User login
Is anxiety normal or pathological? Age of onset is key
NEW YORK – Anxiety has become a common descriptor for fears, worries, or concerns, but the diagnosis of anxiety as a pathological affective disorder in children requires attention to the age of onset and the types of triggers, according to a presentation at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
“Normal anxiety involves predictable triggers like a test in school,” explained John T. Walkup, MD, director of the division of child and adolescent psychiatry at Children’s Hospital, Northwestern University, Chicago. In the absence of the trigger, the symptoms abate or resolve.
“Age of onset is an important clue,” said Dr. Walkup, reporting that signs of pathological anxiety typically develop between the ages of 6 and 12 years. In comparison, symptoms of ADHD and autism spectrum disorder typically begin at younger ages, while the onset of affective disorders, such as depression or bipolar disease, typically occur at older ages.
Persistent symptoms may not be limited to children with pathological anxiety. Dr. Walkup said many children contend with “bad schools, troubled homes, and interpersonal violence,” creating “a huge population that meets the criteria for anxiety disorder,” even when the solution is eliminating the triggers rather than seeking an underlying psychiatric disorder.
Conversely, families of children with clear manifestations of anxiety might resist this diagnostic label.
“Parents tell me that their kids are not anxious; they are stressed out,” Dr. Walkup recounted. “These families see the external world as the problem for a kid who actually has internal problems regulating their anxious state.”
Rather than quibbling about terminology, patients should be educated about the very real threat posed by persistent and untreated symptoms, Dr. Walkup suggested. Pathological anxiety, regardless of the term used, is not a phase.
“Some of these kids do recover from childhood onset anxiety, but more often, the condition tracks to adolescence or adulthood,” Dr. Walkup said. . He contended that many adults with personality disorders are experiencing the consequences of distorted thinking and problematic emotional responses that began with childhood anxiety.
“Children with anxiety need to learn to cope. If you medicate them to control the anxiety, it does not necessarily mean that they will learn how to live anxiety free,” Dr. Walkup said, reiterating that pathological anxiety often persists indefinitely even after effective therapy diminishes the symptom burden. To improve a supportive family environment for an anxious child, he encouraged educating parents about the condition.
“One of the many books published on childhood anxiety may be all they need,” said Dr. Walkup, listing several examples, such as “You and Your Anxious Child” (New York: Avery, 2013) coauthored by Anne Marie Albano, PhD, a professor of child psychiatry at Columbia University in New York.
As anxiety is such a ubiquitous human experience, many parents trivialize the pathological variety, Dr. Walkup said. Educating patients about the immediate and long-term risks of pathological anxiety is important. The associated symptoms are not a phase, as some parents are likely to contend. He believes that early diagnosis and effective management can change the trajectory of a lifelong threat.
Dr. Walkup reported no potential conflicts of interest.
NEW YORK – Anxiety has become a common descriptor for fears, worries, or concerns, but the diagnosis of anxiety as a pathological affective disorder in children requires attention to the age of onset and the types of triggers, according to a presentation at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
“Normal anxiety involves predictable triggers like a test in school,” explained John T. Walkup, MD, director of the division of child and adolescent psychiatry at Children’s Hospital, Northwestern University, Chicago. In the absence of the trigger, the symptoms abate or resolve.
“Age of onset is an important clue,” said Dr. Walkup, reporting that signs of pathological anxiety typically develop between the ages of 6 and 12 years. In comparison, symptoms of ADHD and autism spectrum disorder typically begin at younger ages, while the onset of affective disorders, such as depression or bipolar disease, typically occur at older ages.
Persistent symptoms may not be limited to children with pathological anxiety. Dr. Walkup said many children contend with “bad schools, troubled homes, and interpersonal violence,” creating “a huge population that meets the criteria for anxiety disorder,” even when the solution is eliminating the triggers rather than seeking an underlying psychiatric disorder.
Conversely, families of children with clear manifestations of anxiety might resist this diagnostic label.
“Parents tell me that their kids are not anxious; they are stressed out,” Dr. Walkup recounted. “These families see the external world as the problem for a kid who actually has internal problems regulating their anxious state.”
Rather than quibbling about terminology, patients should be educated about the very real threat posed by persistent and untreated symptoms, Dr. Walkup suggested. Pathological anxiety, regardless of the term used, is not a phase.
“Some of these kids do recover from childhood onset anxiety, but more often, the condition tracks to adolescence or adulthood,” Dr. Walkup said. . He contended that many adults with personality disorders are experiencing the consequences of distorted thinking and problematic emotional responses that began with childhood anxiety.
“Children with anxiety need to learn to cope. If you medicate them to control the anxiety, it does not necessarily mean that they will learn how to live anxiety free,” Dr. Walkup said, reiterating that pathological anxiety often persists indefinitely even after effective therapy diminishes the symptom burden. To improve a supportive family environment for an anxious child, he encouraged educating parents about the condition.
“One of the many books published on childhood anxiety may be all they need,” said Dr. Walkup, listing several examples, such as “You and Your Anxious Child” (New York: Avery, 2013) coauthored by Anne Marie Albano, PhD, a professor of child psychiatry at Columbia University in New York.
As anxiety is such a ubiquitous human experience, many parents trivialize the pathological variety, Dr. Walkup said. Educating patients about the immediate and long-term risks of pathological anxiety is important. The associated symptoms are not a phase, as some parents are likely to contend. He believes that early diagnosis and effective management can change the trajectory of a lifelong threat.
Dr. Walkup reported no potential conflicts of interest.
NEW YORK – Anxiety has become a common descriptor for fears, worries, or concerns, but the diagnosis of anxiety as a pathological affective disorder in children requires attention to the age of onset and the types of triggers, according to a presentation at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
“Normal anxiety involves predictable triggers like a test in school,” explained John T. Walkup, MD, director of the division of child and adolescent psychiatry at Children’s Hospital, Northwestern University, Chicago. In the absence of the trigger, the symptoms abate or resolve.
“Age of onset is an important clue,” said Dr. Walkup, reporting that signs of pathological anxiety typically develop between the ages of 6 and 12 years. In comparison, symptoms of ADHD and autism spectrum disorder typically begin at younger ages, while the onset of affective disorders, such as depression or bipolar disease, typically occur at older ages.
Persistent symptoms may not be limited to children with pathological anxiety. Dr. Walkup said many children contend with “bad schools, troubled homes, and interpersonal violence,” creating “a huge population that meets the criteria for anxiety disorder,” even when the solution is eliminating the triggers rather than seeking an underlying psychiatric disorder.
Conversely, families of children with clear manifestations of anxiety might resist this diagnostic label.
“Parents tell me that their kids are not anxious; they are stressed out,” Dr. Walkup recounted. “These families see the external world as the problem for a kid who actually has internal problems regulating their anxious state.”
Rather than quibbling about terminology, patients should be educated about the very real threat posed by persistent and untreated symptoms, Dr. Walkup suggested. Pathological anxiety, regardless of the term used, is not a phase.
“Some of these kids do recover from childhood onset anxiety, but more often, the condition tracks to adolescence or adulthood,” Dr. Walkup said. . He contended that many adults with personality disorders are experiencing the consequences of distorted thinking and problematic emotional responses that began with childhood anxiety.
“Children with anxiety need to learn to cope. If you medicate them to control the anxiety, it does not necessarily mean that they will learn how to live anxiety free,” Dr. Walkup said, reiterating that pathological anxiety often persists indefinitely even after effective therapy diminishes the symptom burden. To improve a supportive family environment for an anxious child, he encouraged educating parents about the condition.
“One of the many books published on childhood anxiety may be all they need,” said Dr. Walkup, listing several examples, such as “You and Your Anxious Child” (New York: Avery, 2013) coauthored by Anne Marie Albano, PhD, a professor of child psychiatry at Columbia University in New York.
As anxiety is such a ubiquitous human experience, many parents trivialize the pathological variety, Dr. Walkup said. Educating patients about the immediate and long-term risks of pathological anxiety is important. The associated symptoms are not a phase, as some parents are likely to contend. He believes that early diagnosis and effective management can change the trajectory of a lifelong threat.
Dr. Walkup reported no potential conflicts of interest.
EXPERT ANALYSIS FROM THE PSYCHOPHARMACOLOGY UPDATE INSTITUTE
Latest PANS trials suggest cause may be treatable
NEW YORK – New controlled trials in the treatment of pediatric acute neuropsychiatric syndrome (PANS) support the hypothesis that the cause may, in fact, be treatable, an expert said at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
PANS and pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) are controversial diagnoses. But ongoing research has expanded the body of literature describing symptoms and evaluating treatments, according to an overview from Barbara J. Coffey, MD, division chief in child and adolescent psychiatry at the University of Miami.
PANS and PANDAS, which are clinical diagnoses of exclusion, are characterized by an abrupt onset of one or more neuropsychiatric symptoms in children that can include signs of obsessive-compulsive disorder (OCD), tics, anxiety, irritability, and behavioral changes. Despite more than 15 years of clinical and experimental studies, almost all aspects of PANS and PANDAS remain controversial, Dr. Coffey said.
“Many pediatricians I work with do not want to see these kids, because they really do not know what to do,” she reported.
This prevailing conception has led to treatment trials with antibiotics for the underlying infection and, most recently, with intravenous immunoglobulins (IVIG) to prevent cross-reactive antibodies induced by infection. Dr. Coffey, reviewing several recently published studies, noted that there have been signals of activity suggesting “there may be something there.” However, she cautioned that the data are inconclusive.
Of recent studies, a trial with azithromycin in children with PANS generated somewhat positive findings (J Child Adolesc Psychopharmacol. 2017;27[7]:640-51). In this study, 31 children aged 4-14 years were randomized to receive azithromycin or placebo for 4 weeks. They were evaluated via the Children’s Yale–Brown Obsessive Compulsive Scale (CY-BOCS) and the OCD Clinical Global Impression Severity (CGI-S OCD) scale.
The study associated azithromycin with a significant reduction in symptoms as measured with CGI-S OCD (41.2% vs. 7.1%; P = .045), but no difference was found in response as measured with the CY-BOCS, which Dr. Coffey described as the more conservative measure. Even when measured with the CGI-S OCD scale, symptom improvements were modest. But the authors concluded that azithromycin “may be helpful” for the control of neuropsychiatric symptoms.
In a trial with IVIG, 35 children with PANDAS were randomized to IVIG or placebo (J Am Acad Child Adolesc Psychiatry. 2016;55[10]:860-7). The primary outcome was at least a 30% reduction in CY-BOCS at 12 weeks. Nonresponders at 12 weeks were permitted 12 more weeks of treatment with open-label IVIG.
Twice as many patients receiving IVIG, compared with those on placebo, reached the primary outcome (24% vs. 12%), but the study was small and the difference did not reach significance. However, the authors reported that the mean CY-BOCS improvement from baseline on IVIG, which was well tolerated, was 55% at week 12 and 62% at week 24. The authors suggested that larger trials are warranted.
“One critique of this study is that all of the patients were placed on prophylactic antibiotics, which may have attenuated the response,” Dr. Coffey said. In outlining these results, she emphasized: “This is not something I am recommending. I just want to acquaint you with what is going on out there.”
None of the most recent trials provide conclusive support for therapy targeted at infection or an autoimmune process in PANS or PANDAS, but Dr. Coffey indicated that . One of the most recent sets of data come from a recently published Scandinavian cohort study with 17 years of follow-up (JAMA Psychiatry. 2017;74[7]:740-6). That study associated pediatric infections of any kind, not just streptococcal infections, with an elevated risk of mental disorders – particularly OCD and tics.
Overall, the evidence base is growing to suggest “antibiotics and immune therapy may be beneficial, but the jury is not in yet for which patients, how much, and how long,” Dr. Coffey said. She is aware of clinicians who are now using antibiotics empirically to control neuropsychiatric symptoms in PANDAS but cautioned that more investigation is needed.
Dr. Coffey reports financial relationships with Genco Sciences, Neurocrine Biosciences, Shire, and Teva/Nuvelution.
NEW YORK – New controlled trials in the treatment of pediatric acute neuropsychiatric syndrome (PANS) support the hypothesis that the cause may, in fact, be treatable, an expert said at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
PANS and pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) are controversial diagnoses. But ongoing research has expanded the body of literature describing symptoms and evaluating treatments, according to an overview from Barbara J. Coffey, MD, division chief in child and adolescent psychiatry at the University of Miami.
PANS and PANDAS, which are clinical diagnoses of exclusion, are characterized by an abrupt onset of one or more neuropsychiatric symptoms in children that can include signs of obsessive-compulsive disorder (OCD), tics, anxiety, irritability, and behavioral changes. Despite more than 15 years of clinical and experimental studies, almost all aspects of PANS and PANDAS remain controversial, Dr. Coffey said.
“Many pediatricians I work with do not want to see these kids, because they really do not know what to do,” she reported.
This prevailing conception has led to treatment trials with antibiotics for the underlying infection and, most recently, with intravenous immunoglobulins (IVIG) to prevent cross-reactive antibodies induced by infection. Dr. Coffey, reviewing several recently published studies, noted that there have been signals of activity suggesting “there may be something there.” However, she cautioned that the data are inconclusive.
Of recent studies, a trial with azithromycin in children with PANS generated somewhat positive findings (J Child Adolesc Psychopharmacol. 2017;27[7]:640-51). In this study, 31 children aged 4-14 years were randomized to receive azithromycin or placebo for 4 weeks. They were evaluated via the Children’s Yale–Brown Obsessive Compulsive Scale (CY-BOCS) and the OCD Clinical Global Impression Severity (CGI-S OCD) scale.
The study associated azithromycin with a significant reduction in symptoms as measured with CGI-S OCD (41.2% vs. 7.1%; P = .045), but no difference was found in response as measured with the CY-BOCS, which Dr. Coffey described as the more conservative measure. Even when measured with the CGI-S OCD scale, symptom improvements were modest. But the authors concluded that azithromycin “may be helpful” for the control of neuropsychiatric symptoms.
In a trial with IVIG, 35 children with PANDAS were randomized to IVIG or placebo (J Am Acad Child Adolesc Psychiatry. 2016;55[10]:860-7). The primary outcome was at least a 30% reduction in CY-BOCS at 12 weeks. Nonresponders at 12 weeks were permitted 12 more weeks of treatment with open-label IVIG.
Twice as many patients receiving IVIG, compared with those on placebo, reached the primary outcome (24% vs. 12%), but the study was small and the difference did not reach significance. However, the authors reported that the mean CY-BOCS improvement from baseline on IVIG, which was well tolerated, was 55% at week 12 and 62% at week 24. The authors suggested that larger trials are warranted.
“One critique of this study is that all of the patients were placed on prophylactic antibiotics, which may have attenuated the response,” Dr. Coffey said. In outlining these results, she emphasized: “This is not something I am recommending. I just want to acquaint you with what is going on out there.”
None of the most recent trials provide conclusive support for therapy targeted at infection or an autoimmune process in PANS or PANDAS, but Dr. Coffey indicated that . One of the most recent sets of data come from a recently published Scandinavian cohort study with 17 years of follow-up (JAMA Psychiatry. 2017;74[7]:740-6). That study associated pediatric infections of any kind, not just streptococcal infections, with an elevated risk of mental disorders – particularly OCD and tics.
Overall, the evidence base is growing to suggest “antibiotics and immune therapy may be beneficial, but the jury is not in yet for which patients, how much, and how long,” Dr. Coffey said. She is aware of clinicians who are now using antibiotics empirically to control neuropsychiatric symptoms in PANDAS but cautioned that more investigation is needed.
Dr. Coffey reports financial relationships with Genco Sciences, Neurocrine Biosciences, Shire, and Teva/Nuvelution.
NEW YORK – New controlled trials in the treatment of pediatric acute neuropsychiatric syndrome (PANS) support the hypothesis that the cause may, in fact, be treatable, an expert said at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
PANS and pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) are controversial diagnoses. But ongoing research has expanded the body of literature describing symptoms and evaluating treatments, according to an overview from Barbara J. Coffey, MD, division chief in child and adolescent psychiatry at the University of Miami.
PANS and PANDAS, which are clinical diagnoses of exclusion, are characterized by an abrupt onset of one or more neuropsychiatric symptoms in children that can include signs of obsessive-compulsive disorder (OCD), tics, anxiety, irritability, and behavioral changes. Despite more than 15 years of clinical and experimental studies, almost all aspects of PANS and PANDAS remain controversial, Dr. Coffey said.
“Many pediatricians I work with do not want to see these kids, because they really do not know what to do,” she reported.
This prevailing conception has led to treatment trials with antibiotics for the underlying infection and, most recently, with intravenous immunoglobulins (IVIG) to prevent cross-reactive antibodies induced by infection. Dr. Coffey, reviewing several recently published studies, noted that there have been signals of activity suggesting “there may be something there.” However, she cautioned that the data are inconclusive.
Of recent studies, a trial with azithromycin in children with PANS generated somewhat positive findings (J Child Adolesc Psychopharmacol. 2017;27[7]:640-51). In this study, 31 children aged 4-14 years were randomized to receive azithromycin or placebo for 4 weeks. They were evaluated via the Children’s Yale–Brown Obsessive Compulsive Scale (CY-BOCS) and the OCD Clinical Global Impression Severity (CGI-S OCD) scale.
The study associated azithromycin with a significant reduction in symptoms as measured with CGI-S OCD (41.2% vs. 7.1%; P = .045), but no difference was found in response as measured with the CY-BOCS, which Dr. Coffey described as the more conservative measure. Even when measured with the CGI-S OCD scale, symptom improvements were modest. But the authors concluded that azithromycin “may be helpful” for the control of neuropsychiatric symptoms.
In a trial with IVIG, 35 children with PANDAS were randomized to IVIG or placebo (J Am Acad Child Adolesc Psychiatry. 2016;55[10]:860-7). The primary outcome was at least a 30% reduction in CY-BOCS at 12 weeks. Nonresponders at 12 weeks were permitted 12 more weeks of treatment with open-label IVIG.
Twice as many patients receiving IVIG, compared with those on placebo, reached the primary outcome (24% vs. 12%), but the study was small and the difference did not reach significance. However, the authors reported that the mean CY-BOCS improvement from baseline on IVIG, which was well tolerated, was 55% at week 12 and 62% at week 24. The authors suggested that larger trials are warranted.
“One critique of this study is that all of the patients were placed on prophylactic antibiotics, which may have attenuated the response,” Dr. Coffey said. In outlining these results, she emphasized: “This is not something I am recommending. I just want to acquaint you with what is going on out there.”
None of the most recent trials provide conclusive support for therapy targeted at infection or an autoimmune process in PANS or PANDAS, but Dr. Coffey indicated that . One of the most recent sets of data come from a recently published Scandinavian cohort study with 17 years of follow-up (JAMA Psychiatry. 2017;74[7]:740-6). That study associated pediatric infections of any kind, not just streptococcal infections, with an elevated risk of mental disorders – particularly OCD and tics.
Overall, the evidence base is growing to suggest “antibiotics and immune therapy may be beneficial, but the jury is not in yet for which patients, how much, and how long,” Dr. Coffey said. She is aware of clinicians who are now using antibiotics empirically to control neuropsychiatric symptoms in PANDAS but cautioned that more investigation is needed.
Dr. Coffey reports financial relationships with Genco Sciences, Neurocrine Biosciences, Shire, and Teva/Nuvelution.
REPORTING FROM THE PSYCHOPHARMACOLOGY UPDATE INSTITUTE
Psychiatric pharmacogenomics not ‘ready for prime time’
NEW YORK – Pharmacogenomics testing for guiding drug choices in psychiatric disease is “not completely ready for prime time,” based on a critical review of published guidelines and expert opinions on the use of those tests, according to Erika L. Nurmi, MD, PhD.
It is important to understand the limitations of such tests because many patients or family members are asking clinicians to be guided by the results of tests they have ordered on their own, said Dr. Nurmi, a researcher and clinician at the UCLA Semel Institute for Neuroscience and Human Behavior, Los Angeles.
Published guidelines and expert opinions based on objective data support these conclusions, she said. Dr. Nurmi suggested that .
“Basically, what it says is if you do not have the testing in hand, don’t order it. If you have the testing in hand when a poor metabolizer of CYP2D6 or CYP2C19 has been identified, switch to a med that is not metabolized by those enzymes. That’s it,” Dr. Nurmi reported at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
The guidelines from the Clinical Pharmacogenetics Implementation Consortium (CPIC) were only modestly more detailed. Only a moderate level of evidence supported most recommendations, she said, and these were labeled optional. The exception regarded treating ultrafast metabolizers of CYP2D6 who are taking paroxetine: In these, the use of a drug metabolized by a different enzyme was strongly recommended.
Similar recommendations in the CPIC guidelines were made for fluoxetine, fluvoxamine, and sertraline. In patients on citalopram or escitalopram, ultrafast metabolizers of CYP2C19 are considered candidates for a non-CYP2C19 drug. If they are poor metabolizers, the CPIC guidelines recommended a non-CYP2C19 drug or reducing the starting dose by 50%.
However, in all of these cases, pharmacogenomics testing is best reserved for patients who have had an inadequate response to therapy or, in the case of poor metabolizers, have had unacceptable adverse events.
Of the limitations Dr. Nurmi outlined for pharmacogenomics testing, one of the most important is that these tests typically focus on a single genetic variant. According to Dr. Nurmi, the problem with a single variant is that “our bodies are more complex.” She said she believes that genetic information for drug selection will not be useful until testing is able to synthesize information from multiple genetic variants and place this in context with confounders such as age and exposure to other substances, such as hormones, caffeine, or grapefruit juice.
This complexity is likely to be mastered eventually, Dr. Nurmi said, but patients now have unrealistic expectations. For their part, clinicians need to develop an understanding of the limitations of these tests in order to provide informed counsel. As pharmacogenomics testing is being marketed directly to consumers with inflated claims about its value, clinicians often must defend their decision to use or not use this information.
“Commercially available products combine variants of widely discrepant validity using proprietary, undisclosed algorithms into sweeping treatment recommendations,” said Dr. Nurmi, who noted that she has found some of her own data misappropriated to make claims. Often, the companies that develop the tests have conducted the validation studies without any replication by independent investigators. She noted that many studies have been declared positive on the basis of secondary outcomes after the primary outcome was negative.
“There are very few positive prospective, randomized, double-blind trials,” Dr. Nurmi said. Even when such trials have been conducted, they typically are not designed to show a clinically meaningful outcome.
By attempting to look at a single or a limited number of variants in which to guide choice of medication in psychiatric disease, pharmacogenomics testing is being “vastly oversimplified,” Dr. Nurmi said. Although she said she believes this field is enormously promising and that medical records for each patient eventually will contain the genome sequence, she emphasized that, at this time, pharmacogenomics testing has a very limited role to play for the management of psychiatric diseases.
Dr. Nurmi reported she had no financial relationships relevant to this topic.
NEW YORK – Pharmacogenomics testing for guiding drug choices in psychiatric disease is “not completely ready for prime time,” based on a critical review of published guidelines and expert opinions on the use of those tests, according to Erika L. Nurmi, MD, PhD.
It is important to understand the limitations of such tests because many patients or family members are asking clinicians to be guided by the results of tests they have ordered on their own, said Dr. Nurmi, a researcher and clinician at the UCLA Semel Institute for Neuroscience and Human Behavior, Los Angeles.
Published guidelines and expert opinions based on objective data support these conclusions, she said. Dr. Nurmi suggested that .
“Basically, what it says is if you do not have the testing in hand, don’t order it. If you have the testing in hand when a poor metabolizer of CYP2D6 or CYP2C19 has been identified, switch to a med that is not metabolized by those enzymes. That’s it,” Dr. Nurmi reported at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
The guidelines from the Clinical Pharmacogenetics Implementation Consortium (CPIC) were only modestly more detailed. Only a moderate level of evidence supported most recommendations, she said, and these were labeled optional. The exception regarded treating ultrafast metabolizers of CYP2D6 who are taking paroxetine: In these, the use of a drug metabolized by a different enzyme was strongly recommended.
Similar recommendations in the CPIC guidelines were made for fluoxetine, fluvoxamine, and sertraline. In patients on citalopram or escitalopram, ultrafast metabolizers of CYP2C19 are considered candidates for a non-CYP2C19 drug. If they are poor metabolizers, the CPIC guidelines recommended a non-CYP2C19 drug or reducing the starting dose by 50%.
However, in all of these cases, pharmacogenomics testing is best reserved for patients who have had an inadequate response to therapy or, in the case of poor metabolizers, have had unacceptable adverse events.
Of the limitations Dr. Nurmi outlined for pharmacogenomics testing, one of the most important is that these tests typically focus on a single genetic variant. According to Dr. Nurmi, the problem with a single variant is that “our bodies are more complex.” She said she believes that genetic information for drug selection will not be useful until testing is able to synthesize information from multiple genetic variants and place this in context with confounders such as age and exposure to other substances, such as hormones, caffeine, or grapefruit juice.
This complexity is likely to be mastered eventually, Dr. Nurmi said, but patients now have unrealistic expectations. For their part, clinicians need to develop an understanding of the limitations of these tests in order to provide informed counsel. As pharmacogenomics testing is being marketed directly to consumers with inflated claims about its value, clinicians often must defend their decision to use or not use this information.
“Commercially available products combine variants of widely discrepant validity using proprietary, undisclosed algorithms into sweeping treatment recommendations,” said Dr. Nurmi, who noted that she has found some of her own data misappropriated to make claims. Often, the companies that develop the tests have conducted the validation studies without any replication by independent investigators. She noted that many studies have been declared positive on the basis of secondary outcomes after the primary outcome was negative.
“There are very few positive prospective, randomized, double-blind trials,” Dr. Nurmi said. Even when such trials have been conducted, they typically are not designed to show a clinically meaningful outcome.
By attempting to look at a single or a limited number of variants in which to guide choice of medication in psychiatric disease, pharmacogenomics testing is being “vastly oversimplified,” Dr. Nurmi said. Although she said she believes this field is enormously promising and that medical records for each patient eventually will contain the genome sequence, she emphasized that, at this time, pharmacogenomics testing has a very limited role to play for the management of psychiatric diseases.
Dr. Nurmi reported she had no financial relationships relevant to this topic.
NEW YORK – Pharmacogenomics testing for guiding drug choices in psychiatric disease is “not completely ready for prime time,” based on a critical review of published guidelines and expert opinions on the use of those tests, according to Erika L. Nurmi, MD, PhD.
It is important to understand the limitations of such tests because many patients or family members are asking clinicians to be guided by the results of tests they have ordered on their own, said Dr. Nurmi, a researcher and clinician at the UCLA Semel Institute for Neuroscience and Human Behavior, Los Angeles.
Published guidelines and expert opinions based on objective data support these conclusions, she said. Dr. Nurmi suggested that .
“Basically, what it says is if you do not have the testing in hand, don’t order it. If you have the testing in hand when a poor metabolizer of CYP2D6 or CYP2C19 has been identified, switch to a med that is not metabolized by those enzymes. That’s it,” Dr. Nurmi reported at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
The guidelines from the Clinical Pharmacogenetics Implementation Consortium (CPIC) were only modestly more detailed. Only a moderate level of evidence supported most recommendations, she said, and these were labeled optional. The exception regarded treating ultrafast metabolizers of CYP2D6 who are taking paroxetine: In these, the use of a drug metabolized by a different enzyme was strongly recommended.
Similar recommendations in the CPIC guidelines were made for fluoxetine, fluvoxamine, and sertraline. In patients on citalopram or escitalopram, ultrafast metabolizers of CYP2C19 are considered candidates for a non-CYP2C19 drug. If they are poor metabolizers, the CPIC guidelines recommended a non-CYP2C19 drug or reducing the starting dose by 50%.
However, in all of these cases, pharmacogenomics testing is best reserved for patients who have had an inadequate response to therapy or, in the case of poor metabolizers, have had unacceptable adverse events.
Of the limitations Dr. Nurmi outlined for pharmacogenomics testing, one of the most important is that these tests typically focus on a single genetic variant. According to Dr. Nurmi, the problem with a single variant is that “our bodies are more complex.” She said she believes that genetic information for drug selection will not be useful until testing is able to synthesize information from multiple genetic variants and place this in context with confounders such as age and exposure to other substances, such as hormones, caffeine, or grapefruit juice.
This complexity is likely to be mastered eventually, Dr. Nurmi said, but patients now have unrealistic expectations. For their part, clinicians need to develop an understanding of the limitations of these tests in order to provide informed counsel. As pharmacogenomics testing is being marketed directly to consumers with inflated claims about its value, clinicians often must defend their decision to use or not use this information.
“Commercially available products combine variants of widely discrepant validity using proprietary, undisclosed algorithms into sweeping treatment recommendations,” said Dr. Nurmi, who noted that she has found some of her own data misappropriated to make claims. Often, the companies that develop the tests have conducted the validation studies without any replication by independent investigators. She noted that many studies have been declared positive on the basis of secondary outcomes after the primary outcome was negative.
“There are very few positive prospective, randomized, double-blind trials,” Dr. Nurmi said. Even when such trials have been conducted, they typically are not designed to show a clinically meaningful outcome.
By attempting to look at a single or a limited number of variants in which to guide choice of medication in psychiatric disease, pharmacogenomics testing is being “vastly oversimplified,” Dr. Nurmi said. Although she said she believes this field is enormously promising and that medical records for each patient eventually will contain the genome sequence, she emphasized that, at this time, pharmacogenomics testing has a very limited role to play for the management of psychiatric diseases.
Dr. Nurmi reported she had no financial relationships relevant to this topic.
EXPERT ANALYSIS FROM THE PSYCHOPHARMACOLOGY UPDATE INSTITUTE
Abrupt behavior changes in autism? ID medical triggers first
NEW YORK – When treating children with autism spectrum disorder who develop an abrupt increase in symptoms, it is best to identify and treat the precipitating event or events – rather than intensify ASD drug therapy, an expert said.
“These acute behavior changes are almost always triggered by something,” Jeremy Veenstra-VanderWeele, MD, reported at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry. Triggers are not always identifiable, but Dr. Veenstra-VanderWeele said solutions may prove simple when they are.
In ASD patients with an acute change in behavior, caregivers typically think first of environmental triggers, including adverse interactions with peers or siblings. But Dr. Veenstra-VanderWeele emphasized that medical problems should be considered first. This makes sense because of the importance of quickly resolving health problems. However, pain and discomfort, particularly in those with difficulty verbalizing these complaints, can be overlooked.
Moreover, even highly verbal ASD patients may not volunteer physical complaints without prompting, Dr. Veenstra-VanderWeele said. Among the health issues in children, constipation and other gastrointestinal issues are “incredibly common” in ASD patients. Dr. Veenstra-VanderWeele looks for clues, such as body posturing suggesting abdominal pain or flatulence, when a history is ambiguous.
“I will order an abdominal flat plate when I hear enough symptoms to make me wonder when the family is not sure,” Dr. Veenstra-VanderWeele reported. “Almost always it comes back with evidence of constipation. We treat it, and they are less irritable like all of us would be.”
All common conditions in a pediatric population, including ear infections, dental caries, and food allergies, should be considered, according to Dr. Veenstra-VanderWeele, who recommended a practice pathway for evaluating triggers in children with ASD (Pediatrics. 2016 Feb;137 Suppl 2:S136-48). A coauthor on this pathway, Dr. Veenstra-VanderWeele emphasized the importance of pursuing a systematic approach to medical issues before considering other triggers, such as psychosocial stressors.
In adolescents, headache caused by migraine and late-onset epilepsy, often in the form of complex partial seizures, should be added to the list of potential triggers for irritation or aggression, Dr. Veenstra-VanderWeele said. Epilepsy often precedes the diagnosis of ASD in young children, and Dr. Veenstra-VanderWeele noted that a second peak incidence sometimes occurs in late adolescence.
After ruling out medical problems, helping patients recognize and verbalize stressors can serve as both diagnosis and treatment. In ASD patients with limited verbal skills who are suffering from stress, “aggression is one form of communication,” Dr. Veenstra-VanderWeele said.
However, Dr. Veenstra-VanderWeele cautioned that, even if a trigger is successfully addressed, inadvertently reinforced aggression might persist.
“Aggression can be rewarded sometimes by removing the patient from the classroom, sometimes by giving in, and then that becomes a maladaptive reinforcement pattern that needs to be broken,” Dr. Veenstra-VanderWeele said. “Even if you are treating their irritability and agitation with, say, risperidone, you still need to break the maladaptive reinforcement pattern or they will keep engaging in what has become instrumental aggression.”
Dr. Veenstra-VanderWeele reported financial relationships with Hoffmann-La Roche, Novartis, Seaside Therapeutics, and SynapDx.
NEW YORK – When treating children with autism spectrum disorder who develop an abrupt increase in symptoms, it is best to identify and treat the precipitating event or events – rather than intensify ASD drug therapy, an expert said.
“These acute behavior changes are almost always triggered by something,” Jeremy Veenstra-VanderWeele, MD, reported at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry. Triggers are not always identifiable, but Dr. Veenstra-VanderWeele said solutions may prove simple when they are.
In ASD patients with an acute change in behavior, caregivers typically think first of environmental triggers, including adverse interactions with peers or siblings. But Dr. Veenstra-VanderWeele emphasized that medical problems should be considered first. This makes sense because of the importance of quickly resolving health problems. However, pain and discomfort, particularly in those with difficulty verbalizing these complaints, can be overlooked.
Moreover, even highly verbal ASD patients may not volunteer physical complaints without prompting, Dr. Veenstra-VanderWeele said. Among the health issues in children, constipation and other gastrointestinal issues are “incredibly common” in ASD patients. Dr. Veenstra-VanderWeele looks for clues, such as body posturing suggesting abdominal pain or flatulence, when a history is ambiguous.
“I will order an abdominal flat plate when I hear enough symptoms to make me wonder when the family is not sure,” Dr. Veenstra-VanderWeele reported. “Almost always it comes back with evidence of constipation. We treat it, and they are less irritable like all of us would be.”
All common conditions in a pediatric population, including ear infections, dental caries, and food allergies, should be considered, according to Dr. Veenstra-VanderWeele, who recommended a practice pathway for evaluating triggers in children with ASD (Pediatrics. 2016 Feb;137 Suppl 2:S136-48). A coauthor on this pathway, Dr. Veenstra-VanderWeele emphasized the importance of pursuing a systematic approach to medical issues before considering other triggers, such as psychosocial stressors.
In adolescents, headache caused by migraine and late-onset epilepsy, often in the form of complex partial seizures, should be added to the list of potential triggers for irritation or aggression, Dr. Veenstra-VanderWeele said. Epilepsy often precedes the diagnosis of ASD in young children, and Dr. Veenstra-VanderWeele noted that a second peak incidence sometimes occurs in late adolescence.
After ruling out medical problems, helping patients recognize and verbalize stressors can serve as both diagnosis and treatment. In ASD patients with limited verbal skills who are suffering from stress, “aggression is one form of communication,” Dr. Veenstra-VanderWeele said.
However, Dr. Veenstra-VanderWeele cautioned that, even if a trigger is successfully addressed, inadvertently reinforced aggression might persist.
“Aggression can be rewarded sometimes by removing the patient from the classroom, sometimes by giving in, and then that becomes a maladaptive reinforcement pattern that needs to be broken,” Dr. Veenstra-VanderWeele said. “Even if you are treating their irritability and agitation with, say, risperidone, you still need to break the maladaptive reinforcement pattern or they will keep engaging in what has become instrumental aggression.”
Dr. Veenstra-VanderWeele reported financial relationships with Hoffmann-La Roche, Novartis, Seaside Therapeutics, and SynapDx.
NEW YORK – When treating children with autism spectrum disorder who develop an abrupt increase in symptoms, it is best to identify and treat the precipitating event or events – rather than intensify ASD drug therapy, an expert said.
“These acute behavior changes are almost always triggered by something,” Jeremy Veenstra-VanderWeele, MD, reported at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry. Triggers are not always identifiable, but Dr. Veenstra-VanderWeele said solutions may prove simple when they are.
In ASD patients with an acute change in behavior, caregivers typically think first of environmental triggers, including adverse interactions with peers or siblings. But Dr. Veenstra-VanderWeele emphasized that medical problems should be considered first. This makes sense because of the importance of quickly resolving health problems. However, pain and discomfort, particularly in those with difficulty verbalizing these complaints, can be overlooked.
Moreover, even highly verbal ASD patients may not volunteer physical complaints without prompting, Dr. Veenstra-VanderWeele said. Among the health issues in children, constipation and other gastrointestinal issues are “incredibly common” in ASD patients. Dr. Veenstra-VanderWeele looks for clues, such as body posturing suggesting abdominal pain or flatulence, when a history is ambiguous.
“I will order an abdominal flat plate when I hear enough symptoms to make me wonder when the family is not sure,” Dr. Veenstra-VanderWeele reported. “Almost always it comes back with evidence of constipation. We treat it, and they are less irritable like all of us would be.”
All common conditions in a pediatric population, including ear infections, dental caries, and food allergies, should be considered, according to Dr. Veenstra-VanderWeele, who recommended a practice pathway for evaluating triggers in children with ASD (Pediatrics. 2016 Feb;137 Suppl 2:S136-48). A coauthor on this pathway, Dr. Veenstra-VanderWeele emphasized the importance of pursuing a systematic approach to medical issues before considering other triggers, such as psychosocial stressors.
In adolescents, headache caused by migraine and late-onset epilepsy, often in the form of complex partial seizures, should be added to the list of potential triggers for irritation or aggression, Dr. Veenstra-VanderWeele said. Epilepsy often precedes the diagnosis of ASD in young children, and Dr. Veenstra-VanderWeele noted that a second peak incidence sometimes occurs in late adolescence.
After ruling out medical problems, helping patients recognize and verbalize stressors can serve as both diagnosis and treatment. In ASD patients with limited verbal skills who are suffering from stress, “aggression is one form of communication,” Dr. Veenstra-VanderWeele said.
However, Dr. Veenstra-VanderWeele cautioned that, even if a trigger is successfully addressed, inadvertently reinforced aggression might persist.
“Aggression can be rewarded sometimes by removing the patient from the classroom, sometimes by giving in, and then that becomes a maladaptive reinforcement pattern that needs to be broken,” Dr. Veenstra-VanderWeele said. “Even if you are treating their irritability and agitation with, say, risperidone, you still need to break the maladaptive reinforcement pattern or they will keep engaging in what has become instrumental aggression.”
Dr. Veenstra-VanderWeele reported financial relationships with Hoffmann-La Roche, Novartis, Seaside Therapeutics, and SynapDx.
EXPERT ANALYSIS FROM the PSYCHOPHARMACOLOGY UPDATE INSTITUTE
Reactive aggressive disorder in children with ADHD is looking for a name
NEW YORK – according to Robert L. Findling, MD.
Emphasizing the reactive component to this behavioral problem, he said: “They look okay until someone bumps into them at school. They do not have a mood disorder. They have a disorder of reactivity.”
The hurdle is that there is no accepted terminology to encourage clinicians to identify and initiate treatment in children with this behavior. The term conduct disorder has been used in the past, but Dr. Findling said that care delivered for conduct disorder is not reimbursable. This may be among the reasons that aggressive reactive behavior of ADHD is overlooked – even though treatment is likely to improve long-term outcome.
“I wish I had a magic label for this, but I don’t,” Dr. Findling said. However, he maintained that most clinicians who work with ADHD children are familiar with this type of behavior. Indeed, clinicians “grapple with this day to day. We all see these kids, and they are oftentimes the most impaired kids in our practices,” he said at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
This behavior should not be confused with the aggression associated with mood disorders, such as disruptive mood dysregulation disorder (DMDD) or bipolar disease, according to Dr. Findling. Children with DMDD, for example, are chronically irritable or angry. Although bipolar disorder patients with aggressive behavior are not necessarily angry between episodes, they also have persistent mood disturbances.
In contrast, preadolescent children with ADHD who have episodes of aggression, a symptom far more common among males than females, do not otherwise exhibit disturbances in mood. In addition, the episodes of impulsive, reactive aggression are provoked. They require a perceived insult, threat, or similar trigger.
While many of these children continue to have episodes of impulsive aggressive behavior even on treatment effective for other ADHD symptoms, Dr. Findling said, “The good news is that there are treatments for aggression.” In addition to psychosocial support aimed at reducing aggressive behavior, once the diagnosis has been made, these include adjusting ADHD treatments to better target symptoms of episodic aggression. If needed, therapies known to treat aggression, such as atypical antipsychotics, anticonvulsants, or lithium also are options.
Dr. Findling did review one older double-blind study that associated methylphenidate with a reduction in aggression in children with conduct disorder, but said he believes that there is no guarantee for a response from any treatment. Rather, he recommended empirical strategies for symptom management and keeping in mind the benefit-to-risk relationship when considering treatments that impose a high burden of adverse events.
However, the first step to treatment is recognizing the problem.
“In my opinion, what is missing is the nosology for these kids,” Dr. Findling said. An evidence-based label will help increase awareness of the problem and encourage more extensive clinical study, he said.
“These children are not rare and they are really impaired. It is heartbreaking, because when you talk to them when they are still little, they know what people think of them. They know their teachers don’t like them. They know their parents think they’re bad. They know their peers are scared of them, and they cannot make friends,” he said. However, there is a potential for reversing these problems if treatment is initiated early.
“As you watch them get older, you watch them scarring over,” he added.
Dr. Findling reported financial ties with numerous pharmaceutical companies.
SOURCE: Findling RL. Psychopharmacology Update Institute
NEW YORK – according to Robert L. Findling, MD.
Emphasizing the reactive component to this behavioral problem, he said: “They look okay until someone bumps into them at school. They do not have a mood disorder. They have a disorder of reactivity.”
The hurdle is that there is no accepted terminology to encourage clinicians to identify and initiate treatment in children with this behavior. The term conduct disorder has been used in the past, but Dr. Findling said that care delivered for conduct disorder is not reimbursable. This may be among the reasons that aggressive reactive behavior of ADHD is overlooked – even though treatment is likely to improve long-term outcome.
“I wish I had a magic label for this, but I don’t,” Dr. Findling said. However, he maintained that most clinicians who work with ADHD children are familiar with this type of behavior. Indeed, clinicians “grapple with this day to day. We all see these kids, and they are oftentimes the most impaired kids in our practices,” he said at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
This behavior should not be confused with the aggression associated with mood disorders, such as disruptive mood dysregulation disorder (DMDD) or bipolar disease, according to Dr. Findling. Children with DMDD, for example, are chronically irritable or angry. Although bipolar disorder patients with aggressive behavior are not necessarily angry between episodes, they also have persistent mood disturbances.
In contrast, preadolescent children with ADHD who have episodes of aggression, a symptom far more common among males than females, do not otherwise exhibit disturbances in mood. In addition, the episodes of impulsive, reactive aggression are provoked. They require a perceived insult, threat, or similar trigger.
While many of these children continue to have episodes of impulsive aggressive behavior even on treatment effective for other ADHD symptoms, Dr. Findling said, “The good news is that there are treatments for aggression.” In addition to psychosocial support aimed at reducing aggressive behavior, once the diagnosis has been made, these include adjusting ADHD treatments to better target symptoms of episodic aggression. If needed, therapies known to treat aggression, such as atypical antipsychotics, anticonvulsants, or lithium also are options.
Dr. Findling did review one older double-blind study that associated methylphenidate with a reduction in aggression in children with conduct disorder, but said he believes that there is no guarantee for a response from any treatment. Rather, he recommended empirical strategies for symptom management and keeping in mind the benefit-to-risk relationship when considering treatments that impose a high burden of adverse events.
However, the first step to treatment is recognizing the problem.
“In my opinion, what is missing is the nosology for these kids,” Dr. Findling said. An evidence-based label will help increase awareness of the problem and encourage more extensive clinical study, he said.
“These children are not rare and they are really impaired. It is heartbreaking, because when you talk to them when they are still little, they know what people think of them. They know their teachers don’t like them. They know their parents think they’re bad. They know their peers are scared of them, and they cannot make friends,” he said. However, there is a potential for reversing these problems if treatment is initiated early.
“As you watch them get older, you watch them scarring over,” he added.
Dr. Findling reported financial ties with numerous pharmaceutical companies.
SOURCE: Findling RL. Psychopharmacology Update Institute
NEW YORK – according to Robert L. Findling, MD.
Emphasizing the reactive component to this behavioral problem, he said: “They look okay until someone bumps into them at school. They do not have a mood disorder. They have a disorder of reactivity.”
The hurdle is that there is no accepted terminology to encourage clinicians to identify and initiate treatment in children with this behavior. The term conduct disorder has been used in the past, but Dr. Findling said that care delivered for conduct disorder is not reimbursable. This may be among the reasons that aggressive reactive behavior of ADHD is overlooked – even though treatment is likely to improve long-term outcome.
“I wish I had a magic label for this, but I don’t,” Dr. Findling said. However, he maintained that most clinicians who work with ADHD children are familiar with this type of behavior. Indeed, clinicians “grapple with this day to day. We all see these kids, and they are oftentimes the most impaired kids in our practices,” he said at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
This behavior should not be confused with the aggression associated with mood disorders, such as disruptive mood dysregulation disorder (DMDD) or bipolar disease, according to Dr. Findling. Children with DMDD, for example, are chronically irritable or angry. Although bipolar disorder patients with aggressive behavior are not necessarily angry between episodes, they also have persistent mood disturbances.
In contrast, preadolescent children with ADHD who have episodes of aggression, a symptom far more common among males than females, do not otherwise exhibit disturbances in mood. In addition, the episodes of impulsive, reactive aggression are provoked. They require a perceived insult, threat, or similar trigger.
While many of these children continue to have episodes of impulsive aggressive behavior even on treatment effective for other ADHD symptoms, Dr. Findling said, “The good news is that there are treatments for aggression.” In addition to psychosocial support aimed at reducing aggressive behavior, once the diagnosis has been made, these include adjusting ADHD treatments to better target symptoms of episodic aggression. If needed, therapies known to treat aggression, such as atypical antipsychotics, anticonvulsants, or lithium also are options.
Dr. Findling did review one older double-blind study that associated methylphenidate with a reduction in aggression in children with conduct disorder, but said he believes that there is no guarantee for a response from any treatment. Rather, he recommended empirical strategies for symptom management and keeping in mind the benefit-to-risk relationship when considering treatments that impose a high burden of adverse events.
However, the first step to treatment is recognizing the problem.
“In my opinion, what is missing is the nosology for these kids,” Dr. Findling said. An evidence-based label will help increase awareness of the problem and encourage more extensive clinical study, he said.
“These children are not rare and they are really impaired. It is heartbreaking, because when you talk to them when they are still little, they know what people think of them. They know their teachers don’t like them. They know their parents think they’re bad. They know their peers are scared of them, and they cannot make friends,” he said. However, there is a potential for reversing these problems if treatment is initiated early.
“As you watch them get older, you watch them scarring over,” he added.
Dr. Findling reported financial ties with numerous pharmaceutical companies.
SOURCE: Findling RL. Psychopharmacology Update Institute
REPORTING FROM THE PSYCHOPHARMACOLOGY UPDATE INSTITUTE
Characterize duration when seeking etiology of tantrums in children
NEW YORK – Although explosive outbursts or tantrums accompany nearly every psychiatric illness that affects children, the specific features may help identify an etiology, according to Gabrielle A. Carlson, MD.
“There are two components of irritability,” explained Dr. Carlson, professor of psychiatry and pediatrics, Stony Brook (N.Y.) University Medical Center. “One is how often the child loses his or her temper, and the other is what they do when they lose their temper.”
To be useful in identifying the source, the characterization of explosive outbursts must be undertaken in the context of the patient’s history and the duration and types of tantrum-related behaviors, particularly aggressive behavior toward others, according to Dr. Carlson.
Presenting a diagnostic algorithm relevant to children with frequent explosive outbursts, Dr. Carlson suggested that pathways differ for young children and adolescents. Yet, the first step – which is evaluating whether or not irritability is a feature of the patient’s disposition when not in the midst of a tantrum – is common to both groups.
In young children with new onset of explosive outbursts, stressors in school, such as bullying, or family, such as abuse, represent an appropriate initial focus. In adolescents, initial attention should be paid to the potential role of mood disorders, particularly depression, mania, or anxiety, according to Dr. Carlson.
For most patients and most etiologies, tantrums follow a trigger and then resolve quickly. When tantrums do not resolve quickly in patients who remain generally irritable even when they are not having a tantrum, there is an increased likelihood of disruptive mood dysregulation disorder (DMDD).
Relative to tantrums associated with attention deficit hyperactive disorder (ADHD), oppositional defiant disorder (ODD), or affective disorders, explosive outbursts associated with DMDD are also more likely to include aggression toward others.
Physical restraint to safeguard the patient or others during a tantrum is uncommon in most conditions associated with tantrums, with the exception of DMDD. Greater aggression tracks with greater DMDD severity. According to data presented by Dr. Carlson, 92% of a clinical sample of DMDD patients exhibited physical aggression, compared with none of those in a community sample.
Tantrums lasting more than 30 minutes were observed in 60% of the clinic sample, versus only 12.5% of the community sample.
Explosive outbursts “are not an uncommon or trivial problem,” according to Dr. Carlson, who cited data suggesting that 70% of children between the ages of 5 and 12 years hospitalized for a psychiatric diseases are referred for an explosive outburst.
She believes that a systematic approach toward characterizing the tantrum will be helpful in understanding the underlying etiology and appropriate treatment. Using such tools as the Irritability and Rages Inventory or the Affective Reactivity Index Child Form, clinicians should seek to evaluate the frequency of tantrums, the duration, and the patient’s symptom burden between tantrums.
If explosive outbursts are rare, they are unlikely to be due to DMDD or affective disorders, such as bipolar disease. If frequent in a patient with chronic psychopathology, those who are generally “fine until frustrated” are the ones more likely to have ADHD or even oppositional defiant disorder (ODD).
The less common profile, which is rage that does not completely resolve, suggests DMDD, a condition that Dr. Carlson described with the mnemonic OI VEY to convey key features. The letters stand for Outbursts that are frequent, Irritable mood in the absence of an outburst, Very chronic (more than 1 per year), Explained by other co-existing conditions, such as mania, and Young (starts between ages 6 and 10 years).
Although tantrums are the way in which children with a broad array of psychiatric conditions express frustration, Dr. Carlson said it is not clear if the mechanisms for irritability and explosive outbursts are shared across conditions. Despite the guidance she offered for linking specific tantrum features with DMDD, she also reiterated that tantrums cannot be considered a symptom specific to any single etiology. The difference between etiologies for irritable children having a tantrum “is not how they feel, the difference is what they do,” Dr. Carlson suggested.
Dr. Carlson reported no relevant financial relationships.
NEW YORK – Although explosive outbursts or tantrums accompany nearly every psychiatric illness that affects children, the specific features may help identify an etiology, according to Gabrielle A. Carlson, MD.
“There are two components of irritability,” explained Dr. Carlson, professor of psychiatry and pediatrics, Stony Brook (N.Y.) University Medical Center. “One is how often the child loses his or her temper, and the other is what they do when they lose their temper.”
To be useful in identifying the source, the characterization of explosive outbursts must be undertaken in the context of the patient’s history and the duration and types of tantrum-related behaviors, particularly aggressive behavior toward others, according to Dr. Carlson.
Presenting a diagnostic algorithm relevant to children with frequent explosive outbursts, Dr. Carlson suggested that pathways differ for young children and adolescents. Yet, the first step – which is evaluating whether or not irritability is a feature of the patient’s disposition when not in the midst of a tantrum – is common to both groups.
In young children with new onset of explosive outbursts, stressors in school, such as bullying, or family, such as abuse, represent an appropriate initial focus. In adolescents, initial attention should be paid to the potential role of mood disorders, particularly depression, mania, or anxiety, according to Dr. Carlson.
For most patients and most etiologies, tantrums follow a trigger and then resolve quickly. When tantrums do not resolve quickly in patients who remain generally irritable even when they are not having a tantrum, there is an increased likelihood of disruptive mood dysregulation disorder (DMDD).
Relative to tantrums associated with attention deficit hyperactive disorder (ADHD), oppositional defiant disorder (ODD), or affective disorders, explosive outbursts associated with DMDD are also more likely to include aggression toward others.
Physical restraint to safeguard the patient or others during a tantrum is uncommon in most conditions associated with tantrums, with the exception of DMDD. Greater aggression tracks with greater DMDD severity. According to data presented by Dr. Carlson, 92% of a clinical sample of DMDD patients exhibited physical aggression, compared with none of those in a community sample.
Tantrums lasting more than 30 minutes were observed in 60% of the clinic sample, versus only 12.5% of the community sample.
Explosive outbursts “are not an uncommon or trivial problem,” according to Dr. Carlson, who cited data suggesting that 70% of children between the ages of 5 and 12 years hospitalized for a psychiatric diseases are referred for an explosive outburst.
She believes that a systematic approach toward characterizing the tantrum will be helpful in understanding the underlying etiology and appropriate treatment. Using such tools as the Irritability and Rages Inventory or the Affective Reactivity Index Child Form, clinicians should seek to evaluate the frequency of tantrums, the duration, and the patient’s symptom burden between tantrums.
If explosive outbursts are rare, they are unlikely to be due to DMDD or affective disorders, such as bipolar disease. If frequent in a patient with chronic psychopathology, those who are generally “fine until frustrated” are the ones more likely to have ADHD or even oppositional defiant disorder (ODD).
The less common profile, which is rage that does not completely resolve, suggests DMDD, a condition that Dr. Carlson described with the mnemonic OI VEY to convey key features. The letters stand for Outbursts that are frequent, Irritable mood in the absence of an outburst, Very chronic (more than 1 per year), Explained by other co-existing conditions, such as mania, and Young (starts between ages 6 and 10 years).
Although tantrums are the way in which children with a broad array of psychiatric conditions express frustration, Dr. Carlson said it is not clear if the mechanisms for irritability and explosive outbursts are shared across conditions. Despite the guidance she offered for linking specific tantrum features with DMDD, she also reiterated that tantrums cannot be considered a symptom specific to any single etiology. The difference between etiologies for irritable children having a tantrum “is not how they feel, the difference is what they do,” Dr. Carlson suggested.
Dr. Carlson reported no relevant financial relationships.
NEW YORK – Although explosive outbursts or tantrums accompany nearly every psychiatric illness that affects children, the specific features may help identify an etiology, according to Gabrielle A. Carlson, MD.
“There are two components of irritability,” explained Dr. Carlson, professor of psychiatry and pediatrics, Stony Brook (N.Y.) University Medical Center. “One is how often the child loses his or her temper, and the other is what they do when they lose their temper.”
To be useful in identifying the source, the characterization of explosive outbursts must be undertaken in the context of the patient’s history and the duration and types of tantrum-related behaviors, particularly aggressive behavior toward others, according to Dr. Carlson.
Presenting a diagnostic algorithm relevant to children with frequent explosive outbursts, Dr. Carlson suggested that pathways differ for young children and adolescents. Yet, the first step – which is evaluating whether or not irritability is a feature of the patient’s disposition when not in the midst of a tantrum – is common to both groups.
In young children with new onset of explosive outbursts, stressors in school, such as bullying, or family, such as abuse, represent an appropriate initial focus. In adolescents, initial attention should be paid to the potential role of mood disorders, particularly depression, mania, or anxiety, according to Dr. Carlson.
For most patients and most etiologies, tantrums follow a trigger and then resolve quickly. When tantrums do not resolve quickly in patients who remain generally irritable even when they are not having a tantrum, there is an increased likelihood of disruptive mood dysregulation disorder (DMDD).
Relative to tantrums associated with attention deficit hyperactive disorder (ADHD), oppositional defiant disorder (ODD), or affective disorders, explosive outbursts associated with DMDD are also more likely to include aggression toward others.
Physical restraint to safeguard the patient or others during a tantrum is uncommon in most conditions associated with tantrums, with the exception of DMDD. Greater aggression tracks with greater DMDD severity. According to data presented by Dr. Carlson, 92% of a clinical sample of DMDD patients exhibited physical aggression, compared with none of those in a community sample.
Tantrums lasting more than 30 minutes were observed in 60% of the clinic sample, versus only 12.5% of the community sample.
Explosive outbursts “are not an uncommon or trivial problem,” according to Dr. Carlson, who cited data suggesting that 70% of children between the ages of 5 and 12 years hospitalized for a psychiatric diseases are referred for an explosive outburst.
She believes that a systematic approach toward characterizing the tantrum will be helpful in understanding the underlying etiology and appropriate treatment. Using such tools as the Irritability and Rages Inventory or the Affective Reactivity Index Child Form, clinicians should seek to evaluate the frequency of tantrums, the duration, and the patient’s symptom burden between tantrums.
If explosive outbursts are rare, they are unlikely to be due to DMDD or affective disorders, such as bipolar disease. If frequent in a patient with chronic psychopathology, those who are generally “fine until frustrated” are the ones more likely to have ADHD or even oppositional defiant disorder (ODD).
The less common profile, which is rage that does not completely resolve, suggests DMDD, a condition that Dr. Carlson described with the mnemonic OI VEY to convey key features. The letters stand for Outbursts that are frequent, Irritable mood in the absence of an outburst, Very chronic (more than 1 per year), Explained by other co-existing conditions, such as mania, and Young (starts between ages 6 and 10 years).
Although tantrums are the way in which children with a broad array of psychiatric conditions express frustration, Dr. Carlson said it is not clear if the mechanisms for irritability and explosive outbursts are shared across conditions. Despite the guidance she offered for linking specific tantrum features with DMDD, she also reiterated that tantrums cannot be considered a symptom specific to any single etiology. The difference between etiologies for irritable children having a tantrum “is not how they feel, the difference is what they do,” Dr. Carlson suggested.
Dr. Carlson reported no relevant financial relationships.
REPORTING FROM THE PSYCHOPHARMACOLOGY UPDATE INSTITUTE