump psychoses together as schizophrenia.2,3 Eugen Bleuler first suggested the existence of a “group of schizophrenias.”4 It is possible that his group encompasses our 5 psychoses from 5 inbuilt emotional instincts,5 each corresponding to a specific anxiety or depressive subtype.
The 5 anxiety and depressive subtypes noted in this article are common, but psychosis is not. Considerable research suggests that certain global “psychotogenic” factors create susceptibility to all psychoses.6,7 While many genetic, neuroanatomical, experiential, and other factors have been reported, the most important may be “hypofrontality” (genetically reduced frontal lobe function, size, or neuronal activity) and dopaminergic hyperfunction (genetically increased dopamine activity).5-7
An evolutionary perspective
One evolutionary theory of psychopathology starts with the subtypes of depression and anxiety. For example, major depressive disorder and generalized anxiety disorder may encompass 5 commonplace and more specific anxiety and depressive subtypes. Consideration of the emotional, cognitive, and functional aspects of those subtypes suggests that they may have once been advantageous for primeval human herds. Those primeval altruistic instincts may have helped survival, reproduction, and preservation of kin group DNA.5
More than any other species, humans can draw upon consciousness and culture to rationally overcome the influences of unconscious instincts. But those instincts can then emerge from the deep, and painfully encourage obedience to their guidance. In nonpsychotic anxiety and depressive disorders, the specific messages are experienced as specific anxiety and depressive symptoms.5 In psychotic disorders, the messages can emerge as unreasoned and frightful fears, perceptions, beliefs, and behaviors. With newer research, clinical observation, and an evolutionary perspective, a novel and counterintuitive approach may improve our ability to help patients.8
Continue to: Five affective comorbidities evolved from primeval altruistic instincts...
Five affective comorbidities evolved from primeval altruistic instincts
Melancholic depression5
Melancholic depression is often triggered by serious illness, group exclusion, pronounced loss, or purposelessness. We hear patients talk painfully about illness, guilt, and death. Indeed, some increased risk of death, especially from infectious disease, may result from hypercortisolemia (documented by the dexamethasone suppression test). Hypercortisolemic death also occurs in salmon after spawning, and in male marsupial mice after mating. The tragic passing of an individual saves scarce resources for the remainder of the herd.
Obsessive-compulsive disorder5
Factor-analytic studies suggest 4 main obsessive-compulsive disorder (OCD) subtypes: cleanliness, hoarding, intrusive thoughts, and organizing. Obsessive-compulsive traits can help maintain a safe and efficient environment in humans and other species, but OCD is dysfunctional.
Panic anxiety5
Panic anxiety is triggered by real, symbolic, or emotional separation from home and family. In toddlers, separation anxiety can reduce the odds of getting lost and hurt.
Social anxiety5
Social anxiety includes fear of self-embarrassment, exposure as a pretender to higher social rank, and thus often a reluctant avoidance of increased social rank. While consciousness and cultural encouragement can overcome that hesitation and thus lead to greater success, social anxiety activation can still cause painful anxiety. The social hierarchies of many species include comparable biological influences, and help preserve group DNA by reducing hierarchical infighting.
Atypical depression and bipolar I mania5
Atypical depression includes increased rejection sensitivity, resulting in inoffensive behavior to avoid social rejection. This reduces risk of isolation from the group, and improves group harmony. Unlike the 4 other syndromes, atypical depression and bipolar I mania may reflect 2 separate seasonal mood phases. Atypical depression (including seasonal affective disorder) often worsens with shortened winter daylight hours, akin to hibernation. Initial bipolar I mania is more common with springtime daylight, with symptoms not unlike exaggerated hibernation awakening.9
Primeval biological altruism has great evolutionary value in many species, and even somewhat in modern humans. But it is quite different from modern rational altruism. Although we sometimes override our instincts, they respond with messages experienced as emotional pain—they still tell us to follow instructions for primeval herd survival. In an earlier book, I (JPK) provide a lengthier description of the evidence for this evolutionary psychopathology theory, including interplay of the 5 instincts with psychotogenic factors.5
Continue to: Five comorbidity psychoses from 5 primeval instincts.....
Five comorbidity psychoses from 5 primeval instincts
The 5 affective comorbidities described above contribute to the presence, subtype, and treatment approaches of 5 corresponding psychoses. Ordinary panic attacks might occur when feeling trapped or separated from home, so people want to flee to safety. Nonhuman species with limited consciousness and language are unlikely to think “time to head for safety.” Instead, instincts encourage flight from danger through internally generated perceptions of threat. Likewise, people with psychosis and panic, without sufficient conscious modulation, may experience sensory perceptions of actual danger when feeling symbolically trapped.1,10
One pilot study carefully examined the prevalence of these 5 comorbidities in an unselected group of psychotic patients.10 At least 85% met criteria for ≥1 of the 5 subtypes.10 Moreover, organic psychoses related to physical illness, substances, and iatrogenesis may also predict future episodes of functional psychoses.1
Using statistical analysis of psychosis rating scales, 2 studies took a “transdiagnostic” look at psychoses, and each found 5 psychosis subtypes and a generalized psychosis susceptibility factor.11,12 Replication of that transdiagnostic approach, newly including psychosis symptoms and our 5 specific comorbidities, might well find that the 5 subtype models resemble each other.11,12
Our proposed 5 comorbidity subtypes are1:
Delusional depression (melancholic depression). Most common in geriatric patients, this psychosis can also occur at younger ages. Prodromal melancholic depression can include guilt and hopelessness, and is acute, rather than the chronic course of our other 4 syndromes. Subsequent delusional depression includes delusions of bodily decay, illness, or death, as well as overwhelming guilt, shame, and remorse. The classic vegetative symptoms of depression continue. In addition to infectious disease issues, high suicide risk makes hospitalization imperative.
Obsessive-compulsive schizophrenia. Just as OCD has an early age of onset, obsessive-compulsive schizophrenia begins earlier than other psychoses. Despite preserved cognition, some nonpsychotic patients with OCD have diminished symptom insight. OCD may be comorbid with schizophrenia in 12% of cases, typically preceding psychosis onset. Obsessive-compulsive schizophrenia symptoms may include highly exaggerated doubt or ambivalence; contamination concerns; eccentric, ritualistic, motor stereotypy, checking, disorganized, and other behaviors; and paranoia.
Schizophrenia with voices (panic anxiety). Classic paranoid schizophrenia with voices appears to be the most similar to a “panic psychosis.” Patients with nonpsychotic panic anxiety have increased paranoid ideation and ideas of reference as measured on the Symptom Checklist-90. Schizophrenia is highly comorbid with panic anxiety, estimated at 45% in the Epidemiologic Catchment Area study.13 These are likely underestimates: cognitive impairment hinders reporting, and psychotic panic is masked as auditory hallucinations. A pilot study of schizophrenia with voices using a carbon dioxide panic induction challenge found that 100% had panic anxiety.14 That study and another found that virtually all participants reported voices concurrent with panic using our Panic and Schizophrenia Interview (PaSI) (Box 1). Panic onset precedes schizophrenia onset, and panic may reappear if antipsychotic medications sufficiently control voices: “voices without the voices,” say some.
Box 1
Let’s talk for a minute about your voices.
[IDENTIFYING PAROXYSMAL MOMENTS OF VOICE ONSET]
Do you hear voices at every single moment, or are they sometimes silent? Think about those times when you are not actually hearing any voices.
Now, there may be reasons why the voices start talking when they do, but let’s leave that aside for now.
So, whenever the voices do begin speaking—and for whatever reason they do—is it all of a sudden, or do they start very softly and then very gradually get louder?
If your voices are nearly always there, then are there times when the voices suddenly come back, get louder, get more insistent, or just get more obvious to you?
[Focus patient on sudden moment of voice onset, intensification, or awareness]
Let’s talk about that sudden moment when the voices begin (or intensify, or become obvious), even if you know the reason why they start.
I’m going to ask you about some symptoms that you might have at that same sudden moment when the voices start (or intensify, or become obvious). If you have any of these symptoms at the other times, they do not count for now.
So, when I ask about each symptom, tell me whether it comes on at the same sudden moments as the voices, and also if it used to come on with the voices in the past.
For each sudden symptom, just say “YES” or “NO” or “SOMETIMES.”
[Begin each query with: “At the same sudden moment that the voices come on”]
- Sudden anxiety, fear, or panic on the inside?
- Sudden anger or rage on the inside? [ANGER QUERY]
- Sudden heart racing? Heart pounding?
- Sudden chest pain? Chest pressure?
- Sudden sweating?
- Sudden trembling or shaking?
- Sudden shortness of breath, or like you can’t catch your breath?
- Sudden choking or a lump in your throat?
- Sudden nausea or queasiness?
- Sudden dizziness, lightheadedness, or faintness?
- Sudden feeling of detachment, sort of like you are in a glass box?
- Sudden fear of losing control? Fear of going crazy?
- Sudden fear afraid of dying? Afraid of having a heart attack?
- Sudden numbness or tingling, especially in your hands or face?
- Sudden feeling of heat, or cold?
- Sudden itching in your teeth? [VALIDITY CHECK]
- Sudden fear that people want to hurt you? [EXCESS FEAR QUERY]
- Sudden voices? [VOICES QUERY]
[PAST & PRODROMAL PANIC HISTORY]
At what age did you first see a therapist or psychiatrist?
At what age were you first hospitalized for an emotional problem?
At what age did you first start hearing voices?
At what age did you first start having strong fears of other people?
Before you ever heard voices, did you ever have any of the other sudden symptoms like the ones we just talked about?
Did those episodes back then feel sort of like your voices or sudden fears do now, except that there were no voices or sudden fears of people back then?
At what age did those sudden anxiety (or panic or rage) episodes begin?
Back then, was there MORE (M) sudden anxiety, or the SAME (S) sudden anxiety, or LESS (L) sudden anxiety than with your sudden voices now?
[PAST & PRODROMAL PANIC SYMPTOMS]
Now let’s talk about some symptoms that you might have had at those same sudden anxiety moments, in the time before you ever heard any voices. So, for each sudden symptom just say “YES” or “NO” or “SOMETIMES.”
[Begin each query with: “At the same moment the sudden anxiety came on—but only during the time before you ever heard sudden voices”]
[Ask about the same 18 panic-related symptoms listed above]
[PHOBIA-RELATED PANIC AND VOICES]
Have you ever been afraid to go into a (car, bus, plane, train, subway, elevator, mall, tunnel, bridge, heights, small place, CAT scan or MRI, being alone, crowds)?
[If yes or maybe: Ask about panic symptoms in phobic situations]
Now let’s talk about some symptoms that you might have had at some of those times you were afraid. So, for each symptom just say “YES” or “NO” or “MAYBE.”
[Ask about the same 18 panic-related symptoms listed above]
At what age did you last have sudden anxiety without voices?
Has medication ever completely stopped your voices? Somewhat?
If so, did those other sudden symptoms still happen sometimes?
Thank you for your help, and for answering all of these questions!
Persecutory delusional disorder (social anxiety). Some “schizophrenia” without voices may be misdiagnosis of persecutory (paranoid) delusional disorder (PDD). Therefore, the reported population prevalence (0.02%) may be underestimated. Social anxiety is highly comorbid with “schizophrenia” (15%).16 Case reports and clinical experience suggest that PDD is commonly preceded by social anxiety.17 Some nonpsychotic social anxiety symptoms closely resemble the PDD psychotic ideas of reference (a perception that low social rank attracts critical scrutiny by authorities). Patients with PDD may remain relatively functional, with few negative symptoms, despite pronounced paranoia. Outward manifestation of paranoia may be limited, unless quite intense. The typical age of onset (40 years) is later than that of schizophrenia, and symptoms can last a long time.18
Continue to: Bipolar 1 mania with delusions...
Bipolar I mania with delusions (atypical depression). Atypical depression is the most common depression in bipolar I disorder. Often more pronounced in winter, it may intensify at any time of year. Long ago, hypersomnia, lethargy, inactivity, inoffensiveness, and craving high-calorie food may have been conducive to hibernation.
Bipolar I mania includes delusions of special accomplishments or abilities, energetically focused on a grandiose mission to help everyone. These intense symptoms may be related to reduced frontal lobe modulation. In some milder form, bipolar I mania may once have encouraged hibernation awakening. Indeed, initial bipolar I mania episodes are more common in spring, as is the spring cleaning that helps us prepare for summer.
Recognizing affective trees in a psychotic forest
Though long observed, comorbid affective symptoms have generally been considered a hodgepodge of distress caused by painful psychotic illness. But the affective symptoms precede psychosis onset, can be masked during acute psychosis, and will revert to ordinary form if psychosis abates.11-13
Rather than affective symptoms being a consequence of psychosis, it may well be the other way around. Affective disorders could be important causal and differentiating components of psychotic disorders.11-13 Research and clinical experience suggest that adjunctive treatment of the comorbidities with correct medication can greatly enhance outcome.
Diagnostic approaches
Because interviews of patients with psychosis are often complicated by confusion, irritability, paranoid evasiveness, cognitive impairment, and medication, nuanced diagnosis is difficult. Interviews should explore psychotic syndromes and subtypes that correlate with comorbidity psychoses, including pre-psychotic anxiety and depressive diagnoses that are chronic (though unlike our 4 other diagnoses, melancholic depression is not chronic).
Establishing pre-psychotic diagnosis of chronic syndromes suggests that they are still present, even if they are difficult to assess during psychosis. Re-interview after some improvement allows for a significantly better diagnosis. Just as in nonpsychotic affective disorders, multiple comorbidities are common, and can lead to a mixed psychotic diagnosis and treatment plan.1
Structured interview tools can assist diagnosis. The PaSI (Box 1,15) elicits past, present, and detailed history of DSM panic, and has been validated in a small pilot randomized controlled trial. The PaSI focuses patient attention on paroxysmal onset voices, and then evaluates the presence of concurrent DSM panic symptoms. If voices are mostly psychotic panic, they may well be a proxy for panic. Ultimately, diagnosis of 5 comorbidities and associated psychotic symptoms may allow simpler categorization into 1 (or more) of the 5 psychosis subtypes.
Continue to: Treatment by comorbidity subtype...
Treatment by comorbidity subtype
Treatment of psychosis generally begins with antipsychotics. Nominal psychotherapy (presence of a professionally detached, compassionate clinician) improves compliance and leads to supportive therapy. Cognitive-behavioral therapy and dialectical behavior therapy may help later, with limited interpersonal approaches further on for some patients.
The suggested approaches to pharmacotherapy noted here draw on research and clinical experience.1,14,19-21 All medications used to treat comorbidities noted here are approved or generally accepted for that diagnosis. Estimated doses are similar to those for comorbidities when patients are nonpsychotic, and vary among patients. Doses, dosing schedules, and titration are extremely important for full benefit. Always consider compliance issues, suicidality, possible adverse effects, and potential drug/drug interactions. Although the medications we suggest using to treat the comorbidities may appear to also benefit psychosis, only antipsychotics are approved for psychosis per se.
Delusional depression. Antipsychotic + antidepressant. Tricyclic antidepressants are possibly most effective, but increase the risk of overdose and dangerous falls among fragile patients. Electroconvulsive therapy is sometimes used.
Obsessive-compulsive schizophrenia. Antipsychotic + selective serotonin reuptake inhibitor (SSRI). Consider aripiprazole (
Schizophrenia with voices. Antipsychotic + clonazepam. Concurrent usage may stabilize psychosis more rapidly, and with a lower antipsychotic dose.23 Titrate a fixed dose of clonazepam every 12 hours (avoid as-needed doses), starting low (ie, 0.5 mg) to limit initial drowsiness (which typically diminishes in 3 to 10 days). Titrate to full voice and panic cessation (1 to 2.5 mg every 12 hours).14 Exercise caution about excessive drowsiness, as well as outpatient compliance and abuse. Besides alprazolam, other antipanic medications have little incidental benefit for psychosis.
Persecutory delusional disorder. Antipsychotic + SSRI. Aripiprazole (consider long-acting injectable for compliance) also enhances the benefits of fluoxetine for social anxiety. Long half-life fluoxetine (20 mg/d) improves compliance and near-term outcomes.
Bipolar I mania: mania with delusions. Consider olanzapine for acute phase, then add other antimanic medication (commonly lithium or valproic acid), check blood level, and then taper olanzapine some weeks later. Importantly, lamotrigine is not effective for bipolar I mania. Consider suicide risk, medical conditions, and outpatient compliance. Comorbid panic anxiety is also common in bipolar I mania, often presenting as nonthreatening voices.
Seasonality: Following research that bipolar I mania is more common in spring and summer, studies have shown beneficial clinical augmentation from dark therapy as provided by reduced light exposure, blue-blocking glasses, and exogenous melatonin (a darkness-signaling hormone).24
Bipolar I mania atypical depression (significant current or historical symptoms). SSRI + booster medication. An SSRI (ie, escitalopram, 10 mg/d) is best started several weeks after full bipolar I mania resolution, while also continuing long-term antimanic medication. Booster medications (ie, buspirone 15 mg every 12 hours; lithium 300 mg/d; or trazodone 50 mg every 12 hours) can enhance SSRI benefits. Meta-analysis suggests SSRIs may have limited risk of inducing bipolar I mania.25 Although not yet specifically tested for atypical depression, lamotrigine may be effective, and may be safer still.25 However, lamotrigine requires very gradual dose titration to prevent a potentially dangerous rash, including after periods of outpatient noncompliance.
Seasonality: Atypical depression is often worse in winter (seasonal affective disorder). Light therapy can produce some clinically helpful benefits year-round.
To illustrate this new approach to psychosis diagnosis and treatment, our book
Box 2
Ms. B, a studious 19-year-old, has been very shy since childhood, with few friends. Meeting new people always gave her gradually increasing anxiety, thinking that she would embarrass herself in their eyes. She had that same anxiety, along with sweating and tachycardia, when she couldn’t avoid speaking in front of class. Sometimes, while walking down the street she would think that strangers were casting a disdainful eye on her, though she knew that wasn’t true. Another anxiety started when she was 16. While looking for paper in a small supply closet, she suddenly felt panicky. With a racing heart and short of breath, she desperately fled the closet. These episodes continued, sometimes for no apparent reason, and nearly always unnoticed by others.
At age 17, she began to believe that those strangers on the street were looking down on her with evil intent, and even following her around. She became afraid to walk around town. A few months later, she also started to hear angry and critical voices at sudden moments. Although the paroxysmal voices always coincided with her panicky symptoms, the threatening voices now felt more important to her than the panic itself. Nonpsychotic panics had stopped. Mostly a recluse, she saw less of her family, left her job, and stopped going to the movies.
After a family dinner, she was detached, scared, and quieter than usual. She sought help from her primary care physician, who referred her to a psychiatrist. A thorough history from Ms. B and her family revealed her disturbing fears, as well as her history of social anxiety. Interviewing for panic was prompted by her mother’s recollection of the supply closet story.
In view of Ms. B’s cooperativeness and supportive family, outpatient treatment of her recent-onset psychosis began with aripiprazole, 10 mg/d, and clonazepam, 0.5 mg every 12 hours. Clonazepam was gradually increased until voices (and panic) ceased. She was then able to describe how earlier panics had felt just like voices, but without the voices. The fears of strangers continued. Escitalopram, 20 mg/d, was added for social anxiety (aripiprazole enhances the benefits of selective serotonin reuptake inhibitors).
One month later, her fears of strangers diminished, and she felt more comfortable around people than ever before. On the same medications, and in psychotherapy over the next year, she began to increase her social network while making plans to start college.
Larger studies are needed
Current research supports the concept of a 5-diagnosis classification of psychoses, which may correlate with our comorbid anxiety and depression model. Larger diagnostic and treatment studies would invaluably examine existing research and clinical experience, and potentially encourage more clinically useful diagnoses, specific treatments, and improved outcomes.
Bottom Line
New insights from evolutionary psychopathology, clinical research and observation, psychotogenesis, genetics, and epidemiology suggest that most functional psychoses may fall into 1 of 5 comorbidity-defined subtypes, for which specific treatments can lead to much improved outcomes.
How can we treat psychosis if we don’t know what we are treating? Over the years, attempts at defining psychosis subtypes have met with dead ends. However, recent research supports a new approach that offers a rational classification model organized according to 5 specific comorbid anxiety and depressive disorder diagnoses.
Anxiety and depressive symptoms are not just the result of psychotic despair. They are specific diagnoses, they precede psychosis onset, they help define psychotic syndromes, and they can point to much more effective treatment approaches. Most of the psychotic diagnoses in this schema are already recognized or posited. And, just as patients who do not have psychotic illness can have more than 1 anxiety or depressive disorder, patients with psychosis can present with a mixed picture that reflects more than 1 contributing comorbidity. Research further suggests that each of the 5 psychosis comorbidity diagnoses may involve some similar underlying factors that facilitate the formation of psychosis.
This article describes the basics of 5 psychosis subtypes, and provides initial guidelines to diagnosis, symptomatology, and treatment. Though clinical experience and existing research support the clinical presence and treatment value of this classification model, further verification will require considerably more controlled studies. An eventual validation of this approach could largely supplant ill-defined diagnoses of “schizophrenia” and other functional psychoses.
Recognizing the comorbidities in the context of their corresponding psychoses entails learning new interviewing skills and devoting more time to both initial and subsequent diagnosis and treatment. In our recently published book,1 we provide extensive details on the approach we describe in this article, including case examples, new interview tools to simplify the diagnostic journey, and novel treatment approaches.
Psychosis-proneness underlies functional psychoses
Functional (idiopathic) schizophrenia and psychotic disorders have long been difficult to separate, and many categorizations have been discarded. Despite clinical dissimilarities, today we too often casually lump psychoses together as schizophrenia.2,3 Eugen Bleuler first suggested the existence of a “group of schizophrenias.”4 It is possible that his group encompasses our 5 psychoses from 5 inbuilt emotional instincts,5 each corresponding to a specific anxiety or depressive subtype.
The 5 anxiety and depressive subtypes noted in this article are common, but psychosis is not. Considerable research suggests that certain global “psychotogenic” factors create susceptibility to all psychoses.6,7 While many genetic, neuroanatomical, experiential, and other factors have been reported, the most important may be “hypofrontality” (genetically reduced frontal lobe function, size, or neuronal activity) and dopaminergic hyperfunction (genetically increased dopamine activity).5-7
An evolutionary perspective
One evolutionary theory of psychopathology starts with the subtypes of depression and anxiety. For example, major depressive disorder and generalized anxiety disorder may encompass 5 commonplace and more specific anxiety and depressive subtypes. Consideration of the emotional, cognitive, and functional aspects of those subtypes suggests that they may have once been advantageous for primeval human herds. Those primeval altruistic instincts may have helped survival, reproduction, and preservation of kin group DNA.5
More than any other species, humans can draw upon consciousness and culture to rationally overcome the influences of unconscious instincts. But those instincts can then emerge from the deep, and painfully encourage obedience to their guidance. In nonpsychotic anxiety and depressive disorders, the specific messages are experienced as specific anxiety and depressive symptoms.5 In psychotic disorders, the messages can emerge as unreasoned and frightful fears, perceptions, beliefs, and behaviors. With newer research, clinical observation, and an evolutionary perspective, a novel and counterintuitive approach may improve our ability to help patients.8
Continue to: Five affective comorbidities evolved from primeval altruistic instincts...
Five affective comorbidities evolved from primeval altruistic instincts
Melancholic depression5
Melancholic depression is often triggered by serious illness, group exclusion, pronounced loss, or purposelessness. We hear patients talk painfully about illness, guilt, and death. Indeed, some increased risk of death, especially from infectious disease, may result from hypercortisolemia (documented by the dexamethasone suppression test). Hypercortisolemic death also occurs in salmon after spawning, and in male marsupial mice after mating. The tragic passing of an individual saves scarce resources for the remainder of the herd.
Obsessive-compulsive disorder5
Factor-analytic studies suggest 4 main obsessive-compulsive disorder (OCD) subtypes: cleanliness, hoarding, intrusive thoughts, and organizing. Obsessive-compulsive traits can help maintain a safe and efficient environment in humans and other species, but OCD is dysfunctional.
Panic anxiety5
Panic anxiety is triggered by real, symbolic, or emotional separation from home and family. In toddlers, separation anxiety can reduce the odds of getting lost and hurt.
Social anxiety5
Social anxiety includes fear of self-embarrassment, exposure as a pretender to higher social rank, and thus often a reluctant avoidance of increased social rank. While consciousness and cultural encouragement can overcome that hesitation and thus lead to greater success, social anxiety activation can still cause painful anxiety. The social hierarchies of many species include comparable biological influences, and help preserve group DNA by reducing hierarchical infighting.
Atypical depression and bipolar I mania5
Atypical depression includes increased rejection sensitivity, resulting in inoffensive behavior to avoid social rejection. This reduces risk of isolation from the group, and improves group harmony. Unlike the 4 other syndromes, atypical depression and bipolar I mania may reflect 2 separate seasonal mood phases. Atypical depression (including seasonal affective disorder) often worsens with shortened winter daylight hours, akin to hibernation. Initial bipolar I mania is more common with springtime daylight, with symptoms not unlike exaggerated hibernation awakening.9
Primeval biological altruism has great evolutionary value in many species, and even somewhat in modern humans. But it is quite different from modern rational altruism. Although we sometimes override our instincts, they respond with messages experienced as emotional pain—they still tell us to follow instructions for primeval herd survival. In an earlier book, I (JPK) provide a lengthier description of the evidence for this evolutionary psychopathology theory, including interplay of the 5 instincts with psychotogenic factors.5
Continue to: Five comorbidity psychoses from 5 primeval instincts.....
Five comorbidity psychoses from 5 primeval instincts
The 5 affective comorbidities described above contribute to the presence, subtype, and treatment approaches of 5 corresponding psychoses. Ordinary panic attacks might occur when feeling trapped or separated from home, so people want to flee to safety. Nonhuman species with limited consciousness and language are unlikely to think “time to head for safety.” Instead, instincts encourage flight from danger through internally generated perceptions of threat. Likewise, people with psychosis and panic, without sufficient conscious modulation, may experience sensory perceptions of actual danger when feeling symbolically trapped.1,10
One pilot study carefully examined the prevalence of these 5 comorbidities in an unselected group of psychotic patients.10 At least 85% met criteria for ≥1 of the 5 subtypes.10 Moreover, organic psychoses related to physical illness, substances, and iatrogenesis may also predict future episodes of functional psychoses.1
Using statistical analysis of psychosis rating scales, 2 studies took a “transdiagnostic” look at psychoses, and each found 5 psychosis subtypes and a generalized psychosis susceptibility factor.11,12 Replication of that transdiagnostic approach, newly including psychosis symptoms and our 5 specific comorbidities, might well find that the 5 subtype models resemble each other.11,12
Our proposed 5 comorbidity subtypes are1:
Delusional depression (melancholic depression). Most common in geriatric patients, this psychosis can also occur at younger ages. Prodromal melancholic depression can include guilt and hopelessness, and is acute, rather than the chronic course of our other 4 syndromes. Subsequent delusional depression includes delusions of bodily decay, illness, or death, as well as overwhelming guilt, shame, and remorse. The classic vegetative symptoms of depression continue. In addition to infectious disease issues, high suicide risk makes hospitalization imperative.
Obsessive-compulsive schizophrenia. Just as OCD has an early age of onset, obsessive-compulsive schizophrenia begins earlier than other psychoses. Despite preserved cognition, some nonpsychotic patients with OCD have diminished symptom insight. OCD may be comorbid with schizophrenia in 12% of cases, typically preceding psychosis onset. Obsessive-compulsive schizophrenia symptoms may include highly exaggerated doubt or ambivalence; contamination concerns; eccentric, ritualistic, motor stereotypy, checking, disorganized, and other behaviors; and paranoia.
Schizophrenia with voices (panic anxiety). Classic paranoid schizophrenia with voices appears to be the most similar to a “panic psychosis.” Patients with nonpsychotic panic anxiety have increased paranoid ideation and ideas of reference as measured on the Symptom Checklist-90. Schizophrenia is highly comorbid with panic anxiety, estimated at 45% in the Epidemiologic Catchment Area study.13 These are likely underestimates: cognitive impairment hinders reporting, and psychotic panic is masked as auditory hallucinations. A pilot study of schizophrenia with voices using a carbon dioxide panic induction challenge found that 100% had panic anxiety.14 That study and another found that virtually all participants reported voices concurrent with panic using our Panic and Schizophrenia Interview (PaSI) (Box 1). Panic onset precedes schizophrenia onset, and panic may reappear if antipsychotic medications sufficiently control voices: “voices without the voices,” say some.
Box 1
Let’s talk for a minute about your voices.
[IDENTIFYING PAROXYSMAL MOMENTS OF VOICE ONSET]
Do you hear voices at every single moment, or are they sometimes silent? Think about those times when you are not actually hearing any voices.
Now, there may be reasons why the voices start talking when they do, but let’s leave that aside for now.
So, whenever the voices do begin speaking—and for whatever reason they do—is it all of a sudden, or do they start very softly and then very gradually get louder?
If your voices are nearly always there, then are there times when the voices suddenly come back, get louder, get more insistent, or just get more obvious to you?
[Focus patient on sudden moment of voice onset, intensification, or awareness]
Let’s talk about that sudden moment when the voices begin (or intensify, or become obvious), even if you know the reason why they start.
I’m going to ask you about some symptoms that you might have at that same sudden moment when the voices start (or intensify, or become obvious). If you have any of these symptoms at the other times, they do not count for now.
So, when I ask about each symptom, tell me whether it comes on at the same sudden moments as the voices, and also if it used to come on with the voices in the past.
For each sudden symptom, just say “YES” or “NO” or “SOMETIMES.”
[Begin each query with: “At the same sudden moment that the voices come on”]
- Sudden anxiety, fear, or panic on the inside?
- Sudden anger or rage on the inside? [ANGER QUERY]
- Sudden heart racing? Heart pounding?
- Sudden chest pain? Chest pressure?
- Sudden sweating?
- Sudden trembling or shaking?
- Sudden shortness of breath, or like you can’t catch your breath?
- Sudden choking or a lump in your throat?
- Sudden nausea or queasiness?
- Sudden dizziness, lightheadedness, or faintness?
- Sudden feeling of detachment, sort of like you are in a glass box?
- Sudden fear of losing control? Fear of going crazy?
- Sudden fear afraid of dying? Afraid of having a heart attack?
- Sudden numbness or tingling, especially in your hands or face?
- Sudden feeling of heat, or cold?
- Sudden itching in your teeth? [VALIDITY CHECK]
- Sudden fear that people want to hurt you? [EXCESS FEAR QUERY]
- Sudden voices? [VOICES QUERY]
[PAST & PRODROMAL PANIC HISTORY]
At what age did you first see a therapist or psychiatrist?
At what age were you first hospitalized for an emotional problem?
At what age did you first start hearing voices?
At what age did you first start having strong fears of other people?
Before you ever heard voices, did you ever have any of the other sudden symptoms like the ones we just talked about?
Did those episodes back then feel sort of like your voices or sudden fears do now, except that there were no voices or sudden fears of people back then?
At what age did those sudden anxiety (or panic or rage) episodes begin?
Back then, was there MORE (M) sudden anxiety, or the SAME (S) sudden anxiety, or LESS (L) sudden anxiety than with your sudden voices now?
[PAST & PRODROMAL PANIC SYMPTOMS]
Now let’s talk about some symptoms that you might have had at those same sudden anxiety moments, in the time before you ever heard any voices. So, for each sudden symptom just say “YES” or “NO” or “SOMETIMES.”
[Begin each query with: “At the same moment the sudden anxiety came on—but only during the time before you ever heard sudden voices”]
[Ask about the same 18 panic-related symptoms listed above]
[PHOBIA-RELATED PANIC AND VOICES]
Have you ever been afraid to go into a (car, bus, plane, train, subway, elevator, mall, tunnel, bridge, heights, small place, CAT scan or MRI, being alone, crowds)?
[If yes or maybe: Ask about panic symptoms in phobic situations]
Now let’s talk about some symptoms that you might have had at some of those times you were afraid. So, for each symptom just say “YES” or “NO” or “MAYBE.”
[Ask about the same 18 panic-related symptoms listed above]
At what age did you last have sudden anxiety without voices?
Has medication ever completely stopped your voices? Somewhat?
If so, did those other sudden symptoms still happen sometimes?
Thank you for your help, and for answering all of these questions!
Persecutory delusional disorder (social anxiety). Some “schizophrenia” without voices may be misdiagnosis of persecutory (paranoid) delusional disorder (PDD). Therefore, the reported population prevalence (0.02%) may be underestimated. Social anxiety is highly comorbid with “schizophrenia” (15%).16 Case reports and clinical experience suggest that PDD is commonly preceded by social anxiety.17 Some nonpsychotic social anxiety symptoms closely resemble the PDD psychotic ideas of reference (a perception that low social rank attracts critical scrutiny by authorities). Patients with PDD may remain relatively functional, with few negative symptoms, despite pronounced paranoia. Outward manifestation of paranoia may be limited, unless quite intense. The typical age of onset (40 years) is later than that of schizophrenia, and symptoms can last a long time.18
Continue to: Bipolar 1 mania with delusions...
Bipolar I mania with delusions (atypical depression). Atypical depression is the most common depression in bipolar I disorder. Often more pronounced in winter, it may intensify at any time of year. Long ago, hypersomnia, lethargy, inactivity, inoffensiveness, and craving high-calorie food may have been conducive to hibernation.
Bipolar I mania includes delusions of special accomplishments or abilities, energetically focused on a grandiose mission to help everyone. These intense symptoms may be related to reduced frontal lobe modulation. In some milder form, bipolar I mania may once have encouraged hibernation awakening. Indeed, initial bipolar I mania episodes are more common in spring, as is the spring cleaning that helps us prepare for summer.
Recognizing affective trees in a psychotic forest
Though long observed, comorbid affective symptoms have generally been considered a hodgepodge of distress caused by painful psychotic illness. But the affective symptoms precede psychosis onset, can be masked during acute psychosis, and will revert to ordinary form if psychosis abates.11-13
Rather than affective symptoms being a consequence of psychosis, it may well be the other way around. Affective disorders could be important causal and differentiating components of psychotic disorders.11-13 Research and clinical experience suggest that adjunctive treatment of the comorbidities with correct medication can greatly enhance outcome.
Diagnostic approaches
Because interviews of patients with psychosis are often complicated by confusion, irritability, paranoid evasiveness, cognitive impairment, and medication, nuanced diagnosis is difficult. Interviews should explore psychotic syndromes and subtypes that correlate with comorbidity psychoses, including pre-psychotic anxiety and depressive diagnoses that are chronic (though unlike our 4 other diagnoses, melancholic depression is not chronic).
Establishing pre-psychotic diagnosis of chronic syndromes suggests that they are still present, even if they are difficult to assess during psychosis. Re-interview after some improvement allows for a significantly better diagnosis. Just as in nonpsychotic affective disorders, multiple comorbidities are common, and can lead to a mixed psychotic diagnosis and treatment plan.1
Structured interview tools can assist diagnosis. The PaSI (Box 1,15) elicits past, present, and detailed history of DSM panic, and has been validated in a small pilot randomized controlled trial. The PaSI focuses patient attention on paroxysmal onset voices, and then evaluates the presence of concurrent DSM panic symptoms. If voices are mostly psychotic panic, they may well be a proxy for panic. Ultimately, diagnosis of 5 comorbidities and associated psychotic symptoms may allow simpler categorization into 1 (or more) of the 5 psychosis subtypes.
Continue to: Treatment by comorbidity subtype...
Treatment by comorbidity subtype
Treatment of psychosis generally begins with antipsychotics. Nominal psychotherapy (presence of a professionally detached, compassionate clinician) improves compliance and leads to supportive therapy. Cognitive-behavioral therapy and dialectical behavior therapy may help later, with limited interpersonal approaches further on for some patients.
The suggested approaches to pharmacotherapy noted here draw on research and clinical experience.1,14,19-21 All medications used to treat comorbidities noted here are approved or generally accepted for that diagnosis. Estimated doses are similar to those for comorbidities when patients are nonpsychotic, and vary among patients. Doses, dosing schedules, and titration are extremely important for full benefit. Always consider compliance issues, suicidality, possible adverse effects, and potential drug/drug interactions. Although the medications we suggest using to treat the comorbidities may appear to also benefit psychosis, only antipsychotics are approved for psychosis per se.
Delusional depression. Antipsychotic + antidepressant. Tricyclic antidepressants are possibly most effective, but increase the risk of overdose and dangerous falls among fragile patients. Electroconvulsive therapy is sometimes used.
Obsessive-compulsive schizophrenia. Antipsychotic + selective serotonin reuptake inhibitor (SSRI). Consider aripiprazole (
Schizophrenia with voices. Antipsychotic + clonazepam. Concurrent usage may stabilize psychosis more rapidly, and with a lower antipsychotic dose.23 Titrate a fixed dose of clonazepam every 12 hours (avoid as-needed doses), starting low (ie, 0.5 mg) to limit initial drowsiness (which typically diminishes in 3 to 10 days). Titrate to full voice and panic cessation (1 to 2.5 mg every 12 hours).14 Exercise caution about excessive drowsiness, as well as outpatient compliance and abuse. Besides alprazolam, other antipanic medications have little incidental benefit for psychosis.
Persecutory delusional disorder. Antipsychotic + SSRI. Aripiprazole (consider long-acting injectable for compliance) also enhances the benefits of fluoxetine for social anxiety. Long half-life fluoxetine (20 mg/d) improves compliance and near-term outcomes.
Bipolar I mania: mania with delusions. Consider olanzapine for acute phase, then add other antimanic medication (commonly lithium or valproic acid), check blood level, and then taper olanzapine some weeks later. Importantly, lamotrigine is not effective for bipolar I mania. Consider suicide risk, medical conditions, and outpatient compliance. Comorbid panic anxiety is also common in bipolar I mania, often presenting as nonthreatening voices.
Seasonality: Following research that bipolar I mania is more common in spring and summer, studies have shown beneficial clinical augmentation from dark therapy as provided by reduced light exposure, blue-blocking glasses, and exogenous melatonin (a darkness-signaling hormone).24
Bipolar I mania atypical depression (significant current or historical symptoms). SSRI + booster medication. An SSRI (ie, escitalopram, 10 mg/d) is best started several weeks after full bipolar I mania resolution, while also continuing long-term antimanic medication. Booster medications (ie, buspirone 15 mg every 12 hours; lithium 300 mg/d; or trazodone 50 mg every 12 hours) can enhance SSRI benefits. Meta-analysis suggests SSRIs may have limited risk of inducing bipolar I mania.25 Although not yet specifically tested for atypical depression, lamotrigine may be effective, and may be safer still.25 However, lamotrigine requires very gradual dose titration to prevent a potentially dangerous rash, including after periods of outpatient noncompliance.
Seasonality: Atypical depression is often worse in winter (seasonal affective disorder). Light therapy can produce some clinically helpful benefits year-round.
To illustrate this new approach to psychosis diagnosis and treatment, our book
Box 2
Ms. B, a studious 19-year-old, has been very shy since childhood, with few friends. Meeting new people always gave her gradually increasing anxiety, thinking that she would embarrass herself in their eyes. She had that same anxiety, along with sweating and tachycardia, when she couldn’t avoid speaking in front of class. Sometimes, while walking down the street she would think that strangers were casting a disdainful eye on her, though she knew that wasn’t true. Another anxiety started when she was 16. While looking for paper in a small supply closet, she suddenly felt panicky. With a racing heart and short of breath, she desperately fled the closet. These episodes continued, sometimes for no apparent reason, and nearly always unnoticed by others.
At age 17, she began to believe that those strangers on the street were looking down on her with evil intent, and even following her around. She became afraid to walk around town. A few months later, she also started to hear angry and critical voices at sudden moments. Although the paroxysmal voices always coincided with her panicky symptoms, the threatening voices now felt more important to her than the panic itself. Nonpsychotic panics had stopped. Mostly a recluse, she saw less of her family, left her job, and stopped going to the movies.
After a family dinner, she was detached, scared, and quieter than usual. She sought help from her primary care physician, who referred her to a psychiatrist. A thorough history from Ms. B and her family revealed her disturbing fears, as well as her history of social anxiety. Interviewing for panic was prompted by her mother’s recollection of the supply closet story.
In view of Ms. B’s cooperativeness and supportive family, outpatient treatment of her recent-onset psychosis began with aripiprazole, 10 mg/d, and clonazepam, 0.5 mg every 12 hours. Clonazepam was gradually increased until voices (and panic) ceased. She was then able to describe how earlier panics had felt just like voices, but without the voices. The fears of strangers continued. Escitalopram, 20 mg/d, was added for social anxiety (aripiprazole enhances the benefits of selective serotonin reuptake inhibitors).
One month later, her fears of strangers diminished, and she felt more comfortable around people than ever before. On the same medications, and in psychotherapy over the next year, she began to increase her social network while making plans to start college.
Larger studies are needed
Current research supports the concept of a 5-diagnosis classification of psychoses, which may correlate with our comorbid anxiety and depression model. Larger diagnostic and treatment studies would invaluably examine existing research and clinical experience, and potentially encourage more clinically useful diagnoses, specific treatments, and improved outcomes.
Bottom Line
New insights from evolutionary psychopathology, clinical research and observation, psychotogenesis, genetics, and epidemiology suggest that most functional psychoses may fall into 1 of 5 comorbidity-defined subtypes, for which specific treatments can lead to much improved outcomes.
1. Veras AB, Kahn JP, eds. Psychotic Disorders: Comorbidity Detection Promotes Improved Diagnosis and Treatment. Elsevier; 2021.
2. Gaebel W, Zielasek J. Focus on psychosis. Dialogues Clin Neuroscience. 2015;17(1):9-18.
3. Guloksuz S, Van Os J. The slow death of the concept of schizophrenia and the painful birth of the psychosis spectrum. Psychological Medicine. 2018;48(2):229-244.
4. Bleuler E. Dementia Praecox or the Group of Schizophrenias. International Universities Press; 1950.
5. Kahn JP. Angst: Origins of Depression and Anxiety. Oxford University Press; 2013.
6. Howes OD, McCutcheon R, Owen MJ, et al. The role of genes, stress, and dopamine in the development of schizophrenia. Biol Psychiatry. 2017;81(1):9-20.
7. Mubarik A, Tohid H. Frontal lobe alterations in schizophrenia: a review. Trends Psychiatry Psychother. 2016;38(4):198-206.
8. Murray RM, Bhavsar V, Tripoli G, et al. 30 Years on: How the neurodevelopmental hypothesis of schizophrenia morphed into the developmental risk factor model of psychosis. Schizophr Bull. 2017;43(6):1190-1196.
9. Bauer M, Glenn T, Alda M, et al. Solar insolation in springtime influences age of onset of bipolar I disorder. Acta Psychiatr Scand. 2017;136(6):571-582.
10. Kahn JP, Bombassaro T, Veras AB. Comorbid schizophrenia and panic anxiety: panic psychosis revisited. Psychiatr Ann. 2018;48(12):561-565.
11. Bebbington P, Freeman D. Transdiagnostic extension of delusions: schizophrenia and beyond. Schizophr Bull. 2017;43(2):273-282.
12. Catalan A, Simons CJP, Bustamante S, et al. Data gathering bias: trait vulnerability to psychotic symptoms? PLoS One. 2015;10(7):e0132442. doi:10.1371/journal.pone.0132442
13. Goodwin R, Lyons JS, McNally RJ. Panic attacks in schizophrenia. Schizophr Res. 2002;58(2-3):213-220.
14. Kahn JP, Puertollano MA, Schane MD, et al. Adjunctive alprazolam for schizophrenia with panic anxiety: clinical observation and pathogenetic implications. Am J Psychiatry. 1988;145(6):742-744.
15. Kahn JP. Chapter 4: Paranoid schizophrenia with voices and panic anxiety. In: Veras AB, Kahn JP, eds. Psychotic Disorders: Comorbidity Detection Promotes Improved Diagnosis and Treatment. Elsevier; 2021.
16. Achim AM, Maziade M, Raymond E, et al. How prevalent are anxiety disorders in schizophrenia? A meta-analysis and critical review on a significant association. Schizophr Bull. 2011;37(4):811-821.
17. Veras AB, Souza TG, Ricci TG, et al. Paranoid delusional disorder follows social anxiety disorder in a long-term case series: evolutionary perspective. J Nerv Ment Dis. 2015;203(6):477-479.
18. McIntyre JC, Wickham S, Barr B, et al. Social identity and psychosis: associations and psychological mechanisms. Schizophr Bull. 2018;44(3):681-690.
19. Barbee JG, Mancuso DM, Freed CR. Alprazolam as a neuroleptic adjunct in the emergency treatment of schizophrenia. Am J Psychiatry. 1992;149(4):506-510.
20. Nardi AE, Machado S, Almada LF. Clonazepam for the treatment of panic disorder. Curr Drug Targets. 2013;14(3):353-364.
21. Poyurovsky M. Schizo-Obsessive Disorder. Cambridge University Press; 2013.
22. Reznik I, Sirota P. Obsessive and compulsive symptoms in schizophrenia: a randomized controlled trial with fluvoxamine and neuroleptics. J Clin Psychopharmacol. 2000;20(4):410-416.
23. Bodkin JA. Emerging uses for high-potency benzodiazepines in psychotic disorders. J Clin Psychiatry. 1990;51 Suppl:41-53.
24. Gottlieb JF, Benedetti F, Geoffroy PA, et al. The chronotherapeutic treatment of bipolar disorders: a systematic review and practice recommendations from the ISBD task force on chronotherapy and chronobiology. Bipolar Disord. 2019;21(8):741-773.
25. Pacchiarotti I, Bond DJ, Baldessarini RJ, et al. The International Society for Bipolar Disorders (ISBD) task force report on antidepressant use in bipolar disorders. Am J Psychiatry. 2013;170(11):1249-1262.
1. Veras AB, Kahn JP, eds. Psychotic Disorders: Comorbidity Detection Promotes Improved Diagnosis and Treatment. Elsevier; 2021.
2. Gaebel W, Zielasek J. Focus on psychosis. Dialogues Clin Neuroscience. 2015;17(1):9-18.
3. Guloksuz S, Van Os J. The slow death of the concept of schizophrenia and the painful birth of the psychosis spectrum. Psychological Medicine. 2018;48(2):229-244.
4. Bleuler E. Dementia Praecox or the Group of Schizophrenias. International Universities Press; 1950.
5. Kahn JP. Angst: Origins of Depression and Anxiety. Oxford University Press; 2013.
6. Howes OD, McCutcheon R, Owen MJ, et al. The role of genes, stress, and dopamine in the development of schizophrenia. Biol Psychiatry. 2017;81(1):9-20.
7. Mubarik A, Tohid H. Frontal lobe alterations in schizophrenia: a review. Trends Psychiatry Psychother. 2016;38(4):198-206.
8. Murray RM, Bhavsar V, Tripoli G, et al. 30 Years on: How the neurodevelopmental hypothesis of schizophrenia morphed into the developmental risk factor model of psychosis. Schizophr Bull. 2017;43(6):1190-1196.
9. Bauer M, Glenn T, Alda M, et al. Solar insolation in springtime influences age of onset of bipolar I disorder. Acta Psychiatr Scand. 2017;136(6):571-582.
10. Kahn JP, Bombassaro T, Veras AB. Comorbid schizophrenia and panic anxiety: panic psychosis revisited. Psychiatr Ann. 2018;48(12):561-565.
11. Bebbington P, Freeman D. Transdiagnostic extension of delusions: schizophrenia and beyond. Schizophr Bull. 2017;43(2):273-282.
12. Catalan A, Simons CJP, Bustamante S, et al. Data gathering bias: trait vulnerability to psychotic symptoms? PLoS One. 2015;10(7):e0132442. doi:10.1371/journal.pone.0132442
13. Goodwin R, Lyons JS, McNally RJ. Panic attacks in schizophrenia. Schizophr Res. 2002;58(2-3):213-220.
14. Kahn JP, Puertollano MA, Schane MD, et al. Adjunctive alprazolam for schizophrenia with panic anxiety: clinical observation and pathogenetic implications. Am J Psychiatry. 1988;145(6):742-744.
15. Kahn JP. Chapter 4: Paranoid schizophrenia with voices and panic anxiety. In: Veras AB, Kahn JP, eds. Psychotic Disorders: Comorbidity Detection Promotes Improved Diagnosis and Treatment. Elsevier; 2021.
16. Achim AM, Maziade M, Raymond E, et al. How prevalent are anxiety disorders in schizophrenia? A meta-analysis and critical review on a significant association. Schizophr Bull. 2011;37(4):811-821.
17. Veras AB, Souza TG, Ricci TG, et al. Paranoid delusional disorder follows social anxiety disorder in a long-term case series: evolutionary perspective. J Nerv Ment Dis. 2015;203(6):477-479.
18. McIntyre JC, Wickham S, Barr B, et al. Social identity and psychosis: associations and psychological mechanisms. Schizophr Bull. 2018;44(3):681-690.
19. Barbee JG, Mancuso DM, Freed CR. Alprazolam as a neuroleptic adjunct in the emergency treatment of schizophrenia. Am J Psychiatry. 1992;149(4):506-510.
20. Nardi AE, Machado S, Almada LF. Clonazepam for the treatment of panic disorder. Curr Drug Targets. 2013;14(3):353-364.
21. Poyurovsky M. Schizo-Obsessive Disorder. Cambridge University Press; 2013.
22. Reznik I, Sirota P. Obsessive and compulsive symptoms in schizophrenia: a randomized controlled trial with fluvoxamine and neuroleptics. J Clin Psychopharmacol. 2000;20(4):410-416.
23. Bodkin JA. Emerging uses for high-potency benzodiazepines in psychotic disorders. J Clin Psychiatry. 1990;51 Suppl:41-53.
24. Gottlieb JF, Benedetti F, Geoffroy PA, et al. The chronotherapeutic treatment of bipolar disorders: a systematic review and practice recommendations from the ISBD task force on chronotherapy and chronobiology. Bipolar Disord. 2019;21(8):741-773.
25. Pacchiarotti I, Bond DJ, Baldessarini RJ, et al. The International Society for Bipolar Disorders (ISBD) task force report on antidepressant use in bipolar disorders. Am J Psychiatry. 2013;170(11):1249-1262.
The importance of a post-COVID wellness program for medical staff
LAS VEGAS – , according to Jon A. Levenson, MD.
“We can learn from previous pandemics and epidemics, which will be important for us going forward from COVID-19,” Dr. Levenson, associate professor of psychiatry at Columbia University Irving Medical Center, New York, said during an annual psychopharmacology update held by the Nevada Psychiatric Association.
During the severe acute respiratory syndrome (SARS) epidemic in 2005, 68% of health care workers reported significant job-related stress, including increased workload, changing work duties, redeployment, shortage of medical supplies, concerns about insufficient personal protective equipment (PPE), lack of safety at work, absence of effective treatment protocols, inconsistent organizational support and information and misinformation from hospital management, and witnessing intense pain, isolation, and loss on a daily basis with few opportunities to take breaks (Psychiatr Serv. 2020 Oct 6. doi: 10.1176/appi.ps.202000274).
Personal concerns associated with psychopathological symptoms included spreading infection to family members; feeling responsibility for family members’ social isolation; self-isolating to avoid infecting family, which can lead to increased loneliness and sadness. “For those who were working remotely, this level of work is hard and challenging,” Dr. Levenson said. “For those who are parents, the 24-hour childcare responsibilities exist on top of work. They often found they can’t unwind with friends.”
Across SARS, MERS, Ebola, and swine flu, a wide range of prevalence in symptoms of distress, stress, anxiety, depressive symptoms, and substance use emerged, he continued. During COVID-19, at least three studies reported significant percentages of distress, depression, anxiety, insomnia, and PTSD among health care workers (JAMA Netw Open. 2020;3[3]:e203976, Front Psychol. 2020 Dec 8;11:608986., and Gen Hosp Psychiatry. Sep-Oct 2020;66:1-8).
“Who is at most-increased risk?” Dr. Levenson asked. “Women; those who are younger and have fewer years of work experience; those working on the front lines such as nurses and advanced practice professionals; and people with preexisting vulnerabilities to psychiatric disorders including anxiety, depression, obsessional symptoms, substance use, suicidal behavior, and impulse control disorders are likely to be especially vulnerable to stress-related symptoms.”
At CUIMC, there were certain “tipping points,” to the vulnerability of health care worker well-being in the early stage of the COVID-19 pandemic, he said, including the loss of an emergency medicine physician colleague from death by suicide. “On the national level there were so many other issues going on such as health care disparities of the COVID-19 infection itself, the murder of George Floyd in Minneapolis, other issues of racial injustice, a tense political climate with an upcoming election at the time, and other factors related to the natural climate concerns,” he said. This prompted several faculty members in the CUIMC department of psychiatry including Claude Ann Mellins, PhD, Laurel S. Mayer, MD, and Lourival Baptista-Neto, MD, to partner with ColumbiaDoctors and New York-Presbyterian Hospital and develop a model of care for health care workers known as CopeColumbia, a virtual program intended to address staff burnout and fatigue, with an emphasis on prevention and promotion of resilience.* It launched in March of 2020 and consists of 1:1 peer support, a peer support group program, town halls/webinars, and an active web site.
The 1:1 peer support sessions typically last 20-30 minutes and provide easy access for all distressed hospital and medical center staff. “We have a phone line staffed by Columbia psychiatrists and psychologists so that a distressed staff member can reach support directly,” he said. The format of these sessions includes a brief discussion of challenges and brainstorming around potential coping strategies. “This is not a psychotherapy session,” Dr. Levenson said. “Each session can be individualized to further assess the type of distress or to implement rating scales such as the Generalized Anxiety Disorder-7 scale to assess for signs and symptoms consistent with GAD. There are options to schedule a second or third peer support session, or a prompt referral within Columbia psychiatry when indicated.”
A typical peer support group meeting lasts about 30 minutes and comprises individual divisions or departments. Some goals of the peer groups are to discuss unique challenges of the work environment and to encourage the members of the group to come up with solutions; to promote team support and coping; to teach resilience-enhancing strategies from empirically based treatments such as CBT, “and to end each meeting with expressions of gratitude and of thanks within the group,” he said.
According to Dr. Levenson, sample questions CopeColumbia faculty use to facilitate coping, include “which coping skills are working for you?”; “Are you able to be present?”; “Have you honored loss with any specific ways or traditions?”; “Do you have any work buddies who support you and vice versa?”; “Can your work community build off each other’s individual strengths to help both the individual and the work group cope optimally?”; and “How can your work team help facilitate each other to best support each other?”
Other aspects of the CopeColumbia program include town halls/grand rounds that range from 30 to 60 minutes in length. “It may be a virtual presentation from a mental health professional on specific aspects of coping such as relaxation techniques,” he said. “The focus is how to manage stress, anxiety, trauma, loss, and grief. It also includes an active Q&A to engage staff participants. The advantage of this format is that you can reach many staff in an entire department.” The program also has an active web site for staff with both internal and external support links including mindfulness, meditation, exercise, parenting suggestions/caregiving, and other resources to promote well-being and resilience for staff and family.
To date, certain themes emerged from the 1:1 and peer support group sessions, including expressions of difficulty adapting to “such a new reality,” compared with the pre-COVID era. “Staff would often express anticipatory anxiety and uncertainty, such as is there going to be another surge of COVID-19 cases, and will there be a change in policies?” Dr. Levenson said. “There was a lot of expression of stress and frustration related to politicizing the virus and public containment strategies, both on a local and national level.”
Staff also mentioned the loss of usual coping strategies because of prolonged social isolation, especially for those doing remote work, and the loss of usual support resources that have helped them in the past. “They also reported delayed trauma and grief reactions, including symptoms of depression, anxiety, and posttraumatic stress,” he said. “Health care workers with children mentioned high levels of stress related to childcare, increased workload, and what seems like an impossible work-life balance.” Many reported exhaustion and irritability, “which could affect and cause tension within the work group and challenges to effective team cohesion,” he said. “There were also stressors related to the impact of racial injustices and the [presidential] election that could exacerbate the impact of COVID-19.”
Dr. Levenson hopes that CopeColumbia serves as a model for other health care systems looking for ways to support the mental well-being of their employees. “We want to promote the message that emotional health should have the same priority level as physical health,” he said. “The term that I like to use is total health. Addressing the well-being of health care workers is critical for a healthy workforce and for delivering high-quality patient care.”
He reported having no relevant financial disclosures related to his presentation.
Correction, 2/28/22: An earlier version of this article misstated Dr. Lourival Baptista-Neto's name.
LAS VEGAS – , according to Jon A. Levenson, MD.
“We can learn from previous pandemics and epidemics, which will be important for us going forward from COVID-19,” Dr. Levenson, associate professor of psychiatry at Columbia University Irving Medical Center, New York, said during an annual psychopharmacology update held by the Nevada Psychiatric Association.
During the severe acute respiratory syndrome (SARS) epidemic in 2005, 68% of health care workers reported significant job-related stress, including increased workload, changing work duties, redeployment, shortage of medical supplies, concerns about insufficient personal protective equipment (PPE), lack of safety at work, absence of effective treatment protocols, inconsistent organizational support and information and misinformation from hospital management, and witnessing intense pain, isolation, and loss on a daily basis with few opportunities to take breaks (Psychiatr Serv. 2020 Oct 6. doi: 10.1176/appi.ps.202000274).
Personal concerns associated with psychopathological symptoms included spreading infection to family members; feeling responsibility for family members’ social isolation; self-isolating to avoid infecting family, which can lead to increased loneliness and sadness. “For those who were working remotely, this level of work is hard and challenging,” Dr. Levenson said. “For those who are parents, the 24-hour childcare responsibilities exist on top of work. They often found they can’t unwind with friends.”
Across SARS, MERS, Ebola, and swine flu, a wide range of prevalence in symptoms of distress, stress, anxiety, depressive symptoms, and substance use emerged, he continued. During COVID-19, at least three studies reported significant percentages of distress, depression, anxiety, insomnia, and PTSD among health care workers (JAMA Netw Open. 2020;3[3]:e203976, Front Psychol. 2020 Dec 8;11:608986., and Gen Hosp Psychiatry. Sep-Oct 2020;66:1-8).
“Who is at most-increased risk?” Dr. Levenson asked. “Women; those who are younger and have fewer years of work experience; those working on the front lines such as nurses and advanced practice professionals; and people with preexisting vulnerabilities to psychiatric disorders including anxiety, depression, obsessional symptoms, substance use, suicidal behavior, and impulse control disorders are likely to be especially vulnerable to stress-related symptoms.”
At CUIMC, there were certain “tipping points,” to the vulnerability of health care worker well-being in the early stage of the COVID-19 pandemic, he said, including the loss of an emergency medicine physician colleague from death by suicide. “On the national level there were so many other issues going on such as health care disparities of the COVID-19 infection itself, the murder of George Floyd in Minneapolis, other issues of racial injustice, a tense political climate with an upcoming election at the time, and other factors related to the natural climate concerns,” he said. This prompted several faculty members in the CUIMC department of psychiatry including Claude Ann Mellins, PhD, Laurel S. Mayer, MD, and Lourival Baptista-Neto, MD, to partner with ColumbiaDoctors and New York-Presbyterian Hospital and develop a model of care for health care workers known as CopeColumbia, a virtual program intended to address staff burnout and fatigue, with an emphasis on prevention and promotion of resilience.* It launched in March of 2020 and consists of 1:1 peer support, a peer support group program, town halls/webinars, and an active web site.
The 1:1 peer support sessions typically last 20-30 minutes and provide easy access for all distressed hospital and medical center staff. “We have a phone line staffed by Columbia psychiatrists and psychologists so that a distressed staff member can reach support directly,” he said. The format of these sessions includes a brief discussion of challenges and brainstorming around potential coping strategies. “This is not a psychotherapy session,” Dr. Levenson said. “Each session can be individualized to further assess the type of distress or to implement rating scales such as the Generalized Anxiety Disorder-7 scale to assess for signs and symptoms consistent with GAD. There are options to schedule a second or third peer support session, or a prompt referral within Columbia psychiatry when indicated.”
A typical peer support group meeting lasts about 30 minutes and comprises individual divisions or departments. Some goals of the peer groups are to discuss unique challenges of the work environment and to encourage the members of the group to come up with solutions; to promote team support and coping; to teach resilience-enhancing strategies from empirically based treatments such as CBT, “and to end each meeting with expressions of gratitude and of thanks within the group,” he said.
According to Dr. Levenson, sample questions CopeColumbia faculty use to facilitate coping, include “which coping skills are working for you?”; “Are you able to be present?”; “Have you honored loss with any specific ways or traditions?”; “Do you have any work buddies who support you and vice versa?”; “Can your work community build off each other’s individual strengths to help both the individual and the work group cope optimally?”; and “How can your work team help facilitate each other to best support each other?”
Other aspects of the CopeColumbia program include town halls/grand rounds that range from 30 to 60 minutes in length. “It may be a virtual presentation from a mental health professional on specific aspects of coping such as relaxation techniques,” he said. “The focus is how to manage stress, anxiety, trauma, loss, and grief. It also includes an active Q&A to engage staff participants. The advantage of this format is that you can reach many staff in an entire department.” The program also has an active web site for staff with both internal and external support links including mindfulness, meditation, exercise, parenting suggestions/caregiving, and other resources to promote well-being and resilience for staff and family.
To date, certain themes emerged from the 1:1 and peer support group sessions, including expressions of difficulty adapting to “such a new reality,” compared with the pre-COVID era. “Staff would often express anticipatory anxiety and uncertainty, such as is there going to be another surge of COVID-19 cases, and will there be a change in policies?” Dr. Levenson said. “There was a lot of expression of stress and frustration related to politicizing the virus and public containment strategies, both on a local and national level.”
Staff also mentioned the loss of usual coping strategies because of prolonged social isolation, especially for those doing remote work, and the loss of usual support resources that have helped them in the past. “They also reported delayed trauma and grief reactions, including symptoms of depression, anxiety, and posttraumatic stress,” he said. “Health care workers with children mentioned high levels of stress related to childcare, increased workload, and what seems like an impossible work-life balance.” Many reported exhaustion and irritability, “which could affect and cause tension within the work group and challenges to effective team cohesion,” he said. “There were also stressors related to the impact of racial injustices and the [presidential] election that could exacerbate the impact of COVID-19.”
Dr. Levenson hopes that CopeColumbia serves as a model for other health care systems looking for ways to support the mental well-being of their employees. “We want to promote the message that emotional health should have the same priority level as physical health,” he said. “The term that I like to use is total health. Addressing the well-being of health care workers is critical for a healthy workforce and for delivering high-quality patient care.”
He reported having no relevant financial disclosures related to his presentation.
Correction, 2/28/22: An earlier version of this article misstated Dr. Lourival Baptista-Neto's name.
LAS VEGAS – , according to Jon A. Levenson, MD.
“We can learn from previous pandemics and epidemics, which will be important for us going forward from COVID-19,” Dr. Levenson, associate professor of psychiatry at Columbia University Irving Medical Center, New York, said during an annual psychopharmacology update held by the Nevada Psychiatric Association.
During the severe acute respiratory syndrome (SARS) epidemic in 2005, 68% of health care workers reported significant job-related stress, including increased workload, changing work duties, redeployment, shortage of medical supplies, concerns about insufficient personal protective equipment (PPE), lack of safety at work, absence of effective treatment protocols, inconsistent organizational support and information and misinformation from hospital management, and witnessing intense pain, isolation, and loss on a daily basis with few opportunities to take breaks (Psychiatr Serv. 2020 Oct 6. doi: 10.1176/appi.ps.202000274).
Personal concerns associated with psychopathological symptoms included spreading infection to family members; feeling responsibility for family members’ social isolation; self-isolating to avoid infecting family, which can lead to increased loneliness and sadness. “For those who were working remotely, this level of work is hard and challenging,” Dr. Levenson said. “For those who are parents, the 24-hour childcare responsibilities exist on top of work. They often found they can’t unwind with friends.”
Across SARS, MERS, Ebola, and swine flu, a wide range of prevalence in symptoms of distress, stress, anxiety, depressive symptoms, and substance use emerged, he continued. During COVID-19, at least three studies reported significant percentages of distress, depression, anxiety, insomnia, and PTSD among health care workers (JAMA Netw Open. 2020;3[3]:e203976, Front Psychol. 2020 Dec 8;11:608986., and Gen Hosp Psychiatry. Sep-Oct 2020;66:1-8).
“Who is at most-increased risk?” Dr. Levenson asked. “Women; those who are younger and have fewer years of work experience; those working on the front lines such as nurses and advanced practice professionals; and people with preexisting vulnerabilities to psychiatric disorders including anxiety, depression, obsessional symptoms, substance use, suicidal behavior, and impulse control disorders are likely to be especially vulnerable to stress-related symptoms.”
At CUIMC, there were certain “tipping points,” to the vulnerability of health care worker well-being in the early stage of the COVID-19 pandemic, he said, including the loss of an emergency medicine physician colleague from death by suicide. “On the national level there were so many other issues going on such as health care disparities of the COVID-19 infection itself, the murder of George Floyd in Minneapolis, other issues of racial injustice, a tense political climate with an upcoming election at the time, and other factors related to the natural climate concerns,” he said. This prompted several faculty members in the CUIMC department of psychiatry including Claude Ann Mellins, PhD, Laurel S. Mayer, MD, and Lourival Baptista-Neto, MD, to partner with ColumbiaDoctors and New York-Presbyterian Hospital and develop a model of care for health care workers known as CopeColumbia, a virtual program intended to address staff burnout and fatigue, with an emphasis on prevention and promotion of resilience.* It launched in March of 2020 and consists of 1:1 peer support, a peer support group program, town halls/webinars, and an active web site.
The 1:1 peer support sessions typically last 20-30 minutes and provide easy access for all distressed hospital and medical center staff. “We have a phone line staffed by Columbia psychiatrists and psychologists so that a distressed staff member can reach support directly,” he said. The format of these sessions includes a brief discussion of challenges and brainstorming around potential coping strategies. “This is not a psychotherapy session,” Dr. Levenson said. “Each session can be individualized to further assess the type of distress or to implement rating scales such as the Generalized Anxiety Disorder-7 scale to assess for signs and symptoms consistent with GAD. There are options to schedule a second or third peer support session, or a prompt referral within Columbia psychiatry when indicated.”
A typical peer support group meeting lasts about 30 minutes and comprises individual divisions or departments. Some goals of the peer groups are to discuss unique challenges of the work environment and to encourage the members of the group to come up with solutions; to promote team support and coping; to teach resilience-enhancing strategies from empirically based treatments such as CBT, “and to end each meeting with expressions of gratitude and of thanks within the group,” he said.
According to Dr. Levenson, sample questions CopeColumbia faculty use to facilitate coping, include “which coping skills are working for you?”; “Are you able to be present?”; “Have you honored loss with any specific ways or traditions?”; “Do you have any work buddies who support you and vice versa?”; “Can your work community build off each other’s individual strengths to help both the individual and the work group cope optimally?”; and “How can your work team help facilitate each other to best support each other?”
Other aspects of the CopeColumbia program include town halls/grand rounds that range from 30 to 60 minutes in length. “It may be a virtual presentation from a mental health professional on specific aspects of coping such as relaxation techniques,” he said. “The focus is how to manage stress, anxiety, trauma, loss, and grief. It also includes an active Q&A to engage staff participants. The advantage of this format is that you can reach many staff in an entire department.” The program also has an active web site for staff with both internal and external support links including mindfulness, meditation, exercise, parenting suggestions/caregiving, and other resources to promote well-being and resilience for staff and family.
To date, certain themes emerged from the 1:1 and peer support group sessions, including expressions of difficulty adapting to “such a new reality,” compared with the pre-COVID era. “Staff would often express anticipatory anxiety and uncertainty, such as is there going to be another surge of COVID-19 cases, and will there be a change in policies?” Dr. Levenson said. “There was a lot of expression of stress and frustration related to politicizing the virus and public containment strategies, both on a local and national level.”
Staff also mentioned the loss of usual coping strategies because of prolonged social isolation, especially for those doing remote work, and the loss of usual support resources that have helped them in the past. “They also reported delayed trauma and grief reactions, including symptoms of depression, anxiety, and posttraumatic stress,” he said. “Health care workers with children mentioned high levels of stress related to childcare, increased workload, and what seems like an impossible work-life balance.” Many reported exhaustion and irritability, “which could affect and cause tension within the work group and challenges to effective team cohesion,” he said. “There were also stressors related to the impact of racial injustices and the [presidential] election that could exacerbate the impact of COVID-19.”
Dr. Levenson hopes that CopeColumbia serves as a model for other health care systems looking for ways to support the mental well-being of their employees. “We want to promote the message that emotional health should have the same priority level as physical health,” he said. “The term that I like to use is total health. Addressing the well-being of health care workers is critical for a healthy workforce and for delivering high-quality patient care.”
He reported having no relevant financial disclosures related to his presentation.
Correction, 2/28/22: An earlier version of this article misstated Dr. Lourival Baptista-Neto's name.
FROM NPA 2022
PTSD symptoms common in families of COVID-19 patients
The pandemic has significantly affected the mental health of family members of patients with COVID-19, including high rates of posttraumatic stress disorder (PTSD), anxiety, and depression, new research suggests.
They also had a higher prevalence of depression and anxiety symptoms.
The results illustrate how the mental health of families has been adversely affected by strict isolation measures instituted at the height of the COVID pandemic, lead author Elie Azoulay, MD, PhD, professor of medicine at Diderot University and director of the Medical Intensive Care Unit, Saint Louis Hospital, Paris, told this news organization.
Such restrictions were unnecessary, Dr. Azoulay noted, adding that everyone, including health care professionals, benefits when families are allowed to interact with their loved ones in the ICU.
He added the study findings also emphasize the importance of social supports.
“We need to develop and really increase what we can do for family members” of patients staying in the ICU, said Dr. Azoulay.
The findings were published online Feb. 18 in JAMA.
Twenty-three ICUs in France
The study included adult family members of patients admitted with ARDS to 23 ICUs in France from January to October 2020.
Patients had a partial pressure of arterial oxygen to fraction of inspired oxygen ratio (PaO2/FiO2) of less than 300, and bilateral opacities on chest radiography not fully explained by cardiac failure or fluid overload.
Two trained clinical psychologists interviewed family members and patients by telephone a median of 112 days after ICU discharge. During this interview, participants completed the Impact of Event Scale Revised (IES-R) and the Hospital Anxiety and Depression Scale (HADS).
The IES-R score ranges from 0 (best) to 88 (worst) with a score of more than 22 indicating presence of PTSD-related symptoms of clinical concern. The HADS has separate subscales for anxiety and depression, with a score of 7 or greater on a 21-point scale indicating symptoms of anxiety or depression.
Family members also rated social supports on a scale from 0 (extremely limited) to 10 (extremely effective). Dr. Azoulay noted that social support is the subjective perception of the extent to which friends, mental health specialists, and others are available and helpful.
Investigators divided patients into two groups depending on whether or not the cause of ARDS was COVID-19. Causes other than COVID-19 mainly included community-acquired pneumonia and influenza.
The primary outcome was the prevalence of PTSD-related symptoms among family members. Secondary outcomes were the prevalence of anxiety and depression in family members.
The analysis included 303 family members of patients with COVID-19 ARDS and 214 family members of patients with non–COVID-19 ARDS. Almost half of the family members were spouses.
Those with family members with COVID-19 were younger than the non-COVID group (median age, 50 vs. 55 years). They were less frequently allowed to visit the ICU (35% vs. 88%) and more commonly received patient information by phone (84% vs. 20%).
Better strategies needed
Results showed PTSD symptoms were significantly more common in family members of patients with than without COVID-10 (35% vs. 19%; difference of 16%; 95% confidence interval, 8%-24%; P < .001).
Anxiety symptoms were significantly more common in the COVID-19 group (41% vs. 34%; difference of 8%; 95% CI, 0%-16%; P = .05), as were depression symptoms (31% vs. 18%; difference of 13%; 95% CI, 6%-21%; P < .001).
About 26% of the hospitalized relatives died. PTSD symptoms were more common among bereaved family members of patients who died from COVID-19 than of patients without COVID-19 (63% vs. 39%; difference of 24%; 95% CI, 7%-40%; P = .008).
In the COVID-19 group, significantly fewer family members reported having attended the funeral (77% vs. 91%, P = .04). This could be because of concerns over transmitting the virus, the investigators noted.
After adjustment for age, sex, and level of social support in a multivariable analysis, COVID-19 ARDS was significantly associated with increased risk for PTSD-related symptoms in family members (odds ratio, 2.05; 95% CI, 1.30-3.23; P =.002).
Other factors independently associated with PTSD symptoms were age, level of social support, and being male.
Factors associated with anxiety included having COVID-19 ARDS, age, being male, and level of social support. COVID-19 ARDS and level of social support were independently associated with depression.
Although isolation measures were implemented to prevent viral transmission during the pandemic, severely restricting family members from interacting with their sick loved ones in the ICU is “very destructive [and] deeply distressing,” said Dr. Azoulay. “It’s almost cruel.”
Fear may be at the heart of the “psycho-trauma” experienced by family members, he said.
“I would say one of the main sources is fear of getting infected, fear of abandoning family members, fear of leaving the kids alone without any support, and fear of infecting others,” he added.
Health care providers should develop strategies to better communicate with family members, who also feel a lot of guilt when they’re unable to be with their sick loved ones, said Dr. Azoulay.
‘Element of fear’
Commenting on the findings for this news organization, O. Joseph Bienvenu, MD, PhD, professor of psychiatry and behavioral sciences at Johns Hopkins Medicine, Baltimore, called the study “solid” and noted the lead author is “a well-recognized clinical researcher.”
It was “remarkable” that investigators were able to include a control group of family members of patients with ARDS not due to COVID-19, added Dr. Bienvenu, who was not involved with the research.
“It sounds like the bottom line is COVID adds an additional element of fear in loved ones,” he said.
Dr. Bienvenu added this fits with his own clinical experience – and noted that some COVID-19 follow-up clinics now include family members in their assessments and care.
“I think this study nicely illustrates the utility of this,” he concluded.
The study received funding from the French Ministry of Health. Dr. Azoulay reported receipt of personal fees from lectures from Pfizer, Gilead, Baxter, and Alexion, and institutional research grants from Merck Sharp and Dohme, Pfizer, Baxter, and Alexion. Dr. Bienvenu has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The pandemic has significantly affected the mental health of family members of patients with COVID-19, including high rates of posttraumatic stress disorder (PTSD), anxiety, and depression, new research suggests.
They also had a higher prevalence of depression and anxiety symptoms.
The results illustrate how the mental health of families has been adversely affected by strict isolation measures instituted at the height of the COVID pandemic, lead author Elie Azoulay, MD, PhD, professor of medicine at Diderot University and director of the Medical Intensive Care Unit, Saint Louis Hospital, Paris, told this news organization.
Such restrictions were unnecessary, Dr. Azoulay noted, adding that everyone, including health care professionals, benefits when families are allowed to interact with their loved ones in the ICU.
He added the study findings also emphasize the importance of social supports.
“We need to develop and really increase what we can do for family members” of patients staying in the ICU, said Dr. Azoulay.
The findings were published online Feb. 18 in JAMA.
Twenty-three ICUs in France
The study included adult family members of patients admitted with ARDS to 23 ICUs in France from January to October 2020.
Patients had a partial pressure of arterial oxygen to fraction of inspired oxygen ratio (PaO2/FiO2) of less than 300, and bilateral opacities on chest radiography not fully explained by cardiac failure or fluid overload.
Two trained clinical psychologists interviewed family members and patients by telephone a median of 112 days after ICU discharge. During this interview, participants completed the Impact of Event Scale Revised (IES-R) and the Hospital Anxiety and Depression Scale (HADS).
The IES-R score ranges from 0 (best) to 88 (worst) with a score of more than 22 indicating presence of PTSD-related symptoms of clinical concern. The HADS has separate subscales for anxiety and depression, with a score of 7 or greater on a 21-point scale indicating symptoms of anxiety or depression.
Family members also rated social supports on a scale from 0 (extremely limited) to 10 (extremely effective). Dr. Azoulay noted that social support is the subjective perception of the extent to which friends, mental health specialists, and others are available and helpful.
Investigators divided patients into two groups depending on whether or not the cause of ARDS was COVID-19. Causes other than COVID-19 mainly included community-acquired pneumonia and influenza.
The primary outcome was the prevalence of PTSD-related symptoms among family members. Secondary outcomes were the prevalence of anxiety and depression in family members.
The analysis included 303 family members of patients with COVID-19 ARDS and 214 family members of patients with non–COVID-19 ARDS. Almost half of the family members were spouses.
Those with family members with COVID-19 were younger than the non-COVID group (median age, 50 vs. 55 years). They were less frequently allowed to visit the ICU (35% vs. 88%) and more commonly received patient information by phone (84% vs. 20%).
Better strategies needed
Results showed PTSD symptoms were significantly more common in family members of patients with than without COVID-10 (35% vs. 19%; difference of 16%; 95% confidence interval, 8%-24%; P < .001).
Anxiety symptoms were significantly more common in the COVID-19 group (41% vs. 34%; difference of 8%; 95% CI, 0%-16%; P = .05), as were depression symptoms (31% vs. 18%; difference of 13%; 95% CI, 6%-21%; P < .001).
About 26% of the hospitalized relatives died. PTSD symptoms were more common among bereaved family members of patients who died from COVID-19 than of patients without COVID-19 (63% vs. 39%; difference of 24%; 95% CI, 7%-40%; P = .008).
In the COVID-19 group, significantly fewer family members reported having attended the funeral (77% vs. 91%, P = .04). This could be because of concerns over transmitting the virus, the investigators noted.
After adjustment for age, sex, and level of social support in a multivariable analysis, COVID-19 ARDS was significantly associated with increased risk for PTSD-related symptoms in family members (odds ratio, 2.05; 95% CI, 1.30-3.23; P =.002).
Other factors independently associated with PTSD symptoms were age, level of social support, and being male.
Factors associated with anxiety included having COVID-19 ARDS, age, being male, and level of social support. COVID-19 ARDS and level of social support were independently associated with depression.
Although isolation measures were implemented to prevent viral transmission during the pandemic, severely restricting family members from interacting with their sick loved ones in the ICU is “very destructive [and] deeply distressing,” said Dr. Azoulay. “It’s almost cruel.”
Fear may be at the heart of the “psycho-trauma” experienced by family members, he said.
“I would say one of the main sources is fear of getting infected, fear of abandoning family members, fear of leaving the kids alone without any support, and fear of infecting others,” he added.
Health care providers should develop strategies to better communicate with family members, who also feel a lot of guilt when they’re unable to be with their sick loved ones, said Dr. Azoulay.
‘Element of fear’
Commenting on the findings for this news organization, O. Joseph Bienvenu, MD, PhD, professor of psychiatry and behavioral sciences at Johns Hopkins Medicine, Baltimore, called the study “solid” and noted the lead author is “a well-recognized clinical researcher.”
It was “remarkable” that investigators were able to include a control group of family members of patients with ARDS not due to COVID-19, added Dr. Bienvenu, who was not involved with the research.
“It sounds like the bottom line is COVID adds an additional element of fear in loved ones,” he said.
Dr. Bienvenu added this fits with his own clinical experience – and noted that some COVID-19 follow-up clinics now include family members in their assessments and care.
“I think this study nicely illustrates the utility of this,” he concluded.
The study received funding from the French Ministry of Health. Dr. Azoulay reported receipt of personal fees from lectures from Pfizer, Gilead, Baxter, and Alexion, and institutional research grants from Merck Sharp and Dohme, Pfizer, Baxter, and Alexion. Dr. Bienvenu has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The pandemic has significantly affected the mental health of family members of patients with COVID-19, including high rates of posttraumatic stress disorder (PTSD), anxiety, and depression, new research suggests.
They also had a higher prevalence of depression and anxiety symptoms.
The results illustrate how the mental health of families has been adversely affected by strict isolation measures instituted at the height of the COVID pandemic, lead author Elie Azoulay, MD, PhD, professor of medicine at Diderot University and director of the Medical Intensive Care Unit, Saint Louis Hospital, Paris, told this news organization.
Such restrictions were unnecessary, Dr. Azoulay noted, adding that everyone, including health care professionals, benefits when families are allowed to interact with their loved ones in the ICU.
He added the study findings also emphasize the importance of social supports.
“We need to develop and really increase what we can do for family members” of patients staying in the ICU, said Dr. Azoulay.
The findings were published online Feb. 18 in JAMA.
Twenty-three ICUs in France
The study included adult family members of patients admitted with ARDS to 23 ICUs in France from January to October 2020.
Patients had a partial pressure of arterial oxygen to fraction of inspired oxygen ratio (PaO2/FiO2) of less than 300, and bilateral opacities on chest radiography not fully explained by cardiac failure or fluid overload.
Two trained clinical psychologists interviewed family members and patients by telephone a median of 112 days after ICU discharge. During this interview, participants completed the Impact of Event Scale Revised (IES-R) and the Hospital Anxiety and Depression Scale (HADS).
The IES-R score ranges from 0 (best) to 88 (worst) with a score of more than 22 indicating presence of PTSD-related symptoms of clinical concern. The HADS has separate subscales for anxiety and depression, with a score of 7 or greater on a 21-point scale indicating symptoms of anxiety or depression.
Family members also rated social supports on a scale from 0 (extremely limited) to 10 (extremely effective). Dr. Azoulay noted that social support is the subjective perception of the extent to which friends, mental health specialists, and others are available and helpful.
Investigators divided patients into two groups depending on whether or not the cause of ARDS was COVID-19. Causes other than COVID-19 mainly included community-acquired pneumonia and influenza.
The primary outcome was the prevalence of PTSD-related symptoms among family members. Secondary outcomes were the prevalence of anxiety and depression in family members.
The analysis included 303 family members of patients with COVID-19 ARDS and 214 family members of patients with non–COVID-19 ARDS. Almost half of the family members were spouses.
Those with family members with COVID-19 were younger than the non-COVID group (median age, 50 vs. 55 years). They were less frequently allowed to visit the ICU (35% vs. 88%) and more commonly received patient information by phone (84% vs. 20%).
Better strategies needed
Results showed PTSD symptoms were significantly more common in family members of patients with than without COVID-10 (35% vs. 19%; difference of 16%; 95% confidence interval, 8%-24%; P < .001).
Anxiety symptoms were significantly more common in the COVID-19 group (41% vs. 34%; difference of 8%; 95% CI, 0%-16%; P = .05), as were depression symptoms (31% vs. 18%; difference of 13%; 95% CI, 6%-21%; P < .001).
About 26% of the hospitalized relatives died. PTSD symptoms were more common among bereaved family members of patients who died from COVID-19 than of patients without COVID-19 (63% vs. 39%; difference of 24%; 95% CI, 7%-40%; P = .008).
In the COVID-19 group, significantly fewer family members reported having attended the funeral (77% vs. 91%, P = .04). This could be because of concerns over transmitting the virus, the investigators noted.
After adjustment for age, sex, and level of social support in a multivariable analysis, COVID-19 ARDS was significantly associated with increased risk for PTSD-related symptoms in family members (odds ratio, 2.05; 95% CI, 1.30-3.23; P =.002).
Other factors independently associated with PTSD symptoms were age, level of social support, and being male.
Factors associated with anxiety included having COVID-19 ARDS, age, being male, and level of social support. COVID-19 ARDS and level of social support were independently associated with depression.
Although isolation measures were implemented to prevent viral transmission during the pandemic, severely restricting family members from interacting with their sick loved ones in the ICU is “very destructive [and] deeply distressing,” said Dr. Azoulay. “It’s almost cruel.”
Fear may be at the heart of the “psycho-trauma” experienced by family members, he said.
“I would say one of the main sources is fear of getting infected, fear of abandoning family members, fear of leaving the kids alone without any support, and fear of infecting others,” he added.
Health care providers should develop strategies to better communicate with family members, who also feel a lot of guilt when they’re unable to be with their sick loved ones, said Dr. Azoulay.
‘Element of fear’
Commenting on the findings for this news organization, O. Joseph Bienvenu, MD, PhD, professor of psychiatry and behavioral sciences at Johns Hopkins Medicine, Baltimore, called the study “solid” and noted the lead author is “a well-recognized clinical researcher.”
It was “remarkable” that investigators were able to include a control group of family members of patients with ARDS not due to COVID-19, added Dr. Bienvenu, who was not involved with the research.
“It sounds like the bottom line is COVID adds an additional element of fear in loved ones,” he said.
Dr. Bienvenu added this fits with his own clinical experience – and noted that some COVID-19 follow-up clinics now include family members in their assessments and care.
“I think this study nicely illustrates the utility of this,” he concluded.
The study received funding from the French Ministry of Health. Dr. Azoulay reported receipt of personal fees from lectures from Pfizer, Gilead, Baxter, and Alexion, and institutional research grants from Merck Sharp and Dohme, Pfizer, Baxter, and Alexion. Dr. Bienvenu has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA
Pandemic-stressed youths call runaway hotline
The calls kept coming into the National Runaway Safeline during the pandemic: the desperate kids who wanted to bike away from home in the middle of the night, the isolated youths who felt suicidal, the teens whose parents had forced them out of the house.
To the surprise of experts who help runaway youths, the pandemic didn’t appear to produce a big rise or fall in the numbers of children and teens who had left home. Still, the crisis hit hard. As schools closed and households sheltered in place, youths reached out to the National Runaway Safeline to report heightened family conflicts and worsening mental health.
The Safeline, based in Chicago, is the country’s 24/7, federally designated communications system for runaway and homeless youths. Each year, it makes about 125,000 connections with young people and their family members through its hotline and other services.
In a typical year, teens aged 15-17 years are the main group that gets in touch by phone, live chat, email, or an online crisis forum, according to Jeff Stern, chief engagement officer at the Safeline.
But in the past 2 years, “contacts have skewed younger,” including many more children under age 12.
“I think this is showing what a hit this is taking on young children,” he said.
Without school, sports, and other activities, younger children might be reaching out because they’ve lost trusted sources of support. Callers have been as young as 9.
“Those ones stand out,” said a crisis center supervisor who asked to go by Michael, which is not his real name, to protect the privacy of his clients.
In November 2020, a child posted in the crisis forum: “I’m 11 and my parents treat me poorly. They have told me many times to ‘kill myself’ and I didn’t let that settle well with me. ... I have tried to run away one time from my house, but they found out, so they took my phone away and put screws on my windows so I couldn’t leave.”
Increasing numbers of children told Safeline counselors that their parents were emotionally or verbally abusive, while others reported physical abuse. Some said they experienced neglect, while others had been thrown out.
“We absolutely have had youths who have either been physically kicked out of the house or just verbally told to leave,” Michael said, “and then the kid does.”
Heightened family conflicts
The Safeline partners with the National Center for Missing and Exploited Children, which, despite widespread public perception, doesn’t work mainly with child abduction cases. Each year, the center assists with 29,000-31,000 cases, and 92% involve “endangered runaways,” said John Bischoff, vice president of the Missing Children Division. These children could be running away from home or foster care.
During the pandemic, the center didn’t spot major changes in its missing child numbers, “which honestly was shocking,” Mr. Bischoff said. “We figured we were either going to see an extreme rise or a decrease.
“But the reasons for the run were changing,” he said.
Many youths were fleeing out of frustration with quarantine restrictions, Mr. Bischoff said, as well as frustration with the unknown and their own lack of control over many situations.
At the runaway hotline, calls have been longer and more intense, with family problems topping the list of concerns. In 2019, about 57% of all contacts mentioned family dynamics. In 2020, that number jumped to 88%, according to Mr. Stern.
Some kids sought support for family problems that involved school. In October 2020, one 13-year-old wrote in the Safeline forum: “My mom constantly yells at me for no reason. I want to leave, but I don’t know how. I have also been really stressed about school because they haven’t been giving me the grades I would normally receive during actual school. She thinks I’m lying and that I don’t care. I just need somebody to help me.”
Many adults are under tremendous strain, too, Michael said.
“Parents might have gotten COVID last month and haven’t been able to work for 2 weeks, and they’re missing a paycheck now. Money is tight, there might not be food, everyone’s angry at everything.”
During the pandemic, the National Runaway Safeline found a 16% increase in contacts citing financial challenges.
Some children have felt confined in unsafe homes or have endured violence, as one 15-year-old reported in the forum: “I am the scapegoat out of four kids. Unfortunately, my mom has always been a toxic person. ... I’m the only kid she still hits really hard. She’s left bruises and scratches recently. ... I just have no solution to this.”
Worsening mental health
Besides family dynamics, mental health emerged as a top concern that youths reported in 2020. “This is something notable. It increased by 30% just in 1 year,” Mr. Stern said.
In November 2020, a 16-year-old wrote: “I can’t ever go outside. I’ve been stuck in the house for a very long time now since quarantine started. I’m scared. ... My mother has been taking her anger out on me emotionally. ... I have severe depression and I need help. Please, if there’s any way I can get out of here, let me know.”
The Safeline also has seen a rise in suicide-related contacts. Among children and teens who had cited a mental health concern, 18% said they were suicidal, Stern said. Most were between ages 12 and 16, but some were younger than 12.
When children couldn’t hang out with peers, they felt even more isolated if parents confiscated their phones, a common punishment, Michael said.
During the winter of 2020-21, “It felt like almost every digital contact was a youth reaching out on their Chromebook because they had gotten their phone taken away and they were either suicidal or considering running away,” he said. “That’s kind of their entire social sphere getting taken away.”
Reality check
Roughly 7 in 10 youths report still being at home when they reach out to the Safeline. Among those who do leave, Michael said, “They’re going sometimes to friends’ houses, oftentimes to a significant other’s house, sometimes to extended family members’ houses. Often, they don’t have a place that they’re planning to go. They just left, and that’s why they’re calling us.”
While some youths have been afraid of catching COVID-19 in general, the coronavirus threat hasn’t deterred those who have decided to run away, Michael said. “Usually, they’re more worried about being returned home.”
Many can’t comprehend the risks of setting off on their own.
In October 2021, a 15-year-old boy posted on the forum that his verbally abusive parents had called him a mistake and said they couldn’t wait for him to move out.
“So I’m going to make their dreams come true,” he wrote. “I’m going to go live in California with my friend who is a young YouTuber. I need help getting money to either fly or get a bus ticket, even though I’m all right with trying to ride a bike or fixing my dirt bike and getting the wagon to pull my stuff. But I’m looking for apartments in Los Angeles so I’m not living on the streets and I’m looking for a job. Please help me. My friend can’t send me money because I don’t have a bank account.”
“Often,” Michael said, “we’re reality-checking kids who want to hitchhike 5 hours away to either a friend’s or the closest shelter that we could find them. Or walk for 5 hours at 3 a.m. or bike, so we try to safety-check that.”
Another concern: online enticement by predators. During the pandemic, the National Center for Missing and Exploited Children saw cases in which children ran away from home “to go meet with someone who may not be who they thought they were talking to online,” Mr. Bischoff said. “It’s certainly something we’re keeping a close eye on.”
Fewer resources in the pandemic
The National Runaway Safeline provides information and referrals to other hotlines and services, including suicide prevention and mental health organizations. When youths have already run away and have no place to go, Michael said, the Safeline tries to find shelter options or seek out a relative who can provide a safe place to stay.
But finding shelters became tougher during the pandemic, when many had no room or shelter supply was limited. Some had to shut down for COVID-19–related deep cleanings, Michael said. Helping youths find transportation, especially with public transportation shutdowns, also was tough.
The Huckleberry House, a six-bed youth shelter in San Francisco, has stayed open throughout the pandemic with limited staffing, said Douglas Styles, PsyD. He’s the executive director of the Huckleberry Youth Programs, which runs the house.
The shelter, which serves Bay Area runaway and homeless youths ages 12-17, hasn’t seen an overall spike in demand, Dr. Styles said. But “what’s expanded is undocumented [youths] and young people who don’t have any family connections in the area, so they’re unaccompanied as well. We’ve seen that here and there throughout the years, but during the pandemic, that population has actually increased quite a bit.”
The Huckleberry House has sheltered children and teens who have run away from all kinds of homes, including affluent ones, Dr. Styles said.
Once children leave home, the lack of adult supervision leaves them vulnerable. They face multiple dangers, including child sex trafficking and exploitation, substance abuse, gang involvement, and violence. “As an organization, that scares us,” Mr. Bischoff said. “What’s happening at home, we’ll sort that out. The biggest thing we as an organization are trying to do is locate them and ensure their safety.”
To help runaways and their families get in touch, the National Runaway Safeline provides a message service and conference calling. “We can play the middleman, really acting on behalf of the young person – not because they’re right or wrong, but to ensure that their voice is really heard,” Mr. Stern said.
Through its national Home Free program, the Safeline partners with Greyhound to bring children back home or into an alternative, safe living environment by providing a free bus ticket.
These days, technology can expose children to harm online, but it can also speed their return home.
“When I was growing up, if you weren’t home by 5 o’clock, Mom would start to worry, but she really didn’t have any way of reaching you,” Mr. Bischoff said. “More children today have cellphones. More children are easily reachable. That’s a benefit.”
A version of this article first appeared on WebMD.com.
The calls kept coming into the National Runaway Safeline during the pandemic: the desperate kids who wanted to bike away from home in the middle of the night, the isolated youths who felt suicidal, the teens whose parents had forced them out of the house.
To the surprise of experts who help runaway youths, the pandemic didn’t appear to produce a big rise or fall in the numbers of children and teens who had left home. Still, the crisis hit hard. As schools closed and households sheltered in place, youths reached out to the National Runaway Safeline to report heightened family conflicts and worsening mental health.
The Safeline, based in Chicago, is the country’s 24/7, federally designated communications system for runaway and homeless youths. Each year, it makes about 125,000 connections with young people and their family members through its hotline and other services.
In a typical year, teens aged 15-17 years are the main group that gets in touch by phone, live chat, email, or an online crisis forum, according to Jeff Stern, chief engagement officer at the Safeline.
But in the past 2 years, “contacts have skewed younger,” including many more children under age 12.
“I think this is showing what a hit this is taking on young children,” he said.
Without school, sports, and other activities, younger children might be reaching out because they’ve lost trusted sources of support. Callers have been as young as 9.
“Those ones stand out,” said a crisis center supervisor who asked to go by Michael, which is not his real name, to protect the privacy of his clients.
In November 2020, a child posted in the crisis forum: “I’m 11 and my parents treat me poorly. They have told me many times to ‘kill myself’ and I didn’t let that settle well with me. ... I have tried to run away one time from my house, but they found out, so they took my phone away and put screws on my windows so I couldn’t leave.”
Increasing numbers of children told Safeline counselors that their parents were emotionally or verbally abusive, while others reported physical abuse. Some said they experienced neglect, while others had been thrown out.
“We absolutely have had youths who have either been physically kicked out of the house or just verbally told to leave,” Michael said, “and then the kid does.”
Heightened family conflicts
The Safeline partners with the National Center for Missing and Exploited Children, which, despite widespread public perception, doesn’t work mainly with child abduction cases. Each year, the center assists with 29,000-31,000 cases, and 92% involve “endangered runaways,” said John Bischoff, vice president of the Missing Children Division. These children could be running away from home or foster care.
During the pandemic, the center didn’t spot major changes in its missing child numbers, “which honestly was shocking,” Mr. Bischoff said. “We figured we were either going to see an extreme rise or a decrease.
“But the reasons for the run were changing,” he said.
Many youths were fleeing out of frustration with quarantine restrictions, Mr. Bischoff said, as well as frustration with the unknown and their own lack of control over many situations.
At the runaway hotline, calls have been longer and more intense, with family problems topping the list of concerns. In 2019, about 57% of all contacts mentioned family dynamics. In 2020, that number jumped to 88%, according to Mr. Stern.
Some kids sought support for family problems that involved school. In October 2020, one 13-year-old wrote in the Safeline forum: “My mom constantly yells at me for no reason. I want to leave, but I don’t know how. I have also been really stressed about school because they haven’t been giving me the grades I would normally receive during actual school. She thinks I’m lying and that I don’t care. I just need somebody to help me.”
Many adults are under tremendous strain, too, Michael said.
“Parents might have gotten COVID last month and haven’t been able to work for 2 weeks, and they’re missing a paycheck now. Money is tight, there might not be food, everyone’s angry at everything.”
During the pandemic, the National Runaway Safeline found a 16% increase in contacts citing financial challenges.
Some children have felt confined in unsafe homes or have endured violence, as one 15-year-old reported in the forum: “I am the scapegoat out of four kids. Unfortunately, my mom has always been a toxic person. ... I’m the only kid she still hits really hard. She’s left bruises and scratches recently. ... I just have no solution to this.”
Worsening mental health
Besides family dynamics, mental health emerged as a top concern that youths reported in 2020. “This is something notable. It increased by 30% just in 1 year,” Mr. Stern said.
In November 2020, a 16-year-old wrote: “I can’t ever go outside. I’ve been stuck in the house for a very long time now since quarantine started. I’m scared. ... My mother has been taking her anger out on me emotionally. ... I have severe depression and I need help. Please, if there’s any way I can get out of here, let me know.”
The Safeline also has seen a rise in suicide-related contacts. Among children and teens who had cited a mental health concern, 18% said they were suicidal, Stern said. Most were between ages 12 and 16, but some were younger than 12.
When children couldn’t hang out with peers, they felt even more isolated if parents confiscated their phones, a common punishment, Michael said.
During the winter of 2020-21, “It felt like almost every digital contact was a youth reaching out on their Chromebook because they had gotten their phone taken away and they were either suicidal or considering running away,” he said. “That’s kind of their entire social sphere getting taken away.”
Reality check
Roughly 7 in 10 youths report still being at home when they reach out to the Safeline. Among those who do leave, Michael said, “They’re going sometimes to friends’ houses, oftentimes to a significant other’s house, sometimes to extended family members’ houses. Often, they don’t have a place that they’re planning to go. They just left, and that’s why they’re calling us.”
While some youths have been afraid of catching COVID-19 in general, the coronavirus threat hasn’t deterred those who have decided to run away, Michael said. “Usually, they’re more worried about being returned home.”
Many can’t comprehend the risks of setting off on their own.
In October 2021, a 15-year-old boy posted on the forum that his verbally abusive parents had called him a mistake and said they couldn’t wait for him to move out.
“So I’m going to make their dreams come true,” he wrote. “I’m going to go live in California with my friend who is a young YouTuber. I need help getting money to either fly or get a bus ticket, even though I’m all right with trying to ride a bike or fixing my dirt bike and getting the wagon to pull my stuff. But I’m looking for apartments in Los Angeles so I’m not living on the streets and I’m looking for a job. Please help me. My friend can’t send me money because I don’t have a bank account.”
“Often,” Michael said, “we’re reality-checking kids who want to hitchhike 5 hours away to either a friend’s or the closest shelter that we could find them. Or walk for 5 hours at 3 a.m. or bike, so we try to safety-check that.”
Another concern: online enticement by predators. During the pandemic, the National Center for Missing and Exploited Children saw cases in which children ran away from home “to go meet with someone who may not be who they thought they were talking to online,” Mr. Bischoff said. “It’s certainly something we’re keeping a close eye on.”
Fewer resources in the pandemic
The National Runaway Safeline provides information and referrals to other hotlines and services, including suicide prevention and mental health organizations. When youths have already run away and have no place to go, Michael said, the Safeline tries to find shelter options or seek out a relative who can provide a safe place to stay.
But finding shelters became tougher during the pandemic, when many had no room or shelter supply was limited. Some had to shut down for COVID-19–related deep cleanings, Michael said. Helping youths find transportation, especially with public transportation shutdowns, also was tough.
The Huckleberry House, a six-bed youth shelter in San Francisco, has stayed open throughout the pandemic with limited staffing, said Douglas Styles, PsyD. He’s the executive director of the Huckleberry Youth Programs, which runs the house.
The shelter, which serves Bay Area runaway and homeless youths ages 12-17, hasn’t seen an overall spike in demand, Dr. Styles said. But “what’s expanded is undocumented [youths] and young people who don’t have any family connections in the area, so they’re unaccompanied as well. We’ve seen that here and there throughout the years, but during the pandemic, that population has actually increased quite a bit.”
The Huckleberry House has sheltered children and teens who have run away from all kinds of homes, including affluent ones, Dr. Styles said.
Once children leave home, the lack of adult supervision leaves them vulnerable. They face multiple dangers, including child sex trafficking and exploitation, substance abuse, gang involvement, and violence. “As an organization, that scares us,” Mr. Bischoff said. “What’s happening at home, we’ll sort that out. The biggest thing we as an organization are trying to do is locate them and ensure their safety.”
To help runaways and their families get in touch, the National Runaway Safeline provides a message service and conference calling. “We can play the middleman, really acting on behalf of the young person – not because they’re right or wrong, but to ensure that their voice is really heard,” Mr. Stern said.
Through its national Home Free program, the Safeline partners with Greyhound to bring children back home or into an alternative, safe living environment by providing a free bus ticket.
These days, technology can expose children to harm online, but it can also speed their return home.
“When I was growing up, if you weren’t home by 5 o’clock, Mom would start to worry, but she really didn’t have any way of reaching you,” Mr. Bischoff said. “More children today have cellphones. More children are easily reachable. That’s a benefit.”
A version of this article first appeared on WebMD.com.
The calls kept coming into the National Runaway Safeline during the pandemic: the desperate kids who wanted to bike away from home in the middle of the night, the isolated youths who felt suicidal, the teens whose parents had forced them out of the house.
To the surprise of experts who help runaway youths, the pandemic didn’t appear to produce a big rise or fall in the numbers of children and teens who had left home. Still, the crisis hit hard. As schools closed and households sheltered in place, youths reached out to the National Runaway Safeline to report heightened family conflicts and worsening mental health.
The Safeline, based in Chicago, is the country’s 24/7, federally designated communications system for runaway and homeless youths. Each year, it makes about 125,000 connections with young people and their family members through its hotline and other services.
In a typical year, teens aged 15-17 years are the main group that gets in touch by phone, live chat, email, or an online crisis forum, according to Jeff Stern, chief engagement officer at the Safeline.
But in the past 2 years, “contacts have skewed younger,” including many more children under age 12.
“I think this is showing what a hit this is taking on young children,” he said.
Without school, sports, and other activities, younger children might be reaching out because they’ve lost trusted sources of support. Callers have been as young as 9.
“Those ones stand out,” said a crisis center supervisor who asked to go by Michael, which is not his real name, to protect the privacy of his clients.
In November 2020, a child posted in the crisis forum: “I’m 11 and my parents treat me poorly. They have told me many times to ‘kill myself’ and I didn’t let that settle well with me. ... I have tried to run away one time from my house, but they found out, so they took my phone away and put screws on my windows so I couldn’t leave.”
Increasing numbers of children told Safeline counselors that their parents were emotionally or verbally abusive, while others reported physical abuse. Some said they experienced neglect, while others had been thrown out.
“We absolutely have had youths who have either been physically kicked out of the house or just verbally told to leave,” Michael said, “and then the kid does.”
Heightened family conflicts
The Safeline partners with the National Center for Missing and Exploited Children, which, despite widespread public perception, doesn’t work mainly with child abduction cases. Each year, the center assists with 29,000-31,000 cases, and 92% involve “endangered runaways,” said John Bischoff, vice president of the Missing Children Division. These children could be running away from home or foster care.
During the pandemic, the center didn’t spot major changes in its missing child numbers, “which honestly was shocking,” Mr. Bischoff said. “We figured we were either going to see an extreme rise or a decrease.
“But the reasons for the run were changing,” he said.
Many youths were fleeing out of frustration with quarantine restrictions, Mr. Bischoff said, as well as frustration with the unknown and their own lack of control over many situations.
At the runaway hotline, calls have been longer and more intense, with family problems topping the list of concerns. In 2019, about 57% of all contacts mentioned family dynamics. In 2020, that number jumped to 88%, according to Mr. Stern.
Some kids sought support for family problems that involved school. In October 2020, one 13-year-old wrote in the Safeline forum: “My mom constantly yells at me for no reason. I want to leave, but I don’t know how. I have also been really stressed about school because they haven’t been giving me the grades I would normally receive during actual school. She thinks I’m lying and that I don’t care. I just need somebody to help me.”
Many adults are under tremendous strain, too, Michael said.
“Parents might have gotten COVID last month and haven’t been able to work for 2 weeks, and they’re missing a paycheck now. Money is tight, there might not be food, everyone’s angry at everything.”
During the pandemic, the National Runaway Safeline found a 16% increase in contacts citing financial challenges.
Some children have felt confined in unsafe homes or have endured violence, as one 15-year-old reported in the forum: “I am the scapegoat out of four kids. Unfortunately, my mom has always been a toxic person. ... I’m the only kid she still hits really hard. She’s left bruises and scratches recently. ... I just have no solution to this.”
Worsening mental health
Besides family dynamics, mental health emerged as a top concern that youths reported in 2020. “This is something notable. It increased by 30% just in 1 year,” Mr. Stern said.
In November 2020, a 16-year-old wrote: “I can’t ever go outside. I’ve been stuck in the house for a very long time now since quarantine started. I’m scared. ... My mother has been taking her anger out on me emotionally. ... I have severe depression and I need help. Please, if there’s any way I can get out of here, let me know.”
The Safeline also has seen a rise in suicide-related contacts. Among children and teens who had cited a mental health concern, 18% said they were suicidal, Stern said. Most were between ages 12 and 16, but some were younger than 12.
When children couldn’t hang out with peers, they felt even more isolated if parents confiscated their phones, a common punishment, Michael said.
During the winter of 2020-21, “It felt like almost every digital contact was a youth reaching out on their Chromebook because they had gotten their phone taken away and they were either suicidal or considering running away,” he said. “That’s kind of their entire social sphere getting taken away.”
Reality check
Roughly 7 in 10 youths report still being at home when they reach out to the Safeline. Among those who do leave, Michael said, “They’re going sometimes to friends’ houses, oftentimes to a significant other’s house, sometimes to extended family members’ houses. Often, they don’t have a place that they’re planning to go. They just left, and that’s why they’re calling us.”
While some youths have been afraid of catching COVID-19 in general, the coronavirus threat hasn’t deterred those who have decided to run away, Michael said. “Usually, they’re more worried about being returned home.”
Many can’t comprehend the risks of setting off on their own.
In October 2021, a 15-year-old boy posted on the forum that his verbally abusive parents had called him a mistake and said they couldn’t wait for him to move out.
“So I’m going to make their dreams come true,” he wrote. “I’m going to go live in California with my friend who is a young YouTuber. I need help getting money to either fly or get a bus ticket, even though I’m all right with trying to ride a bike or fixing my dirt bike and getting the wagon to pull my stuff. But I’m looking for apartments in Los Angeles so I’m not living on the streets and I’m looking for a job. Please help me. My friend can’t send me money because I don’t have a bank account.”
“Often,” Michael said, “we’re reality-checking kids who want to hitchhike 5 hours away to either a friend’s or the closest shelter that we could find them. Or walk for 5 hours at 3 a.m. or bike, so we try to safety-check that.”
Another concern: online enticement by predators. During the pandemic, the National Center for Missing and Exploited Children saw cases in which children ran away from home “to go meet with someone who may not be who they thought they were talking to online,” Mr. Bischoff said. “It’s certainly something we’re keeping a close eye on.”
Fewer resources in the pandemic
The National Runaway Safeline provides information and referrals to other hotlines and services, including suicide prevention and mental health organizations. When youths have already run away and have no place to go, Michael said, the Safeline tries to find shelter options or seek out a relative who can provide a safe place to stay.
But finding shelters became tougher during the pandemic, when many had no room or shelter supply was limited. Some had to shut down for COVID-19–related deep cleanings, Michael said. Helping youths find transportation, especially with public transportation shutdowns, also was tough.
The Huckleberry House, a six-bed youth shelter in San Francisco, has stayed open throughout the pandemic with limited staffing, said Douglas Styles, PsyD. He’s the executive director of the Huckleberry Youth Programs, which runs the house.
The shelter, which serves Bay Area runaway and homeless youths ages 12-17, hasn’t seen an overall spike in demand, Dr. Styles said. But “what’s expanded is undocumented [youths] and young people who don’t have any family connections in the area, so they’re unaccompanied as well. We’ve seen that here and there throughout the years, but during the pandemic, that population has actually increased quite a bit.”
The Huckleberry House has sheltered children and teens who have run away from all kinds of homes, including affluent ones, Dr. Styles said.
Once children leave home, the lack of adult supervision leaves them vulnerable. They face multiple dangers, including child sex trafficking and exploitation, substance abuse, gang involvement, and violence. “As an organization, that scares us,” Mr. Bischoff said. “What’s happening at home, we’ll sort that out. The biggest thing we as an organization are trying to do is locate them and ensure their safety.”
To help runaways and their families get in touch, the National Runaway Safeline provides a message service and conference calling. “We can play the middleman, really acting on behalf of the young person – not because they’re right or wrong, but to ensure that their voice is really heard,” Mr. Stern said.
Through its national Home Free program, the Safeline partners with Greyhound to bring children back home or into an alternative, safe living environment by providing a free bus ticket.
These days, technology can expose children to harm online, but it can also speed their return home.
“When I was growing up, if you weren’t home by 5 o’clock, Mom would start to worry, but she really didn’t have any way of reaching you,” Mr. Bischoff said. “More children today have cellphones. More children are easily reachable. That’s a benefit.”
A version of this article first appeared on WebMD.com.
Imaging links insula and frontal cortex to anxiety in Parkinson’s disease
Anxiety occurs in approximately 31% of Parkinson’s disease patients, but the underlying mechanisms are not well understood, wrote Nacim Betrouni, MD, of the University of Lille, France, and colleagues. Previous research has shown associations between anxiety severity and increased activity in brain areas of emotion processing, based on MRI and positron emission tomography, but electroencephalography (EEG) has not been widely used, they said.
In a study published in Neurophysiologie Clinique , the researchers compared EEG spectral patterns and functional resting-state networks in Parkinson’s disease patients with and without anxiety disorders. They identified data from 33 PD patients who met criteria for anxiety, and 75 without anxiety. The average age of the patients was 65 years, and the average disease duration was 9.76 years in anxiety patients and 7.83 years in patients without anxiety.
Overall, findings on spectral analysis showed an association between anxiety and changes in the alpha activity in the right frontal cortex, the researchers said. They also found the relative power in the alpha1 frequency band in the right prefrontal cortex was lower in patients with anxiety than without; this finding was significantly associated with avoidance behavior on a subscale of the Parkinson’s Anxiety Scale (PAS_C, P = .035). A trend toward a significant association with episodic anxiety was noted (PAS_B, P = .06), but no significant associations were noted for persistent anxiety or the total scale score.
The imaging also showed an increased connectivity between the insula and the posterior cingulate cortex in several frequency bands in the anxiety patients, the researchers said. “The increased connectivity observed here may be a marker of the maintenance of avoidance behaviors that characterize anxiety in PD,” they noted.
The study findings were limited by several factors including the small and unbalanced proportion of the study population with anxiety, and the consideration of global anxiety only, without distinguishing anxiety subtypes, the researchers noted. Another limitation was the use only of static EEC patterns, without using dynamic patterns, they said.
The study is the first known to use EEG to explore the mechanisms of PD-related anxiety and “the reported results provide new insights, supporting findings of previous studies using other modalities, mainly rs-fMRI, and show that EEG could be a relevant technique to explore these disorders,” the researchers wrote.
However, more research is needed to confirm the findings in patients with a larger panel of anxiety disorders, they concluded.
The study was supported by the Michael J. Fox Foundation. The researchers had no financial conflicts to disclose.
Anxiety occurs in approximately 31% of Parkinson’s disease patients, but the underlying mechanisms are not well understood, wrote Nacim Betrouni, MD, of the University of Lille, France, and colleagues. Previous research has shown associations between anxiety severity and increased activity in brain areas of emotion processing, based on MRI and positron emission tomography, but electroencephalography (EEG) has not been widely used, they said.
In a study published in Neurophysiologie Clinique , the researchers compared EEG spectral patterns and functional resting-state networks in Parkinson’s disease patients with and without anxiety disorders. They identified data from 33 PD patients who met criteria for anxiety, and 75 without anxiety. The average age of the patients was 65 years, and the average disease duration was 9.76 years in anxiety patients and 7.83 years in patients without anxiety.
Overall, findings on spectral analysis showed an association between anxiety and changes in the alpha activity in the right frontal cortex, the researchers said. They also found the relative power in the alpha1 frequency band in the right prefrontal cortex was lower in patients with anxiety than without; this finding was significantly associated with avoidance behavior on a subscale of the Parkinson’s Anxiety Scale (PAS_C, P = .035). A trend toward a significant association with episodic anxiety was noted (PAS_B, P = .06), but no significant associations were noted for persistent anxiety or the total scale score.
The imaging also showed an increased connectivity between the insula and the posterior cingulate cortex in several frequency bands in the anxiety patients, the researchers said. “The increased connectivity observed here may be a marker of the maintenance of avoidance behaviors that characterize anxiety in PD,” they noted.
The study findings were limited by several factors including the small and unbalanced proportion of the study population with anxiety, and the consideration of global anxiety only, without distinguishing anxiety subtypes, the researchers noted. Another limitation was the use only of static EEC patterns, without using dynamic patterns, they said.
The study is the first known to use EEG to explore the mechanisms of PD-related anxiety and “the reported results provide new insights, supporting findings of previous studies using other modalities, mainly rs-fMRI, and show that EEG could be a relevant technique to explore these disorders,” the researchers wrote.
However, more research is needed to confirm the findings in patients with a larger panel of anxiety disorders, they concluded.
The study was supported by the Michael J. Fox Foundation. The researchers had no financial conflicts to disclose.
Anxiety occurs in approximately 31% of Parkinson’s disease patients, but the underlying mechanisms are not well understood, wrote Nacim Betrouni, MD, of the University of Lille, France, and colleagues. Previous research has shown associations between anxiety severity and increased activity in brain areas of emotion processing, based on MRI and positron emission tomography, but electroencephalography (EEG) has not been widely used, they said.
In a study published in Neurophysiologie Clinique , the researchers compared EEG spectral patterns and functional resting-state networks in Parkinson’s disease patients with and without anxiety disorders. They identified data from 33 PD patients who met criteria for anxiety, and 75 without anxiety. The average age of the patients was 65 years, and the average disease duration was 9.76 years in anxiety patients and 7.83 years in patients without anxiety.
Overall, findings on spectral analysis showed an association between anxiety and changes in the alpha activity in the right frontal cortex, the researchers said. They also found the relative power in the alpha1 frequency band in the right prefrontal cortex was lower in patients with anxiety than without; this finding was significantly associated with avoidance behavior on a subscale of the Parkinson’s Anxiety Scale (PAS_C, P = .035). A trend toward a significant association with episodic anxiety was noted (PAS_B, P = .06), but no significant associations were noted for persistent anxiety or the total scale score.
The imaging also showed an increased connectivity between the insula and the posterior cingulate cortex in several frequency bands in the anxiety patients, the researchers said. “The increased connectivity observed here may be a marker of the maintenance of avoidance behaviors that characterize anxiety in PD,” they noted.
The study findings were limited by several factors including the small and unbalanced proportion of the study population with anxiety, and the consideration of global anxiety only, without distinguishing anxiety subtypes, the researchers noted. Another limitation was the use only of static EEC patterns, without using dynamic patterns, they said.
The study is the first known to use EEG to explore the mechanisms of PD-related anxiety and “the reported results provide new insights, supporting findings of previous studies using other modalities, mainly rs-fMRI, and show that EEG could be a relevant technique to explore these disorders,” the researchers wrote.
However, more research is needed to confirm the findings in patients with a larger panel of anxiety disorders, they concluded.
The study was supported by the Michael J. Fox Foundation. The researchers had no financial conflicts to disclose.
FROM NEUROPHYSIOLOGIE CLINIQUE
Seizure phobia stands out in epilepsy patients
Anxiety and depression are known to affect quality of life in epilepsy patients, and previous studies have shown that anticipatory anxiety of epileptic seizures (AAS) was present in 53% of patients with focal epilepsy, wrote lead author Aviva Weiss of Psychiatric Hostels affiliated with Kidum Rehabilitation Projects, Jerusalem, and colleagues.
“Although recognized by the epilepsy and the psychiatric communities, seizure phobia as a distinct anxiety disorder among PWE is insufficiently described in the medical literature,” they said.
Seizure phobia has been defined as an anxiety disorder in which patients experience fear related to anticipation of seizures in certain situations.
In a study published in Seizure: European Journal of Epilepsy, the researchers recruited 69 PWE who were treated at an outpatient clinic. Data were collected from interviews, questionnaires, and medical records. The average age of the participants was 36.8 years, 41 were women, and 41 were married.
Overall, 19 individuals (27.5%) were diagnosed with seizure phobia. Compared with PWE without seizure phobia, the seizure phobia patients were significantly more likely to be women (84.2% vs. 44.2%; P = .005) and to have comorbid anxiety disorders (84.2% vs. 34.9%; P = .01). Individuals with seizure phobia also were significantly more likely than those without seizure phobia to have a past major depressive episode (63.2% vs. 20.9%; P = .003), and posttraumatic stress disorder (26.3% vs. 7%; P = .05).
Seizure phobia was significantly associated with comorbid psychogenic nonepileptic seizures (PNES) (36.8% vs. 11.6%; P = .034). PNES have been significantly associated with panic attacks, and “all patients with both panic attacks and comorbid PNES were diagnosed with seizure phobia,” the researchers noted. However, no significant association was found with epilepsy-related variables, they said.
A multivariate logistic regression model to predict seizure phobia showed that anxiety and a past MDE were significant predictors; the odds of seizure phobia were 10.45 times higher if a patient reported any anxiety disorder, and 6.85 times higher if the patient had a history of MDE.
The study findings were limited by several factors, including the use of semistructured interviews to diagnose seizure phobia, which are subject to interviewer bias, and by the small study population with a high proportion of comorbid PNES and epilepsy, the researchers noted. However, the results support seizure phobia as a distinct clinical entity worthy of management with education, psychosocial interventions, and potential medication changes, they said.
“Development of appropriate screening tools and implementation of effective treatment interventions is warranted for individual patients, combined with large-scale population-targeted psychoeducation, aimed to mitigate the risk of developing seizure phobia in PWE,” they concluded.
The study received no outside funding. The researchers had no financial conflicts to disclose.
Anxiety and depression are known to affect quality of life in epilepsy patients, and previous studies have shown that anticipatory anxiety of epileptic seizures (AAS) was present in 53% of patients with focal epilepsy, wrote lead author Aviva Weiss of Psychiatric Hostels affiliated with Kidum Rehabilitation Projects, Jerusalem, and colleagues.
“Although recognized by the epilepsy and the psychiatric communities, seizure phobia as a distinct anxiety disorder among PWE is insufficiently described in the medical literature,” they said.
Seizure phobia has been defined as an anxiety disorder in which patients experience fear related to anticipation of seizures in certain situations.
In a study published in Seizure: European Journal of Epilepsy, the researchers recruited 69 PWE who were treated at an outpatient clinic. Data were collected from interviews, questionnaires, and medical records. The average age of the participants was 36.8 years, 41 were women, and 41 were married.
Overall, 19 individuals (27.5%) were diagnosed with seizure phobia. Compared with PWE without seizure phobia, the seizure phobia patients were significantly more likely to be women (84.2% vs. 44.2%; P = .005) and to have comorbid anxiety disorders (84.2% vs. 34.9%; P = .01). Individuals with seizure phobia also were significantly more likely than those without seizure phobia to have a past major depressive episode (63.2% vs. 20.9%; P = .003), and posttraumatic stress disorder (26.3% vs. 7%; P = .05).
Seizure phobia was significantly associated with comorbid psychogenic nonepileptic seizures (PNES) (36.8% vs. 11.6%; P = .034). PNES have been significantly associated with panic attacks, and “all patients with both panic attacks and comorbid PNES were diagnosed with seizure phobia,” the researchers noted. However, no significant association was found with epilepsy-related variables, they said.
A multivariate logistic regression model to predict seizure phobia showed that anxiety and a past MDE were significant predictors; the odds of seizure phobia were 10.45 times higher if a patient reported any anxiety disorder, and 6.85 times higher if the patient had a history of MDE.
The study findings were limited by several factors, including the use of semistructured interviews to diagnose seizure phobia, which are subject to interviewer bias, and by the small study population with a high proportion of comorbid PNES and epilepsy, the researchers noted. However, the results support seizure phobia as a distinct clinical entity worthy of management with education, psychosocial interventions, and potential medication changes, they said.
“Development of appropriate screening tools and implementation of effective treatment interventions is warranted for individual patients, combined with large-scale population-targeted psychoeducation, aimed to mitigate the risk of developing seizure phobia in PWE,” they concluded.
The study received no outside funding. The researchers had no financial conflicts to disclose.
Anxiety and depression are known to affect quality of life in epilepsy patients, and previous studies have shown that anticipatory anxiety of epileptic seizures (AAS) was present in 53% of patients with focal epilepsy, wrote lead author Aviva Weiss of Psychiatric Hostels affiliated with Kidum Rehabilitation Projects, Jerusalem, and colleagues.
“Although recognized by the epilepsy and the psychiatric communities, seizure phobia as a distinct anxiety disorder among PWE is insufficiently described in the medical literature,” they said.
Seizure phobia has been defined as an anxiety disorder in which patients experience fear related to anticipation of seizures in certain situations.
In a study published in Seizure: European Journal of Epilepsy, the researchers recruited 69 PWE who were treated at an outpatient clinic. Data were collected from interviews, questionnaires, and medical records. The average age of the participants was 36.8 years, 41 were women, and 41 were married.
Overall, 19 individuals (27.5%) were diagnosed with seizure phobia. Compared with PWE without seizure phobia, the seizure phobia patients were significantly more likely to be women (84.2% vs. 44.2%; P = .005) and to have comorbid anxiety disorders (84.2% vs. 34.9%; P = .01). Individuals with seizure phobia also were significantly more likely than those without seizure phobia to have a past major depressive episode (63.2% vs. 20.9%; P = .003), and posttraumatic stress disorder (26.3% vs. 7%; P = .05).
Seizure phobia was significantly associated with comorbid psychogenic nonepileptic seizures (PNES) (36.8% vs. 11.6%; P = .034). PNES have been significantly associated with panic attacks, and “all patients with both panic attacks and comorbid PNES were diagnosed with seizure phobia,” the researchers noted. However, no significant association was found with epilepsy-related variables, they said.
A multivariate logistic regression model to predict seizure phobia showed that anxiety and a past MDE were significant predictors; the odds of seizure phobia were 10.45 times higher if a patient reported any anxiety disorder, and 6.85 times higher if the patient had a history of MDE.
The study findings were limited by several factors, including the use of semistructured interviews to diagnose seizure phobia, which are subject to interviewer bias, and by the small study population with a high proportion of comorbid PNES and epilepsy, the researchers noted. However, the results support seizure phobia as a distinct clinical entity worthy of management with education, psychosocial interventions, and potential medication changes, they said.
“Development of appropriate screening tools and implementation of effective treatment interventions is warranted for individual patients, combined with large-scale population-targeted psychoeducation, aimed to mitigate the risk of developing seizure phobia in PWE,” they concluded.
The study received no outside funding. The researchers had no financial conflicts to disclose.
FROM SEIZURE: EUROPEAN JOURNAL OF EPILEPSY
If you’ve got 3 seconds, then you’ve got time to work out
Goffin’s cockatoo? More like golfin’ cockatoo
Can birds play golf? Of course not; it’s ridiculous. Humans can barely play golf, and we invented the sport. Anyway, moving on to “Brian retraction injury after elective aneurysm clipping.”
Hang on, we’re now hearing that a group of researchers, as part of a large international project comparing children’s innovation and problem-solving skills with those of cockatoos, have in fact taught a group of Goffin’s cockatoos how to play golf. Huh. What an oddly specific project. All right, fine, I guess we’ll go with the golf-playing birds.
Golf may seem very simple at its core. It is, essentially, whacking a ball with a stick. But the Scots who invented the game were undertaking a complex project involving combined usage of multiple tools, and until now, only primates were thought to be capable of utilizing compound tools to play games such as golf.
For this latest research, published in Scientific Reports, our intrepid birds were given a rudimentary form of golf to play (featuring a stick, a ball, and a closed box to get the ball through). Putting the ball through the hole gave the bird a reward. Not every cockatoo was able to hole out, but three did, with each inventing a unique way to manipulate the stick to hit the ball.
As entertaining as it would be to simply teach some birds how to play golf, we do loop back around to medical relevance. While children are perfectly capable of using tools, young children in particular are actually quite bad at using tools to solve novel solutions. Present a 5-year-old with a stick, a ball, and a hole, and that child might not figure out what the cockatoos did. The research really does give insight into the psychology behind the development of complex tools and technology by our ancient ancestors, according to the researchers.
We’re not entirely convinced this isn’t an elaborate ploy to get a bird out onto the PGA Tour. The LOTME staff can see the future headline already: “Painted bunting wins Valspar Championship in epic playoff.”
Work out now, sweat never
Okay, show of hands: Who’s familiar with “Name that tune?” The TV game show got a reboot last year, but some of us are old enough to remember the 1970s version hosted by national treasure Tom Kennedy.
The contestants try to identify a song as quickly as possible, claiming that they “can name that tune in five notes.” Or four notes, or three. Well, welcome to “Name that exercise study.”
Senior author Masatoshi Nakamura, PhD, and associates gathered together 39 students from Niigata (Japan) University of Health and Welfare and had them perform one isometric, concentric, or eccentric bicep curl with a dumbbell for 3 seconds a day at maximum effort for 5 days a week, over 4 weeks. And yes, we did say 3 seconds.
“Lifting the weight sees the bicep in concentric contraction, lowering the weight sees it in eccentric contraction, while holding the weight parallel to the ground is isometric,” they explained in a statement on Eurekalert.
The three exercise groups were compared with a group that did no exercise, and after 4 weeks of rigorous but brief science, the group doing eccentric contractions had the best results, as their overall muscle strength increased by 11.5%. After a total of just 60 seconds of exercise in 4 weeks. That’s 60 seconds. In 4 weeks.
Big news, but maybe we can do better. “Tom, we can do that exercise in 2 seconds.”
And one! And two! Whoa, feel the burn.
Tingling over anxiety
Apparently there are two kinds of people in this world. Those who love ASMR and those who just don’t get it.
ASMR, for those who don’t know, is the autonomous sensory meridian response. An online community has surfaced, with video creators making tapping sounds, whispering, or brushing mannequin hair to elicit “a pleasant tingling sensation originating from the scalp and neck which can spread to the rest of the body” from viewers, Charlotte M. Eid and associates said in PLOS One.
The people who are into these types of videos are more likely to have higher levels of neuroticism than those who aren’t, which gives ASMR the potential to be a nontraditional form of treatment for anxiety and/or neuroticism, they suggested.
The research involved a group of 64 volunteers who watched an ASMR video meant to trigger the tingles and then completed questionnaires to evaluate their levels of neuroticism, trait anxiety, and state anxiety, said Ms. Eid and associates of Northumbria University in Newcastle-upon-Tyne, England.
The people who had a history of producing tingles from ASMR videos in the past had higher levels of anxiety, compared with those who didn’t. Those who responded to triggers also received some benefit from the video in the study, reporting lower levels of neuroticism and anxiety after watching, the investigators found.
Although people who didn’t have a history of tingles didn’t feel any reduction in anxiety after the video, that didn’t stop the people who weren’t familiar with the genre from catching tingles.
So if you find yourself a little high strung or anxious, or if you can’t sleep, consider watching a person pretending to give you a makeover or using fingernails to tap on books for some relaxation. Don’t knock it until you try it!
Living in the past? Not so far-fetched
It’s usually an insult when people tell us to stop living in the past, but the joke’s on them because we really do live in the past. By 15 seconds, to be exact, according to researchers from the University of California, Berkeley.
But wait, did you just read that last sentence 15 seconds ago, even though it feels like real time? Did we just type these words now, or 15 seconds ago?
Think of your brain as a web page you’re constantly refreshing. We are constantly seeing new pictures, images, and colors, and your brain is responsible for keeping everything in chronological order. This new research suggests that our brains show us images from 15 seconds prior. Is your mind blown yet?
“One could say our brain is procrastinating. It’s too much work to constantly update images, so it sticks to the past because the past is a good predictor of the present. We recycle information from the past because it’s faster, more efficient and less work,” senior author David Whitney explained in a statement from the university.
It seems like the 15-second rule helps us not lose our minds by keeping a steady flow of information, but it could be a bit dangerous if someone, such as a surgeon, needs to see things with extreme precision.
And now we are definitely feeling a bit anxious about our upcoming heart/spleen/gallbladder replacement. … Where’s that link to the ASMR video?
Goffin’s cockatoo? More like golfin’ cockatoo
Can birds play golf? Of course not; it’s ridiculous. Humans can barely play golf, and we invented the sport. Anyway, moving on to “Brian retraction injury after elective aneurysm clipping.”
Hang on, we’re now hearing that a group of researchers, as part of a large international project comparing children’s innovation and problem-solving skills with those of cockatoos, have in fact taught a group of Goffin’s cockatoos how to play golf. Huh. What an oddly specific project. All right, fine, I guess we’ll go with the golf-playing birds.
Golf may seem very simple at its core. It is, essentially, whacking a ball with a stick. But the Scots who invented the game were undertaking a complex project involving combined usage of multiple tools, and until now, only primates were thought to be capable of utilizing compound tools to play games such as golf.
For this latest research, published in Scientific Reports, our intrepid birds were given a rudimentary form of golf to play (featuring a stick, a ball, and a closed box to get the ball through). Putting the ball through the hole gave the bird a reward. Not every cockatoo was able to hole out, but three did, with each inventing a unique way to manipulate the stick to hit the ball.
As entertaining as it would be to simply teach some birds how to play golf, we do loop back around to medical relevance. While children are perfectly capable of using tools, young children in particular are actually quite bad at using tools to solve novel solutions. Present a 5-year-old with a stick, a ball, and a hole, and that child might not figure out what the cockatoos did. The research really does give insight into the psychology behind the development of complex tools and technology by our ancient ancestors, according to the researchers.
We’re not entirely convinced this isn’t an elaborate ploy to get a bird out onto the PGA Tour. The LOTME staff can see the future headline already: “Painted bunting wins Valspar Championship in epic playoff.”
Work out now, sweat never
Okay, show of hands: Who’s familiar with “Name that tune?” The TV game show got a reboot last year, but some of us are old enough to remember the 1970s version hosted by national treasure Tom Kennedy.
The contestants try to identify a song as quickly as possible, claiming that they “can name that tune in five notes.” Or four notes, or three. Well, welcome to “Name that exercise study.”
Senior author Masatoshi Nakamura, PhD, and associates gathered together 39 students from Niigata (Japan) University of Health and Welfare and had them perform one isometric, concentric, or eccentric bicep curl with a dumbbell for 3 seconds a day at maximum effort for 5 days a week, over 4 weeks. And yes, we did say 3 seconds.
“Lifting the weight sees the bicep in concentric contraction, lowering the weight sees it in eccentric contraction, while holding the weight parallel to the ground is isometric,” they explained in a statement on Eurekalert.
The three exercise groups were compared with a group that did no exercise, and after 4 weeks of rigorous but brief science, the group doing eccentric contractions had the best results, as their overall muscle strength increased by 11.5%. After a total of just 60 seconds of exercise in 4 weeks. That’s 60 seconds. In 4 weeks.
Big news, but maybe we can do better. “Tom, we can do that exercise in 2 seconds.”
And one! And two! Whoa, feel the burn.
Tingling over anxiety
Apparently there are two kinds of people in this world. Those who love ASMR and those who just don’t get it.
ASMR, for those who don’t know, is the autonomous sensory meridian response. An online community has surfaced, with video creators making tapping sounds, whispering, or brushing mannequin hair to elicit “a pleasant tingling sensation originating from the scalp and neck which can spread to the rest of the body” from viewers, Charlotte M. Eid and associates said in PLOS One.
The people who are into these types of videos are more likely to have higher levels of neuroticism than those who aren’t, which gives ASMR the potential to be a nontraditional form of treatment for anxiety and/or neuroticism, they suggested.
The research involved a group of 64 volunteers who watched an ASMR video meant to trigger the tingles and then completed questionnaires to evaluate their levels of neuroticism, trait anxiety, and state anxiety, said Ms. Eid and associates of Northumbria University in Newcastle-upon-Tyne, England.
The people who had a history of producing tingles from ASMR videos in the past had higher levels of anxiety, compared with those who didn’t. Those who responded to triggers also received some benefit from the video in the study, reporting lower levels of neuroticism and anxiety after watching, the investigators found.
Although people who didn’t have a history of tingles didn’t feel any reduction in anxiety after the video, that didn’t stop the people who weren’t familiar with the genre from catching tingles.
So if you find yourself a little high strung or anxious, or if you can’t sleep, consider watching a person pretending to give you a makeover or using fingernails to tap on books for some relaxation. Don’t knock it until you try it!
Living in the past? Not so far-fetched
It’s usually an insult when people tell us to stop living in the past, but the joke’s on them because we really do live in the past. By 15 seconds, to be exact, according to researchers from the University of California, Berkeley.
But wait, did you just read that last sentence 15 seconds ago, even though it feels like real time? Did we just type these words now, or 15 seconds ago?
Think of your brain as a web page you’re constantly refreshing. We are constantly seeing new pictures, images, and colors, and your brain is responsible for keeping everything in chronological order. This new research suggests that our brains show us images from 15 seconds prior. Is your mind blown yet?
“One could say our brain is procrastinating. It’s too much work to constantly update images, so it sticks to the past because the past is a good predictor of the present. We recycle information from the past because it’s faster, more efficient and less work,” senior author David Whitney explained in a statement from the university.
It seems like the 15-second rule helps us not lose our minds by keeping a steady flow of information, but it could be a bit dangerous if someone, such as a surgeon, needs to see things with extreme precision.
And now we are definitely feeling a bit anxious about our upcoming heart/spleen/gallbladder replacement. … Where’s that link to the ASMR video?
Goffin’s cockatoo? More like golfin’ cockatoo
Can birds play golf? Of course not; it’s ridiculous. Humans can barely play golf, and we invented the sport. Anyway, moving on to “Brian retraction injury after elective aneurysm clipping.”
Hang on, we’re now hearing that a group of researchers, as part of a large international project comparing children’s innovation and problem-solving skills with those of cockatoos, have in fact taught a group of Goffin’s cockatoos how to play golf. Huh. What an oddly specific project. All right, fine, I guess we’ll go with the golf-playing birds.
Golf may seem very simple at its core. It is, essentially, whacking a ball with a stick. But the Scots who invented the game were undertaking a complex project involving combined usage of multiple tools, and until now, only primates were thought to be capable of utilizing compound tools to play games such as golf.
For this latest research, published in Scientific Reports, our intrepid birds were given a rudimentary form of golf to play (featuring a stick, a ball, and a closed box to get the ball through). Putting the ball through the hole gave the bird a reward. Not every cockatoo was able to hole out, but three did, with each inventing a unique way to manipulate the stick to hit the ball.
As entertaining as it would be to simply teach some birds how to play golf, we do loop back around to medical relevance. While children are perfectly capable of using tools, young children in particular are actually quite bad at using tools to solve novel solutions. Present a 5-year-old with a stick, a ball, and a hole, and that child might not figure out what the cockatoos did. The research really does give insight into the psychology behind the development of complex tools and technology by our ancient ancestors, according to the researchers.
We’re not entirely convinced this isn’t an elaborate ploy to get a bird out onto the PGA Tour. The LOTME staff can see the future headline already: “Painted bunting wins Valspar Championship in epic playoff.”
Work out now, sweat never
Okay, show of hands: Who’s familiar with “Name that tune?” The TV game show got a reboot last year, but some of us are old enough to remember the 1970s version hosted by national treasure Tom Kennedy.
The contestants try to identify a song as quickly as possible, claiming that they “can name that tune in five notes.” Or four notes, or three. Well, welcome to “Name that exercise study.”
Senior author Masatoshi Nakamura, PhD, and associates gathered together 39 students from Niigata (Japan) University of Health and Welfare and had them perform one isometric, concentric, or eccentric bicep curl with a dumbbell for 3 seconds a day at maximum effort for 5 days a week, over 4 weeks. And yes, we did say 3 seconds.
“Lifting the weight sees the bicep in concentric contraction, lowering the weight sees it in eccentric contraction, while holding the weight parallel to the ground is isometric,” they explained in a statement on Eurekalert.
The three exercise groups were compared with a group that did no exercise, and after 4 weeks of rigorous but brief science, the group doing eccentric contractions had the best results, as their overall muscle strength increased by 11.5%. After a total of just 60 seconds of exercise in 4 weeks. That’s 60 seconds. In 4 weeks.
Big news, but maybe we can do better. “Tom, we can do that exercise in 2 seconds.”
And one! And two! Whoa, feel the burn.
Tingling over anxiety
Apparently there are two kinds of people in this world. Those who love ASMR and those who just don’t get it.
ASMR, for those who don’t know, is the autonomous sensory meridian response. An online community has surfaced, with video creators making tapping sounds, whispering, or brushing mannequin hair to elicit “a pleasant tingling sensation originating from the scalp and neck which can spread to the rest of the body” from viewers, Charlotte M. Eid and associates said in PLOS One.
The people who are into these types of videos are more likely to have higher levels of neuroticism than those who aren’t, which gives ASMR the potential to be a nontraditional form of treatment for anxiety and/or neuroticism, they suggested.
The research involved a group of 64 volunteers who watched an ASMR video meant to trigger the tingles and then completed questionnaires to evaluate their levels of neuroticism, trait anxiety, and state anxiety, said Ms. Eid and associates of Northumbria University in Newcastle-upon-Tyne, England.
The people who had a history of producing tingles from ASMR videos in the past had higher levels of anxiety, compared with those who didn’t. Those who responded to triggers also received some benefit from the video in the study, reporting lower levels of neuroticism and anxiety after watching, the investigators found.
Although people who didn’t have a history of tingles didn’t feel any reduction in anxiety after the video, that didn’t stop the people who weren’t familiar with the genre from catching tingles.
So if you find yourself a little high strung or anxious, or if you can’t sleep, consider watching a person pretending to give you a makeover or using fingernails to tap on books for some relaxation. Don’t knock it until you try it!
Living in the past? Not so far-fetched
It’s usually an insult when people tell us to stop living in the past, but the joke’s on them because we really do live in the past. By 15 seconds, to be exact, according to researchers from the University of California, Berkeley.
But wait, did you just read that last sentence 15 seconds ago, even though it feels like real time? Did we just type these words now, or 15 seconds ago?
Think of your brain as a web page you’re constantly refreshing. We are constantly seeing new pictures, images, and colors, and your brain is responsible for keeping everything in chronological order. This new research suggests that our brains show us images from 15 seconds prior. Is your mind blown yet?
“One could say our brain is procrastinating. It’s too much work to constantly update images, so it sticks to the past because the past is a good predictor of the present. We recycle information from the past because it’s faster, more efficient and less work,” senior author David Whitney explained in a statement from the university.
It seems like the 15-second rule helps us not lose our minds by keeping a steady flow of information, but it could be a bit dangerous if someone, such as a surgeon, needs to see things with extreme precision.
And now we are definitely feeling a bit anxious about our upcoming heart/spleen/gallbladder replacement. … Where’s that link to the ASMR video?