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Adherence to ADHD meds may lower unemployment risk
Investigators analyzed data for almost 13,000 working-age adults with ADHD and found ADHD medication use during the previous 2 years was associated with a 10% lower risk for long-term unemployment in the following year.
In addition, among the female participants, longer treatment duration was associated with a lower risk for subsequent long-term unemployment. In both genders, within-individual comparisons showed long-term unemployment was lower during periods of ADHD medication treatment, compared with nontreatment periods.
“This evidence should be considered together with the existing knowledge of risks and benefits of ADHD medications when developing treatment plans for working-aged adults,” lead author Lin Li, MSc, a doctoral candidate at the School of Medical Science, Örebro University, Sweden, told this news organization.
“However, the effect size is relatively small in magnitude, indicating that other treatment programs, such as psychotherapy, are also needed to help individuals with ADHD in work-related settings,” Ms. Li said.
The findings were published online in JAMA Network Open.
Evidence gap
Adults with ADHD “have occupational impairments, such as poor work performance, less job stability, financial problems, and increased risk for unemployment,” the investigators write.
However, “less is known about the extent to which pharmacological treatment of ADHD is associated with reductions in unemployment rates,” they add.
“People with ADHD have been reported to have problems in work-related performance,” Ms. Li noted. “ADHD medications could reduce ADHD symptoms and also help with academic achievement, but there is limited evidence on the association between ADHD medication and occupational outcomes.”
To address this gap in evidence, the researchers turned to several major Swedish registries to identify 25,358 individuals with ADHD born between 1958 and 1978 who were aged 30 to 55 years during the study period of Jan. 1, 2008, through Dec. 31, 2013).
Of these, 12,875 (41.5% women; mean age, 37.9 years) were included in the analysis. Most participants (81.19%) had more than 9 years of education.
The registers provided information not only about diagnosis, but also about prescription medications these individuals took for ADHD, including methylphenidate, amphetamine, dexamphetamine, lisdexamfetamine, and atomoxetine.
Administrative records provided data about yearly accumulated unemployment days, with long-term unemployment defined as having at least 90 days of unemployment in a calendar year.
Covariates included age at baseline, sex, country of birth, highest educational level, crime records, and psychiatric comorbidities.
Most patients (69.34%) had at least one psychiatric comorbidity, with depressive, anxiety, and substance use disorders being the most common (in 40.28%, 35.27%, and 28.77%, respectively).
Symptom reduction
The mean length of medication use was 49 days (range, 0-366 days) per year. Of participants in whom these data were available, 31.29% of women and 31.03% of men never used ADHD medications. Among participants treated with ADHD medication (68.71%), only 3.23% of the women and 3.46% of the men had persistent use during the follow-up period.
Among women and men in whom these data were available, (38.85% of the total sample), 35.70% and 41.08%, respectively, were recorded as having one or more long-term unemployment stretches across the study period. In addition, 0.15% and 0.4%, respectively, had long-term unemployment during each of those years.
Use of ADHD medications during the previous 2 years was associated with a 10% lower risk for long-term unemployment in the following year (adjusted relative risk, 0.90; 95% confidence interval, 0.87-0.95).
The researchers also found an association between use of ADHD medications and long-term unemployment among women (RR, 0.82; 95% CI, 0.76-0.89) but not among men (RR, 0.96; 95% CI, 0.91-1.01).
Among women in particular, longer treatment duration was associated with a lower risk of subsequent long-term unemployment (P < .001 for trend).
Within-individual comparisons showed the long-term unemployment rate was lower during periods when individuals were being treated with ADHD medication vs. periods of nontreatment (RR, 0.89; 95% CI, 0.85-0.94).
“Among 12,875 working-aged adults with ADHD in Sweden, we found the use of ADHD medication is associated with a lower risk of long-term unemployment, especially for women,” Ms. Li said.
“The hypothesis of this study is that ADHD medications are effective in reducing ADHD symptoms, which may in turn help to improve work performance among individuals with ADHD,” she added.
However, Ms. Li cautioned, “the information on ADHD symptoms is not available in Swedish National Registers, so more research is needed to test the hypothesis.”
The investigators also suggest that future research “should further explore the effectiveness of stimulant and nonstimulant ADHD medications” and replicate their findings in other settings.
Findings ‘make sense’
Commenting on the study, Ari Tuckman PsyD, expert spokesman for Children and Adults with Attention-Deficit/Hyperactivity Disorder, said, there is “a lot to like about this study, specifically the large sample size and within-individual comparisons that the Scandinavians’ databases allow.”
“We know that ADHD can impact both finding and keeping a job, so it absolutely makes sense that medication use would reduce duration of unemployment,” said Dr. Tuckman, who is in private practice in West Chester, Pa., and was not involved with the research.
However, “I would venture that the results would have been more robust if the authors had been able to only look at those on optimized medication regimens, which is far too few,” he added. “This lack of optimization would have been even more true 10 years ago, which is when the data was from.”
The study was supported by a grant from the Swedish Council for Health, Working Life, and Welfare, an award from the Swedish Research Council, and a grant from Shire International GmbH, a member of the Takeda group of companies. Ms. Li and Dr. Tuckman have disclosed no relevant financial relationships. The other authors’ disclosures are listed in the original paper.
A version of this article first appeared on Medscape.com.
Investigators analyzed data for almost 13,000 working-age adults with ADHD and found ADHD medication use during the previous 2 years was associated with a 10% lower risk for long-term unemployment in the following year.
In addition, among the female participants, longer treatment duration was associated with a lower risk for subsequent long-term unemployment. In both genders, within-individual comparisons showed long-term unemployment was lower during periods of ADHD medication treatment, compared with nontreatment periods.
“This evidence should be considered together with the existing knowledge of risks and benefits of ADHD medications when developing treatment plans for working-aged adults,” lead author Lin Li, MSc, a doctoral candidate at the School of Medical Science, Örebro University, Sweden, told this news organization.
“However, the effect size is relatively small in magnitude, indicating that other treatment programs, such as psychotherapy, are also needed to help individuals with ADHD in work-related settings,” Ms. Li said.
The findings were published online in JAMA Network Open.
Evidence gap
Adults with ADHD “have occupational impairments, such as poor work performance, less job stability, financial problems, and increased risk for unemployment,” the investigators write.
However, “less is known about the extent to which pharmacological treatment of ADHD is associated with reductions in unemployment rates,” they add.
“People with ADHD have been reported to have problems in work-related performance,” Ms. Li noted. “ADHD medications could reduce ADHD symptoms and also help with academic achievement, but there is limited evidence on the association between ADHD medication and occupational outcomes.”
To address this gap in evidence, the researchers turned to several major Swedish registries to identify 25,358 individuals with ADHD born between 1958 and 1978 who were aged 30 to 55 years during the study period of Jan. 1, 2008, through Dec. 31, 2013).
Of these, 12,875 (41.5% women; mean age, 37.9 years) were included in the analysis. Most participants (81.19%) had more than 9 years of education.
The registers provided information not only about diagnosis, but also about prescription medications these individuals took for ADHD, including methylphenidate, amphetamine, dexamphetamine, lisdexamfetamine, and atomoxetine.
Administrative records provided data about yearly accumulated unemployment days, with long-term unemployment defined as having at least 90 days of unemployment in a calendar year.
Covariates included age at baseline, sex, country of birth, highest educational level, crime records, and psychiatric comorbidities.
Most patients (69.34%) had at least one psychiatric comorbidity, with depressive, anxiety, and substance use disorders being the most common (in 40.28%, 35.27%, and 28.77%, respectively).
Symptom reduction
The mean length of medication use was 49 days (range, 0-366 days) per year. Of participants in whom these data were available, 31.29% of women and 31.03% of men never used ADHD medications. Among participants treated with ADHD medication (68.71%), only 3.23% of the women and 3.46% of the men had persistent use during the follow-up period.
Among women and men in whom these data were available, (38.85% of the total sample), 35.70% and 41.08%, respectively, were recorded as having one or more long-term unemployment stretches across the study period. In addition, 0.15% and 0.4%, respectively, had long-term unemployment during each of those years.
Use of ADHD medications during the previous 2 years was associated with a 10% lower risk for long-term unemployment in the following year (adjusted relative risk, 0.90; 95% confidence interval, 0.87-0.95).
The researchers also found an association between use of ADHD medications and long-term unemployment among women (RR, 0.82; 95% CI, 0.76-0.89) but not among men (RR, 0.96; 95% CI, 0.91-1.01).
Among women in particular, longer treatment duration was associated with a lower risk of subsequent long-term unemployment (P < .001 for trend).
Within-individual comparisons showed the long-term unemployment rate was lower during periods when individuals were being treated with ADHD medication vs. periods of nontreatment (RR, 0.89; 95% CI, 0.85-0.94).
“Among 12,875 working-aged adults with ADHD in Sweden, we found the use of ADHD medication is associated with a lower risk of long-term unemployment, especially for women,” Ms. Li said.
“The hypothesis of this study is that ADHD medications are effective in reducing ADHD symptoms, which may in turn help to improve work performance among individuals with ADHD,” she added.
However, Ms. Li cautioned, “the information on ADHD symptoms is not available in Swedish National Registers, so more research is needed to test the hypothesis.”
The investigators also suggest that future research “should further explore the effectiveness of stimulant and nonstimulant ADHD medications” and replicate their findings in other settings.
Findings ‘make sense’
Commenting on the study, Ari Tuckman PsyD, expert spokesman for Children and Adults with Attention-Deficit/Hyperactivity Disorder, said, there is “a lot to like about this study, specifically the large sample size and within-individual comparisons that the Scandinavians’ databases allow.”
“We know that ADHD can impact both finding and keeping a job, so it absolutely makes sense that medication use would reduce duration of unemployment,” said Dr. Tuckman, who is in private practice in West Chester, Pa., and was not involved with the research.
However, “I would venture that the results would have been more robust if the authors had been able to only look at those on optimized medication regimens, which is far too few,” he added. “This lack of optimization would have been even more true 10 years ago, which is when the data was from.”
The study was supported by a grant from the Swedish Council for Health, Working Life, and Welfare, an award from the Swedish Research Council, and a grant from Shire International GmbH, a member of the Takeda group of companies. Ms. Li and Dr. Tuckman have disclosed no relevant financial relationships. The other authors’ disclosures are listed in the original paper.
A version of this article first appeared on Medscape.com.
Investigators analyzed data for almost 13,000 working-age adults with ADHD and found ADHD medication use during the previous 2 years was associated with a 10% lower risk for long-term unemployment in the following year.
In addition, among the female participants, longer treatment duration was associated with a lower risk for subsequent long-term unemployment. In both genders, within-individual comparisons showed long-term unemployment was lower during periods of ADHD medication treatment, compared with nontreatment periods.
“This evidence should be considered together with the existing knowledge of risks and benefits of ADHD medications when developing treatment plans for working-aged adults,” lead author Lin Li, MSc, a doctoral candidate at the School of Medical Science, Örebro University, Sweden, told this news organization.
“However, the effect size is relatively small in magnitude, indicating that other treatment programs, such as psychotherapy, are also needed to help individuals with ADHD in work-related settings,” Ms. Li said.
The findings were published online in JAMA Network Open.
Evidence gap
Adults with ADHD “have occupational impairments, such as poor work performance, less job stability, financial problems, and increased risk for unemployment,” the investigators write.
However, “less is known about the extent to which pharmacological treatment of ADHD is associated with reductions in unemployment rates,” they add.
“People with ADHD have been reported to have problems in work-related performance,” Ms. Li noted. “ADHD medications could reduce ADHD symptoms and also help with academic achievement, but there is limited evidence on the association between ADHD medication and occupational outcomes.”
To address this gap in evidence, the researchers turned to several major Swedish registries to identify 25,358 individuals with ADHD born between 1958 and 1978 who were aged 30 to 55 years during the study period of Jan. 1, 2008, through Dec. 31, 2013).
Of these, 12,875 (41.5% women; mean age, 37.9 years) were included in the analysis. Most participants (81.19%) had more than 9 years of education.
The registers provided information not only about diagnosis, but also about prescription medications these individuals took for ADHD, including methylphenidate, amphetamine, dexamphetamine, lisdexamfetamine, and atomoxetine.
Administrative records provided data about yearly accumulated unemployment days, with long-term unemployment defined as having at least 90 days of unemployment in a calendar year.
Covariates included age at baseline, sex, country of birth, highest educational level, crime records, and psychiatric comorbidities.
Most patients (69.34%) had at least one psychiatric comorbidity, with depressive, anxiety, and substance use disorders being the most common (in 40.28%, 35.27%, and 28.77%, respectively).
Symptom reduction
The mean length of medication use was 49 days (range, 0-366 days) per year. Of participants in whom these data were available, 31.29% of women and 31.03% of men never used ADHD medications. Among participants treated with ADHD medication (68.71%), only 3.23% of the women and 3.46% of the men had persistent use during the follow-up period.
Among women and men in whom these data were available, (38.85% of the total sample), 35.70% and 41.08%, respectively, were recorded as having one or more long-term unemployment stretches across the study period. In addition, 0.15% and 0.4%, respectively, had long-term unemployment during each of those years.
Use of ADHD medications during the previous 2 years was associated with a 10% lower risk for long-term unemployment in the following year (adjusted relative risk, 0.90; 95% confidence interval, 0.87-0.95).
The researchers also found an association between use of ADHD medications and long-term unemployment among women (RR, 0.82; 95% CI, 0.76-0.89) but not among men (RR, 0.96; 95% CI, 0.91-1.01).
Among women in particular, longer treatment duration was associated with a lower risk of subsequent long-term unemployment (P < .001 for trend).
Within-individual comparisons showed the long-term unemployment rate was lower during periods when individuals were being treated with ADHD medication vs. periods of nontreatment (RR, 0.89; 95% CI, 0.85-0.94).
“Among 12,875 working-aged adults with ADHD in Sweden, we found the use of ADHD medication is associated with a lower risk of long-term unemployment, especially for women,” Ms. Li said.
“The hypothesis of this study is that ADHD medications are effective in reducing ADHD symptoms, which may in turn help to improve work performance among individuals with ADHD,” she added.
However, Ms. Li cautioned, “the information on ADHD symptoms is not available in Swedish National Registers, so more research is needed to test the hypothesis.”
The investigators also suggest that future research “should further explore the effectiveness of stimulant and nonstimulant ADHD medications” and replicate their findings in other settings.
Findings ‘make sense’
Commenting on the study, Ari Tuckman PsyD, expert spokesman for Children and Adults with Attention-Deficit/Hyperactivity Disorder, said, there is “a lot to like about this study, specifically the large sample size and within-individual comparisons that the Scandinavians’ databases allow.”
“We know that ADHD can impact both finding and keeping a job, so it absolutely makes sense that medication use would reduce duration of unemployment,” said Dr. Tuckman, who is in private practice in West Chester, Pa., and was not involved with the research.
However, “I would venture that the results would have been more robust if the authors had been able to only look at those on optimized medication regimens, which is far too few,” he added. “This lack of optimization would have been even more true 10 years ago, which is when the data was from.”
The study was supported by a grant from the Swedish Council for Health, Working Life, and Welfare, an award from the Swedish Research Council, and a grant from Shire International GmbH, a member of the Takeda group of companies. Ms. Li and Dr. Tuckman have disclosed no relevant financial relationships. The other authors’ disclosures are listed in the original paper.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN
Depression biomarkers: Which ones matter most?
Multiple biomarkers of depression involved in several brain circuits are altered in patients with unipolar depression.
because they suggest neuroimmunological alterations, disturbances in the blood-brain-barrier, hyperactivity in the hypothalamic-pituitary-adrenal (HPA) axis, and impaired neuroplasticity as factors in depression pathophysiology.
However, said study investigator Michael E. Benros, MD, PhD, professor and head of research at Mental Health Centre Copenhagen and University of Copenhagen, this is on a group level. “So in order to be relevant in a clinical context, the results need to be validated by further high-quality studies identifying subgroups with different biological underpinnings,” he told this news organization.
Identification of potential subgroups of depression with different biomarkers might help explain the diverse symptomatology and variability in treatment response observed in patients with depression, he noted.
The study was published online in JAMA Psychiatry.
Multiple pathways to depression
The systematic review and meta-analysis included 97 studies investigating 165 CSF biomarkers.
Of the 42 biomarkers investigated in at least two studies, patients with unipolar depression had higher CSF levels of interleukin 6, a marker of chronic inflammation; total protein, which signals blood-brain barrier dysfunction and increased permeability; and cortisol, which is linked to psychological stress, compared with healthy controls.
Depression was also associated with:
- Lower CSF levels of homovanillic acid, the major terminal metabolite of dopamine.
- Gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the CNS thought to play a vital role in the control of stress and depression.
- Somatostatin, a neuropeptide often coexpressed with GABA.
- Brain-derived neurotrophic factor (BDNF), a protein involved in neurogenesis, synaptic plasticity, and neurotransmission.
- Amyloid-β 40, implicated in Alzheimer’s disease.
- Transthyretin, involved in transport of thyroxine across the blood-brain barrier.
Collectively, the findings point toward a “dysregulated dopaminergic system, a compromised inhibitory system, HPA axis hyperactivity, increased neuroinflammation and blood-brain barrier permeability, and impaired neuroplasticity as important factors in depression pathophysiology,” the investigators wrote.
“It is notable that we did not find significant difference in the metabolite levels of serotonin and noradrenalin, which are the most targeted neurotransmitters in modern antidepressant treatment,” said Dr. Benros.
However, this could be explained by substantial heterogeneity between studies and the fact that quantification of total CSF biomarker concentrations does not reflect local alteration within the brain, he explained.
Many of the studies had small cohorts and most quantified only a few biomarkers, making it hard to examine potential interactions between biomarkers or identify specific phenotypes of depression.
“Novel high-quality studies including larger cohorts with an integrative approach and extensive numbers of biomarkers are needed to validate these potential biomarkers of depression and set the stage for the development of more effective and precise treatments,” the researchers noted.
Which ones hold water?
Reached for comment, Dean MacKinnon, MD, associate professor of psychiatry and behavioral sciences at Johns Hopkins University, Baltimore, noted that this analysis “extracts the vast amount of knowledge” gained from different studies on biomarkers in the CSF for depression.
“They were able to identify 97 papers that have enough information in them that they could sort of lump them together and see which ones still hold water. It’s always useful to be able to look at patterns in the research and see if you can find some consistent trends,” he told this news organization.
Dr. MacKinnon, who was not part of the research team, also noted that “nonreplicability” is a problem in psychiatry and psychology research, “so being able to show that at least some studies were sufficiently well done, to get a good result, and that they could be replicated in at least one other good study is useful information.”
When it comes to depression, Dr. MacKinnon said, “We just don’t know enough to really pin down a physiologic pathway to explain it. The fact that some people seem to have high cortisol and some people seem to have high permeability of blood-brain barrier, and others have abnormalities in dopamine, is interesting and suggests that depression is likely not a unitary disease with a single cause.”
He cautioned, however, that the findings don’t have immediate clinical implications for individual patients with depression.
“Theoretically, down the road, if you extrapolate from what they found, and if it’s truly the case that this research maps to something that could suggest a different clinical approach, you might be able to determine whether one patient might respond better to an SSRI or an SNRI or something like that,” Dr. MacKinnon said.
Dr. Benros reported grants from Lundbeck Foundation during the conduct of the study. Dr. MacKinnon has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Multiple biomarkers of depression involved in several brain circuits are altered in patients with unipolar depression.
because they suggest neuroimmunological alterations, disturbances in the blood-brain-barrier, hyperactivity in the hypothalamic-pituitary-adrenal (HPA) axis, and impaired neuroplasticity as factors in depression pathophysiology.
However, said study investigator Michael E. Benros, MD, PhD, professor and head of research at Mental Health Centre Copenhagen and University of Copenhagen, this is on a group level. “So in order to be relevant in a clinical context, the results need to be validated by further high-quality studies identifying subgroups with different biological underpinnings,” he told this news organization.
Identification of potential subgroups of depression with different biomarkers might help explain the diverse symptomatology and variability in treatment response observed in patients with depression, he noted.
The study was published online in JAMA Psychiatry.
Multiple pathways to depression
The systematic review and meta-analysis included 97 studies investigating 165 CSF biomarkers.
Of the 42 biomarkers investigated in at least two studies, patients with unipolar depression had higher CSF levels of interleukin 6, a marker of chronic inflammation; total protein, which signals blood-brain barrier dysfunction and increased permeability; and cortisol, which is linked to psychological stress, compared with healthy controls.
Depression was also associated with:
- Lower CSF levels of homovanillic acid, the major terminal metabolite of dopamine.
- Gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the CNS thought to play a vital role in the control of stress and depression.
- Somatostatin, a neuropeptide often coexpressed with GABA.
- Brain-derived neurotrophic factor (BDNF), a protein involved in neurogenesis, synaptic plasticity, and neurotransmission.
- Amyloid-β 40, implicated in Alzheimer’s disease.
- Transthyretin, involved in transport of thyroxine across the blood-brain barrier.
Collectively, the findings point toward a “dysregulated dopaminergic system, a compromised inhibitory system, HPA axis hyperactivity, increased neuroinflammation and blood-brain barrier permeability, and impaired neuroplasticity as important factors in depression pathophysiology,” the investigators wrote.
“It is notable that we did not find significant difference in the metabolite levels of serotonin and noradrenalin, which are the most targeted neurotransmitters in modern antidepressant treatment,” said Dr. Benros.
However, this could be explained by substantial heterogeneity between studies and the fact that quantification of total CSF biomarker concentrations does not reflect local alteration within the brain, he explained.
Many of the studies had small cohorts and most quantified only a few biomarkers, making it hard to examine potential interactions between biomarkers or identify specific phenotypes of depression.
“Novel high-quality studies including larger cohorts with an integrative approach and extensive numbers of biomarkers are needed to validate these potential biomarkers of depression and set the stage for the development of more effective and precise treatments,” the researchers noted.
Which ones hold water?
Reached for comment, Dean MacKinnon, MD, associate professor of psychiatry and behavioral sciences at Johns Hopkins University, Baltimore, noted that this analysis “extracts the vast amount of knowledge” gained from different studies on biomarkers in the CSF for depression.
“They were able to identify 97 papers that have enough information in them that they could sort of lump them together and see which ones still hold water. It’s always useful to be able to look at patterns in the research and see if you can find some consistent trends,” he told this news organization.
Dr. MacKinnon, who was not part of the research team, also noted that “nonreplicability” is a problem in psychiatry and psychology research, “so being able to show that at least some studies were sufficiently well done, to get a good result, and that they could be replicated in at least one other good study is useful information.”
When it comes to depression, Dr. MacKinnon said, “We just don’t know enough to really pin down a physiologic pathway to explain it. The fact that some people seem to have high cortisol and some people seem to have high permeability of blood-brain barrier, and others have abnormalities in dopamine, is interesting and suggests that depression is likely not a unitary disease with a single cause.”
He cautioned, however, that the findings don’t have immediate clinical implications for individual patients with depression.
“Theoretically, down the road, if you extrapolate from what they found, and if it’s truly the case that this research maps to something that could suggest a different clinical approach, you might be able to determine whether one patient might respond better to an SSRI or an SNRI or something like that,” Dr. MacKinnon said.
Dr. Benros reported grants from Lundbeck Foundation during the conduct of the study. Dr. MacKinnon has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Multiple biomarkers of depression involved in several brain circuits are altered in patients with unipolar depression.
because they suggest neuroimmunological alterations, disturbances in the blood-brain-barrier, hyperactivity in the hypothalamic-pituitary-adrenal (HPA) axis, and impaired neuroplasticity as factors in depression pathophysiology.
However, said study investigator Michael E. Benros, MD, PhD, professor and head of research at Mental Health Centre Copenhagen and University of Copenhagen, this is on a group level. “So in order to be relevant in a clinical context, the results need to be validated by further high-quality studies identifying subgroups with different biological underpinnings,” he told this news organization.
Identification of potential subgroups of depression with different biomarkers might help explain the diverse symptomatology and variability in treatment response observed in patients with depression, he noted.
The study was published online in JAMA Psychiatry.
Multiple pathways to depression
The systematic review and meta-analysis included 97 studies investigating 165 CSF biomarkers.
Of the 42 biomarkers investigated in at least two studies, patients with unipolar depression had higher CSF levels of interleukin 6, a marker of chronic inflammation; total protein, which signals blood-brain barrier dysfunction and increased permeability; and cortisol, which is linked to psychological stress, compared with healthy controls.
Depression was also associated with:
- Lower CSF levels of homovanillic acid, the major terminal metabolite of dopamine.
- Gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the CNS thought to play a vital role in the control of stress and depression.
- Somatostatin, a neuropeptide often coexpressed with GABA.
- Brain-derived neurotrophic factor (BDNF), a protein involved in neurogenesis, synaptic plasticity, and neurotransmission.
- Amyloid-β 40, implicated in Alzheimer’s disease.
- Transthyretin, involved in transport of thyroxine across the blood-brain barrier.
Collectively, the findings point toward a “dysregulated dopaminergic system, a compromised inhibitory system, HPA axis hyperactivity, increased neuroinflammation and blood-brain barrier permeability, and impaired neuroplasticity as important factors in depression pathophysiology,” the investigators wrote.
“It is notable that we did not find significant difference in the metabolite levels of serotonin and noradrenalin, which are the most targeted neurotransmitters in modern antidepressant treatment,” said Dr. Benros.
However, this could be explained by substantial heterogeneity between studies and the fact that quantification of total CSF biomarker concentrations does not reflect local alteration within the brain, he explained.
Many of the studies had small cohorts and most quantified only a few biomarkers, making it hard to examine potential interactions between biomarkers or identify specific phenotypes of depression.
“Novel high-quality studies including larger cohorts with an integrative approach and extensive numbers of biomarkers are needed to validate these potential biomarkers of depression and set the stage for the development of more effective and precise treatments,” the researchers noted.
Which ones hold water?
Reached for comment, Dean MacKinnon, MD, associate professor of psychiatry and behavioral sciences at Johns Hopkins University, Baltimore, noted that this analysis “extracts the vast amount of knowledge” gained from different studies on biomarkers in the CSF for depression.
“They were able to identify 97 papers that have enough information in them that they could sort of lump them together and see which ones still hold water. It’s always useful to be able to look at patterns in the research and see if you can find some consistent trends,” he told this news organization.
Dr. MacKinnon, who was not part of the research team, also noted that “nonreplicability” is a problem in psychiatry and psychology research, “so being able to show that at least some studies were sufficiently well done, to get a good result, and that they could be replicated in at least one other good study is useful information.”
When it comes to depression, Dr. MacKinnon said, “We just don’t know enough to really pin down a physiologic pathway to explain it. The fact that some people seem to have high cortisol and some people seem to have high permeability of blood-brain barrier, and others have abnormalities in dopamine, is interesting and suggests that depression is likely not a unitary disease with a single cause.”
He cautioned, however, that the findings don’t have immediate clinical implications for individual patients with depression.
“Theoretically, down the road, if you extrapolate from what they found, and if it’s truly the case that this research maps to something that could suggest a different clinical approach, you might be able to determine whether one patient might respond better to an SSRI or an SNRI or something like that,” Dr. MacKinnon said.
Dr. Benros reported grants from Lundbeck Foundation during the conduct of the study. Dr. MacKinnon has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA PSYCHIATRY
Seven hours of sleep is ideal for middle aged and older
Sleep disturbances are common in older age, and previous studies have shown associations between too much or too little sleep and increased risk of cognitive decline, but the ideal amount of sleep for preserving mental health has not been well described, according to the authors of the new paper.
In the study published in Nature Aging, the team of researchers from China and the United Kingdom reviewed data from the UK Biobank, a national database of individuals in the United Kingdom that includes cognitive assessments, mental health questionnaires, and brain imaging data, as well as genetic information.
Sleep is important for physical and psychological health, and also serves a neuroprotective function by clearing waste products from the brain, lead author Yuzhu Li of Fudan University, Shanghai, China, and colleagues wrote.
The study population included 498,277 participants, aged 38-73 years, who completed touchscreen questionnaires about sleep duration between 2006 and 2010. The average age at baseline was 56.5 years, 54% were female, and the mean sleep duration was 7.15 hours.
The researchers also reviewed brain imaging data and genetic data from 39,692 participants in 2014 to examine the relationships between sleep duration and brain structure and between sleep duration and genetic risk. In addition, 156,884 participants completed an online follow-up mental health questionnaire in 2016-2017 to assess the longitudinal impact of sleep on mental health.
Both excessive and insufficient sleep was associated with impaired cognitive performance, evidenced by the U-shaped curve found by the researchers in their data analysis, which used quadratic associations.
Specific cognitive functions including pair matching, trail making, prospective memory, and reaction time were significantly impaired with too much or too little sleep, the researchers said. “This demonstrated the positive association of both insufficient and excessive sleep duration with inferior performance on cognitive tasks.”
When the researchers analyzed the association between sleep duration and mental health, sleep duration also showed a U-shaped association with symptoms of anxiety, depression, mental distress, mania, and self-harm, while well-being showed an inverted U-shape. All associations between sleep duration and mental health were statistically significant after controlling for confounding variables (P < .001).
On further analysis (using two-line tests), the researchers determined that consistent sleep duration of approximately 7 hours per night was optimal for cognitive performance and for good mental health.
The researchers also used neuroimaging data to examine the relationship between sleep duration and brain structure. Overall, greater changes were seen in the regions of the brain involved in cognitive processing and memory.
“The most significant cortical volumes nonlinearly associated with sleep duration included the precentral cortex, the superior frontal gyrus, the lateral orbitofrontal cortex, the pars orbitalis, the frontal pole, and the middle temporal cortex,” the researchers wrote (P < .05 for all).
The association between sleep duration and cognitive function diminished among individuals older than 65 years, compared with those aged approximately 40 years, which suggests that optimal sleep duration may be more beneficial in middle age, the researchers noted. However, no similar impact of age was seen for mental health. For brain structure, the nonlinear relationship between sleep duration and cortical volumes was greatest in those aged 44-59 years, and gradually flattened with older age.
Research supports sleep discussions with patients
“Primary care physicians can use this study in their discussions with middle-aged and older patients to recommend optimal sleep duration and measures to achieve this sleep target,” Noel Deep, MD, a general internist in group practice in Antigo, Wisc., who was not involved in the study, said in an interview.
“This study is important because it demonstrated that both inadequate and excessive sleep patterns were associated with cognitive and mental health changes,” said Dr. Deep. “It supported previous observations of cognitive decline and mental health disorders being linked to disturbed sleep. But this study was unique because it provides data supporting an optimal sleep duration of 7 hours and the ill effects of both insufficient and excessive sleep duration.
“The usual thought process has been to assume that older individuals may not require as much sleep as the younger individuals, but this study supports an optimal time duration of sleep of 7 hours that benefits the older individuals. It was also interesting to note the mental health effects caused by the inadequate and excessive sleep durations,” he added.
As for additional research, “I would like to look into the quality of the sleep, in addition to the duration of sleep,” said Dr. Deep. For example, whether the excessive sleep was caused by poor quality sleep or fragmented sleep leading to the structural and subsequent cognitive decline.
Study limitations
“The current study relied on self-reporting of the sleep duration and was not observed and recorded data,” Dr. Deep noted. “It would also be beneficial to not only rely on healthy volunteers reporting the sleep duration, but also obtain sleep data from individuals with known brain disorders.”
The study findings were limited by several other factors, including the use of total sleep duration only, without other measures of sleep hygiene, the researchers noted. More research is needed to investigate the mechanisms driving the association between too much and not enough sleep and poor mental health and cognitive function.
The study was supported by the National Key R&D Program of China, the Shanghai Municipal Science and Technology Major Project, the Shanghai Center for Brain Science and Brain-Inspired Technology, the 111 Project, the National Natural Sciences Foundation of China and the Shanghai Rising Star Program.
The researchers had no financial conflicts to disclose. Dr. Deep had no financial conflicts to disclose, but serves on the editorial advisory board of Internal Medicine News.
Sleep disturbances are common in older age, and previous studies have shown associations between too much or too little sleep and increased risk of cognitive decline, but the ideal amount of sleep for preserving mental health has not been well described, according to the authors of the new paper.
In the study published in Nature Aging, the team of researchers from China and the United Kingdom reviewed data from the UK Biobank, a national database of individuals in the United Kingdom that includes cognitive assessments, mental health questionnaires, and brain imaging data, as well as genetic information.
Sleep is important for physical and psychological health, and also serves a neuroprotective function by clearing waste products from the brain, lead author Yuzhu Li of Fudan University, Shanghai, China, and colleagues wrote.
The study population included 498,277 participants, aged 38-73 years, who completed touchscreen questionnaires about sleep duration between 2006 and 2010. The average age at baseline was 56.5 years, 54% were female, and the mean sleep duration was 7.15 hours.
The researchers also reviewed brain imaging data and genetic data from 39,692 participants in 2014 to examine the relationships between sleep duration and brain structure and between sleep duration and genetic risk. In addition, 156,884 participants completed an online follow-up mental health questionnaire in 2016-2017 to assess the longitudinal impact of sleep on mental health.
Both excessive and insufficient sleep was associated with impaired cognitive performance, evidenced by the U-shaped curve found by the researchers in their data analysis, which used quadratic associations.
Specific cognitive functions including pair matching, trail making, prospective memory, and reaction time were significantly impaired with too much or too little sleep, the researchers said. “This demonstrated the positive association of both insufficient and excessive sleep duration with inferior performance on cognitive tasks.”
When the researchers analyzed the association between sleep duration and mental health, sleep duration also showed a U-shaped association with symptoms of anxiety, depression, mental distress, mania, and self-harm, while well-being showed an inverted U-shape. All associations between sleep duration and mental health were statistically significant after controlling for confounding variables (P < .001).
On further analysis (using two-line tests), the researchers determined that consistent sleep duration of approximately 7 hours per night was optimal for cognitive performance and for good mental health.
The researchers also used neuroimaging data to examine the relationship between sleep duration and brain structure. Overall, greater changes were seen in the regions of the brain involved in cognitive processing and memory.
“The most significant cortical volumes nonlinearly associated with sleep duration included the precentral cortex, the superior frontal gyrus, the lateral orbitofrontal cortex, the pars orbitalis, the frontal pole, and the middle temporal cortex,” the researchers wrote (P < .05 for all).
The association between sleep duration and cognitive function diminished among individuals older than 65 years, compared with those aged approximately 40 years, which suggests that optimal sleep duration may be more beneficial in middle age, the researchers noted. However, no similar impact of age was seen for mental health. For brain structure, the nonlinear relationship between sleep duration and cortical volumes was greatest in those aged 44-59 years, and gradually flattened with older age.
Research supports sleep discussions with patients
“Primary care physicians can use this study in their discussions with middle-aged and older patients to recommend optimal sleep duration and measures to achieve this sleep target,” Noel Deep, MD, a general internist in group practice in Antigo, Wisc., who was not involved in the study, said in an interview.
“This study is important because it demonstrated that both inadequate and excessive sleep patterns were associated with cognitive and mental health changes,” said Dr. Deep. “It supported previous observations of cognitive decline and mental health disorders being linked to disturbed sleep. But this study was unique because it provides data supporting an optimal sleep duration of 7 hours and the ill effects of both insufficient and excessive sleep duration.
“The usual thought process has been to assume that older individuals may not require as much sleep as the younger individuals, but this study supports an optimal time duration of sleep of 7 hours that benefits the older individuals. It was also interesting to note the mental health effects caused by the inadequate and excessive sleep durations,” he added.
As for additional research, “I would like to look into the quality of the sleep, in addition to the duration of sleep,” said Dr. Deep. For example, whether the excessive sleep was caused by poor quality sleep or fragmented sleep leading to the structural and subsequent cognitive decline.
Study limitations
“The current study relied on self-reporting of the sleep duration and was not observed and recorded data,” Dr. Deep noted. “It would also be beneficial to not only rely on healthy volunteers reporting the sleep duration, but also obtain sleep data from individuals with known brain disorders.”
The study findings were limited by several other factors, including the use of total sleep duration only, without other measures of sleep hygiene, the researchers noted. More research is needed to investigate the mechanisms driving the association between too much and not enough sleep and poor mental health and cognitive function.
The study was supported by the National Key R&D Program of China, the Shanghai Municipal Science and Technology Major Project, the Shanghai Center for Brain Science and Brain-Inspired Technology, the 111 Project, the National Natural Sciences Foundation of China and the Shanghai Rising Star Program.
The researchers had no financial conflicts to disclose. Dr. Deep had no financial conflicts to disclose, but serves on the editorial advisory board of Internal Medicine News.
Sleep disturbances are common in older age, and previous studies have shown associations between too much or too little sleep and increased risk of cognitive decline, but the ideal amount of sleep for preserving mental health has not been well described, according to the authors of the new paper.
In the study published in Nature Aging, the team of researchers from China and the United Kingdom reviewed data from the UK Biobank, a national database of individuals in the United Kingdom that includes cognitive assessments, mental health questionnaires, and brain imaging data, as well as genetic information.
Sleep is important for physical and psychological health, and also serves a neuroprotective function by clearing waste products from the brain, lead author Yuzhu Li of Fudan University, Shanghai, China, and colleagues wrote.
The study population included 498,277 participants, aged 38-73 years, who completed touchscreen questionnaires about sleep duration between 2006 and 2010. The average age at baseline was 56.5 years, 54% were female, and the mean sleep duration was 7.15 hours.
The researchers also reviewed brain imaging data and genetic data from 39,692 participants in 2014 to examine the relationships between sleep duration and brain structure and between sleep duration and genetic risk. In addition, 156,884 participants completed an online follow-up mental health questionnaire in 2016-2017 to assess the longitudinal impact of sleep on mental health.
Both excessive and insufficient sleep was associated with impaired cognitive performance, evidenced by the U-shaped curve found by the researchers in their data analysis, which used quadratic associations.
Specific cognitive functions including pair matching, trail making, prospective memory, and reaction time were significantly impaired with too much or too little sleep, the researchers said. “This demonstrated the positive association of both insufficient and excessive sleep duration with inferior performance on cognitive tasks.”
When the researchers analyzed the association between sleep duration and mental health, sleep duration also showed a U-shaped association with symptoms of anxiety, depression, mental distress, mania, and self-harm, while well-being showed an inverted U-shape. All associations between sleep duration and mental health were statistically significant after controlling for confounding variables (P < .001).
On further analysis (using two-line tests), the researchers determined that consistent sleep duration of approximately 7 hours per night was optimal for cognitive performance and for good mental health.
The researchers also used neuroimaging data to examine the relationship between sleep duration and brain structure. Overall, greater changes were seen in the regions of the brain involved in cognitive processing and memory.
“The most significant cortical volumes nonlinearly associated with sleep duration included the precentral cortex, the superior frontal gyrus, the lateral orbitofrontal cortex, the pars orbitalis, the frontal pole, and the middle temporal cortex,” the researchers wrote (P < .05 for all).
The association between sleep duration and cognitive function diminished among individuals older than 65 years, compared with those aged approximately 40 years, which suggests that optimal sleep duration may be more beneficial in middle age, the researchers noted. However, no similar impact of age was seen for mental health. For brain structure, the nonlinear relationship between sleep duration and cortical volumes was greatest in those aged 44-59 years, and gradually flattened with older age.
Research supports sleep discussions with patients
“Primary care physicians can use this study in their discussions with middle-aged and older patients to recommend optimal sleep duration and measures to achieve this sleep target,” Noel Deep, MD, a general internist in group practice in Antigo, Wisc., who was not involved in the study, said in an interview.
“This study is important because it demonstrated that both inadequate and excessive sleep patterns were associated with cognitive and mental health changes,” said Dr. Deep. “It supported previous observations of cognitive decline and mental health disorders being linked to disturbed sleep. But this study was unique because it provides data supporting an optimal sleep duration of 7 hours and the ill effects of both insufficient and excessive sleep duration.
“The usual thought process has been to assume that older individuals may not require as much sleep as the younger individuals, but this study supports an optimal time duration of sleep of 7 hours that benefits the older individuals. It was also interesting to note the mental health effects caused by the inadequate and excessive sleep durations,” he added.
As for additional research, “I would like to look into the quality of the sleep, in addition to the duration of sleep,” said Dr. Deep. For example, whether the excessive sleep was caused by poor quality sleep or fragmented sleep leading to the structural and subsequent cognitive decline.
Study limitations
“The current study relied on self-reporting of the sleep duration and was not observed and recorded data,” Dr. Deep noted. “It would also be beneficial to not only rely on healthy volunteers reporting the sleep duration, but also obtain sleep data from individuals with known brain disorders.”
The study findings were limited by several other factors, including the use of total sleep duration only, without other measures of sleep hygiene, the researchers noted. More research is needed to investigate the mechanisms driving the association between too much and not enough sleep and poor mental health and cognitive function.
The study was supported by the National Key R&D Program of China, the Shanghai Municipal Science and Technology Major Project, the Shanghai Center for Brain Science and Brain-Inspired Technology, the 111 Project, the National Natural Sciences Foundation of China and the Shanghai Rising Star Program.
The researchers had no financial conflicts to disclose. Dr. Deep had no financial conflicts to disclose, but serves on the editorial advisory board of Internal Medicine News.
FROM NATURE AGING
Severe COVID-19 adds 20 years of cognitive aging: Study
adding that the impairment is “equivalent to losing 10 IQ points.”
In their study, published in eClinicalMedicine, a team of scientists from the University of Cambridge and Imperial College London said there is growing evidence that COVID-19 can cause lasting cognitive and mental health problems. Patients report fatigue, “brain fog,” problems recalling words, sleep disturbances, anxiety, and even posttraumatic stress disorder months after infection.
The researchers analyzed data from 46 individuals who received critical care for COVID-19 at Addenbrooke’s Hospital between March and July 2020 (27 females, 19 males, mean age 51 years, 16 of whom had mechanical ventilation) and were recruited to the NIHR COVID-19 BioResource project.
At an average of 6 months after acute COVID-19 illness, the study participants underwent detailed computerized cognitive tests via the Cognitron platform, comprising eight tasks deployed on an iPad measuring mental function such as memory, attention, and reasoning. Also assessed were anxiety, depression, and posttraumatic stress disorder via standard mood, anxiety, and posttraumatic stress scales – specifically the Generalized Anxiety Disorder 7 (GAD-7), the Patient Health Questionnaire 9 (PHQ-9), and the PTSD Checklist for Diagnostic and Statistical Manual of Mental Disorders 5 (PCL-5). Their data were compared against 460 controls – matched for age, sex, education, and first language – and the pattern of deficits across tasks was qualitatively compared with normal age-related decline and early-stage dementia.
Less accurate and slower response times
The authors highlighted how this was the first time a “rigorous assessment and comparison” had been carried out in relation to the after-effects of severe COVID-19.
“Cognitive impairment is common to a wide range of neurological disorders, including dementia, and even routine aging, but the patterns we saw – the cognitive ‘fingerprint’ of COVID-19 – was distinct from all of these,” said David Menon, MD, division of anesthesia at the University of Cambridge, England, and the study’s senior author.
The scientists found that COVID-19 survivors were less accurate and had slower response times than the control population, and added that survivors scored particularly poorly on verbal analogical reasoning and showed slower processing speeds.
Critically, the scale of the cognitive deficits correlated with acute illness severity, but not fatigue or mental health status at the time of cognitive assessment, said the authors.
Recovery ‘at best gradual’
The effects were strongest for those with more severe acute illness, and who required mechanical ventilation, said the authors, who found that acute illness severity was “better at predicting the cognitive deficits.”
The authors pointed out how these deficits were still detectable when patients were followed up 6 months later, and that, although patients’ scores and reaction times began to improve over time, any recovery was “at best gradual” and likely to be influenced by factors such as illness severity and its neurological or psychological impacts.
“We followed some patients up as late as 10 months after their acute infection, so were able to see a very slow improvement,” Dr. Menon said. He explained how, while this improvement was not statistically significant, it was “at least heading in the right direction.”
However, he warned it is very possible that some of these individuals “will never fully recover.”
The cognitive deficits observed may be due to several factors in combination, said the authors, including inadequate oxygen or blood supply to the brain, blockage of large or small blood vessels due to clotting, and microscopic bleeds. They highlighted how the most important mechanism, however, may be “damage caused by the body’s own inflammatory response and immune system.”
Adam Hampshire, PhD, of the department of brain sciences at Imperial College London, one of the study’s authors, described how around 40,000 people have been through intensive care with COVID-19 in England alone, with many more despite having been very sick not admitted to hospital. This means there is a “large number of people out there still experiencing problems with cognition many months later,” he said. “We urgently need to look at what can be done to help these people.”
A version of this article first appeared on Univadis.
adding that the impairment is “equivalent to losing 10 IQ points.”
In their study, published in eClinicalMedicine, a team of scientists from the University of Cambridge and Imperial College London said there is growing evidence that COVID-19 can cause lasting cognitive and mental health problems. Patients report fatigue, “brain fog,” problems recalling words, sleep disturbances, anxiety, and even posttraumatic stress disorder months after infection.
The researchers analyzed data from 46 individuals who received critical care for COVID-19 at Addenbrooke’s Hospital between March and July 2020 (27 females, 19 males, mean age 51 years, 16 of whom had mechanical ventilation) and were recruited to the NIHR COVID-19 BioResource project.
At an average of 6 months after acute COVID-19 illness, the study participants underwent detailed computerized cognitive tests via the Cognitron platform, comprising eight tasks deployed on an iPad measuring mental function such as memory, attention, and reasoning. Also assessed were anxiety, depression, and posttraumatic stress disorder via standard mood, anxiety, and posttraumatic stress scales – specifically the Generalized Anxiety Disorder 7 (GAD-7), the Patient Health Questionnaire 9 (PHQ-9), and the PTSD Checklist for Diagnostic and Statistical Manual of Mental Disorders 5 (PCL-5). Their data were compared against 460 controls – matched for age, sex, education, and first language – and the pattern of deficits across tasks was qualitatively compared with normal age-related decline and early-stage dementia.
Less accurate and slower response times
The authors highlighted how this was the first time a “rigorous assessment and comparison” had been carried out in relation to the after-effects of severe COVID-19.
“Cognitive impairment is common to a wide range of neurological disorders, including dementia, and even routine aging, but the patterns we saw – the cognitive ‘fingerprint’ of COVID-19 – was distinct from all of these,” said David Menon, MD, division of anesthesia at the University of Cambridge, England, and the study’s senior author.
The scientists found that COVID-19 survivors were less accurate and had slower response times than the control population, and added that survivors scored particularly poorly on verbal analogical reasoning and showed slower processing speeds.
Critically, the scale of the cognitive deficits correlated with acute illness severity, but not fatigue or mental health status at the time of cognitive assessment, said the authors.
Recovery ‘at best gradual’
The effects were strongest for those with more severe acute illness, and who required mechanical ventilation, said the authors, who found that acute illness severity was “better at predicting the cognitive deficits.”
The authors pointed out how these deficits were still detectable when patients were followed up 6 months later, and that, although patients’ scores and reaction times began to improve over time, any recovery was “at best gradual” and likely to be influenced by factors such as illness severity and its neurological or psychological impacts.
“We followed some patients up as late as 10 months after their acute infection, so were able to see a very slow improvement,” Dr. Menon said. He explained how, while this improvement was not statistically significant, it was “at least heading in the right direction.”
However, he warned it is very possible that some of these individuals “will never fully recover.”
The cognitive deficits observed may be due to several factors in combination, said the authors, including inadequate oxygen or blood supply to the brain, blockage of large or small blood vessels due to clotting, and microscopic bleeds. They highlighted how the most important mechanism, however, may be “damage caused by the body’s own inflammatory response and immune system.”
Adam Hampshire, PhD, of the department of brain sciences at Imperial College London, one of the study’s authors, described how around 40,000 people have been through intensive care with COVID-19 in England alone, with many more despite having been very sick not admitted to hospital. This means there is a “large number of people out there still experiencing problems with cognition many months later,” he said. “We urgently need to look at what can be done to help these people.”
A version of this article first appeared on Univadis.
adding that the impairment is “equivalent to losing 10 IQ points.”
In their study, published in eClinicalMedicine, a team of scientists from the University of Cambridge and Imperial College London said there is growing evidence that COVID-19 can cause lasting cognitive and mental health problems. Patients report fatigue, “brain fog,” problems recalling words, sleep disturbances, anxiety, and even posttraumatic stress disorder months after infection.
The researchers analyzed data from 46 individuals who received critical care for COVID-19 at Addenbrooke’s Hospital between March and July 2020 (27 females, 19 males, mean age 51 years, 16 of whom had mechanical ventilation) and were recruited to the NIHR COVID-19 BioResource project.
At an average of 6 months after acute COVID-19 illness, the study participants underwent detailed computerized cognitive tests via the Cognitron platform, comprising eight tasks deployed on an iPad measuring mental function such as memory, attention, and reasoning. Also assessed were anxiety, depression, and posttraumatic stress disorder via standard mood, anxiety, and posttraumatic stress scales – specifically the Generalized Anxiety Disorder 7 (GAD-7), the Patient Health Questionnaire 9 (PHQ-9), and the PTSD Checklist for Diagnostic and Statistical Manual of Mental Disorders 5 (PCL-5). Their data were compared against 460 controls – matched for age, sex, education, and first language – and the pattern of deficits across tasks was qualitatively compared with normal age-related decline and early-stage dementia.
Less accurate and slower response times
The authors highlighted how this was the first time a “rigorous assessment and comparison” had been carried out in relation to the after-effects of severe COVID-19.
“Cognitive impairment is common to a wide range of neurological disorders, including dementia, and even routine aging, but the patterns we saw – the cognitive ‘fingerprint’ of COVID-19 – was distinct from all of these,” said David Menon, MD, division of anesthesia at the University of Cambridge, England, and the study’s senior author.
The scientists found that COVID-19 survivors were less accurate and had slower response times than the control population, and added that survivors scored particularly poorly on verbal analogical reasoning and showed slower processing speeds.
Critically, the scale of the cognitive deficits correlated with acute illness severity, but not fatigue or mental health status at the time of cognitive assessment, said the authors.
Recovery ‘at best gradual’
The effects were strongest for those with more severe acute illness, and who required mechanical ventilation, said the authors, who found that acute illness severity was “better at predicting the cognitive deficits.”
The authors pointed out how these deficits were still detectable when patients were followed up 6 months later, and that, although patients’ scores and reaction times began to improve over time, any recovery was “at best gradual” and likely to be influenced by factors such as illness severity and its neurological or psychological impacts.
“We followed some patients up as late as 10 months after their acute infection, so were able to see a very slow improvement,” Dr. Menon said. He explained how, while this improvement was not statistically significant, it was “at least heading in the right direction.”
However, he warned it is very possible that some of these individuals “will never fully recover.”
The cognitive deficits observed may be due to several factors in combination, said the authors, including inadequate oxygen or blood supply to the brain, blockage of large or small blood vessels due to clotting, and microscopic bleeds. They highlighted how the most important mechanism, however, may be “damage caused by the body’s own inflammatory response and immune system.”
Adam Hampshire, PhD, of the department of brain sciences at Imperial College London, one of the study’s authors, described how around 40,000 people have been through intensive care with COVID-19 in England alone, with many more despite having been very sick not admitted to hospital. This means there is a “large number of people out there still experiencing problems with cognition many months later,” he said. “We urgently need to look at what can be done to help these people.”
A version of this article first appeared on Univadis.
FROM ECLINICAL MEDICINE
Should you be screening for eating disorders?
The US Preventive Services Task Force recently released its findings on screening for eating disorders—including binge eating, bulimia nervosa, and anorexia nervosa—in adolescents and adults.1 This is the first time the Task Force has addressed this topic.
For those who have no signs or symptoms of an eating disorder, the Task Force found insufficient evidence to assess the benefits and harms of screening. Signs and symptoms of an eating disorder include rapid changes in weight (gain or loss), delayed puberty, bradycardia, oligomenorrhea, or amenorrhea.1
Screening vs diagnostic work-up. The term screening means looking for the presence of a condition in an asymptomatic person. Those who have signs or symptoms that could be due to an eating disorder should be assessed for these conditions, but this would be classified as diagnostic testing rather than preventive screening.
Relatively uncommon but serious. The estimated lifetime prevalence of anorexia is 1.42% in women and 0.12% in men; for bulimia, 0.46% in women and 0.08% in men; and for binge eating, 1.25% in women and 0.42% in men.1 Those suspected of having an eating disorder need psychological, behavioral, medical, and nutritional care provided by those with expertise in diagnosing and treating these disorders. (A systematic review of treatment options was recently published in American Family Physician.2)
If you suspect an eating disorder … Several tools for the assessment of eating disorders have been described in the literature, including the Eating Disorder Screen for Primary Care (EDS-PC) tool, but the Task Force identified enough evidence to comment on the accuracy of only one: the SCOFF questionnaire. There is adequate evidence on its accuracy for use in adult women but not in adolescents or males.1
The SCOFF tool, which originated in the United Kingdom, consists of 5 questions3:
- Do you make yourself Sick because you feel uncomfortably full?
- Do you worry that you have lost Control over how much you eat?
- Have you recently lost more than One stone (14 lb) in a 3-month period?
- Do you believe yourself to be Fat when others say you are too thin?
- Would you say that Food dominates your life?
A threshold of 2 or more “Yes” answers on the SCOFF questionnaire has a pooled sensitivity of 84% for all 3 disorders combined and a pooled specificity of 80%.4
What should you do routinely? For adolescents and adults who have no indication of an eating disorder, there is no proven value to screening. Measuring height and weight, calculating body mass index, and continuing to track these measurements for all patients over time is considered standard practice. For those patients who have signs or symptoms that could be due to an eating disorder, administer the SCOFF tool; further assess those with 2 or more positive responses, and refer for diagnosis and treatment those suspected of having an eating disorder.
1. USPSTF. Screening for eating disorders in adolescents and adults. JAMA. 2022;327:1061-1066. doi: 10.1001/jama.2022.1806
2. Klein DA, Sylvester JE, Schvey NA. Eating disorders in primary care: diagnosis and management. Am Fam Physician. 2021;103:22-32.
3. Morgan JF, Reid F, Lacy JH. The SCOFF questionnaire: a new screening tool for eating disorders. West J Med. 2000;172:164-165. doi: 10.1136/ewjm.172.3.164
4. Feltner C, Peat C, Reddy S, et al. Evidence Synthesis No 212: Screening for eating disorders in adolescents and adults: an evidence review for the US Preventive Services Task Force. Published March 2022. www.uspreventiveservicestaskforce.org/uspstf/document/final-evidence-review/screening-eating-disorders-adolescents-adults
The US Preventive Services Task Force recently released its findings on screening for eating disorders—including binge eating, bulimia nervosa, and anorexia nervosa—in adolescents and adults.1 This is the first time the Task Force has addressed this topic.
For those who have no signs or symptoms of an eating disorder, the Task Force found insufficient evidence to assess the benefits and harms of screening. Signs and symptoms of an eating disorder include rapid changes in weight (gain or loss), delayed puberty, bradycardia, oligomenorrhea, or amenorrhea.1
Screening vs diagnostic work-up. The term screening means looking for the presence of a condition in an asymptomatic person. Those who have signs or symptoms that could be due to an eating disorder should be assessed for these conditions, but this would be classified as diagnostic testing rather than preventive screening.
Relatively uncommon but serious. The estimated lifetime prevalence of anorexia is 1.42% in women and 0.12% in men; for bulimia, 0.46% in women and 0.08% in men; and for binge eating, 1.25% in women and 0.42% in men.1 Those suspected of having an eating disorder need psychological, behavioral, medical, and nutritional care provided by those with expertise in diagnosing and treating these disorders. (A systematic review of treatment options was recently published in American Family Physician.2)
If you suspect an eating disorder … Several tools for the assessment of eating disorders have been described in the literature, including the Eating Disorder Screen for Primary Care (EDS-PC) tool, but the Task Force identified enough evidence to comment on the accuracy of only one: the SCOFF questionnaire. There is adequate evidence on its accuracy for use in adult women but not in adolescents or males.1
The SCOFF tool, which originated in the United Kingdom, consists of 5 questions3:
- Do you make yourself Sick because you feel uncomfortably full?
- Do you worry that you have lost Control over how much you eat?
- Have you recently lost more than One stone (14 lb) in a 3-month period?
- Do you believe yourself to be Fat when others say you are too thin?
- Would you say that Food dominates your life?
A threshold of 2 or more “Yes” answers on the SCOFF questionnaire has a pooled sensitivity of 84% for all 3 disorders combined and a pooled specificity of 80%.4
What should you do routinely? For adolescents and adults who have no indication of an eating disorder, there is no proven value to screening. Measuring height and weight, calculating body mass index, and continuing to track these measurements for all patients over time is considered standard practice. For those patients who have signs or symptoms that could be due to an eating disorder, administer the SCOFF tool; further assess those with 2 or more positive responses, and refer for diagnosis and treatment those suspected of having an eating disorder.
The US Preventive Services Task Force recently released its findings on screening for eating disorders—including binge eating, bulimia nervosa, and anorexia nervosa—in adolescents and adults.1 This is the first time the Task Force has addressed this topic.
For those who have no signs or symptoms of an eating disorder, the Task Force found insufficient evidence to assess the benefits and harms of screening. Signs and symptoms of an eating disorder include rapid changes in weight (gain or loss), delayed puberty, bradycardia, oligomenorrhea, or amenorrhea.1
Screening vs diagnostic work-up. The term screening means looking for the presence of a condition in an asymptomatic person. Those who have signs or symptoms that could be due to an eating disorder should be assessed for these conditions, but this would be classified as diagnostic testing rather than preventive screening.
Relatively uncommon but serious. The estimated lifetime prevalence of anorexia is 1.42% in women and 0.12% in men; for bulimia, 0.46% in women and 0.08% in men; and for binge eating, 1.25% in women and 0.42% in men.1 Those suspected of having an eating disorder need psychological, behavioral, medical, and nutritional care provided by those with expertise in diagnosing and treating these disorders. (A systematic review of treatment options was recently published in American Family Physician.2)
If you suspect an eating disorder … Several tools for the assessment of eating disorders have been described in the literature, including the Eating Disorder Screen for Primary Care (EDS-PC) tool, but the Task Force identified enough evidence to comment on the accuracy of only one: the SCOFF questionnaire. There is adequate evidence on its accuracy for use in adult women but not in adolescents or males.1
The SCOFF tool, which originated in the United Kingdom, consists of 5 questions3:
- Do you make yourself Sick because you feel uncomfortably full?
- Do you worry that you have lost Control over how much you eat?
- Have you recently lost more than One stone (14 lb) in a 3-month period?
- Do you believe yourself to be Fat when others say you are too thin?
- Would you say that Food dominates your life?
A threshold of 2 or more “Yes” answers on the SCOFF questionnaire has a pooled sensitivity of 84% for all 3 disorders combined and a pooled specificity of 80%.4
What should you do routinely? For adolescents and adults who have no indication of an eating disorder, there is no proven value to screening. Measuring height and weight, calculating body mass index, and continuing to track these measurements for all patients over time is considered standard practice. For those patients who have signs or symptoms that could be due to an eating disorder, administer the SCOFF tool; further assess those with 2 or more positive responses, and refer for diagnosis and treatment those suspected of having an eating disorder.
1. USPSTF. Screening for eating disorders in adolescents and adults. JAMA. 2022;327:1061-1066. doi: 10.1001/jama.2022.1806
2. Klein DA, Sylvester JE, Schvey NA. Eating disorders in primary care: diagnosis and management. Am Fam Physician. 2021;103:22-32.
3. Morgan JF, Reid F, Lacy JH. The SCOFF questionnaire: a new screening tool for eating disorders. West J Med. 2000;172:164-165. doi: 10.1136/ewjm.172.3.164
4. Feltner C, Peat C, Reddy S, et al. Evidence Synthesis No 212: Screening for eating disorders in adolescents and adults: an evidence review for the US Preventive Services Task Force. Published March 2022. www.uspreventiveservicestaskforce.org/uspstf/document/final-evidence-review/screening-eating-disorders-adolescents-adults
1. USPSTF. Screening for eating disorders in adolescents and adults. JAMA. 2022;327:1061-1066. doi: 10.1001/jama.2022.1806
2. Klein DA, Sylvester JE, Schvey NA. Eating disorders in primary care: diagnosis and management. Am Fam Physician. 2021;103:22-32.
3. Morgan JF, Reid F, Lacy JH. The SCOFF questionnaire: a new screening tool for eating disorders. West J Med. 2000;172:164-165. doi: 10.1136/ewjm.172.3.164
4. Feltner C, Peat C, Reddy S, et al. Evidence Synthesis No 212: Screening for eating disorders in adolescents and adults: an evidence review for the US Preventive Services Task Force. Published March 2022. www.uspreventiveservicestaskforce.org/uspstf/document/final-evidence-review/screening-eating-disorders-adolescents-adults
CBT or hypnotherapy may help kids’ functional abdominal pain
Functional abdominal pain in childhood and adolescence is extremely stressful for patients and a therapeutic challenge for the physicians treating them. A meta-analysis of 33 randomized-controlled studies published in JAMA Pediatrics shows that cognitive-behavioral therapy or hypnotherapy promises the greatest therapy success.
“If children or adolescents complain about chronic abdominal pain and a detailed diagnostic does not reveal any somatic cause, this is referred to as functional abdominal pain,” Burkhard Rodeck, MD, general secretary of the German Society of Pediatrics and Adolescent Medicine in Berlin, told this news organization.
Signal perception disorder
“These patients are experiencing a signal perception disorder: normal body signals, such as a slight stomach rumble, are assigned to the pain category for them much more quickly than for other people,” said Dr. Rodeck. “The meta-analysis provides confirmation of this – functional abdominal pain is actually a biopsychosocial matter.”
In the standard therapy of functional abdominal pain, however, it is also possible to choose a medicinal approach. “Studies show that herbal preparations such as peppermint oil capsules have some efficacy, since they attenuate the strength of the signals being sent from the gastrointestinal tract to the brain, with the result that they are not perceived so quickly as pain. Probiotics can also potentially help,” added Dr. Rodeck.
“If this is unsuccessful, the child must be offered a psychologic/psychotherapeutic measure, usually cognitive-behavioral therapy.”
Comparison of psychosocial therapies
The meta-analysis was carried out by a research team at the University of Central Lancashire, Preston, United Kingdom. It included 2,657 children and adolescents between the ages of 7 and 17 years, of which two-thirds were girls.
Various psychosocial therapy approaches for functional abdominal pain, such as cognitive-behavioral therapy, educational assistance, hypnotherapy (directed at the digestive system), guided meditation with relaxation, yoga, or (visceral) osteopathy were investigated and compared in the studies – sometimes against each other and sometimes against no intervention.
Lead author Morris Gordon, MBChB, PhD, professor of evidence synthesis and systematic review at the University of Central Lancashire, and his colleagues reported that cognitive-behavioral therapy was 2.37-times more likely to result in therapy success than no intervention. To treat functional abdominal pain successfully in one child or adolescent, five children needed to be treated with cognitive-behavioral therapy.
Rarer, milder pain
The children and adolescents treated with cognitive-behavioral therapy also experienced less frequent and less severe abdominal pain than the children and adolescents who did not receive any intervention. The rate of side effect–related therapy discontinuations did not differ between the groups.
Hypnotherapy could also be associated with an improved outcome, compared with no intervention, added Dr. Gordon and his colleagues. Hypnotherapy was 2.86-times more likely to result in therapy success, and the number needed to treat was five.
The other therapeutic approaches investigated did not perform any better in the studies than no intervention. However, the authors noted that evidence of the effectiveness of cognitive-behavioral therapy and hypnotherapy is moderate or weak, especially owing to the high bias risk.
“The therapy for functional abdominal pain cannot be compared with the therapy for scarlet fever, for example, where penicillin is administered in the knowledge that recovery is guaranteed. There is evidence that cognitive-behavioral therapy and possibly also hypnotherapy may help, but this is not true for every patient,” said Dr. Rodeck.
Start with the pediatrician
Dr. Gordon and his co-authors suggested considering cognitive-behavioral therapy and hypnotherapy for the treatment of functional abdominal pain in children and adolescents. But they added that further randomized controlled studies are necessary to improve the quality of evidence and therefore the reliability of these results.
Children and adolescents with functional abdominal pain do not need to be sent directly to the psychologist for treatment, said Dr. Rodeck. The pediatric or adolescent medicine specialist can also administer the initial behavioral therapy measures. “Some patients manage with the behavioral therapy approaches we offer as pediatric and adolescent medicine specialists; others require professional support with psychologic expertise,” said Dr. Rodeck. Should outpatient treatment be unsuccessful, inpatient therapy in special psychosomatic clinics or wards remains an option.
Education offers relief
For many patients, being informed about the connections and mechanisms that play a role in functional abdominal pain can offer a lot of relief, said Dr. Rodeck. Offering coping strategies that can be used in the event of acute symptoms is also a part of this education.
“If patients have functional abdominal pain for which no organic cause can be found, this can lead to frustration, sadness, and despair. The problem can become even worse if they feel that they are not being taken seriously by the physician,” said Dr. Rodeck. These negative experiences can further exacerbate the pain perception disorder. The aim of behavioral therapy measures is therefore to interrupt and downregulate this vicious cycle.
“Constant investigations are not always helpful for patients with functional abdominal pain. Time must be taken with these patients to talk and explore the options. They have definite abdominal pain, they are not imagining it. They must be taken seriously,” he emphasized.
A version of this article first appeared on Medscape.com.
Functional abdominal pain in childhood and adolescence is extremely stressful for patients and a therapeutic challenge for the physicians treating them. A meta-analysis of 33 randomized-controlled studies published in JAMA Pediatrics shows that cognitive-behavioral therapy or hypnotherapy promises the greatest therapy success.
“If children or adolescents complain about chronic abdominal pain and a detailed diagnostic does not reveal any somatic cause, this is referred to as functional abdominal pain,” Burkhard Rodeck, MD, general secretary of the German Society of Pediatrics and Adolescent Medicine in Berlin, told this news organization.
Signal perception disorder
“These patients are experiencing a signal perception disorder: normal body signals, such as a slight stomach rumble, are assigned to the pain category for them much more quickly than for other people,” said Dr. Rodeck. “The meta-analysis provides confirmation of this – functional abdominal pain is actually a biopsychosocial matter.”
In the standard therapy of functional abdominal pain, however, it is also possible to choose a medicinal approach. “Studies show that herbal preparations such as peppermint oil capsules have some efficacy, since they attenuate the strength of the signals being sent from the gastrointestinal tract to the brain, with the result that they are not perceived so quickly as pain. Probiotics can also potentially help,” added Dr. Rodeck.
“If this is unsuccessful, the child must be offered a psychologic/psychotherapeutic measure, usually cognitive-behavioral therapy.”
Comparison of psychosocial therapies
The meta-analysis was carried out by a research team at the University of Central Lancashire, Preston, United Kingdom. It included 2,657 children and adolescents between the ages of 7 and 17 years, of which two-thirds were girls.
Various psychosocial therapy approaches for functional abdominal pain, such as cognitive-behavioral therapy, educational assistance, hypnotherapy (directed at the digestive system), guided meditation with relaxation, yoga, or (visceral) osteopathy were investigated and compared in the studies – sometimes against each other and sometimes against no intervention.
Lead author Morris Gordon, MBChB, PhD, professor of evidence synthesis and systematic review at the University of Central Lancashire, and his colleagues reported that cognitive-behavioral therapy was 2.37-times more likely to result in therapy success than no intervention. To treat functional abdominal pain successfully in one child or adolescent, five children needed to be treated with cognitive-behavioral therapy.
Rarer, milder pain
The children and adolescents treated with cognitive-behavioral therapy also experienced less frequent and less severe abdominal pain than the children and adolescents who did not receive any intervention. The rate of side effect–related therapy discontinuations did not differ between the groups.
Hypnotherapy could also be associated with an improved outcome, compared with no intervention, added Dr. Gordon and his colleagues. Hypnotherapy was 2.86-times more likely to result in therapy success, and the number needed to treat was five.
The other therapeutic approaches investigated did not perform any better in the studies than no intervention. However, the authors noted that evidence of the effectiveness of cognitive-behavioral therapy and hypnotherapy is moderate or weak, especially owing to the high bias risk.
“The therapy for functional abdominal pain cannot be compared with the therapy for scarlet fever, for example, where penicillin is administered in the knowledge that recovery is guaranteed. There is evidence that cognitive-behavioral therapy and possibly also hypnotherapy may help, but this is not true for every patient,” said Dr. Rodeck.
Start with the pediatrician
Dr. Gordon and his co-authors suggested considering cognitive-behavioral therapy and hypnotherapy for the treatment of functional abdominal pain in children and adolescents. But they added that further randomized controlled studies are necessary to improve the quality of evidence and therefore the reliability of these results.
Children and adolescents with functional abdominal pain do not need to be sent directly to the psychologist for treatment, said Dr. Rodeck. The pediatric or adolescent medicine specialist can also administer the initial behavioral therapy measures. “Some patients manage with the behavioral therapy approaches we offer as pediatric and adolescent medicine specialists; others require professional support with psychologic expertise,” said Dr. Rodeck. Should outpatient treatment be unsuccessful, inpatient therapy in special psychosomatic clinics or wards remains an option.
Education offers relief
For many patients, being informed about the connections and mechanisms that play a role in functional abdominal pain can offer a lot of relief, said Dr. Rodeck. Offering coping strategies that can be used in the event of acute symptoms is also a part of this education.
“If patients have functional abdominal pain for which no organic cause can be found, this can lead to frustration, sadness, and despair. The problem can become even worse if they feel that they are not being taken seriously by the physician,” said Dr. Rodeck. These negative experiences can further exacerbate the pain perception disorder. The aim of behavioral therapy measures is therefore to interrupt and downregulate this vicious cycle.
“Constant investigations are not always helpful for patients with functional abdominal pain. Time must be taken with these patients to talk and explore the options. They have definite abdominal pain, they are not imagining it. They must be taken seriously,” he emphasized.
A version of this article first appeared on Medscape.com.
Functional abdominal pain in childhood and adolescence is extremely stressful for patients and a therapeutic challenge for the physicians treating them. A meta-analysis of 33 randomized-controlled studies published in JAMA Pediatrics shows that cognitive-behavioral therapy or hypnotherapy promises the greatest therapy success.
“If children or adolescents complain about chronic abdominal pain and a detailed diagnostic does not reveal any somatic cause, this is referred to as functional abdominal pain,” Burkhard Rodeck, MD, general secretary of the German Society of Pediatrics and Adolescent Medicine in Berlin, told this news organization.
Signal perception disorder
“These patients are experiencing a signal perception disorder: normal body signals, such as a slight stomach rumble, are assigned to the pain category for them much more quickly than for other people,” said Dr. Rodeck. “The meta-analysis provides confirmation of this – functional abdominal pain is actually a biopsychosocial matter.”
In the standard therapy of functional abdominal pain, however, it is also possible to choose a medicinal approach. “Studies show that herbal preparations such as peppermint oil capsules have some efficacy, since they attenuate the strength of the signals being sent from the gastrointestinal tract to the brain, with the result that they are not perceived so quickly as pain. Probiotics can also potentially help,” added Dr. Rodeck.
“If this is unsuccessful, the child must be offered a psychologic/psychotherapeutic measure, usually cognitive-behavioral therapy.”
Comparison of psychosocial therapies
The meta-analysis was carried out by a research team at the University of Central Lancashire, Preston, United Kingdom. It included 2,657 children and adolescents between the ages of 7 and 17 years, of which two-thirds were girls.
Various psychosocial therapy approaches for functional abdominal pain, such as cognitive-behavioral therapy, educational assistance, hypnotherapy (directed at the digestive system), guided meditation with relaxation, yoga, or (visceral) osteopathy were investigated and compared in the studies – sometimes against each other and sometimes against no intervention.
Lead author Morris Gordon, MBChB, PhD, professor of evidence synthesis and systematic review at the University of Central Lancashire, and his colleagues reported that cognitive-behavioral therapy was 2.37-times more likely to result in therapy success than no intervention. To treat functional abdominal pain successfully in one child or adolescent, five children needed to be treated with cognitive-behavioral therapy.
Rarer, milder pain
The children and adolescents treated with cognitive-behavioral therapy also experienced less frequent and less severe abdominal pain than the children and adolescents who did not receive any intervention. The rate of side effect–related therapy discontinuations did not differ between the groups.
Hypnotherapy could also be associated with an improved outcome, compared with no intervention, added Dr. Gordon and his colleagues. Hypnotherapy was 2.86-times more likely to result in therapy success, and the number needed to treat was five.
The other therapeutic approaches investigated did not perform any better in the studies than no intervention. However, the authors noted that evidence of the effectiveness of cognitive-behavioral therapy and hypnotherapy is moderate or weak, especially owing to the high bias risk.
“The therapy for functional abdominal pain cannot be compared with the therapy for scarlet fever, for example, where penicillin is administered in the knowledge that recovery is guaranteed. There is evidence that cognitive-behavioral therapy and possibly also hypnotherapy may help, but this is not true for every patient,” said Dr. Rodeck.
Start with the pediatrician
Dr. Gordon and his co-authors suggested considering cognitive-behavioral therapy and hypnotherapy for the treatment of functional abdominal pain in children and adolescents. But they added that further randomized controlled studies are necessary to improve the quality of evidence and therefore the reliability of these results.
Children and adolescents with functional abdominal pain do not need to be sent directly to the psychologist for treatment, said Dr. Rodeck. The pediatric or adolescent medicine specialist can also administer the initial behavioral therapy measures. “Some patients manage with the behavioral therapy approaches we offer as pediatric and adolescent medicine specialists; others require professional support with psychologic expertise,” said Dr. Rodeck. Should outpatient treatment be unsuccessful, inpatient therapy in special psychosomatic clinics or wards remains an option.
Education offers relief
For many patients, being informed about the connections and mechanisms that play a role in functional abdominal pain can offer a lot of relief, said Dr. Rodeck. Offering coping strategies that can be used in the event of acute symptoms is also a part of this education.
“If patients have functional abdominal pain for which no organic cause can be found, this can lead to frustration, sadness, and despair. The problem can become even worse if they feel that they are not being taken seriously by the physician,” said Dr. Rodeck. These negative experiences can further exacerbate the pain perception disorder. The aim of behavioral therapy measures is therefore to interrupt and downregulate this vicious cycle.
“Constant investigations are not always helpful for patients with functional abdominal pain. Time must be taken with these patients to talk and explore the options. They have definite abdominal pain, they are not imagining it. They must be taken seriously,” he emphasized.
A version of this article first appeared on Medscape.com.
Maternal autoimmune diseases up risk of mental illness in children
Mental disorders were significantly more likely in children whose mothers had one of five common autoimmune diseases, a new study found.
Previous research has linked both maternal and paternal autoimmune diseases and specific mental disorders, such as attention-deficit/hyperactivity disorder (ADHD), but most of these studies focused on specific conditions in relatively small populations. The new study included data on more than 2 million births, making it one of the largest efforts to date to examine the association, according to the researchers, whose findings were published in JAMA Network Open.
Previous evidence of the possible association between certain maternal autoimmune diseases and mental disorders in offspring has been “scattered and limited,” which “hampered an overall understanding” of the link, Fei Li, MD, the corresponding author of the study, told this news organization.
Dr. Li, of Shanghai Jiao Tong University China, and colleagues reviewed data from a Danish registry cohort of singleton births with up to 38 years of follow-up. They explored associations between a range of maternal autoimmune diseases diagnosed before childbirth and the risks of mental disorders in children in early childhood through young adulthood.
The study population included 2,254,234 births and 38,916,359 person-years. Data on mental health were collected from the Psychiatric Central Research Register and the country’s National Patient Register. The median age of the children at the time of assessment was 16.7 years; approximately half were male.
A total of 50,863 children (2.26%) were born to mothers who had been diagnosed with autoimmune diseases before childbirth. During the follow-up period, 5,460 children of mothers with autoimmune diseases and 303,092 children of mothers without autoimmune diseases were diagnosed with a mental disorder (10.73% vs. 13.76%), according to the researchers.
The risk of being diagnosed with a mental disorder was significantly higher among children of mothers with any autoimmune disease (hazard ratio [HR,], 1.16), with an incidence of 9.38 vs. 7.91 per 1,000 person-years, the researchers reported.
The increased risk persisted when the results were classified by organ system, including connective tissue (HR, 1.11), endocrine (HR, 1.19), gastrointestinal (HR, 1.11), blood (HR, 1.10), nervous (HR, 1.17), and skin (HR, 1.19).
The five autoimmune diseases in mothers that were most commonly associated mental health disorders in children were type 1 diabetes, rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, and psoriasis vulgaris.
The greatest risk for children of mothers with any autoimmune disease was observed for organic conditions such as delirium, (HR, 1.54), followed by obsessive-compulsive disorder (HR, 1.42), schizophrenia (HR, 1.54), and mood problems (HR, 1.12).
Children of mothers with any autoimmune disorder also had a significantly increased risk of autism (HR, 1.21), intellectual disability (HR, 1.19), and ADHD (HR, 1.19).
The results add to evidence that activation of the maternal immune system may drive changes in the brain and behavioral problems, which has been observed in animal studies, the researchers wrote.
Potential underlying mechanisms in need of more exploration include genetic risk factors, maternal transmission of autoantibodies to the fetus during pregnancy, and the increased risk of obstetric complications, such as preterm birth, for women with autoimmune disorders that could affect mental development in children, they added.
The study findings were limited by several factors, including the lack of data on potential exacerbation of autoimmune disease activity during pregnancy and its effect on the fetus, the researchers noted. Other limitations included potential detection bias, lack of data on mental disorders in adulthood, and potential changes in diagnostic criteria over the long study period.
The results were strengthened by the use of a population-based registry, the large sample size, and ability to consider a range of confounders, the researchers said.
“This study could help acquire a comprehensive compilation of the associations between maternal autoimmune disorders diagnosed before childbirth and offspring’s mental disorders from childhood through early adulthood,” Dr. Li said in an interview.
For clinicians, Dr. Li said, the findings suggest that the offspring of mothers with autoimmune diseases may benefit from long-term surveillance for mental health disorders.
“Further studies should provide more evidence on the detailed associations of specific maternal autoimmune diseases with a full spectrum of mental disorders in offspring, and more research on underlying mechanisms is needed as well,” she said.
Pay early attention
M. Susan Jay, MD, an adjunct professor of pediatrics at the Medical College of Wisconsin, Milwaukee, said previous efforts to examine the association between maternal autoimmunity were hampered by study design, small samples, and self-report of disease history – problems the new research avoids.
The large patient population allowed for detailed subgroup analysis of different conditions and outcomes. Another advantage was the availability of sociodemographic and clinical information, which allowed for the elimination of confounding factors, said Dr. Jay, who was not involved in the research.
“It would be prudent to follow children of mothers with autoimmune disorders before or during pregnancy for mental health issues, and if identified clinically, to offer psychological and developmental behavioral support options,” Dr. Jay added.
The authors have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Mental disorders were significantly more likely in children whose mothers had one of five common autoimmune diseases, a new study found.
Previous research has linked both maternal and paternal autoimmune diseases and specific mental disorders, such as attention-deficit/hyperactivity disorder (ADHD), but most of these studies focused on specific conditions in relatively small populations. The new study included data on more than 2 million births, making it one of the largest efforts to date to examine the association, according to the researchers, whose findings were published in JAMA Network Open.
Previous evidence of the possible association between certain maternal autoimmune diseases and mental disorders in offspring has been “scattered and limited,” which “hampered an overall understanding” of the link, Fei Li, MD, the corresponding author of the study, told this news organization.
Dr. Li, of Shanghai Jiao Tong University China, and colleagues reviewed data from a Danish registry cohort of singleton births with up to 38 years of follow-up. They explored associations between a range of maternal autoimmune diseases diagnosed before childbirth and the risks of mental disorders in children in early childhood through young adulthood.
The study population included 2,254,234 births and 38,916,359 person-years. Data on mental health were collected from the Psychiatric Central Research Register and the country’s National Patient Register. The median age of the children at the time of assessment was 16.7 years; approximately half were male.
A total of 50,863 children (2.26%) were born to mothers who had been diagnosed with autoimmune diseases before childbirth. During the follow-up period, 5,460 children of mothers with autoimmune diseases and 303,092 children of mothers without autoimmune diseases were diagnosed with a mental disorder (10.73% vs. 13.76%), according to the researchers.
The risk of being diagnosed with a mental disorder was significantly higher among children of mothers with any autoimmune disease (hazard ratio [HR,], 1.16), with an incidence of 9.38 vs. 7.91 per 1,000 person-years, the researchers reported.
The increased risk persisted when the results were classified by organ system, including connective tissue (HR, 1.11), endocrine (HR, 1.19), gastrointestinal (HR, 1.11), blood (HR, 1.10), nervous (HR, 1.17), and skin (HR, 1.19).
The five autoimmune diseases in mothers that were most commonly associated mental health disorders in children were type 1 diabetes, rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, and psoriasis vulgaris.
The greatest risk for children of mothers with any autoimmune disease was observed for organic conditions such as delirium, (HR, 1.54), followed by obsessive-compulsive disorder (HR, 1.42), schizophrenia (HR, 1.54), and mood problems (HR, 1.12).
Children of mothers with any autoimmune disorder also had a significantly increased risk of autism (HR, 1.21), intellectual disability (HR, 1.19), and ADHD (HR, 1.19).
The results add to evidence that activation of the maternal immune system may drive changes in the brain and behavioral problems, which has been observed in animal studies, the researchers wrote.
Potential underlying mechanisms in need of more exploration include genetic risk factors, maternal transmission of autoantibodies to the fetus during pregnancy, and the increased risk of obstetric complications, such as preterm birth, for women with autoimmune disorders that could affect mental development in children, they added.
The study findings were limited by several factors, including the lack of data on potential exacerbation of autoimmune disease activity during pregnancy and its effect on the fetus, the researchers noted. Other limitations included potential detection bias, lack of data on mental disorders in adulthood, and potential changes in diagnostic criteria over the long study period.
The results were strengthened by the use of a population-based registry, the large sample size, and ability to consider a range of confounders, the researchers said.
“This study could help acquire a comprehensive compilation of the associations between maternal autoimmune disorders diagnosed before childbirth and offspring’s mental disorders from childhood through early adulthood,” Dr. Li said in an interview.
For clinicians, Dr. Li said, the findings suggest that the offspring of mothers with autoimmune diseases may benefit from long-term surveillance for mental health disorders.
“Further studies should provide more evidence on the detailed associations of specific maternal autoimmune diseases with a full spectrum of mental disorders in offspring, and more research on underlying mechanisms is needed as well,” she said.
Pay early attention
M. Susan Jay, MD, an adjunct professor of pediatrics at the Medical College of Wisconsin, Milwaukee, said previous efforts to examine the association between maternal autoimmunity were hampered by study design, small samples, and self-report of disease history – problems the new research avoids.
The large patient population allowed for detailed subgroup analysis of different conditions and outcomes. Another advantage was the availability of sociodemographic and clinical information, which allowed for the elimination of confounding factors, said Dr. Jay, who was not involved in the research.
“It would be prudent to follow children of mothers with autoimmune disorders before or during pregnancy for mental health issues, and if identified clinically, to offer psychological and developmental behavioral support options,” Dr. Jay added.
The authors have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Mental disorders were significantly more likely in children whose mothers had one of five common autoimmune diseases, a new study found.
Previous research has linked both maternal and paternal autoimmune diseases and specific mental disorders, such as attention-deficit/hyperactivity disorder (ADHD), but most of these studies focused on specific conditions in relatively small populations. The new study included data on more than 2 million births, making it one of the largest efforts to date to examine the association, according to the researchers, whose findings were published in JAMA Network Open.
Previous evidence of the possible association between certain maternal autoimmune diseases and mental disorders in offspring has been “scattered and limited,” which “hampered an overall understanding” of the link, Fei Li, MD, the corresponding author of the study, told this news organization.
Dr. Li, of Shanghai Jiao Tong University China, and colleagues reviewed data from a Danish registry cohort of singleton births with up to 38 years of follow-up. They explored associations between a range of maternal autoimmune diseases diagnosed before childbirth and the risks of mental disorders in children in early childhood through young adulthood.
The study population included 2,254,234 births and 38,916,359 person-years. Data on mental health were collected from the Psychiatric Central Research Register and the country’s National Patient Register. The median age of the children at the time of assessment was 16.7 years; approximately half were male.
A total of 50,863 children (2.26%) were born to mothers who had been diagnosed with autoimmune diseases before childbirth. During the follow-up period, 5,460 children of mothers with autoimmune diseases and 303,092 children of mothers without autoimmune diseases were diagnosed with a mental disorder (10.73% vs. 13.76%), according to the researchers.
The risk of being diagnosed with a mental disorder was significantly higher among children of mothers with any autoimmune disease (hazard ratio [HR,], 1.16), with an incidence of 9.38 vs. 7.91 per 1,000 person-years, the researchers reported.
The increased risk persisted when the results were classified by organ system, including connective tissue (HR, 1.11), endocrine (HR, 1.19), gastrointestinal (HR, 1.11), blood (HR, 1.10), nervous (HR, 1.17), and skin (HR, 1.19).
The five autoimmune diseases in mothers that were most commonly associated mental health disorders in children were type 1 diabetes, rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, and psoriasis vulgaris.
The greatest risk for children of mothers with any autoimmune disease was observed for organic conditions such as delirium, (HR, 1.54), followed by obsessive-compulsive disorder (HR, 1.42), schizophrenia (HR, 1.54), and mood problems (HR, 1.12).
Children of mothers with any autoimmune disorder also had a significantly increased risk of autism (HR, 1.21), intellectual disability (HR, 1.19), and ADHD (HR, 1.19).
The results add to evidence that activation of the maternal immune system may drive changes in the brain and behavioral problems, which has been observed in animal studies, the researchers wrote.
Potential underlying mechanisms in need of more exploration include genetic risk factors, maternal transmission of autoantibodies to the fetus during pregnancy, and the increased risk of obstetric complications, such as preterm birth, for women with autoimmune disorders that could affect mental development in children, they added.
The study findings were limited by several factors, including the lack of data on potential exacerbation of autoimmune disease activity during pregnancy and its effect on the fetus, the researchers noted. Other limitations included potential detection bias, lack of data on mental disorders in adulthood, and potential changes in diagnostic criteria over the long study period.
The results were strengthened by the use of a population-based registry, the large sample size, and ability to consider a range of confounders, the researchers said.
“This study could help acquire a comprehensive compilation of the associations between maternal autoimmune disorders diagnosed before childbirth and offspring’s mental disorders from childhood through early adulthood,” Dr. Li said in an interview.
For clinicians, Dr. Li said, the findings suggest that the offspring of mothers with autoimmune diseases may benefit from long-term surveillance for mental health disorders.
“Further studies should provide more evidence on the detailed associations of specific maternal autoimmune diseases with a full spectrum of mental disorders in offspring, and more research on underlying mechanisms is needed as well,” she said.
Pay early attention
M. Susan Jay, MD, an adjunct professor of pediatrics at the Medical College of Wisconsin, Milwaukee, said previous efforts to examine the association between maternal autoimmunity were hampered by study design, small samples, and self-report of disease history – problems the new research avoids.
The large patient population allowed for detailed subgroup analysis of different conditions and outcomes. Another advantage was the availability of sociodemographic and clinical information, which allowed for the elimination of confounding factors, said Dr. Jay, who was not involved in the research.
“It would be prudent to follow children of mothers with autoimmune disorders before or during pregnancy for mental health issues, and if identified clinically, to offer psychological and developmental behavioral support options,” Dr. Jay added.
The authors have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Cutting dementia risk in AFib: Does rhythm control strategy matter?
The risk for dementia goes up in patients with atrial fibrillation (AFib), but some evidence suggests that risk can be blunted with therapies that restore sinus rhythm. However, a new cohort study suggests that the treatment effect’s magnitude might depend on the rhythm control strategy. It hinted that AFib catheter ablation might be more effective than pharmacologic rhythm control alone at cutting the risk for dementia.
The case-matched study of more than 38,000 adults with AFib saw a 41% reduction (P < .0001) in risk for dementia among those who underwent catheter ablation after attempted rhythm control with antiarrhythmic drugs (AAD), compared with those managed with pharmacologic rhythm control therapy alone.
The observational study comprising 20 years of data comes with big limitations and can’t say for sure whether catheter ablation is better than AAD-only at cutting the dementia risk in AFib. But it and other evidence support the idea, which has yet to be explored in a randomized fashion.
In a secondary finding, the analysis showed a similar reduction in dementia risk from catheter ablation, compared with AAD, in women and in men by 40% and 45%, respectively (P < .0001 for both). The findings are particularly relevant “given the higher life-long risk of dementia among women and the lower likelihood that women will be offered ablation, which has been demonstrated repeatedly,” Emily P. Zeitler, MD, MHS, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, told this news organization. “I think this is another reason to try to be more generous in offering ablation to women.”
Management of AFib certainly evolved in important ways from 2000 to 2021, the period covered by the study. But a sensitivity analysis based on data from 2010 to 2021 showed “no meaningful differences” in the results, said Dr. Zeitler, who is slated to present the findings April 30 at the Heart Rhythm Society 2022 Scientific Sessions, conducted virtually and live in San Francisco.
Dr. Zeitler acknowledged that the observational study, even with its propensity-matched ablation and AAD cohorts, can only hint at a preference for ablation over AAD for lowering risk for AFib-associated dementia. “We know there’s unmeasured and unfixable confounding between those two groups, so we see this really as hypothesis-generating.”
It was “a well-done analysis,” and the conclusion that the dementia risk was lower with catheter ablation is “absolutely correct,” but only as far as the study and its limitations allow, agreed David Conen, MD, MPH, McMaster University, Hamilton, Ontario, who is not a coauthor.
“Even with propensity matching, you can get rid of some sorts of confounding, but you can never get rid of all selection bias issues.” That, he said when interviewed, takes randomized trials.
Dr. Conen, who is studying cognitive decline in AFib as a SWISS-AF trial principal investigator, pointed to a secondary finding of the analysis as evidence for such confounding. He said the ablation group’s nearly 50% drop (P < .0001) in competing risk for death, compared with patients managed with AAD, isn’t plausible.
The finding “strongly suggests these people were healthier and that there’s some sort of selection bias. They were at lower risk of death, they were at lower risk of dementia, and they were probably also at lower risk of stroke, myocardial infarction, thrombosis, and cancer because they were just probably a little healthier than the others,” Dr. Conen said. The ablation and AAD groups “were two very different populations from the get-go.”
The analysis was based on U.S. insurance and Medicare claims data from AFib patients who either underwent catheter ablation after at least one AAD trial or filled prescriptions for at least two different antiarrhythmic agents in the year after AFib diagnosis. Patients with history of dementia, catheter or surgical AFib ablation, or a valve procedure were excluded.
The ablation and AAD-only groups each consisted of 19,066 patients after propensity matching, and the groups were balanced with respect to age, sex, type of insurance, CHA2DS2-VASc scores, and use of renin-angiotensin-system inhibitors, oral anticoagulants, and antiplatelets.
The overall risk for dementia was 1.9% for the ablation group and 3.3% for AAD-only patients (hazard ratio, 0.59; 95% confidence interval, 0.52-0.67). Corresponding HRs by sex were 0.55 (95% CI, 0.46-0.66) for men and 0.60 (95% CI, 0.50-0.72) for women.
The competing risk for death was also significantly decreased in the ablation group (HR, 0.51; 95% CI, 0.46-0.55).
Dr. Zeitler pointed to a randomized trial now in the early stages called Neurocognition and Greater Maintenance of Sinus Rhythm in Atrial Fibrillation, or NOGGIN-AF, which will explore relationships between rhythm control therapy and dementia in patients with AFib, whether catheter ablation or AAD can mitigate that risk, and whether either strategy works better than the other, among other goals.
“I’m optimistic,” she said, “and I think it’s going to add to the growing motivations to get patients ablated more quickly and more broadly.”
The analysis was funded by Biosense-Webster. Dr. Zeitler discloses consulting for Biosense-Webster and Arena Pharmaceuticals (now Pfizer); fees for speaking from Medtronic; and receiving research support from Boston Scientific, Sanofi, and Biosense-Webster. Dr. Conen has previously reported receiving speaker fees from Servier Canada.
A version of this article first appeared on Medscape.com.
The risk for dementia goes up in patients with atrial fibrillation (AFib), but some evidence suggests that risk can be blunted with therapies that restore sinus rhythm. However, a new cohort study suggests that the treatment effect’s magnitude might depend on the rhythm control strategy. It hinted that AFib catheter ablation might be more effective than pharmacologic rhythm control alone at cutting the risk for dementia.
The case-matched study of more than 38,000 adults with AFib saw a 41% reduction (P < .0001) in risk for dementia among those who underwent catheter ablation after attempted rhythm control with antiarrhythmic drugs (AAD), compared with those managed with pharmacologic rhythm control therapy alone.
The observational study comprising 20 years of data comes with big limitations and can’t say for sure whether catheter ablation is better than AAD-only at cutting the dementia risk in AFib. But it and other evidence support the idea, which has yet to be explored in a randomized fashion.
In a secondary finding, the analysis showed a similar reduction in dementia risk from catheter ablation, compared with AAD, in women and in men by 40% and 45%, respectively (P < .0001 for both). The findings are particularly relevant “given the higher life-long risk of dementia among women and the lower likelihood that women will be offered ablation, which has been demonstrated repeatedly,” Emily P. Zeitler, MD, MHS, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, told this news organization. “I think this is another reason to try to be more generous in offering ablation to women.”
Management of AFib certainly evolved in important ways from 2000 to 2021, the period covered by the study. But a sensitivity analysis based on data from 2010 to 2021 showed “no meaningful differences” in the results, said Dr. Zeitler, who is slated to present the findings April 30 at the Heart Rhythm Society 2022 Scientific Sessions, conducted virtually and live in San Francisco.
Dr. Zeitler acknowledged that the observational study, even with its propensity-matched ablation and AAD cohorts, can only hint at a preference for ablation over AAD for lowering risk for AFib-associated dementia. “We know there’s unmeasured and unfixable confounding between those two groups, so we see this really as hypothesis-generating.”
It was “a well-done analysis,” and the conclusion that the dementia risk was lower with catheter ablation is “absolutely correct,” but only as far as the study and its limitations allow, agreed David Conen, MD, MPH, McMaster University, Hamilton, Ontario, who is not a coauthor.
“Even with propensity matching, you can get rid of some sorts of confounding, but you can never get rid of all selection bias issues.” That, he said when interviewed, takes randomized trials.
Dr. Conen, who is studying cognitive decline in AFib as a SWISS-AF trial principal investigator, pointed to a secondary finding of the analysis as evidence for such confounding. He said the ablation group’s nearly 50% drop (P < .0001) in competing risk for death, compared with patients managed with AAD, isn’t plausible.
The finding “strongly suggests these people were healthier and that there’s some sort of selection bias. They were at lower risk of death, they were at lower risk of dementia, and they were probably also at lower risk of stroke, myocardial infarction, thrombosis, and cancer because they were just probably a little healthier than the others,” Dr. Conen said. The ablation and AAD groups “were two very different populations from the get-go.”
The analysis was based on U.S. insurance and Medicare claims data from AFib patients who either underwent catheter ablation after at least one AAD trial or filled prescriptions for at least two different antiarrhythmic agents in the year after AFib diagnosis. Patients with history of dementia, catheter or surgical AFib ablation, or a valve procedure were excluded.
The ablation and AAD-only groups each consisted of 19,066 patients after propensity matching, and the groups were balanced with respect to age, sex, type of insurance, CHA2DS2-VASc scores, and use of renin-angiotensin-system inhibitors, oral anticoagulants, and antiplatelets.
The overall risk for dementia was 1.9% for the ablation group and 3.3% for AAD-only patients (hazard ratio, 0.59; 95% confidence interval, 0.52-0.67). Corresponding HRs by sex were 0.55 (95% CI, 0.46-0.66) for men and 0.60 (95% CI, 0.50-0.72) for women.
The competing risk for death was also significantly decreased in the ablation group (HR, 0.51; 95% CI, 0.46-0.55).
Dr. Zeitler pointed to a randomized trial now in the early stages called Neurocognition and Greater Maintenance of Sinus Rhythm in Atrial Fibrillation, or NOGGIN-AF, which will explore relationships between rhythm control therapy and dementia in patients with AFib, whether catheter ablation or AAD can mitigate that risk, and whether either strategy works better than the other, among other goals.
“I’m optimistic,” she said, “and I think it’s going to add to the growing motivations to get patients ablated more quickly and more broadly.”
The analysis was funded by Biosense-Webster. Dr. Zeitler discloses consulting for Biosense-Webster and Arena Pharmaceuticals (now Pfizer); fees for speaking from Medtronic; and receiving research support from Boston Scientific, Sanofi, and Biosense-Webster. Dr. Conen has previously reported receiving speaker fees from Servier Canada.
A version of this article first appeared on Medscape.com.
The risk for dementia goes up in patients with atrial fibrillation (AFib), but some evidence suggests that risk can be blunted with therapies that restore sinus rhythm. However, a new cohort study suggests that the treatment effect’s magnitude might depend on the rhythm control strategy. It hinted that AFib catheter ablation might be more effective than pharmacologic rhythm control alone at cutting the risk for dementia.
The case-matched study of more than 38,000 adults with AFib saw a 41% reduction (P < .0001) in risk for dementia among those who underwent catheter ablation after attempted rhythm control with antiarrhythmic drugs (AAD), compared with those managed with pharmacologic rhythm control therapy alone.
The observational study comprising 20 years of data comes with big limitations and can’t say for sure whether catheter ablation is better than AAD-only at cutting the dementia risk in AFib. But it and other evidence support the idea, which has yet to be explored in a randomized fashion.
In a secondary finding, the analysis showed a similar reduction in dementia risk from catheter ablation, compared with AAD, in women and in men by 40% and 45%, respectively (P < .0001 for both). The findings are particularly relevant “given the higher life-long risk of dementia among women and the lower likelihood that women will be offered ablation, which has been demonstrated repeatedly,” Emily P. Zeitler, MD, MHS, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, told this news organization. “I think this is another reason to try to be more generous in offering ablation to women.”
Management of AFib certainly evolved in important ways from 2000 to 2021, the period covered by the study. But a sensitivity analysis based on data from 2010 to 2021 showed “no meaningful differences” in the results, said Dr. Zeitler, who is slated to present the findings April 30 at the Heart Rhythm Society 2022 Scientific Sessions, conducted virtually and live in San Francisco.
Dr. Zeitler acknowledged that the observational study, even with its propensity-matched ablation and AAD cohorts, can only hint at a preference for ablation over AAD for lowering risk for AFib-associated dementia. “We know there’s unmeasured and unfixable confounding between those two groups, so we see this really as hypothesis-generating.”
It was “a well-done analysis,” and the conclusion that the dementia risk was lower with catheter ablation is “absolutely correct,” but only as far as the study and its limitations allow, agreed David Conen, MD, MPH, McMaster University, Hamilton, Ontario, who is not a coauthor.
“Even with propensity matching, you can get rid of some sorts of confounding, but you can never get rid of all selection bias issues.” That, he said when interviewed, takes randomized trials.
Dr. Conen, who is studying cognitive decline in AFib as a SWISS-AF trial principal investigator, pointed to a secondary finding of the analysis as evidence for such confounding. He said the ablation group’s nearly 50% drop (P < .0001) in competing risk for death, compared with patients managed with AAD, isn’t plausible.
The finding “strongly suggests these people were healthier and that there’s some sort of selection bias. They were at lower risk of death, they were at lower risk of dementia, and they were probably also at lower risk of stroke, myocardial infarction, thrombosis, and cancer because they were just probably a little healthier than the others,” Dr. Conen said. The ablation and AAD groups “were two very different populations from the get-go.”
The analysis was based on U.S. insurance and Medicare claims data from AFib patients who either underwent catheter ablation after at least one AAD trial or filled prescriptions for at least two different antiarrhythmic agents in the year after AFib diagnosis. Patients with history of dementia, catheter or surgical AFib ablation, or a valve procedure were excluded.
The ablation and AAD-only groups each consisted of 19,066 patients after propensity matching, and the groups were balanced with respect to age, sex, type of insurance, CHA2DS2-VASc scores, and use of renin-angiotensin-system inhibitors, oral anticoagulants, and antiplatelets.
The overall risk for dementia was 1.9% for the ablation group and 3.3% for AAD-only patients (hazard ratio, 0.59; 95% confidence interval, 0.52-0.67). Corresponding HRs by sex were 0.55 (95% CI, 0.46-0.66) for men and 0.60 (95% CI, 0.50-0.72) for women.
The competing risk for death was also significantly decreased in the ablation group (HR, 0.51; 95% CI, 0.46-0.55).
Dr. Zeitler pointed to a randomized trial now in the early stages called Neurocognition and Greater Maintenance of Sinus Rhythm in Atrial Fibrillation, or NOGGIN-AF, which will explore relationships between rhythm control therapy and dementia in patients with AFib, whether catheter ablation or AAD can mitigate that risk, and whether either strategy works better than the other, among other goals.
“I’m optimistic,” she said, “and I think it’s going to add to the growing motivations to get patients ablated more quickly and more broadly.”
The analysis was funded by Biosense-Webster. Dr. Zeitler discloses consulting for Biosense-Webster and Arena Pharmaceuticals (now Pfizer); fees for speaking from Medtronic; and receiving research support from Boston Scientific, Sanofi, and Biosense-Webster. Dr. Conen has previously reported receiving speaker fees from Servier Canada.
A version of this article first appeared on Medscape.com.
Nurses, med staff voice their heartache about California nurse suicide
The Santa Clara Police Department “thoroughly investigated” a report April 27 at Kaiser Permanente Santa Clara Medical Center that a male nurse in the emergency department died from a self-inflicted gunshot wound and ruled it a suicide, according to Wahid Kazem, assistant chief of police.
“This tragic event occurred in a closed room that is not used for patient care, adjacent to the emergency department. No other staff or patients were threatened,” according to Rakesh Chaudhary, MD, physician-in-chief of the medical center.
He added that the emergency department remained open for walk-in patients during the investigation, but ambulances were temporarily diverted to nearby hospitals. “The Santa Clara Police Department and our staff immediately took precautions to isolate the affected area and avoid impact to patient care.”
In terms of the effect on those closer to the victim, Dr. Chaudhary said, “Our hearts go out to the family, friends, and coworkers affected by this terrible loss. Our teams are on site providing emotional support and resources for staff.”
Neither the police nor the hospital released the victim’s name. “Out of respect for the privacy of our colleague and their family, we cannot provide any additional details,” Dr. Chaudhary said.
Among those who tweeted reactions to the news the past few days was someone who worked with the victim, according to the post: “My heart goes out to my coworker who thought he had no one to lean on and to my good friend who had to witness this tragedy. Love my ER fam.”
A male critical care RN tweeted: “My heart hurts for the nurse, his loved ones, and colleagues. Anyone working in ER understands the unique stress that we’ve been under. This is so tragic.”
While others cited the need for more mental health services to care for nurses, a psychiatrist on Twitter added, “Nurses are not OK and pizza and pats on the back aren’t going to fix it. This affects all of us.”
Mental health support was listed as a prime demand of striking workers recently at Stanford (Calif.) Health Care and Lucile Packard Children’s Hospital in Palo Alto, about a half hour away from Santa Clara Medical Center.
The nurses’ strike ended May 2 with an agreement between the health systems and the Committee for Recognition of Nursing Achievement union representing the nurses. The contract includes improvements to existing benefits supporting nurses’ health and well-being, according to a StanfordPackardVoice.com newsletter updating the negotiations.
Earlier this year, an intensive care unit RN from Stanford, Michael Odell, reportedly walked off his shift and was found dead 2 days later in San Francisco by the Alameda County Sheriff’s Office dive team. No foul play was suspected and the incident was believed to be a suicide.
A version of this article first appeared on Medscape.com.
The Santa Clara Police Department “thoroughly investigated” a report April 27 at Kaiser Permanente Santa Clara Medical Center that a male nurse in the emergency department died from a self-inflicted gunshot wound and ruled it a suicide, according to Wahid Kazem, assistant chief of police.
“This tragic event occurred in a closed room that is not used for patient care, adjacent to the emergency department. No other staff or patients were threatened,” according to Rakesh Chaudhary, MD, physician-in-chief of the medical center.
He added that the emergency department remained open for walk-in patients during the investigation, but ambulances were temporarily diverted to nearby hospitals. “The Santa Clara Police Department and our staff immediately took precautions to isolate the affected area and avoid impact to patient care.”
In terms of the effect on those closer to the victim, Dr. Chaudhary said, “Our hearts go out to the family, friends, and coworkers affected by this terrible loss. Our teams are on site providing emotional support and resources for staff.”
Neither the police nor the hospital released the victim’s name. “Out of respect for the privacy of our colleague and their family, we cannot provide any additional details,” Dr. Chaudhary said.
Among those who tweeted reactions to the news the past few days was someone who worked with the victim, according to the post: “My heart goes out to my coworker who thought he had no one to lean on and to my good friend who had to witness this tragedy. Love my ER fam.”
A male critical care RN tweeted: “My heart hurts for the nurse, his loved ones, and colleagues. Anyone working in ER understands the unique stress that we’ve been under. This is so tragic.”
While others cited the need for more mental health services to care for nurses, a psychiatrist on Twitter added, “Nurses are not OK and pizza and pats on the back aren’t going to fix it. This affects all of us.”
Mental health support was listed as a prime demand of striking workers recently at Stanford (Calif.) Health Care and Lucile Packard Children’s Hospital in Palo Alto, about a half hour away from Santa Clara Medical Center.
The nurses’ strike ended May 2 with an agreement between the health systems and the Committee for Recognition of Nursing Achievement union representing the nurses. The contract includes improvements to existing benefits supporting nurses’ health and well-being, according to a StanfordPackardVoice.com newsletter updating the negotiations.
Earlier this year, an intensive care unit RN from Stanford, Michael Odell, reportedly walked off his shift and was found dead 2 days later in San Francisco by the Alameda County Sheriff’s Office dive team. No foul play was suspected and the incident was believed to be a suicide.
A version of this article first appeared on Medscape.com.
The Santa Clara Police Department “thoroughly investigated” a report April 27 at Kaiser Permanente Santa Clara Medical Center that a male nurse in the emergency department died from a self-inflicted gunshot wound and ruled it a suicide, according to Wahid Kazem, assistant chief of police.
“This tragic event occurred in a closed room that is not used for patient care, adjacent to the emergency department. No other staff or patients were threatened,” according to Rakesh Chaudhary, MD, physician-in-chief of the medical center.
He added that the emergency department remained open for walk-in patients during the investigation, but ambulances were temporarily diverted to nearby hospitals. “The Santa Clara Police Department and our staff immediately took precautions to isolate the affected area and avoid impact to patient care.”
In terms of the effect on those closer to the victim, Dr. Chaudhary said, “Our hearts go out to the family, friends, and coworkers affected by this terrible loss. Our teams are on site providing emotional support and resources for staff.”
Neither the police nor the hospital released the victim’s name. “Out of respect for the privacy of our colleague and their family, we cannot provide any additional details,” Dr. Chaudhary said.
Among those who tweeted reactions to the news the past few days was someone who worked with the victim, according to the post: “My heart goes out to my coworker who thought he had no one to lean on and to my good friend who had to witness this tragedy. Love my ER fam.”
A male critical care RN tweeted: “My heart hurts for the nurse, his loved ones, and colleagues. Anyone working in ER understands the unique stress that we’ve been under. This is so tragic.”
While others cited the need for more mental health services to care for nurses, a psychiatrist on Twitter added, “Nurses are not OK and pizza and pats on the back aren’t going to fix it. This affects all of us.”
Mental health support was listed as a prime demand of striking workers recently at Stanford (Calif.) Health Care and Lucile Packard Children’s Hospital in Palo Alto, about a half hour away from Santa Clara Medical Center.
The nurses’ strike ended May 2 with an agreement between the health systems and the Committee for Recognition of Nursing Achievement union representing the nurses. The contract includes improvements to existing benefits supporting nurses’ health and well-being, according to a StanfordPackardVoice.com newsletter updating the negotiations.
Earlier this year, an intensive care unit RN from Stanford, Michael Odell, reportedly walked off his shift and was found dead 2 days later in San Francisco by the Alameda County Sheriff’s Office dive team. No foul play was suspected and the incident was believed to be a suicide.
A version of this article first appeared on Medscape.com.
Higher ‘chemical restraint’ rates in Black psych patients in the ED
Black patients presenting with psychiatric disorders to hospital emergency departments across the United States have significantly higher rates of chemical restraint than their White counterparts, new research shows.
The investigators also found White patients were more likely to receive chemical sedation at hospitals with a higher proportion of Black patients – a finding that suggests hospital demographics influence practice patterns and that structural racism may be a root cause.
“There is a large disparity in the rates at which patients who presented to EDs nationally in the United States are restrained by race. You are 63% more likely, for the same set of chief complaints, to be chemically sedated if you are Black versus if you’re White,” senior investigator Ari Friedman, MD, PhD, an assistant professor of emergency medicine, and medical ethics and health policy, University of Pennsylvania, Philadelphia, told this news organization.
“The major mediator of that difference is the institution you are at – hospitals that primarily serve Black patients are more likely to chemically sedate their patients for these chief complaints – including White patients. So, it’s mediated by the practice pattern and environment,” Dr. Friedman added.
The study was published in the May issue of Annals of Epidemiology.
First large-scale study
Chemical sedation, also known as chemical restraint, is used to calm and help protect patients from harming themselves or others. Previous research on racial differences in the care of ED psychiatric patients with agitation suggests that there may be treatment disparities.
“Previous research from single institutions [has] shown that Black patients are more likely than White patients to be physically restrained, and this has been shown to be true among adult patients and pediatric patients,” lead author Utsha Khatri, MD, assistant professor of emergency medicine at the Icahn School of Medicine, New York, told this news organization.
Specifically, two single-institution studies within the last year revealed similar disparities, with higher rates of physical restraint for Black and Hispanic psychiatric patients in the ED. Another recent study showed an association with race, ethnicity, and pharmacological restraint use among pediatric patients presenting to the ED for mental health concerns.
“There has been work in psychiatry on disparities in this context, although there is less work in emergency departments,” said Dr. Friedman. “We looked across all U.S. EDs as opposed to within a single health system. The major trade-offs for us were that we weren’t able to observe restraint orders, which don’t find their way into national datasets, so we had to make some inferences based on the type of medications given.”
For the study the investigators analyzed data from 2008-2018 through the National Hospital Ambulatory Medical Survey (NHAMCS) database. They examined the association of race and the administration of chemical sedation, with either an antipsychotic or ketamine, in ED visits for psychiatric disorders. These were any visit where the reason for the visit was “symptoms referable to psychological and mental disorders.”
Of the 76.2 million total ED visits evaluated, the researchers found that Black patients presenting with a psychiatric disorder were significantly more likely to receive chemical sedation with antipsychotics or ketamine than White patients presenting with the same conditions (5.3% vs. 3.0%; P < .01). This difference remained significant when accounting for admission or transfer to psychiatric facilities.
Combatting the forces of racism
When researchers accounted for the percent of hospital population that was Black, they found that patient race no longer affected the likelihood of chemical restraint.
“We found the key source of this racial disparity in use of chemical sedation is accounted for by the fact that hospitals that treat a higher proportion of Black patients tend to use more sedation,” said Dr. Khatri.
“Our findings suggest that patients who present to hospitals that serve a patient population that is 60% Black would have [a] roughly 1.8 times likelihood of getting chemically sedated, compared with a hospital that serves a population that is 10% Black,” she added.
“When a hospital has fewer resources, they often don’t have the staff or time to de-escalate a patient in distress and can have to resort to chemical sedation more quickly than a hospital with ample staff and resources,” said Dr. Friedman in a release.
Dr. Khatri added that the study highlights the need to combat the forces of racism by focusing not just on provider bias but by addressing the “underlying structural issues that lead to Black patients getting worse care based on where they live.”
“Hospitals have unequal distribution of resources and quality, largely patterned on the racial makeup of their patients. Dedicated training and funding for de-escalation techniques as well as sufficient staffing and availability of outpatient mental health care may help keep both patients and staff safe by reducing the use of physical restraint and chemical sedation in appropriate circumstances,” said Dr. Khatri.
Dr. Friedman noted that there will always be a need for restraint use to facilitate rapid medical evaluation and stabilization of patients, but “we want to make it as humane, thoughtful, and rare as possible, and to have a large armamentarium of alternative strategies that can be equitably applied across emergency departments.”
Need for widespread, systemic change
Commenting on the findings, Regina James, MD, the American Psychiatric Association’s chief of Diversity and Health Equity and deputy medical director, said the large-scale study confirms the widespread existence of racial and ethnic disparities in patients with psychiatric disorders.
“This study and previous studies, not only in psychiatry but in other areas of medicine, all bring to light that there continues to be evidence of racial and ethnic disparities in health care, and this is consistent across a range of illnesses and health care services,” said Dr. James.
“It’s important that as we think about the solution, we also think about the etiology of the problem and the layers that have contributed to it – understanding, embracing, and recognizing that these differences didn’t just come up de novo. It’s policies, practices, and behaviors that got us to this point, and it’s going to be policies, practices, and behaviors that are going to move us away from this point,” noted Dr. James.
She added that future research should focus on further understanding which factors exacerbate agitation among patients and what resources directed at the hospital level, including de-escalation training, nursing staff, and waiting room crowding, may be effective at reducing the use of chemical sedation when clinically appropriate.
The authors and Dr. James report no relevant financial conflicts of interest.
A version of this article first appeared on Medscape.com.
Black patients presenting with psychiatric disorders to hospital emergency departments across the United States have significantly higher rates of chemical restraint than their White counterparts, new research shows.
The investigators also found White patients were more likely to receive chemical sedation at hospitals with a higher proportion of Black patients – a finding that suggests hospital demographics influence practice patterns and that structural racism may be a root cause.
“There is a large disparity in the rates at which patients who presented to EDs nationally in the United States are restrained by race. You are 63% more likely, for the same set of chief complaints, to be chemically sedated if you are Black versus if you’re White,” senior investigator Ari Friedman, MD, PhD, an assistant professor of emergency medicine, and medical ethics and health policy, University of Pennsylvania, Philadelphia, told this news organization.
“The major mediator of that difference is the institution you are at – hospitals that primarily serve Black patients are more likely to chemically sedate their patients for these chief complaints – including White patients. So, it’s mediated by the practice pattern and environment,” Dr. Friedman added.
The study was published in the May issue of Annals of Epidemiology.
First large-scale study
Chemical sedation, also known as chemical restraint, is used to calm and help protect patients from harming themselves or others. Previous research on racial differences in the care of ED psychiatric patients with agitation suggests that there may be treatment disparities.
“Previous research from single institutions [has] shown that Black patients are more likely than White patients to be physically restrained, and this has been shown to be true among adult patients and pediatric patients,” lead author Utsha Khatri, MD, assistant professor of emergency medicine at the Icahn School of Medicine, New York, told this news organization.
Specifically, two single-institution studies within the last year revealed similar disparities, with higher rates of physical restraint for Black and Hispanic psychiatric patients in the ED. Another recent study showed an association with race, ethnicity, and pharmacological restraint use among pediatric patients presenting to the ED for mental health concerns.
“There has been work in psychiatry on disparities in this context, although there is less work in emergency departments,” said Dr. Friedman. “We looked across all U.S. EDs as opposed to within a single health system. The major trade-offs for us were that we weren’t able to observe restraint orders, which don’t find their way into national datasets, so we had to make some inferences based on the type of medications given.”
For the study the investigators analyzed data from 2008-2018 through the National Hospital Ambulatory Medical Survey (NHAMCS) database. They examined the association of race and the administration of chemical sedation, with either an antipsychotic or ketamine, in ED visits for psychiatric disorders. These were any visit where the reason for the visit was “symptoms referable to psychological and mental disorders.”
Of the 76.2 million total ED visits evaluated, the researchers found that Black patients presenting with a psychiatric disorder were significantly more likely to receive chemical sedation with antipsychotics or ketamine than White patients presenting with the same conditions (5.3% vs. 3.0%; P < .01). This difference remained significant when accounting for admission or transfer to psychiatric facilities.
Combatting the forces of racism
When researchers accounted for the percent of hospital population that was Black, they found that patient race no longer affected the likelihood of chemical restraint.
“We found the key source of this racial disparity in use of chemical sedation is accounted for by the fact that hospitals that treat a higher proportion of Black patients tend to use more sedation,” said Dr. Khatri.
“Our findings suggest that patients who present to hospitals that serve a patient population that is 60% Black would have [a] roughly 1.8 times likelihood of getting chemically sedated, compared with a hospital that serves a population that is 10% Black,” she added.
“When a hospital has fewer resources, they often don’t have the staff or time to de-escalate a patient in distress and can have to resort to chemical sedation more quickly than a hospital with ample staff and resources,” said Dr. Friedman in a release.
Dr. Khatri added that the study highlights the need to combat the forces of racism by focusing not just on provider bias but by addressing the “underlying structural issues that lead to Black patients getting worse care based on where they live.”
“Hospitals have unequal distribution of resources and quality, largely patterned on the racial makeup of their patients. Dedicated training and funding for de-escalation techniques as well as sufficient staffing and availability of outpatient mental health care may help keep both patients and staff safe by reducing the use of physical restraint and chemical sedation in appropriate circumstances,” said Dr. Khatri.
Dr. Friedman noted that there will always be a need for restraint use to facilitate rapid medical evaluation and stabilization of patients, but “we want to make it as humane, thoughtful, and rare as possible, and to have a large armamentarium of alternative strategies that can be equitably applied across emergency departments.”
Need for widespread, systemic change
Commenting on the findings, Regina James, MD, the American Psychiatric Association’s chief of Diversity and Health Equity and deputy medical director, said the large-scale study confirms the widespread existence of racial and ethnic disparities in patients with psychiatric disorders.
“This study and previous studies, not only in psychiatry but in other areas of medicine, all bring to light that there continues to be evidence of racial and ethnic disparities in health care, and this is consistent across a range of illnesses and health care services,” said Dr. James.
“It’s important that as we think about the solution, we also think about the etiology of the problem and the layers that have contributed to it – understanding, embracing, and recognizing that these differences didn’t just come up de novo. It’s policies, practices, and behaviors that got us to this point, and it’s going to be policies, practices, and behaviors that are going to move us away from this point,” noted Dr. James.
She added that future research should focus on further understanding which factors exacerbate agitation among patients and what resources directed at the hospital level, including de-escalation training, nursing staff, and waiting room crowding, may be effective at reducing the use of chemical sedation when clinically appropriate.
The authors and Dr. James report no relevant financial conflicts of interest.
A version of this article first appeared on Medscape.com.
Black patients presenting with psychiatric disorders to hospital emergency departments across the United States have significantly higher rates of chemical restraint than their White counterparts, new research shows.
The investigators also found White patients were more likely to receive chemical sedation at hospitals with a higher proportion of Black patients – a finding that suggests hospital demographics influence practice patterns and that structural racism may be a root cause.
“There is a large disparity in the rates at which patients who presented to EDs nationally in the United States are restrained by race. You are 63% more likely, for the same set of chief complaints, to be chemically sedated if you are Black versus if you’re White,” senior investigator Ari Friedman, MD, PhD, an assistant professor of emergency medicine, and medical ethics and health policy, University of Pennsylvania, Philadelphia, told this news organization.
“The major mediator of that difference is the institution you are at – hospitals that primarily serve Black patients are more likely to chemically sedate their patients for these chief complaints – including White patients. So, it’s mediated by the practice pattern and environment,” Dr. Friedman added.
The study was published in the May issue of Annals of Epidemiology.
First large-scale study
Chemical sedation, also known as chemical restraint, is used to calm and help protect patients from harming themselves or others. Previous research on racial differences in the care of ED psychiatric patients with agitation suggests that there may be treatment disparities.
“Previous research from single institutions [has] shown that Black patients are more likely than White patients to be physically restrained, and this has been shown to be true among adult patients and pediatric patients,” lead author Utsha Khatri, MD, assistant professor of emergency medicine at the Icahn School of Medicine, New York, told this news organization.
Specifically, two single-institution studies within the last year revealed similar disparities, with higher rates of physical restraint for Black and Hispanic psychiatric patients in the ED. Another recent study showed an association with race, ethnicity, and pharmacological restraint use among pediatric patients presenting to the ED for mental health concerns.
“There has been work in psychiatry on disparities in this context, although there is less work in emergency departments,” said Dr. Friedman. “We looked across all U.S. EDs as opposed to within a single health system. The major trade-offs for us were that we weren’t able to observe restraint orders, which don’t find their way into national datasets, so we had to make some inferences based on the type of medications given.”
For the study the investigators analyzed data from 2008-2018 through the National Hospital Ambulatory Medical Survey (NHAMCS) database. They examined the association of race and the administration of chemical sedation, with either an antipsychotic or ketamine, in ED visits for psychiatric disorders. These were any visit where the reason for the visit was “symptoms referable to psychological and mental disorders.”
Of the 76.2 million total ED visits evaluated, the researchers found that Black patients presenting with a psychiatric disorder were significantly more likely to receive chemical sedation with antipsychotics or ketamine than White patients presenting with the same conditions (5.3% vs. 3.0%; P < .01). This difference remained significant when accounting for admission or transfer to psychiatric facilities.
Combatting the forces of racism
When researchers accounted for the percent of hospital population that was Black, they found that patient race no longer affected the likelihood of chemical restraint.
“We found the key source of this racial disparity in use of chemical sedation is accounted for by the fact that hospitals that treat a higher proportion of Black patients tend to use more sedation,” said Dr. Khatri.
“Our findings suggest that patients who present to hospitals that serve a patient population that is 60% Black would have [a] roughly 1.8 times likelihood of getting chemically sedated, compared with a hospital that serves a population that is 10% Black,” she added.
“When a hospital has fewer resources, they often don’t have the staff or time to de-escalate a patient in distress and can have to resort to chemical sedation more quickly than a hospital with ample staff and resources,” said Dr. Friedman in a release.
Dr. Khatri added that the study highlights the need to combat the forces of racism by focusing not just on provider bias but by addressing the “underlying structural issues that lead to Black patients getting worse care based on where they live.”
“Hospitals have unequal distribution of resources and quality, largely patterned on the racial makeup of their patients. Dedicated training and funding for de-escalation techniques as well as sufficient staffing and availability of outpatient mental health care may help keep both patients and staff safe by reducing the use of physical restraint and chemical sedation in appropriate circumstances,” said Dr. Khatri.
Dr. Friedman noted that there will always be a need for restraint use to facilitate rapid medical evaluation and stabilization of patients, but “we want to make it as humane, thoughtful, and rare as possible, and to have a large armamentarium of alternative strategies that can be equitably applied across emergency departments.”
Need for widespread, systemic change
Commenting on the findings, Regina James, MD, the American Psychiatric Association’s chief of Diversity and Health Equity and deputy medical director, said the large-scale study confirms the widespread existence of racial and ethnic disparities in patients with psychiatric disorders.
“This study and previous studies, not only in psychiatry but in other areas of medicine, all bring to light that there continues to be evidence of racial and ethnic disparities in health care, and this is consistent across a range of illnesses and health care services,” said Dr. James.
“It’s important that as we think about the solution, we also think about the etiology of the problem and the layers that have contributed to it – understanding, embracing, and recognizing that these differences didn’t just come up de novo. It’s policies, practices, and behaviors that got us to this point, and it’s going to be policies, practices, and behaviors that are going to move us away from this point,” noted Dr. James.
She added that future research should focus on further understanding which factors exacerbate agitation among patients and what resources directed at the hospital level, including de-escalation training, nursing staff, and waiting room crowding, may be effective at reducing the use of chemical sedation when clinically appropriate.
The authors and Dr. James report no relevant financial conflicts of interest.
A version of this article first appeared on Medscape.com.