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Internet intervention improved insomnia in Black women
Data from previous studies suggest that women are up to 40% more likely to experience insomnia disorder compared with men, Eric S. Zhou, PhD, of Harvard Medical School, Boston, and colleagues wrote. The risk is even higher among Black women, but research on tailored treatments for this particular population has been limited.
In their study, published in JAMA Psychiatry, the researchers recruited women with elevated insomnia symptoms who were enrolled in the Black Women’s Health Study, an ongoing national, longitudinal research cohort in the United States. Participants were recruited between October 2019 and June 2020.The participants were randomized to an Internet-delivered behavior intervention (108 women), a stakeholder-informed Internet intervention tailored to Black women (110 women), or non-Internet patient education about sleep (115 women).
The Internet intervention, known as Sleep Healthy Using the Internet (SHUTi), was a 6-session program lasting 45-60 minutes per session and delivered over 6-9 weeks. The program included core elements of cognitive behavioral therapy and took into account information provided by patients about their baseline sleep function, treatment adherence, and sleep progress.
The tailored version of SHUTi for Black women (SHUTi-BWHS) was similar, but included Black actors for video vignettes and the inclusion of content about the cultural and social contexts in which insomnia often occurs for Black women, such while managing neighborhood noise and or living in crowded environments.
A third group received standard patient education material about sleep through a noninteractive website, and served as the control group.
The primary outcome of insomnia severity was measured using the Insomnia Severity Index (ISI), a 0- to 28-point scale. Scores for the ISI are based on responses to seven questions, including some that ask participants to rate the severity of their insomnia symptoms.
Clinically significant improvement in insomnia was defined as a reduction in score of more than 7 points. Patients were assessed at baseline, at 9 weeks, and again at approximately 6 months.
Significantly greater reductions in insomnia severity seen in intervention groups vs. control group
Overall, women randomized to SHUTi or SHUTi-BWHS) reported a significantly greater reduction in insomnia symptoms from baseline to 6 months, compared with the control group (P < .001), with ISI score decreases of 10.0, 9.3, and 3.6, respectively. No statistically significant differences in ISI score changes appeared between the between the SHUTi-BWHS and SHUTi groups.
Also, significantly more women in the SHUTi-BWHS group than in the SHUTi group completed the intervention (78.2% vs. 64.8%).
Treatment response was similar between the SHUTI-BWHS and SHUTi groups; 47.3% and 46.3%, respectively, had a decrease in ISI score of more than 7 points. In addition, 37% of women in the SHUTi-BWHS and 38% of women in the SHUTi groups reached ISI scores of less than 8 points, defined as full resolution of insomnia, by the last follow-up visit.
Both the SHUTi and SHUTi-BWHS interventions had dramatic effects on insomnia, but the increased number of women who completed the intervention in the SHUTi-BWHS group supports the value of tailored intervention, the researchers noted. “Similar to prior SHUTi trials, there was a direct association between the participant’s level of intervention engagement and their improvement in sleep.”
The average age of the participants was 60 years, 62% were single, and 44% had a graduate degree or higher. Approximately 5% were being actively treated for sleep apnea.
The study findings were limited by several factors including the relatively high socioeconomic status of the study participants, lack of data on medical mistrust, and inability to detect smaller differences between SHUTi and SHUTi-BWHS, the researchers noted.
Choose Internet-based CBT first for insomnia
“This was an excellent paper that sought to see the relative efficacy of standard version of Internet-delivered CBT-I [cognitive-behavioral therapy for insomnia] versus a culturally tailored version for Black women,” said Neil Skolnik, MD, professor of family and community medicine at Thomas Jefferson University, Philadelphia, in an interview. “The trial confirmed that, compared with sleep education, which was used as the control, Internet-delivered CBT-I is effective in the treatment of insomnia.”
“These results demonstrate two important things,” said Dr. Skolnik. “The most important is that Internet-delivered CBT-I works, and since it is both safe and effective, should be the first-line therapy for patients who want treatment for insomnia.”
Secondly, “the fact that more people completed culturally tailored versions suggests that, when culturally tailored versions are available, their use is preferable, as it might facilitate a higher proportion of patients being successful in their insomnia treatment,” he added.
The study was supported by the Patient-Centered Outcomes Research Institute. The Black Women’s Health Study is supported by the National Cancer Institute. Dr. Zhou disclosed support from both PCORI and the NCI during the study. Dr. Skolnik, who was not involved in the study, disclosed serving on the advisory board for Idorsia Pharmaceuticals. He is also a member of the editorial advisory board of Family Practice News.
Data from previous studies suggest that women are up to 40% more likely to experience insomnia disorder compared with men, Eric S. Zhou, PhD, of Harvard Medical School, Boston, and colleagues wrote. The risk is even higher among Black women, but research on tailored treatments for this particular population has been limited.
In their study, published in JAMA Psychiatry, the researchers recruited women with elevated insomnia symptoms who were enrolled in the Black Women’s Health Study, an ongoing national, longitudinal research cohort in the United States. Participants were recruited between October 2019 and June 2020.The participants were randomized to an Internet-delivered behavior intervention (108 women), a stakeholder-informed Internet intervention tailored to Black women (110 women), or non-Internet patient education about sleep (115 women).
The Internet intervention, known as Sleep Healthy Using the Internet (SHUTi), was a 6-session program lasting 45-60 minutes per session and delivered over 6-9 weeks. The program included core elements of cognitive behavioral therapy and took into account information provided by patients about their baseline sleep function, treatment adherence, and sleep progress.
The tailored version of SHUTi for Black women (SHUTi-BWHS) was similar, but included Black actors for video vignettes and the inclusion of content about the cultural and social contexts in which insomnia often occurs for Black women, such while managing neighborhood noise and or living in crowded environments.
A third group received standard patient education material about sleep through a noninteractive website, and served as the control group.
The primary outcome of insomnia severity was measured using the Insomnia Severity Index (ISI), a 0- to 28-point scale. Scores for the ISI are based on responses to seven questions, including some that ask participants to rate the severity of their insomnia symptoms.
Clinically significant improvement in insomnia was defined as a reduction in score of more than 7 points. Patients were assessed at baseline, at 9 weeks, and again at approximately 6 months.
Significantly greater reductions in insomnia severity seen in intervention groups vs. control group
Overall, women randomized to SHUTi or SHUTi-BWHS) reported a significantly greater reduction in insomnia symptoms from baseline to 6 months, compared with the control group (P < .001), with ISI score decreases of 10.0, 9.3, and 3.6, respectively. No statistically significant differences in ISI score changes appeared between the between the SHUTi-BWHS and SHUTi groups.
Also, significantly more women in the SHUTi-BWHS group than in the SHUTi group completed the intervention (78.2% vs. 64.8%).
Treatment response was similar between the SHUTI-BWHS and SHUTi groups; 47.3% and 46.3%, respectively, had a decrease in ISI score of more than 7 points. In addition, 37% of women in the SHUTi-BWHS and 38% of women in the SHUTi groups reached ISI scores of less than 8 points, defined as full resolution of insomnia, by the last follow-up visit.
Both the SHUTi and SHUTi-BWHS interventions had dramatic effects on insomnia, but the increased number of women who completed the intervention in the SHUTi-BWHS group supports the value of tailored intervention, the researchers noted. “Similar to prior SHUTi trials, there was a direct association between the participant’s level of intervention engagement and their improvement in sleep.”
The average age of the participants was 60 years, 62% were single, and 44% had a graduate degree or higher. Approximately 5% were being actively treated for sleep apnea.
The study findings were limited by several factors including the relatively high socioeconomic status of the study participants, lack of data on medical mistrust, and inability to detect smaller differences between SHUTi and SHUTi-BWHS, the researchers noted.
Choose Internet-based CBT first for insomnia
“This was an excellent paper that sought to see the relative efficacy of standard version of Internet-delivered CBT-I [cognitive-behavioral therapy for insomnia] versus a culturally tailored version for Black women,” said Neil Skolnik, MD, professor of family and community medicine at Thomas Jefferson University, Philadelphia, in an interview. “The trial confirmed that, compared with sleep education, which was used as the control, Internet-delivered CBT-I is effective in the treatment of insomnia.”
“These results demonstrate two important things,” said Dr. Skolnik. “The most important is that Internet-delivered CBT-I works, and since it is both safe and effective, should be the first-line therapy for patients who want treatment for insomnia.”
Secondly, “the fact that more people completed culturally tailored versions suggests that, when culturally tailored versions are available, their use is preferable, as it might facilitate a higher proportion of patients being successful in their insomnia treatment,” he added.
The study was supported by the Patient-Centered Outcomes Research Institute. The Black Women’s Health Study is supported by the National Cancer Institute. Dr. Zhou disclosed support from both PCORI and the NCI during the study. Dr. Skolnik, who was not involved in the study, disclosed serving on the advisory board for Idorsia Pharmaceuticals. He is also a member of the editorial advisory board of Family Practice News.
Data from previous studies suggest that women are up to 40% more likely to experience insomnia disorder compared with men, Eric S. Zhou, PhD, of Harvard Medical School, Boston, and colleagues wrote. The risk is even higher among Black women, but research on tailored treatments for this particular population has been limited.
In their study, published in JAMA Psychiatry, the researchers recruited women with elevated insomnia symptoms who were enrolled in the Black Women’s Health Study, an ongoing national, longitudinal research cohort in the United States. Participants were recruited between October 2019 and June 2020.The participants were randomized to an Internet-delivered behavior intervention (108 women), a stakeholder-informed Internet intervention tailored to Black women (110 women), or non-Internet patient education about sleep (115 women).
The Internet intervention, known as Sleep Healthy Using the Internet (SHUTi), was a 6-session program lasting 45-60 minutes per session and delivered over 6-9 weeks. The program included core elements of cognitive behavioral therapy and took into account information provided by patients about their baseline sleep function, treatment adherence, and sleep progress.
The tailored version of SHUTi for Black women (SHUTi-BWHS) was similar, but included Black actors for video vignettes and the inclusion of content about the cultural and social contexts in which insomnia often occurs for Black women, such while managing neighborhood noise and or living in crowded environments.
A third group received standard patient education material about sleep through a noninteractive website, and served as the control group.
The primary outcome of insomnia severity was measured using the Insomnia Severity Index (ISI), a 0- to 28-point scale. Scores for the ISI are based on responses to seven questions, including some that ask participants to rate the severity of their insomnia symptoms.
Clinically significant improvement in insomnia was defined as a reduction in score of more than 7 points. Patients were assessed at baseline, at 9 weeks, and again at approximately 6 months.
Significantly greater reductions in insomnia severity seen in intervention groups vs. control group
Overall, women randomized to SHUTi or SHUTi-BWHS) reported a significantly greater reduction in insomnia symptoms from baseline to 6 months, compared with the control group (P < .001), with ISI score decreases of 10.0, 9.3, and 3.6, respectively. No statistically significant differences in ISI score changes appeared between the between the SHUTi-BWHS and SHUTi groups.
Also, significantly more women in the SHUTi-BWHS group than in the SHUTi group completed the intervention (78.2% vs. 64.8%).
Treatment response was similar between the SHUTI-BWHS and SHUTi groups; 47.3% and 46.3%, respectively, had a decrease in ISI score of more than 7 points. In addition, 37% of women in the SHUTi-BWHS and 38% of women in the SHUTi groups reached ISI scores of less than 8 points, defined as full resolution of insomnia, by the last follow-up visit.
Both the SHUTi and SHUTi-BWHS interventions had dramatic effects on insomnia, but the increased number of women who completed the intervention in the SHUTi-BWHS group supports the value of tailored intervention, the researchers noted. “Similar to prior SHUTi trials, there was a direct association between the participant’s level of intervention engagement and their improvement in sleep.”
The average age of the participants was 60 years, 62% were single, and 44% had a graduate degree or higher. Approximately 5% were being actively treated for sleep apnea.
The study findings were limited by several factors including the relatively high socioeconomic status of the study participants, lack of data on medical mistrust, and inability to detect smaller differences between SHUTi and SHUTi-BWHS, the researchers noted.
Choose Internet-based CBT first for insomnia
“This was an excellent paper that sought to see the relative efficacy of standard version of Internet-delivered CBT-I [cognitive-behavioral therapy for insomnia] versus a culturally tailored version for Black women,” said Neil Skolnik, MD, professor of family and community medicine at Thomas Jefferson University, Philadelphia, in an interview. “The trial confirmed that, compared with sleep education, which was used as the control, Internet-delivered CBT-I is effective in the treatment of insomnia.”
“These results demonstrate two important things,” said Dr. Skolnik. “The most important is that Internet-delivered CBT-I works, and since it is both safe and effective, should be the first-line therapy for patients who want treatment for insomnia.”
Secondly, “the fact that more people completed culturally tailored versions suggests that, when culturally tailored versions are available, their use is preferable, as it might facilitate a higher proportion of patients being successful in their insomnia treatment,” he added.
The study was supported by the Patient-Centered Outcomes Research Institute. The Black Women’s Health Study is supported by the National Cancer Institute. Dr. Zhou disclosed support from both PCORI and the NCI during the study. Dr. Skolnik, who was not involved in the study, disclosed serving on the advisory board for Idorsia Pharmaceuticals. He is also a member of the editorial advisory board of Family Practice News.
FROM JAMA PSYCHIATRY
Do personality traits predict cognitive decline?
new research shows.
Investigators analyzed data from almost 2,000 individuals enrolled in the Rush Memory and Aging Project (MAP) – a longitudinal study of older adults living in the greater Chicago metropolitan region and northeastern Illinois – with recruitment that began in 1997 and continues through today. Participants received a personality assessment as well as annual assessments of their cognitive abilities.
Those with high scores on measures of conscientiousness were significantly less likely to progress from normal cognition to mild cognitive impairment (MCI) during the study. In fact, scoring an extra 1 standard deviation on the conscientiousness scale was associated with a 22% lower risk of transitioning from no cognitive impairment (NCI) to MCI. On the other hand, scoring an additional 1 SD on a neuroticism scale was associated with a 12% increased risk of transitioning to MCI.
Participants who scored high on extraversion, as well as those who scored high on conscientiousness or low on neuroticism, tended to maintain normal cognitive functioning longer than other participants.
“Personality traits reflect relatively enduring patterns of thinking and behaving, which may cumulatively affect engagement in healthy and unhealthy behaviors and thought patterns across the lifespan,” lead author Tomiko Yoneda, PhD, a postdoctoral researcher in the department of medical social sciences, Northwestern University, Chicago, said in an interview.
“The accumulation of lifelong experiences may then contribute to susceptibility of particular diseases or disorders, such as mild cognitive impairment, or contribute to individual differences in the ability to withstand age-related neurological changes,” she added.
The study was published online in the Journal of Personality and Social Psychology.
Competing risk factors
Personality traits “reflect an individual’s persistent patterns of thinking, feeling, and behaving,” Dr. Yoneda said.
“For example, conscientiousness is characterized by competence, dutifulness, and self-discipline, while neuroticism is characterized by anxiety, depressive symptoms, and emotional instability. Likewise, individuals high in extraversion tend to be enthusiastic, gregarious, talkative, and assertive,” she added.
Previous research “suggests that low conscientiousness and high neuroticism are associated with an increased risk of cognitive impairment,” she continued. However, “there is also an increased risk of death in older adulthood – in other words, these outcomes are ‘competing risk factors.’”
Dr. Yoneda said her team wanted to “examine the impact of personality traits on the simultaneous risk of transitioning to mild cognitive impairment, dementia, and death.”
For the study, the researchers analyzed data from 1,954 participants in MAP (mean age at baseline 80 years, 73.7% female, 86.8% White), who received a personality assessment and annual assessments of their cognitive abilities.
To assess personality traits – in particular, conscientiousness, neuroticism, and extraversion – the researchers used the NEO Five Factor Inventory (NEO-FFI). They also used multistate survival modeling to examine the potential association between these traits and transitions from one cognitive status category to another (NCI, MCI, and dementia) and to death.
Cognitive healthspan
By the end of the study, over half of the sample (54%) had died.
Most transitions showed “relative stability in cognitive status across measurement occasions.”
- NCI to NCI (n = 7,368)
- MCI to MCI (n = 1,244)
- Dementia to dementia (n = 876)
There were 725 “backward transitions” from MCI to NCI, “which may reflect improvement or within-person variability in cognitive functioning, or learning effects,” the authors note.
There were only 114 “backward transitions” from dementia to MCI and only 12 from dementia to NCI, “suggesting that improvement in cognitive status was relatively rare, particularly once an individual progresses to dementia.”
After adjusting for demographics, depressive symptoms, and apolipoprotein (APOE) ε4 allele, the researchers found that personality traits were the most important factors in the transition from NCI to MCI.
Higher conscientiousness was associated with a decreased risk of transitioning from NCI to MCI (hazard ratio, 0.78; 95% confidence interval, 0.72-0.85). Conversely, higher neuroticism was associated with an increased risk of transitioning from NCI to MCI (HR, 1.12; 95% CI, 1.04-1.21) and a significantly decreased likelihood of transition back from MCI to NCI (HR, 0.90; 95% CI, 0.81-1.00).
Scoring ~6 points on a conscientiousness scale ranging from 0-48 (that is, 1 SD on the scale) was significantly associated with ~22% lower risk of transitioning forward from NCI to MCI, while scoring ~7 more points on a neuroticism scale (1 SD) was significantly associated with ~12% higher risk of transitioning from NCI to MCI.
Higher extraversion was associated with an increased likelihood of transitioning from MCI back to NCI (HR, 1.12; 95% CI, 1.03-1.22), and although extraversion was not associated with a longer total lifespan, participants who scored high on extraversion, as well as those who scored low on conscientiousness or low on neuroticism, maintained normal cognitive function longer than other participants.
“Our results suggest that high conscientiousness and low neuroticism may protect individuals against mild cognitive impairment,” said Dr. Yoneda.
Importantly, individuals who were either higher in conscientiousness, higher in extraversion, or lower in neuroticism had more years of “cognitive healthspan,” meaning more years without cognitive impairment,” she added.
In addition, “individuals lower in neuroticism and higher in extraversion were more likely to recover after receiving an MCI diagnosis, suggesting that these traits may be protective even after an individual starts to progress to dementia,” she said.
The authors note that the study focused on only three of the Big Five personality traits, while the other 2 – openness to experience and agreeableness – may also be associated with cognitive aging processes and mortality.
Nevertheless, given the current results, alongside extensive research in the personality field, aiming to increase conscientiousness through persistent behavioral change is one potential strategy for promoting healthy cognitive aging, Dr. Yoneda said.
‘Invaluable window’
In a comment, Brent Roberts, PhD, professor of psychology, University of Illinois Urbana-Champaign, said the study provides an “invaluable window into how personality affects the process of decline and either accelerates it, as in the role of neuroticism, or decelerates it, as in the role of conscientiousness.”
“I think the most fascinating finding was the fact that extraversion was related to transitioning from MCI back to NCI. These types of transitions have simply not been part of prior research, and it provides utterly unique insights and opportunities for interventions that may actually help people recover from a decline,” said Dr. Roberts, who was not involved in the research.
Claire Sexton, DPhil, Alzheimer’s Association director of scientific programs and outreach, called the paper “novel” because it investigated the transitions between normal cognition and mild impairment and between mild impairment and dementia.
Dr. Sexton, who was associated with this research team, cautioned that is it observational, “so it can illuminate associations or correlations, but not causes. As a result, we can’t say for sure what the mechanisms are behind these potential connections between personality and cognition, and more research is needed.”
The research was supported by the Alzheimer Society Research Program, Social Sciences and Humanities Research Council, and the National Institute on Aging of the National Institutes of Health. Dr. Yoneda and co-authors, Dr. Roberts, and Dr. Sexton have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research shows.
Investigators analyzed data from almost 2,000 individuals enrolled in the Rush Memory and Aging Project (MAP) – a longitudinal study of older adults living in the greater Chicago metropolitan region and northeastern Illinois – with recruitment that began in 1997 and continues through today. Participants received a personality assessment as well as annual assessments of their cognitive abilities.
Those with high scores on measures of conscientiousness were significantly less likely to progress from normal cognition to mild cognitive impairment (MCI) during the study. In fact, scoring an extra 1 standard deviation on the conscientiousness scale was associated with a 22% lower risk of transitioning from no cognitive impairment (NCI) to MCI. On the other hand, scoring an additional 1 SD on a neuroticism scale was associated with a 12% increased risk of transitioning to MCI.
Participants who scored high on extraversion, as well as those who scored high on conscientiousness or low on neuroticism, tended to maintain normal cognitive functioning longer than other participants.
“Personality traits reflect relatively enduring patterns of thinking and behaving, which may cumulatively affect engagement in healthy and unhealthy behaviors and thought patterns across the lifespan,” lead author Tomiko Yoneda, PhD, a postdoctoral researcher in the department of medical social sciences, Northwestern University, Chicago, said in an interview.
“The accumulation of lifelong experiences may then contribute to susceptibility of particular diseases or disorders, such as mild cognitive impairment, or contribute to individual differences in the ability to withstand age-related neurological changes,” she added.
The study was published online in the Journal of Personality and Social Psychology.
Competing risk factors
Personality traits “reflect an individual’s persistent patterns of thinking, feeling, and behaving,” Dr. Yoneda said.
“For example, conscientiousness is characterized by competence, dutifulness, and self-discipline, while neuroticism is characterized by anxiety, depressive symptoms, and emotional instability. Likewise, individuals high in extraversion tend to be enthusiastic, gregarious, talkative, and assertive,” she added.
Previous research “suggests that low conscientiousness and high neuroticism are associated with an increased risk of cognitive impairment,” she continued. However, “there is also an increased risk of death in older adulthood – in other words, these outcomes are ‘competing risk factors.’”
Dr. Yoneda said her team wanted to “examine the impact of personality traits on the simultaneous risk of transitioning to mild cognitive impairment, dementia, and death.”
For the study, the researchers analyzed data from 1,954 participants in MAP (mean age at baseline 80 years, 73.7% female, 86.8% White), who received a personality assessment and annual assessments of their cognitive abilities.
To assess personality traits – in particular, conscientiousness, neuroticism, and extraversion – the researchers used the NEO Five Factor Inventory (NEO-FFI). They also used multistate survival modeling to examine the potential association between these traits and transitions from one cognitive status category to another (NCI, MCI, and dementia) and to death.
Cognitive healthspan
By the end of the study, over half of the sample (54%) had died.
Most transitions showed “relative stability in cognitive status across measurement occasions.”
- NCI to NCI (n = 7,368)
- MCI to MCI (n = 1,244)
- Dementia to dementia (n = 876)
There were 725 “backward transitions” from MCI to NCI, “which may reflect improvement or within-person variability in cognitive functioning, or learning effects,” the authors note.
There were only 114 “backward transitions” from dementia to MCI and only 12 from dementia to NCI, “suggesting that improvement in cognitive status was relatively rare, particularly once an individual progresses to dementia.”
After adjusting for demographics, depressive symptoms, and apolipoprotein (APOE) ε4 allele, the researchers found that personality traits were the most important factors in the transition from NCI to MCI.
Higher conscientiousness was associated with a decreased risk of transitioning from NCI to MCI (hazard ratio, 0.78; 95% confidence interval, 0.72-0.85). Conversely, higher neuroticism was associated with an increased risk of transitioning from NCI to MCI (HR, 1.12; 95% CI, 1.04-1.21) and a significantly decreased likelihood of transition back from MCI to NCI (HR, 0.90; 95% CI, 0.81-1.00).
Scoring ~6 points on a conscientiousness scale ranging from 0-48 (that is, 1 SD on the scale) was significantly associated with ~22% lower risk of transitioning forward from NCI to MCI, while scoring ~7 more points on a neuroticism scale (1 SD) was significantly associated with ~12% higher risk of transitioning from NCI to MCI.
Higher extraversion was associated with an increased likelihood of transitioning from MCI back to NCI (HR, 1.12; 95% CI, 1.03-1.22), and although extraversion was not associated with a longer total lifespan, participants who scored high on extraversion, as well as those who scored low on conscientiousness or low on neuroticism, maintained normal cognitive function longer than other participants.
“Our results suggest that high conscientiousness and low neuroticism may protect individuals against mild cognitive impairment,” said Dr. Yoneda.
Importantly, individuals who were either higher in conscientiousness, higher in extraversion, or lower in neuroticism had more years of “cognitive healthspan,” meaning more years without cognitive impairment,” she added.
In addition, “individuals lower in neuroticism and higher in extraversion were more likely to recover after receiving an MCI diagnosis, suggesting that these traits may be protective even after an individual starts to progress to dementia,” she said.
The authors note that the study focused on only three of the Big Five personality traits, while the other 2 – openness to experience and agreeableness – may also be associated with cognitive aging processes and mortality.
Nevertheless, given the current results, alongside extensive research in the personality field, aiming to increase conscientiousness through persistent behavioral change is one potential strategy for promoting healthy cognitive aging, Dr. Yoneda said.
‘Invaluable window’
In a comment, Brent Roberts, PhD, professor of psychology, University of Illinois Urbana-Champaign, said the study provides an “invaluable window into how personality affects the process of decline and either accelerates it, as in the role of neuroticism, or decelerates it, as in the role of conscientiousness.”
“I think the most fascinating finding was the fact that extraversion was related to transitioning from MCI back to NCI. These types of transitions have simply not been part of prior research, and it provides utterly unique insights and opportunities for interventions that may actually help people recover from a decline,” said Dr. Roberts, who was not involved in the research.
Claire Sexton, DPhil, Alzheimer’s Association director of scientific programs and outreach, called the paper “novel” because it investigated the transitions between normal cognition and mild impairment and between mild impairment and dementia.
Dr. Sexton, who was associated with this research team, cautioned that is it observational, “so it can illuminate associations or correlations, but not causes. As a result, we can’t say for sure what the mechanisms are behind these potential connections between personality and cognition, and more research is needed.”
The research was supported by the Alzheimer Society Research Program, Social Sciences and Humanities Research Council, and the National Institute on Aging of the National Institutes of Health. Dr. Yoneda and co-authors, Dr. Roberts, and Dr. Sexton have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research shows.
Investigators analyzed data from almost 2,000 individuals enrolled in the Rush Memory and Aging Project (MAP) – a longitudinal study of older adults living in the greater Chicago metropolitan region and northeastern Illinois – with recruitment that began in 1997 and continues through today. Participants received a personality assessment as well as annual assessments of their cognitive abilities.
Those with high scores on measures of conscientiousness were significantly less likely to progress from normal cognition to mild cognitive impairment (MCI) during the study. In fact, scoring an extra 1 standard deviation on the conscientiousness scale was associated with a 22% lower risk of transitioning from no cognitive impairment (NCI) to MCI. On the other hand, scoring an additional 1 SD on a neuroticism scale was associated with a 12% increased risk of transitioning to MCI.
Participants who scored high on extraversion, as well as those who scored high on conscientiousness or low on neuroticism, tended to maintain normal cognitive functioning longer than other participants.
“Personality traits reflect relatively enduring patterns of thinking and behaving, which may cumulatively affect engagement in healthy and unhealthy behaviors and thought patterns across the lifespan,” lead author Tomiko Yoneda, PhD, a postdoctoral researcher in the department of medical social sciences, Northwestern University, Chicago, said in an interview.
“The accumulation of lifelong experiences may then contribute to susceptibility of particular diseases or disorders, such as mild cognitive impairment, or contribute to individual differences in the ability to withstand age-related neurological changes,” she added.
The study was published online in the Journal of Personality and Social Psychology.
Competing risk factors
Personality traits “reflect an individual’s persistent patterns of thinking, feeling, and behaving,” Dr. Yoneda said.
“For example, conscientiousness is characterized by competence, dutifulness, and self-discipline, while neuroticism is characterized by anxiety, depressive symptoms, and emotional instability. Likewise, individuals high in extraversion tend to be enthusiastic, gregarious, talkative, and assertive,” she added.
Previous research “suggests that low conscientiousness and high neuroticism are associated with an increased risk of cognitive impairment,” she continued. However, “there is also an increased risk of death in older adulthood – in other words, these outcomes are ‘competing risk factors.’”
Dr. Yoneda said her team wanted to “examine the impact of personality traits on the simultaneous risk of transitioning to mild cognitive impairment, dementia, and death.”
For the study, the researchers analyzed data from 1,954 participants in MAP (mean age at baseline 80 years, 73.7% female, 86.8% White), who received a personality assessment and annual assessments of their cognitive abilities.
To assess personality traits – in particular, conscientiousness, neuroticism, and extraversion – the researchers used the NEO Five Factor Inventory (NEO-FFI). They also used multistate survival modeling to examine the potential association between these traits and transitions from one cognitive status category to another (NCI, MCI, and dementia) and to death.
Cognitive healthspan
By the end of the study, over half of the sample (54%) had died.
Most transitions showed “relative stability in cognitive status across measurement occasions.”
- NCI to NCI (n = 7,368)
- MCI to MCI (n = 1,244)
- Dementia to dementia (n = 876)
There were 725 “backward transitions” from MCI to NCI, “which may reflect improvement or within-person variability in cognitive functioning, or learning effects,” the authors note.
There were only 114 “backward transitions” from dementia to MCI and only 12 from dementia to NCI, “suggesting that improvement in cognitive status was relatively rare, particularly once an individual progresses to dementia.”
After adjusting for demographics, depressive symptoms, and apolipoprotein (APOE) ε4 allele, the researchers found that personality traits were the most important factors in the transition from NCI to MCI.
Higher conscientiousness was associated with a decreased risk of transitioning from NCI to MCI (hazard ratio, 0.78; 95% confidence interval, 0.72-0.85). Conversely, higher neuroticism was associated with an increased risk of transitioning from NCI to MCI (HR, 1.12; 95% CI, 1.04-1.21) and a significantly decreased likelihood of transition back from MCI to NCI (HR, 0.90; 95% CI, 0.81-1.00).
Scoring ~6 points on a conscientiousness scale ranging from 0-48 (that is, 1 SD on the scale) was significantly associated with ~22% lower risk of transitioning forward from NCI to MCI, while scoring ~7 more points on a neuroticism scale (1 SD) was significantly associated with ~12% higher risk of transitioning from NCI to MCI.
Higher extraversion was associated with an increased likelihood of transitioning from MCI back to NCI (HR, 1.12; 95% CI, 1.03-1.22), and although extraversion was not associated with a longer total lifespan, participants who scored high on extraversion, as well as those who scored low on conscientiousness or low on neuroticism, maintained normal cognitive function longer than other participants.
“Our results suggest that high conscientiousness and low neuroticism may protect individuals against mild cognitive impairment,” said Dr. Yoneda.
Importantly, individuals who were either higher in conscientiousness, higher in extraversion, or lower in neuroticism had more years of “cognitive healthspan,” meaning more years without cognitive impairment,” she added.
In addition, “individuals lower in neuroticism and higher in extraversion were more likely to recover after receiving an MCI diagnosis, suggesting that these traits may be protective even after an individual starts to progress to dementia,” she said.
The authors note that the study focused on only three of the Big Five personality traits, while the other 2 – openness to experience and agreeableness – may also be associated with cognitive aging processes and mortality.
Nevertheless, given the current results, alongside extensive research in the personality field, aiming to increase conscientiousness through persistent behavioral change is one potential strategy for promoting healthy cognitive aging, Dr. Yoneda said.
‘Invaluable window’
In a comment, Brent Roberts, PhD, professor of psychology, University of Illinois Urbana-Champaign, said the study provides an “invaluable window into how personality affects the process of decline and either accelerates it, as in the role of neuroticism, or decelerates it, as in the role of conscientiousness.”
“I think the most fascinating finding was the fact that extraversion was related to transitioning from MCI back to NCI. These types of transitions have simply not been part of prior research, and it provides utterly unique insights and opportunities for interventions that may actually help people recover from a decline,” said Dr. Roberts, who was not involved in the research.
Claire Sexton, DPhil, Alzheimer’s Association director of scientific programs and outreach, called the paper “novel” because it investigated the transitions between normal cognition and mild impairment and between mild impairment and dementia.
Dr. Sexton, who was associated with this research team, cautioned that is it observational, “so it can illuminate associations or correlations, but not causes. As a result, we can’t say for sure what the mechanisms are behind these potential connections between personality and cognition, and more research is needed.”
The research was supported by the Alzheimer Society Research Program, Social Sciences and Humanities Research Council, and the National Institute on Aging of the National Institutes of Health. Dr. Yoneda and co-authors, Dr. Roberts, and Dr. Sexton have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF PERSONALITY AND SOCIAL PSYCHOLOGY
Mental illness tied to COVID-19 breakthrough infection
“Psychiatric disorders remained significantly associated with incident breakthrough infections above and beyond sociodemographic and medical factors, suggesting that mental health is important to consider in conjunction with other risk factors,” wrote the investigators, led by Aoife O’Donovan, PhD, University of California, San Francisco.
Individuals with psychiatric disorders “should be prioritized for booster vaccinations and other critical preventive efforts, including increased SARS-CoV-2 screening, public health campaigns, or COVID-19 discussions during clinical care,” they added.
The study was published online in JAMA Network Open.
Elderly most vulnerable
The researchers reviewed the records of 263,697 veterans who were fully vaccinated against COVID-19.
Just over a half (51.4%) had one or more psychiatric diagnoses within the last 5 years and 14.8% developed breakthrough COVID-19 infections, confirmed by a positive SARS-CoV-2 test.
Psychiatric diagnoses among the veterans included depression, posttraumatic stress, anxiety, adjustment disorder, substance use disorder, bipolar disorder, psychosis, ADHD, dissociation, and eating disorders.
In the overall sample, a history of any psychiatric disorder was associated with a 7% higher incidence of breakthrough COVID-19 infection in models adjusted for potential confounders (adjusted relative risk, 1.07; 95% confidence interval, 1.05-1.09) and a 3% higher incidence in models additionally adjusted for underlying medical comorbidities and smoking (aRR, 1.03; 95% CI, 1.01-1.05).
Most psychiatric disorders were associated with a higher incidence of breakthrough infection, with the highest relative risk observed for substance use disorders (aRR, 1.16; 95% CI, 1.12 -1.21) and adjustment disorder (aRR, 1.13; 95% CI, 1.10-1.16) in fully adjusted models.
Older vaccinated veterans with psychiatric illnesses appear to be most vulnerable to COVID-19 reinfection.
In veterans aged 65 and older, all psychiatric disorders were associated with an increased incidence of breakthrough infection, with increases in the incidence rate ranging from 3% to 24% in fully adjusted models.
In the younger veterans, in contrast, only anxiety, adjustment, and substance use disorders were associated with an increased incidence of breakthrough infection in fully adjusted models.
Psychotic disorders were associated with a 10% lower incidence of breakthrough infection among younger veterans, perhaps because of greater social isolation, the researchers said.
Risky behavior or impaired immunity?
“Although some of the larger observed effect sizes are compelling at an individual level, even the relatively modest effect sizes may have a large effect at the population level when considering the high prevalence of psychiatric disorders and the global reach and scale of the pandemic,” Dr. O’Donovan and colleagues wrote.
They noted that psychiatric disorders, including depression, schizophrenia, and bipolar disorders, have been associated with impaired cellular immunity and blunted response to vaccines. Therefore, it’s possible that those with psychiatric disorders have poorer responses to COVID-19 vaccination.
It’s also possible that immunity following vaccination wanes more quickly or more strongly in people with psychiatric disorders and they could have less protection against new variants, they added.
Patients with psychiatric disorders could be more apt to engage in risky behaviors for contracting COVID-19, which could also increase the risk for breakthrough infection, they said.
The study was supported by a UCSF Department of Psychiatry Rapid Award and UCSF Faculty Resource Fund Award. Dr. O’Donovan reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
“Psychiatric disorders remained significantly associated with incident breakthrough infections above and beyond sociodemographic and medical factors, suggesting that mental health is important to consider in conjunction with other risk factors,” wrote the investigators, led by Aoife O’Donovan, PhD, University of California, San Francisco.
Individuals with psychiatric disorders “should be prioritized for booster vaccinations and other critical preventive efforts, including increased SARS-CoV-2 screening, public health campaigns, or COVID-19 discussions during clinical care,” they added.
The study was published online in JAMA Network Open.
Elderly most vulnerable
The researchers reviewed the records of 263,697 veterans who were fully vaccinated against COVID-19.
Just over a half (51.4%) had one or more psychiatric diagnoses within the last 5 years and 14.8% developed breakthrough COVID-19 infections, confirmed by a positive SARS-CoV-2 test.
Psychiatric diagnoses among the veterans included depression, posttraumatic stress, anxiety, adjustment disorder, substance use disorder, bipolar disorder, psychosis, ADHD, dissociation, and eating disorders.
In the overall sample, a history of any psychiatric disorder was associated with a 7% higher incidence of breakthrough COVID-19 infection in models adjusted for potential confounders (adjusted relative risk, 1.07; 95% confidence interval, 1.05-1.09) and a 3% higher incidence in models additionally adjusted for underlying medical comorbidities and smoking (aRR, 1.03; 95% CI, 1.01-1.05).
Most psychiatric disorders were associated with a higher incidence of breakthrough infection, with the highest relative risk observed for substance use disorders (aRR, 1.16; 95% CI, 1.12 -1.21) and adjustment disorder (aRR, 1.13; 95% CI, 1.10-1.16) in fully adjusted models.
Older vaccinated veterans with psychiatric illnesses appear to be most vulnerable to COVID-19 reinfection.
In veterans aged 65 and older, all psychiatric disorders were associated with an increased incidence of breakthrough infection, with increases in the incidence rate ranging from 3% to 24% in fully adjusted models.
In the younger veterans, in contrast, only anxiety, adjustment, and substance use disorders were associated with an increased incidence of breakthrough infection in fully adjusted models.
Psychotic disorders were associated with a 10% lower incidence of breakthrough infection among younger veterans, perhaps because of greater social isolation, the researchers said.
Risky behavior or impaired immunity?
“Although some of the larger observed effect sizes are compelling at an individual level, even the relatively modest effect sizes may have a large effect at the population level when considering the high prevalence of psychiatric disorders and the global reach and scale of the pandemic,” Dr. O’Donovan and colleagues wrote.
They noted that psychiatric disorders, including depression, schizophrenia, and bipolar disorders, have been associated with impaired cellular immunity and blunted response to vaccines. Therefore, it’s possible that those with psychiatric disorders have poorer responses to COVID-19 vaccination.
It’s also possible that immunity following vaccination wanes more quickly or more strongly in people with psychiatric disorders and they could have less protection against new variants, they added.
Patients with psychiatric disorders could be more apt to engage in risky behaviors for contracting COVID-19, which could also increase the risk for breakthrough infection, they said.
The study was supported by a UCSF Department of Psychiatry Rapid Award and UCSF Faculty Resource Fund Award. Dr. O’Donovan reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
“Psychiatric disorders remained significantly associated with incident breakthrough infections above and beyond sociodemographic and medical factors, suggesting that mental health is important to consider in conjunction with other risk factors,” wrote the investigators, led by Aoife O’Donovan, PhD, University of California, San Francisco.
Individuals with psychiatric disorders “should be prioritized for booster vaccinations and other critical preventive efforts, including increased SARS-CoV-2 screening, public health campaigns, or COVID-19 discussions during clinical care,” they added.
The study was published online in JAMA Network Open.
Elderly most vulnerable
The researchers reviewed the records of 263,697 veterans who were fully vaccinated against COVID-19.
Just over a half (51.4%) had one or more psychiatric diagnoses within the last 5 years and 14.8% developed breakthrough COVID-19 infections, confirmed by a positive SARS-CoV-2 test.
Psychiatric diagnoses among the veterans included depression, posttraumatic stress, anxiety, adjustment disorder, substance use disorder, bipolar disorder, psychosis, ADHD, dissociation, and eating disorders.
In the overall sample, a history of any psychiatric disorder was associated with a 7% higher incidence of breakthrough COVID-19 infection in models adjusted for potential confounders (adjusted relative risk, 1.07; 95% confidence interval, 1.05-1.09) and a 3% higher incidence in models additionally adjusted for underlying medical comorbidities and smoking (aRR, 1.03; 95% CI, 1.01-1.05).
Most psychiatric disorders were associated with a higher incidence of breakthrough infection, with the highest relative risk observed for substance use disorders (aRR, 1.16; 95% CI, 1.12 -1.21) and adjustment disorder (aRR, 1.13; 95% CI, 1.10-1.16) in fully adjusted models.
Older vaccinated veterans with psychiatric illnesses appear to be most vulnerable to COVID-19 reinfection.
In veterans aged 65 and older, all psychiatric disorders were associated with an increased incidence of breakthrough infection, with increases in the incidence rate ranging from 3% to 24% in fully adjusted models.
In the younger veterans, in contrast, only anxiety, adjustment, and substance use disorders were associated with an increased incidence of breakthrough infection in fully adjusted models.
Psychotic disorders were associated with a 10% lower incidence of breakthrough infection among younger veterans, perhaps because of greater social isolation, the researchers said.
Risky behavior or impaired immunity?
“Although some of the larger observed effect sizes are compelling at an individual level, even the relatively modest effect sizes may have a large effect at the population level when considering the high prevalence of psychiatric disorders and the global reach and scale of the pandemic,” Dr. O’Donovan and colleagues wrote.
They noted that psychiatric disorders, including depression, schizophrenia, and bipolar disorders, have been associated with impaired cellular immunity and blunted response to vaccines. Therefore, it’s possible that those with psychiatric disorders have poorer responses to COVID-19 vaccination.
It’s also possible that immunity following vaccination wanes more quickly or more strongly in people with psychiatric disorders and they could have less protection against new variants, they added.
Patients with psychiatric disorders could be more apt to engage in risky behaviors for contracting COVID-19, which could also increase the risk for breakthrough infection, they said.
The study was supported by a UCSF Department of Psychiatry Rapid Award and UCSF Faculty Resource Fund Award. Dr. O’Donovan reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN
Diagnosing PTSD: Heart rate variability may help
, according to a study published in Frontiers in Psychiatry.
It is estimated that between 8% and 15% of clinically recognized pregnancies and up to 30% of all pregnancies result in miscarriage – a loss that can be devastating for everyone. There are limited data on the strength of the association between perinatal loss and subsequent common mental health disorders, such as anxiety, depression, and PTSD. The prevalence of PTSD among this group is still unknown, and one of the factors that contribute to the absence of data is that diagnostic evaluation is subjective.
To address this issue, researchers from Anhembi Morumbi University (UAM) in São José dos Campos, Brazil, along with teams in the United States and United Arab Emirates (UAE), investigated biomarkers for the severity of PTSD. The hope is that the research will enable psychiatrists to assess women who experience pregnancy loss more objectively. Study author Ovidiu Constantin Baltatu, MD, PhD, a professor at Brazil’s UAM and the UAE’s Khalifa University, spoke to this news organization about the study.
Under the guidance of Dr. Baltatu, psychologist Cláudia de Faria Cardoso carried out the research as part of her studies in biomedical engineering at UAM. Fifty-three women were recruited; the average age of the cohort was 33 years. All participants had a history of at least one perinatal loss. Pregnancy loss intervals ranged from less than 40 days to more than 6 months.
Participants completed a clinical interview and a questionnaire; PTSD symptoms were assessed on the basis of criteria in the DSM-5. The instrument used for the assessment was the Brazilian version of the Post-traumatic Stress Disorder Checklist (PCL-5). In addition, to evaluate general autonomic dysfunction, patients completed the Composite Autonomic Symptom Score 31 (COMPASS-31) questionnaire.
HRV was assessed during a deep breathing test using an HRV scanner system with wireless electrocardiography that enabled real-time data analysis and visualization. The investigators examined the following HRV measures: standard deviation (SD) of normal R-R wave intervals (SDNN), square root of the mean of the sum of the squares of differences between adjacent normal R wave intervals, and the number of all R-R intervals in which the change in consecutive normal sinus intervals exceeds 50 ms divided by the total number of R-R intervals measured.
Of the 53 participants, 25 had been diagnosed with pregnancy loss–induced PTSD. The results indicated a significant association between PCL-5 scores and HRV indices. The SDNN index effectively distinguished between patients with PTSD and those without.
To Dr. Baltatu, HRV indices reflect dysfunction of the autonomic nervous system (ANS), one of the major neural pathways activated by stress.
Although the deep breathing test has been around for a long time, it’s not widely used in current clinical practice, he said. According to him, maximum and minimum heart rates during breathing at six cycles per minute can typically be used to calculate the inspiratory-to-expiratory ratio, thus providing an indication of ANS function. “Our group introduced the study of HRV during deep breathing test, which is a step forward,” he said.
The methodology used by the team was well received by the participants. “With the deep breathing test, the women were able to look at a screen and see real-time graphics displaying the stress that they were experiencing after having suffered trauma. This visualization of objective measures was perceived as an improved care,” said Dr. Baltatu.
In general, HRV provides a more objective means of diagnosing PTSD. “Normally, PTSD is assessed through a questionnaire and an interview with psychologists,” said Dr. Baltatu. The subjectivity of the assessment is one of the main factors associated with the underdiagnosis of this condition, he explained.
It is important to remember that other factors, such as a lack of awareness about the problem, also hinder the diagnosis of PTSD in this population, Dr. Baltatu added. Women who have had a miscarriage often don’t think that their symptoms may result from PTSD. This fact highlights why it is so important that hospitals have a clinical psychologist on staff. In addition, Dr. Baltatu pointed out that a woman who experiences a pregnancy loss usually has negative memories of the hospital and is therefore reluctant to reach out for professional help. “In our study, all psychological care and assessments took place outside of a hospital setting, which the participants seemed to appreciate,” he emphasized.
Dr. Baltatu and his team are conducting follow-up research. The preliminary results indicate that the biomarkers identified in the study are promising in the assessment of patients’ clinical progress. This finding may reflect the fact that the HRV indices have proven useful not only in diagnosing but also in monitoring women in treatment, because they are able to identify which patients are responding better to treatment.
A version of this article first appeared on Medscape.com.
, according to a study published in Frontiers in Psychiatry.
It is estimated that between 8% and 15% of clinically recognized pregnancies and up to 30% of all pregnancies result in miscarriage – a loss that can be devastating for everyone. There are limited data on the strength of the association between perinatal loss and subsequent common mental health disorders, such as anxiety, depression, and PTSD. The prevalence of PTSD among this group is still unknown, and one of the factors that contribute to the absence of data is that diagnostic evaluation is subjective.
To address this issue, researchers from Anhembi Morumbi University (UAM) in São José dos Campos, Brazil, along with teams in the United States and United Arab Emirates (UAE), investigated biomarkers for the severity of PTSD. The hope is that the research will enable psychiatrists to assess women who experience pregnancy loss more objectively. Study author Ovidiu Constantin Baltatu, MD, PhD, a professor at Brazil’s UAM and the UAE’s Khalifa University, spoke to this news organization about the study.
Under the guidance of Dr. Baltatu, psychologist Cláudia de Faria Cardoso carried out the research as part of her studies in biomedical engineering at UAM. Fifty-three women were recruited; the average age of the cohort was 33 years. All participants had a history of at least one perinatal loss. Pregnancy loss intervals ranged from less than 40 days to more than 6 months.
Participants completed a clinical interview and a questionnaire; PTSD symptoms were assessed on the basis of criteria in the DSM-5. The instrument used for the assessment was the Brazilian version of the Post-traumatic Stress Disorder Checklist (PCL-5). In addition, to evaluate general autonomic dysfunction, patients completed the Composite Autonomic Symptom Score 31 (COMPASS-31) questionnaire.
HRV was assessed during a deep breathing test using an HRV scanner system with wireless electrocardiography that enabled real-time data analysis and visualization. The investigators examined the following HRV measures: standard deviation (SD) of normal R-R wave intervals (SDNN), square root of the mean of the sum of the squares of differences between adjacent normal R wave intervals, and the number of all R-R intervals in which the change in consecutive normal sinus intervals exceeds 50 ms divided by the total number of R-R intervals measured.
Of the 53 participants, 25 had been diagnosed with pregnancy loss–induced PTSD. The results indicated a significant association between PCL-5 scores and HRV indices. The SDNN index effectively distinguished between patients with PTSD and those without.
To Dr. Baltatu, HRV indices reflect dysfunction of the autonomic nervous system (ANS), one of the major neural pathways activated by stress.
Although the deep breathing test has been around for a long time, it’s not widely used in current clinical practice, he said. According to him, maximum and minimum heart rates during breathing at six cycles per minute can typically be used to calculate the inspiratory-to-expiratory ratio, thus providing an indication of ANS function. “Our group introduced the study of HRV during deep breathing test, which is a step forward,” he said.
The methodology used by the team was well received by the participants. “With the deep breathing test, the women were able to look at a screen and see real-time graphics displaying the stress that they were experiencing after having suffered trauma. This visualization of objective measures was perceived as an improved care,” said Dr. Baltatu.
In general, HRV provides a more objective means of diagnosing PTSD. “Normally, PTSD is assessed through a questionnaire and an interview with psychologists,” said Dr. Baltatu. The subjectivity of the assessment is one of the main factors associated with the underdiagnosis of this condition, he explained.
It is important to remember that other factors, such as a lack of awareness about the problem, also hinder the diagnosis of PTSD in this population, Dr. Baltatu added. Women who have had a miscarriage often don’t think that their symptoms may result from PTSD. This fact highlights why it is so important that hospitals have a clinical psychologist on staff. In addition, Dr. Baltatu pointed out that a woman who experiences a pregnancy loss usually has negative memories of the hospital and is therefore reluctant to reach out for professional help. “In our study, all psychological care and assessments took place outside of a hospital setting, which the participants seemed to appreciate,” he emphasized.
Dr. Baltatu and his team are conducting follow-up research. The preliminary results indicate that the biomarkers identified in the study are promising in the assessment of patients’ clinical progress. This finding may reflect the fact that the HRV indices have proven useful not only in diagnosing but also in monitoring women in treatment, because they are able to identify which patients are responding better to treatment.
A version of this article first appeared on Medscape.com.
, according to a study published in Frontiers in Psychiatry.
It is estimated that between 8% and 15% of clinically recognized pregnancies and up to 30% of all pregnancies result in miscarriage – a loss that can be devastating for everyone. There are limited data on the strength of the association between perinatal loss and subsequent common mental health disorders, such as anxiety, depression, and PTSD. The prevalence of PTSD among this group is still unknown, and one of the factors that contribute to the absence of data is that diagnostic evaluation is subjective.
To address this issue, researchers from Anhembi Morumbi University (UAM) in São José dos Campos, Brazil, along with teams in the United States and United Arab Emirates (UAE), investigated biomarkers for the severity of PTSD. The hope is that the research will enable psychiatrists to assess women who experience pregnancy loss more objectively. Study author Ovidiu Constantin Baltatu, MD, PhD, a professor at Brazil’s UAM and the UAE’s Khalifa University, spoke to this news organization about the study.
Under the guidance of Dr. Baltatu, psychologist Cláudia de Faria Cardoso carried out the research as part of her studies in biomedical engineering at UAM. Fifty-three women were recruited; the average age of the cohort was 33 years. All participants had a history of at least one perinatal loss. Pregnancy loss intervals ranged from less than 40 days to more than 6 months.
Participants completed a clinical interview and a questionnaire; PTSD symptoms were assessed on the basis of criteria in the DSM-5. The instrument used for the assessment was the Brazilian version of the Post-traumatic Stress Disorder Checklist (PCL-5). In addition, to evaluate general autonomic dysfunction, patients completed the Composite Autonomic Symptom Score 31 (COMPASS-31) questionnaire.
HRV was assessed during a deep breathing test using an HRV scanner system with wireless electrocardiography that enabled real-time data analysis and visualization. The investigators examined the following HRV measures: standard deviation (SD) of normal R-R wave intervals (SDNN), square root of the mean of the sum of the squares of differences between adjacent normal R wave intervals, and the number of all R-R intervals in which the change in consecutive normal sinus intervals exceeds 50 ms divided by the total number of R-R intervals measured.
Of the 53 participants, 25 had been diagnosed with pregnancy loss–induced PTSD. The results indicated a significant association between PCL-5 scores and HRV indices. The SDNN index effectively distinguished between patients with PTSD and those without.
To Dr. Baltatu, HRV indices reflect dysfunction of the autonomic nervous system (ANS), one of the major neural pathways activated by stress.
Although the deep breathing test has been around for a long time, it’s not widely used in current clinical practice, he said. According to him, maximum and minimum heart rates during breathing at six cycles per minute can typically be used to calculate the inspiratory-to-expiratory ratio, thus providing an indication of ANS function. “Our group introduced the study of HRV during deep breathing test, which is a step forward,” he said.
The methodology used by the team was well received by the participants. “With the deep breathing test, the women were able to look at a screen and see real-time graphics displaying the stress that they were experiencing after having suffered trauma. This visualization of objective measures was perceived as an improved care,” said Dr. Baltatu.
In general, HRV provides a more objective means of diagnosing PTSD. “Normally, PTSD is assessed through a questionnaire and an interview with psychologists,” said Dr. Baltatu. The subjectivity of the assessment is one of the main factors associated with the underdiagnosis of this condition, he explained.
It is important to remember that other factors, such as a lack of awareness about the problem, also hinder the diagnosis of PTSD in this population, Dr. Baltatu added. Women who have had a miscarriage often don’t think that their symptoms may result from PTSD. This fact highlights why it is so important that hospitals have a clinical psychologist on staff. In addition, Dr. Baltatu pointed out that a woman who experiences a pregnancy loss usually has negative memories of the hospital and is therefore reluctant to reach out for professional help. “In our study, all psychological care and assessments took place outside of a hospital setting, which the participants seemed to appreciate,” he emphasized.
Dr. Baltatu and his team are conducting follow-up research. The preliminary results indicate that the biomarkers identified in the study are promising in the assessment of patients’ clinical progress. This finding may reflect the fact that the HRV indices have proven useful not only in diagnosing but also in monitoring women in treatment, because they are able to identify which patients are responding better to treatment.
A version of this article first appeared on Medscape.com.
FROM FRONTIERS IN PSYCHIATRY
Methylphenidate is overprescribed to children in France
The prevalence of attention-deficit/hyperactivity disorder is difficult to evaluate, and the diagnosis is based primarily on clinical criteria. In 2008, a French study estimated the prevalence to be between 3.5% and 5.6%, but the study’s design was questionable.
Treatment of this disorder consists first and foremost of educational, social, and psychotherapeutic management. Only if such treatment fails is methylphenidate (MPH), the only drug that has been approved in France for this indication, to be considered, according to the recommendations.
The drug’s short-term efficacy has been proven, but it has not shown any effect on the long-term risks for academic failure, delinquency, and drug addiction associated with ADHD. In contrast, its adverse effects are numerous. Cases of nervousness, sleep disorders, headaches, weight loss, risk for aggravation of psychiatric conditions, and progression to violent or suicidal behavior have all been documented extensively, as well as cases of cardiovascular and cerebrovascular disease. Moreover, MPH is classified as a narcotic.
Inappropriate prescribing conditions
A study that appeared in the French journal of neuropsychiatry in minors, Neuropsychiatrie de l’Enfance et de l’Adolescence, investigated the prescribing procedures for this drug in France. Researchers examined Social Security data for 144,509 patients between the ages of 0 and 17 years who had received at least one prescription between 2010 and 2019. The researchers made the following observations about prescribing patterns and usage during this period:
- New MPH prescriptions increased by 56% per year, and the total number of annual prescriptions increased by 116%. In 3- to 17-year-olds, the prevalence was estimated at 0.61% to 0.75% of the pediatric population in 2019. Boys accounted for most of this consumption (82.5% to 80.8% over this period).
- In 2011, the median duration of consumption by children 6 years of age and older was 5.5 years. For 25% of those children, it was more than 8 years.
- Contrary to the labeling, some prescriptions were written for children younger than 6 years.
- Twenty-five percent of initial prescriptions and 50% of annual renewals were not written by a hospital specialist, in violation of the regulatory requirements in effect until Sept. 13, 2021. On that date, the French National Authority for Health (HAS) decided that initial hospital prescription of MPH should end.
- Eighty-four percent of children did not have any medical consultations at the prescribing hospital department in the 13 months after starting MPH. While the prevalence of ADHD has more than doubled, the number of consultations at specialist French medical, psychological, and educational centers for minors (CMPPs) is now less than a fourth of what it was – a drop from 4.1% to 0.8%.
- The prescribing of MPH is not always associated with an ADHD diagnosis, even though ADHD is its only indication.
- Of children and adolescents who use MPH, 22.8% received one or more other psychotropic drugs in the year following the initial prescription, including the following: neuroleptics (64.5%), anxiolytics (35.5%), antidepressants (16.2%), antiepileptics (11%), hypnotics (4.8%), and antiparkinsonian drugs (3%). “These co-prescriptions are often way off-label and are not within HAS recommendations,” according to the authors.
- For the youngest children in school classes (those born in December rather than in January), between 2010 and 2019, there was on average a 54% increased risk of being medicated.
- In 2019, 21.7% of children who received MPH lived in families with Universal Health Coverage or a similar plan. Yet, according to the French National Institute of Statistics and Economic Studies, only 7.8% of the French population had this type of assistance.
A minority of practitioners
The authors of this article state that “the distribution of consumption suggests a predominant role of a minority of practitioners and hospital departments in the prescription of methylphenidate.” They note that “in European countries and in North America, the prescription rate of psychotropic drugs for ADHD has stabilized or shown a clear trend toward stabilization since 2008. The same cannot be said for France, where this rate is continuously increasing; so much so that in 2019, it reached a higher level than in other European countries like Great Britain.” The reasons for this are disputed.
A version of this article first appeared on Medscape.com.
The prevalence of attention-deficit/hyperactivity disorder is difficult to evaluate, and the diagnosis is based primarily on clinical criteria. In 2008, a French study estimated the prevalence to be between 3.5% and 5.6%, but the study’s design was questionable.
Treatment of this disorder consists first and foremost of educational, social, and psychotherapeutic management. Only if such treatment fails is methylphenidate (MPH), the only drug that has been approved in France for this indication, to be considered, according to the recommendations.
The drug’s short-term efficacy has been proven, but it has not shown any effect on the long-term risks for academic failure, delinquency, and drug addiction associated with ADHD. In contrast, its adverse effects are numerous. Cases of nervousness, sleep disorders, headaches, weight loss, risk for aggravation of psychiatric conditions, and progression to violent or suicidal behavior have all been documented extensively, as well as cases of cardiovascular and cerebrovascular disease. Moreover, MPH is classified as a narcotic.
Inappropriate prescribing conditions
A study that appeared in the French journal of neuropsychiatry in minors, Neuropsychiatrie de l’Enfance et de l’Adolescence, investigated the prescribing procedures for this drug in France. Researchers examined Social Security data for 144,509 patients between the ages of 0 and 17 years who had received at least one prescription between 2010 and 2019. The researchers made the following observations about prescribing patterns and usage during this period:
- New MPH prescriptions increased by 56% per year, and the total number of annual prescriptions increased by 116%. In 3- to 17-year-olds, the prevalence was estimated at 0.61% to 0.75% of the pediatric population in 2019. Boys accounted for most of this consumption (82.5% to 80.8% over this period).
- In 2011, the median duration of consumption by children 6 years of age and older was 5.5 years. For 25% of those children, it was more than 8 years.
- Contrary to the labeling, some prescriptions were written for children younger than 6 years.
- Twenty-five percent of initial prescriptions and 50% of annual renewals were not written by a hospital specialist, in violation of the regulatory requirements in effect until Sept. 13, 2021. On that date, the French National Authority for Health (HAS) decided that initial hospital prescription of MPH should end.
- Eighty-four percent of children did not have any medical consultations at the prescribing hospital department in the 13 months after starting MPH. While the prevalence of ADHD has more than doubled, the number of consultations at specialist French medical, psychological, and educational centers for minors (CMPPs) is now less than a fourth of what it was – a drop from 4.1% to 0.8%.
- The prescribing of MPH is not always associated with an ADHD diagnosis, even though ADHD is its only indication.
- Of children and adolescents who use MPH, 22.8% received one or more other psychotropic drugs in the year following the initial prescription, including the following: neuroleptics (64.5%), anxiolytics (35.5%), antidepressants (16.2%), antiepileptics (11%), hypnotics (4.8%), and antiparkinsonian drugs (3%). “These co-prescriptions are often way off-label and are not within HAS recommendations,” according to the authors.
- For the youngest children in school classes (those born in December rather than in January), between 2010 and 2019, there was on average a 54% increased risk of being medicated.
- In 2019, 21.7% of children who received MPH lived in families with Universal Health Coverage or a similar plan. Yet, according to the French National Institute of Statistics and Economic Studies, only 7.8% of the French population had this type of assistance.
A minority of practitioners
The authors of this article state that “the distribution of consumption suggests a predominant role of a minority of practitioners and hospital departments in the prescription of methylphenidate.” They note that “in European countries and in North America, the prescription rate of psychotropic drugs for ADHD has stabilized or shown a clear trend toward stabilization since 2008. The same cannot be said for France, where this rate is continuously increasing; so much so that in 2019, it reached a higher level than in other European countries like Great Britain.” The reasons for this are disputed.
A version of this article first appeared on Medscape.com.
The prevalence of attention-deficit/hyperactivity disorder is difficult to evaluate, and the diagnosis is based primarily on clinical criteria. In 2008, a French study estimated the prevalence to be between 3.5% and 5.6%, but the study’s design was questionable.
Treatment of this disorder consists first and foremost of educational, social, and psychotherapeutic management. Only if such treatment fails is methylphenidate (MPH), the only drug that has been approved in France for this indication, to be considered, according to the recommendations.
The drug’s short-term efficacy has been proven, but it has not shown any effect on the long-term risks for academic failure, delinquency, and drug addiction associated with ADHD. In contrast, its adverse effects are numerous. Cases of nervousness, sleep disorders, headaches, weight loss, risk for aggravation of psychiatric conditions, and progression to violent or suicidal behavior have all been documented extensively, as well as cases of cardiovascular and cerebrovascular disease. Moreover, MPH is classified as a narcotic.
Inappropriate prescribing conditions
A study that appeared in the French journal of neuropsychiatry in minors, Neuropsychiatrie de l’Enfance et de l’Adolescence, investigated the prescribing procedures for this drug in France. Researchers examined Social Security data for 144,509 patients between the ages of 0 and 17 years who had received at least one prescription between 2010 and 2019. The researchers made the following observations about prescribing patterns and usage during this period:
- New MPH prescriptions increased by 56% per year, and the total number of annual prescriptions increased by 116%. In 3- to 17-year-olds, the prevalence was estimated at 0.61% to 0.75% of the pediatric population in 2019. Boys accounted for most of this consumption (82.5% to 80.8% over this period).
- In 2011, the median duration of consumption by children 6 years of age and older was 5.5 years. For 25% of those children, it was more than 8 years.
- Contrary to the labeling, some prescriptions were written for children younger than 6 years.
- Twenty-five percent of initial prescriptions and 50% of annual renewals were not written by a hospital specialist, in violation of the regulatory requirements in effect until Sept. 13, 2021. On that date, the French National Authority for Health (HAS) decided that initial hospital prescription of MPH should end.
- Eighty-four percent of children did not have any medical consultations at the prescribing hospital department in the 13 months after starting MPH. While the prevalence of ADHD has more than doubled, the number of consultations at specialist French medical, psychological, and educational centers for minors (CMPPs) is now less than a fourth of what it was – a drop from 4.1% to 0.8%.
- The prescribing of MPH is not always associated with an ADHD diagnosis, even though ADHD is its only indication.
- Of children and adolescents who use MPH, 22.8% received one or more other psychotropic drugs in the year following the initial prescription, including the following: neuroleptics (64.5%), anxiolytics (35.5%), antidepressants (16.2%), antiepileptics (11%), hypnotics (4.8%), and antiparkinsonian drugs (3%). “These co-prescriptions are often way off-label and are not within HAS recommendations,” according to the authors.
- For the youngest children in school classes (those born in December rather than in January), between 2010 and 2019, there was on average a 54% increased risk of being medicated.
- In 2019, 21.7% of children who received MPH lived in families with Universal Health Coverage or a similar plan. Yet, according to the French National Institute of Statistics and Economic Studies, only 7.8% of the French population had this type of assistance.
A minority of practitioners
The authors of this article state that “the distribution of consumption suggests a predominant role of a minority of practitioners and hospital departments in the prescription of methylphenidate.” They note that “in European countries and in North America, the prescription rate of psychotropic drugs for ADHD has stabilized or shown a clear trend toward stabilization since 2008. The same cannot be said for France, where this rate is continuously increasing; so much so that in 2019, it reached a higher level than in other European countries like Great Britain.” The reasons for this are disputed.
A version of this article first appeared on Medscape.com.
Weigh but don’t tell
Reports of long waiting times at mental health clinics and anecdotal observations by health care providers suggest the pandemic has generated a dramatic increase in the incidence of eating disorders among the pediatric population. Of course this should come as no surprise to pediatricians.
Eating disorders come in many different forms and a triggering event is sometimes difficult to define. Often the adolescent or preadolescent is searching for some sense of stability in a life tossed on a stormy sea roiled by hormonal and physical change. Wresting control of their bodies during a period of uncertainty may result in a downward spiral into dangerously unhealthy weight loss. If nothing else, the pandemic has been a period of dramatic uncertainty unlike what most children and few adults in this country have ever experienced.
With the unprecedented increase in eating disorder cases, providers in several disciplines are searching for novel strategies to ease the burden on their patients and their practices. I recently learned of a pediatric practice in California that is considering blinding all patients aged 12 and older to the body mass measurements obtained at their health maintenance visits.
Blind weight checks for children with eating disorders, particularly those who seem to be nearing recovery, has been a common and often helpful practice. However, I am unaware of any practice that has made it a universal office policy. I’m unsure of the rationale behind this practice’s policy, but on several fronts, suppressing body mass measurements in the age group most vulnerable to eating disorders makes some sense.
Universal blind weight checks could minimize the risk of in-office shaming. However, careful training of support staff and thoughtful placement of the scales could serve the same purpose. This new policy acknowledges not only the ubiquity of the problem but also that many, maybe even most, children with eating disorders appear normal. And of course, there is the unfortunate fact that body mass is a poor screening test for eating disorders.
As I thought more about this novel approach I came to see its educational value for patients, parents, and even physicians. I can envision how a 13-year-old’s first health maintenance visit would go after the roll-out of the new policy. “Dr. Smith, aren’t you going to tell us how much I (or my daughter Jenny) weigh(s)?” This could, or more likely, should launch a discussion about weight and body image. It might continue with questions like, “How much do you think you weigh?” Or, “Do you think you are too heavy or too thin?”
Or, the conversation could include the provider’s observations that weight is just one measure of health and in fact not a very good one. Other ingredients in a healthy life style, such as sleep and physical activity, are not as easy to measure as weight but in many cases are more important.
As my mind struggled to restructure a health maintenance schedule that included blind weight checks, I wondered why we should wait until age 12. Of course, it is unreasonable to expect parents to stick with a pediatric practice that seems to ignore their infant’s weight. I’m sure that, like me, you have always discouraged new parents from having a baby scale at home because in the first few months too-frequent weighings can usually cause more angst than good.
It might make sense to remove a within-earshot discussion of a child’s weight from the health maintenance visit as soon as the child can absorb and digest the discussion; say, around age 3 years. In a perfect world, the provider should have already elicited a history that suggested a young child’s vulnerability to obesity before the scale and the growth chart told the unfortunate story. But, neither you nor I are perfect providers and so we will always need the scale to document our concerns. However, when and how we report that one vital sign to the patient and his or her parents is a topic ripe for discussion and improvement.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Reports of long waiting times at mental health clinics and anecdotal observations by health care providers suggest the pandemic has generated a dramatic increase in the incidence of eating disorders among the pediatric population. Of course this should come as no surprise to pediatricians.
Eating disorders come in many different forms and a triggering event is sometimes difficult to define. Often the adolescent or preadolescent is searching for some sense of stability in a life tossed on a stormy sea roiled by hormonal and physical change. Wresting control of their bodies during a period of uncertainty may result in a downward spiral into dangerously unhealthy weight loss. If nothing else, the pandemic has been a period of dramatic uncertainty unlike what most children and few adults in this country have ever experienced.
With the unprecedented increase in eating disorder cases, providers in several disciplines are searching for novel strategies to ease the burden on their patients and their practices. I recently learned of a pediatric practice in California that is considering blinding all patients aged 12 and older to the body mass measurements obtained at their health maintenance visits.
Blind weight checks for children with eating disorders, particularly those who seem to be nearing recovery, has been a common and often helpful practice. However, I am unaware of any practice that has made it a universal office policy. I’m unsure of the rationale behind this practice’s policy, but on several fronts, suppressing body mass measurements in the age group most vulnerable to eating disorders makes some sense.
Universal blind weight checks could minimize the risk of in-office shaming. However, careful training of support staff and thoughtful placement of the scales could serve the same purpose. This new policy acknowledges not only the ubiquity of the problem but also that many, maybe even most, children with eating disorders appear normal. And of course, there is the unfortunate fact that body mass is a poor screening test for eating disorders.
As I thought more about this novel approach I came to see its educational value for patients, parents, and even physicians. I can envision how a 13-year-old’s first health maintenance visit would go after the roll-out of the new policy. “Dr. Smith, aren’t you going to tell us how much I (or my daughter Jenny) weigh(s)?” This could, or more likely, should launch a discussion about weight and body image. It might continue with questions like, “How much do you think you weigh?” Or, “Do you think you are too heavy or too thin?”
Or, the conversation could include the provider’s observations that weight is just one measure of health and in fact not a very good one. Other ingredients in a healthy life style, such as sleep and physical activity, are not as easy to measure as weight but in many cases are more important.
As my mind struggled to restructure a health maintenance schedule that included blind weight checks, I wondered why we should wait until age 12. Of course, it is unreasonable to expect parents to stick with a pediatric practice that seems to ignore their infant’s weight. I’m sure that, like me, you have always discouraged new parents from having a baby scale at home because in the first few months too-frequent weighings can usually cause more angst than good.
It might make sense to remove a within-earshot discussion of a child’s weight from the health maintenance visit as soon as the child can absorb and digest the discussion; say, around age 3 years. In a perfect world, the provider should have already elicited a history that suggested a young child’s vulnerability to obesity before the scale and the growth chart told the unfortunate story. But, neither you nor I are perfect providers and so we will always need the scale to document our concerns. However, when and how we report that one vital sign to the patient and his or her parents is a topic ripe for discussion and improvement.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
Reports of long waiting times at mental health clinics and anecdotal observations by health care providers suggest the pandemic has generated a dramatic increase in the incidence of eating disorders among the pediatric population. Of course this should come as no surprise to pediatricians.
Eating disorders come in many different forms and a triggering event is sometimes difficult to define. Often the adolescent or preadolescent is searching for some sense of stability in a life tossed on a stormy sea roiled by hormonal and physical change. Wresting control of their bodies during a period of uncertainty may result in a downward spiral into dangerously unhealthy weight loss. If nothing else, the pandemic has been a period of dramatic uncertainty unlike what most children and few adults in this country have ever experienced.
With the unprecedented increase in eating disorder cases, providers in several disciplines are searching for novel strategies to ease the burden on their patients and their practices. I recently learned of a pediatric practice in California that is considering blinding all patients aged 12 and older to the body mass measurements obtained at their health maintenance visits.
Blind weight checks for children with eating disorders, particularly those who seem to be nearing recovery, has been a common and often helpful practice. However, I am unaware of any practice that has made it a universal office policy. I’m unsure of the rationale behind this practice’s policy, but on several fronts, suppressing body mass measurements in the age group most vulnerable to eating disorders makes some sense.
Universal blind weight checks could minimize the risk of in-office shaming. However, careful training of support staff and thoughtful placement of the scales could serve the same purpose. This new policy acknowledges not only the ubiquity of the problem but also that many, maybe even most, children with eating disorders appear normal. And of course, there is the unfortunate fact that body mass is a poor screening test for eating disorders.
As I thought more about this novel approach I came to see its educational value for patients, parents, and even physicians. I can envision how a 13-year-old’s first health maintenance visit would go after the roll-out of the new policy. “Dr. Smith, aren’t you going to tell us how much I (or my daughter Jenny) weigh(s)?” This could, or more likely, should launch a discussion about weight and body image. It might continue with questions like, “How much do you think you weigh?” Or, “Do you think you are too heavy or too thin?”
Or, the conversation could include the provider’s observations that weight is just one measure of health and in fact not a very good one. Other ingredients in a healthy life style, such as sleep and physical activity, are not as easy to measure as weight but in many cases are more important.
As my mind struggled to restructure a health maintenance schedule that included blind weight checks, I wondered why we should wait until age 12. Of course, it is unreasonable to expect parents to stick with a pediatric practice that seems to ignore their infant’s weight. I’m sure that, like me, you have always discouraged new parents from having a baby scale at home because in the first few months too-frequent weighings can usually cause more angst than good.
It might make sense to remove a within-earshot discussion of a child’s weight from the health maintenance visit as soon as the child can absorb and digest the discussion; say, around age 3 years. In a perfect world, the provider should have already elicited a history that suggested a young child’s vulnerability to obesity before the scale and the growth chart told the unfortunate story. But, neither you nor I are perfect providers and so we will always need the scale to document our concerns. However, when and how we report that one vital sign to the patient and his or her parents is a topic ripe for discussion and improvement.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].
USPSTF recommends for the first time that kids 8 and older get screened for anxiety
The U.S. Preventive Services Task Force on Apr. 12 posted draft recommendations on screening for depression and anxiety in children and adolescents.
For the first time, the USPSTF is recommending screening children ages 8 and older for anxiety.
It also recommended screening children ages 12 and older for depression, which was consistent with the USPSTF’s prior recommendations on the topic.
These B-grade draft recommendations are for children and teens who are not showing signs or symptoms of these conditions. The task force emphasized that anyone who has concerns about or shows signs of these conditions should be connected to care.
Task force member Martha Kubik, PhD, RN, a professor with George Mason University, Fairfax, Va, said in a statement: “Fortunately, we found that screening older children for anxiety and depression is effective in identifying these conditions so children and teens can be connected to the support they need.”
The group cited in its recommendation on anxiety the 2018-2019 National Survey of Children’s Health, which found that 7.8% of children and adolescents ages 3-17 years had a current anxiety disorder. It also noted that the National Survey on LGBTQ Youth Mental Health found that 72% of LGBTQ youth and 77% of transgender and nonbinary youth described general anxiety disorder symptoms.
“Anxiety disorders in childhood and adolescence are associated with an increased likelihood of a future anxiety disorder or depression,” the task force authors wrote.
They highlighted that “the prevalence of anxiety in Black youth may be evolving.” Previously, studies had suggested that young Black people may have had lower rates of mental health disorders, compared with their White counterparts.
“However, recent cohorts of Black children or adolescents have reported a higher prevalence of anxiety disorders than in the past,” the authors wrote.
Joanna Quigley, MD, clinical associate professor and associate medical director for child & adolescent services at the University of Michigan, Ann Arbor, said in an interview she was not surprised the USPSTF recommended screening for anxiety starting at age 8.
That’s when parents and providers see anxiety disorders begin to present or become more problematic, she said.
“It’s also acknowledging the importance of prevention,” she said. “The sooner we can identify these challenges for kids, the sooner we can intervene and have better outcomes for that child across their lifespan.”
Screening gets providers and families in the habit of thinking about these concerns when a child or adolescent comes in for another kind of visit, Dr. Quigley said. Chest pains in a well-child check, for example, may trigger thoughts to consider anxiety later if the child is brought in for a cardiac check for chest pains.
“It creates a culture of awareness that is important as well,” Dr. Quigley said. “I think part of what the task force is trying to do is saying that identifying anxiety can be a precursor to what could turn out to be related to depression or related to ADHD and factors we think about when we think about suicide risk as well.
“We’re seeing an increase in suicide in the younger age group as well, which is a huge concern, “ she noted.
Dr. Quigley said, if these recommendations are adopted after the comment period, pediatricians and family practice providers will likely be doing most of the screening for anxiety, but there may also be a role for the screening in pediatric subspecialty care, such as those treating children with chronic illness and in specialized mental health care.
She added: “This builds on the national conversation going on about the mental health crisis, declared a national emergency in the fall. This deserves attention in continuing the momentum.”
Factors that may signal higher risk for depression
While the USPSTF recommends screening for major depressive disorder in all adolescents aged 12 years and older, the USPSTF notes that several risk factors might help identify those at higher risk.
Markers for higher risk include a combination of factors such as a family history of depression, prior episode of depression, and other mental health or behavioral problems.
“Other psychosocial risk factors include childhood abuse or neglect, exposure to traumatic events, bullying (either as perpetrators or as victims), adverse life events, early exposure to stress, maltreatment, and an insecure parental relationship,” the task force authors wrote.
There was limited evidence, however, on the benefits and harms of screening children younger than 8 for anxiety and screening kids younger than 12 for depression.
Not enough evidence for suicide risk screening
The authors of the recommendations acknowledged that, while suicide is a leading cause of death for older children and teens, evidence is still too sparse to make recommendations regarding screening for suicide risk in those without signs or symptoms at any age.
They also explained that evidence is lacking and inconsistent on the effectiveness of treatment (psychotherapy, pharmacotherapy, or collaborative care) for suicide risk in improving outcomes in children and adolescents.
Comments on the USPSTF recommendations may be submitted until May 9, 2022. The USPSTF topic leads review all comments, revise the draft recommendations, put them to a vote by the full task force, and then post the final versions to the website.
The task force authors and Dr. Quigley reported no financial disclosures.
The U.S. Preventive Services Task Force on Apr. 12 posted draft recommendations on screening for depression and anxiety in children and adolescents.
For the first time, the USPSTF is recommending screening children ages 8 and older for anxiety.
It also recommended screening children ages 12 and older for depression, which was consistent with the USPSTF’s prior recommendations on the topic.
These B-grade draft recommendations are for children and teens who are not showing signs or symptoms of these conditions. The task force emphasized that anyone who has concerns about or shows signs of these conditions should be connected to care.
Task force member Martha Kubik, PhD, RN, a professor with George Mason University, Fairfax, Va, said in a statement: “Fortunately, we found that screening older children for anxiety and depression is effective in identifying these conditions so children and teens can be connected to the support they need.”
The group cited in its recommendation on anxiety the 2018-2019 National Survey of Children’s Health, which found that 7.8% of children and adolescents ages 3-17 years had a current anxiety disorder. It also noted that the National Survey on LGBTQ Youth Mental Health found that 72% of LGBTQ youth and 77% of transgender and nonbinary youth described general anxiety disorder symptoms.
“Anxiety disorders in childhood and adolescence are associated with an increased likelihood of a future anxiety disorder or depression,” the task force authors wrote.
They highlighted that “the prevalence of anxiety in Black youth may be evolving.” Previously, studies had suggested that young Black people may have had lower rates of mental health disorders, compared with their White counterparts.
“However, recent cohorts of Black children or adolescents have reported a higher prevalence of anxiety disorders than in the past,” the authors wrote.
Joanna Quigley, MD, clinical associate professor and associate medical director for child & adolescent services at the University of Michigan, Ann Arbor, said in an interview she was not surprised the USPSTF recommended screening for anxiety starting at age 8.
That’s when parents and providers see anxiety disorders begin to present or become more problematic, she said.
“It’s also acknowledging the importance of prevention,” she said. “The sooner we can identify these challenges for kids, the sooner we can intervene and have better outcomes for that child across their lifespan.”
Screening gets providers and families in the habit of thinking about these concerns when a child or adolescent comes in for another kind of visit, Dr. Quigley said. Chest pains in a well-child check, for example, may trigger thoughts to consider anxiety later if the child is brought in for a cardiac check for chest pains.
“It creates a culture of awareness that is important as well,” Dr. Quigley said. “I think part of what the task force is trying to do is saying that identifying anxiety can be a precursor to what could turn out to be related to depression or related to ADHD and factors we think about when we think about suicide risk as well.
“We’re seeing an increase in suicide in the younger age group as well, which is a huge concern, “ she noted.
Dr. Quigley said, if these recommendations are adopted after the comment period, pediatricians and family practice providers will likely be doing most of the screening for anxiety, but there may also be a role for the screening in pediatric subspecialty care, such as those treating children with chronic illness and in specialized mental health care.
She added: “This builds on the national conversation going on about the mental health crisis, declared a national emergency in the fall. This deserves attention in continuing the momentum.”
Factors that may signal higher risk for depression
While the USPSTF recommends screening for major depressive disorder in all adolescents aged 12 years and older, the USPSTF notes that several risk factors might help identify those at higher risk.
Markers for higher risk include a combination of factors such as a family history of depression, prior episode of depression, and other mental health or behavioral problems.
“Other psychosocial risk factors include childhood abuse or neglect, exposure to traumatic events, bullying (either as perpetrators or as victims), adverse life events, early exposure to stress, maltreatment, and an insecure parental relationship,” the task force authors wrote.
There was limited evidence, however, on the benefits and harms of screening children younger than 8 for anxiety and screening kids younger than 12 for depression.
Not enough evidence for suicide risk screening
The authors of the recommendations acknowledged that, while suicide is a leading cause of death for older children and teens, evidence is still too sparse to make recommendations regarding screening for suicide risk in those without signs or symptoms at any age.
They also explained that evidence is lacking and inconsistent on the effectiveness of treatment (psychotherapy, pharmacotherapy, or collaborative care) for suicide risk in improving outcomes in children and adolescents.
Comments on the USPSTF recommendations may be submitted until May 9, 2022. The USPSTF topic leads review all comments, revise the draft recommendations, put them to a vote by the full task force, and then post the final versions to the website.
The task force authors and Dr. Quigley reported no financial disclosures.
The U.S. Preventive Services Task Force on Apr. 12 posted draft recommendations on screening for depression and anxiety in children and adolescents.
For the first time, the USPSTF is recommending screening children ages 8 and older for anxiety.
It also recommended screening children ages 12 and older for depression, which was consistent with the USPSTF’s prior recommendations on the topic.
These B-grade draft recommendations are for children and teens who are not showing signs or symptoms of these conditions. The task force emphasized that anyone who has concerns about or shows signs of these conditions should be connected to care.
Task force member Martha Kubik, PhD, RN, a professor with George Mason University, Fairfax, Va, said in a statement: “Fortunately, we found that screening older children for anxiety and depression is effective in identifying these conditions so children and teens can be connected to the support they need.”
The group cited in its recommendation on anxiety the 2018-2019 National Survey of Children’s Health, which found that 7.8% of children and adolescents ages 3-17 years had a current anxiety disorder. It also noted that the National Survey on LGBTQ Youth Mental Health found that 72% of LGBTQ youth and 77% of transgender and nonbinary youth described general anxiety disorder symptoms.
“Anxiety disorders in childhood and adolescence are associated with an increased likelihood of a future anxiety disorder or depression,” the task force authors wrote.
They highlighted that “the prevalence of anxiety in Black youth may be evolving.” Previously, studies had suggested that young Black people may have had lower rates of mental health disorders, compared with their White counterparts.
“However, recent cohorts of Black children or adolescents have reported a higher prevalence of anxiety disorders than in the past,” the authors wrote.
Joanna Quigley, MD, clinical associate professor and associate medical director for child & adolescent services at the University of Michigan, Ann Arbor, said in an interview she was not surprised the USPSTF recommended screening for anxiety starting at age 8.
That’s when parents and providers see anxiety disorders begin to present or become more problematic, she said.
“It’s also acknowledging the importance of prevention,” she said. “The sooner we can identify these challenges for kids, the sooner we can intervene and have better outcomes for that child across their lifespan.”
Screening gets providers and families in the habit of thinking about these concerns when a child or adolescent comes in for another kind of visit, Dr. Quigley said. Chest pains in a well-child check, for example, may trigger thoughts to consider anxiety later if the child is brought in for a cardiac check for chest pains.
“It creates a culture of awareness that is important as well,” Dr. Quigley said. “I think part of what the task force is trying to do is saying that identifying anxiety can be a precursor to what could turn out to be related to depression or related to ADHD and factors we think about when we think about suicide risk as well.
“We’re seeing an increase in suicide in the younger age group as well, which is a huge concern, “ she noted.
Dr. Quigley said, if these recommendations are adopted after the comment period, pediatricians and family practice providers will likely be doing most of the screening for anxiety, but there may also be a role for the screening in pediatric subspecialty care, such as those treating children with chronic illness and in specialized mental health care.
She added: “This builds on the national conversation going on about the mental health crisis, declared a national emergency in the fall. This deserves attention in continuing the momentum.”
Factors that may signal higher risk for depression
While the USPSTF recommends screening for major depressive disorder in all adolescents aged 12 years and older, the USPSTF notes that several risk factors might help identify those at higher risk.
Markers for higher risk include a combination of factors such as a family history of depression, prior episode of depression, and other mental health or behavioral problems.
“Other psychosocial risk factors include childhood abuse or neglect, exposure to traumatic events, bullying (either as perpetrators or as victims), adverse life events, early exposure to stress, maltreatment, and an insecure parental relationship,” the task force authors wrote.
There was limited evidence, however, on the benefits and harms of screening children younger than 8 for anxiety and screening kids younger than 12 for depression.
Not enough evidence for suicide risk screening
The authors of the recommendations acknowledged that, while suicide is a leading cause of death for older children and teens, evidence is still too sparse to make recommendations regarding screening for suicide risk in those without signs or symptoms at any age.
They also explained that evidence is lacking and inconsistent on the effectiveness of treatment (psychotherapy, pharmacotherapy, or collaborative care) for suicide risk in improving outcomes in children and adolescents.
Comments on the USPSTF recommendations may be submitted until May 9, 2022. The USPSTF topic leads review all comments, revise the draft recommendations, put them to a vote by the full task force, and then post the final versions to the website.
The task force authors and Dr. Quigley reported no financial disclosures.
Somatic symptom disorder in primary care: A collaborative approach
THE CASE
James R* is a 30-year-old man who presented for a primary care walk-in visit due to dizziness, 2 days after he visited an emergency department (ED) for the same concern. He reported episodic symptoms lasting seconds to minutes, specifically when lying down. He said he had not fallen or experienced other physical trauma, did not have blurred vision or hearing loss, and was taking no medications. He also reported panic attacks, during which he experienced palpitations, trembling, paresthesia, and fear of dying. He stated that dizziness did not occur exclusively during panic episodes. His medical history was significant for hypertension; however, he reported significant anxiety related to medical visits. All home blood pressure readings he reported were within normal limits.
Upon examination, the patient had a blood pressure reading of 142/90 mm Hg and no evidence of nystagmus at rest. A neurologic exam was normal and a Dix-Hallpike maneuver reproduced subjective vertigo without nystagmus. Laboratory findings from the patient’s ED visit were negative for troponin and drug use, and blood oxygenation levels were within normal limits. At the time of this current visit, an electrocardiogram was unremarkable, with the exception of some tachycardia.
The presumptive diagnosis was benign paroxysmal positional vertigo (BPPV). An Epley maneuver was performed in the clinic and resulted in minimal symptom improvement. The physician taught Mr. R how to perform the Epley maneuver himself, prescribed a short course of meclizine, and referred him to the integrated mental health care service to address his panic attacks and anxiety.
Over the next few months, Mr. R continued to report significant distress about the dizzy spells, which persisted even after performing the Epley maneuver, and he reported that the meclizine was causing worsening vertigo. He received an ear-nose-and-throat consultation and cognitive behavioral therapy (CBT)–based consultation/interventions. He also reported avoiding multiple activities due to concerns about his dizziness.
●
*The patient’s name and other personally identifying information have been changed to protect his identity.
Somatic symptom disorder (SSD) is characterized by one or more physical symptoms associated with “excessive thoughts, feelings, or behaviors that result in distress and/or functional impairment.”1 Individuals with SSD are preoccupied with symptom-related severity, experience high symptom-related anxiety, or devote significant time and energy to the symptoms or heath concerns. With a diagnosis of SSD, physical symptoms experienced by the patient may or may not be medically explained. The same symptom need not be continuously present as long as the overall symptomatic presentation lasts 6 months or longer.
The specifier “with predominant pain” is used when pain dominates the presentation.1 Estimated prevalence of SSD in primary care ranges from 5% to 35%.2 The true scope of SSD is difficult to assess accurately since research tends to focus on medically unexplained symptoms, rather than excessive symptom-related concerns. Furthermore, terms such as “medically unexplained symptoms” and “functional syndromes” (including fibromyalgia and irritable bowel syndrome) are frequently used when describing SSD.3
One or more factors may contribute to unexplained symptoms: limitations of medical procedures and techniques, partial clinical information, patients’ inability to follow management recommendations, challenges in differential diagnostics, and access-to-care limitations preventing regular care and appropriate diagnostic work up.
What’s important to remember is that it’s the patient’s reaction to physical symptoms, rather than the presence of symptoms per se, that defines SSD.
Considerations in the differential diagnosis
When making a diagnosis of SSD, symptoms cannot:4
- be feigned or deliberately produced as in malingering or factitious disorder.
- result from physiologic effects of a substance (eg, intoxication, withdrawal, or adverse medication effects).
- constitute somatic delusions, as occur in psychotic disorders.
- constitute symptoms or deficits affecting voluntary motor or sensory function that are better explained by neurologic, medical, or psychiatric conditions (consider conversion disorder).
- be preoccupations with physical appearance flaws, as in body dysmorphic disorder.
- be accounted for by an anxiety disorder (eg, palpitations associated with panic attacks).
Continue to: Illness anxiety disorder...
Illness anxiety disorder is also characterized by significant health-related concerns; however, physical symptoms are either mild or absent.
Possible causes of SSD are varied and complex, including genetic and biological factors, family dynamics, behavioral modeling/learning, personality traits, difficulties with emotional regulation, and awareness.5 Patients may present with ongoing requests for symptom explanations, feelings of helplessness, fear of having concerns dismissed, and low motivation for change.3
Aids in supporting a diagnosis of SSD
It’s not appropriate to rely solely on questionnaires to make the diagnosis of SSD. However, brief screening tools are a time-efficient way to capture patients’ experiences and perceptions.6 Along with other components of clinical evaluation, brief symptom screens can both support the diagnosis and help in longitudinal symptom assessment.
Patient Health Questionnaire-15 (PHQ-15), developed for self-report screening in primary care, has desirable psychometric properties including appropriate internal reliability; convergent validity with measures of functional status, disability days, and symptom-related burden; and discriminant validity from measures of depressive symptoms.7 The PHQ-15 is an open access tool that is available in several languages. The respondent is asked to rate the extent of being bothered by a range of medical symptoms in the proceeding 4 weeks. Total scores range from 0 to 30, with higher scores indicating greater symptom aggravation. Cutoffs of 5, 10, and 15 correspond to mild, moderate, and severe symptom levels.8
Somatic Symptom Disorder - B Criteria Scale (SSD-12) aims to capture SSD symptoms in line with Diagnostic and Statistical Manual of Mental Disorders (DSM-5) diagnostic criteria. It assesses cognitive, affective, and behavioral aspects of SSD.9 The SSD-12 is copyrighted and its use requires registration and purchase. Cutoffs by age and gender are available. SSD-12 has demonstrated appropriate reliability and validity.9
Continue to: Structured Clinical Interview for DSM Disorders
Structured Clinical Interview for DSM Disorders (SCID)10,11 is perhaps the most rigorous differential diagnostic tool. However, SCID administration requires training and skill; time for administration and cost of the materials may be prohibitive in primary care.
Finally, SSD symptoms are highly associated with depression and anxiety. Ongoing elevated screening scores for anxiety and depression refractory to interventions may indicate the possibility of overlooked SSD. Furthermore, use of SSD screening tools with anxiety and depression screening tools can provide a more comprehensive picture of impairment, as well as symptom progress.
Treatment: Avoid a split approach
Diagnosing and treating SSD can be challenging for physicians who focus on biomedically based approaches in patient care. Additional tests, studies, and prescriptions are likely to fuel (rather than pacify) patients’ concerns, as such steps divert attention from the underlying psychological needs and mechanisms which maintain SSD. Avoid using a split biopsychosocial approach—ie, beginning the inquiry and treatment planning from a biomedical perspective, and then falling back on psychosocial formulation when treatment efforts have been ineffective. Such an approach leads to understandable patient dissatisfaction and can be interpreted by them as the caregiver suggesting that physical symptoms are “all in [their] head.”12
These 4 tips can help
1. Use a biopsychosocial formulation when initiating treatment. Be familiar with biopsychosocial factors in SSD and develop a narrative for discussing this formulation with patients. For example: “Mr. R, we are going to use the following [medical tests/studies/medications] to understand the cause of your symptoms and better manage them. We also need to think about the role of stress and distress in your symptoms because these can also be at play with dizziness.” This may be particularly beneficial for a functional disorder, such as chronic pain. Incorporating patient education resources is an important step toward shared understanding (see Hunter Integrated Pain Service for chronic pain educational videos; www.tga.gov.au/chronic-pain-management-video-resource-brainman13).
2. Combine education about pathophysiology with patient-centered interviewing. Significant SSD symptom improvements were noted following a single 30-minute educational session, while motivational interviewing techniques were used to probe patients’ concerns.2
Continue to: Maintain professionalism and good clinical practice
3. Maintain professionalism and good clinical practice. Consider SSD a medical matter and address it accordingly: explore concerns fully, provide evidence-based responses, communicate empathy, and employ objective management strategies.14
4. Do not overlook the value of the relationship. A recent systematic review concluded that the relationship between the patient and care provider was central to the success of the interventions for symptom reduction.15
A controversial approach. Pharmacotherapy for SSD is controversial. While several trials of antidepressants and St. John’s wort have been positive and some authors have stated that all classes of antidepressants are effective for SSD, others maintain that questions regarding dosing, treatment duration, and sustainability of improvement have not been sufficiently addressed in research.16,17
Coordination of care issues
Primary care continues to be the de facto mental health system, and specialty services may be unavailable or declined by patients.18 CBT delivered in person or online is empirically supported as a treatment approach to medically unexplained symptoms and SSD.17,19-22
A recent meta-analysis of randomized controlled trials published by Jing and colleagues23 reported that CBT was effective for SSD symptom reduction, and that treatment gains were maintained 3 to 12 months post treatment. However, concerns about the practical implementation of CBT in primary care were raised because CBT was not shown to be effective in improving social functioning or reducing the number of medical visits. Symptom improvement was maximized with longer durations of treatment (> 10 sessions) and greater session lengths (> 50 minutes). Additionally, Abbass and colleagues24 brought up several methodologic (sampling and analysis) concerns related to Jing et al’s work.
Continue to: Overally, CBT's effect sizes...
Overall, CBT’s effect sizes are small, and patients who are open to biopsychosocial explanations for their symptoms and to receiving psychological services may differ from most patients seen in primary care practices.21 Furthermore, mental health providers may hesitate to diagnose SSD because they are concerned about missing a somatic illness.3 Therefore, when coordinating care with mental health providers, it may be beneficial to discuss the treatment approach, assess familiarity with the SSD diagnosis, and closely coordinate and collaborate on the treatment plan.
While physicians cannot be expected to function as psychotherapists, an understanding of CBT and techniques for SSD treatment can be beneficial. Integrated mental health services may hold promise in addressing SSD in primary care. Onsite availability of a behavioral health provider competent in providing evidence-based care can target SSD symptoms and support both patients and physicians.
THE CASE
Mr. R’s treatment course included multiple primary care appointments (scheduled and walk in), ED visits, and specialist visits (ENT/vestibular rehabilitation). He sought care as symptoms intensified, lasted longer, or occurred in new circumstances. He reported persistent fear of the symptoms and anxiety that serious medical causes had been overlooked. He also described distress associated with vertigo and his anxiety sensitivity (anxiety about being anxious).
The behavioral health consultant (BHC; psychologist) and physician talked to the patient about the biopsychosocial antecedents of his condition and the factors that perpetuate the anxiety and stress response. The BHC described the fight/flight/freeze response to the patient and explained its role in the physiologic stress response associated with somatic symptoms and panic. Educational materials (videos and handouts) were also provided to the patient to further illustrate these concepts. The BHC also discussed the role of interoceptive and situational avoidance and active coping (eg, engaging in safe activities); taught the patient relaxation and grounding techniques; and used cognitive disputation aimed at challenging catastrophic symptom interpretations.
The BHC and the patient’s physician established joint treatment goals that included improving functioning, promoting active coping, and decreasing distress associated with symptoms. After the initial medical and BHC visits, both vertigo and anxiety symptoms appeared to abate somewhat, but symptoms have been ongoing and distress and impairment have been variable. The patient’s family physician and BHC continue to work with him to optimize the care plan and treatment goals.
CORRESPONDENCE
Nataliya Pilipenko, PhD, ABPP, Center for Family and Community Medicine, Columbia University Vagelos College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032; [email protected]
ACKNOWLEDGEMENT
The author thanks Dr. Molly Warren for her collaboration and guidance.
1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th edition (DSM-5). American Psychiatric Publishing; 2013.
2. Johnson KK, Bennett C, Rochani H. Significant improvement of somatic symptom disorder with brief psychoeducational intervention by PMHNP in primary care. J Am Psychiatr Nurses Assoc. 2020;28:171-180. doi: 10.1177/1078390320960524
3. Weigel A, Maehder K, Witt M, et al. Psychotherapists’ perspective on the treatment of patients with somatic symptom disorders. J Psychosom Res. 2020;138:110228. doi: 10.1016/j.jpsychores.2020.110228
4. American Psychiatric Association. Handbook of Differential Diagnosis. American Psychiatric Publishing; 2014;234-235.
5. Mayo Clinic. Somatic symptom disorder. Accessed February 21, 2022. www.mayoclinic.org/diseases-conditions/somatic-symptom-disorder/symptoms-causes/syc-20377776?p=1
6. Toussaint A, Riedl B, Kehrer S, et al. Validity of the Somatic Symptom Disorder-B Criteria Scale (SSD-12) in primary care. Fam Pract. 2018;35:342-347. doi: 10.1093/fampra/cmx116
7. Kroenke K, Spitzer RL, Williams JB. The PHQ-15: validity of a new measure for evaluating the severity of somatic symptoms. Psychosom Med. 2002;64:258-66. doi: 10.1097/00006842-200203000-00008
8. Kroenke K, Spitzer RL, Williams JB, et al. The Patient Health Questionnaire Somatic, Anxiety, and Depressive Symptom Scales: a systematic review. Gen Hosp Psychiatry. 2010;32:345-359. doi: 10.1016/j.genhosppsych.2010.03.006
9. Toussaint A, Löwe B, Brähler E, et al. The Somatic Symptom Disorder - B Criteria Scale (SSD-12): factorial structure, validity and population-based norms. J Psychosom Res. 2017;97:9-17. doi: 10.1016/j.jpsychores.2017.03.017
10. First MB, Williams JBW, Karg RS, Spitzer RL, eds. Structured Clinical Interview for DSM-5 Disorders, Research Version. American Psychiatric Association, 2015.
11. First MB, Williams JBW, Karg RS, Spitzer RL, eds. Structured Clinical Interview for DSM-5 Disorders, Clinician Version. American Psychiatric Publishing; 2016.
12. McDaniel SH, Hepworth J, Campbell TL, et al, eds. Family Oriented Primary Care. Springer Publishing Co; 2005:1-15.
13. Hunter Integrated Pain Service (2016). Brainman videos. Hunter New England Local Health District. New South Wales, Australia. Accessed February 21, 2022. www.tga.gov.au/chronic-pain-management-video-resource-brainman
14. Murray AM, Toussaint A, Althaus A, et al. The challenge of diagnosing non-specific, functional, and somatoform disorders: a systematic review of barriers to diagnosis in primary care. J Psychosom Res. 2016;80:1-10. doi: 10.1016/j.jpsychores.2015.11.002
15. Leaviss J, Davis S, Ren S, et al. Behavioral modification interventions for medically unexplained symptoms in primary care: systematic reviews and economic evaluation. Health Technol Assess. 2020;24:1-490. doi: 10.3310/hta24460
16. Kroenke K. Efficacy of treatment for somatoform disorders: a review of randomized controlled trials. Psychosom Med. 2007;69:881-888. doi: 10.1097/PSY.0b013e31815b00c4
17. Steinbrecher N, Koerber S, Frieser D, et al. The prevalence of medically unexplained symptoms in primary care. Psychosomatics. 2011;52:263-271. doi: 10.1016/j.psym.2011.01.007
18. Kessler R, Stafford D. Primary care is the de facto mental health system. In Kessler R, Stafford D, eds. Collaborative Medicine Case Studies: Evidence in Practice. Springer Publishing Co, 2008; 9-21.
19. Barsky AJ, Ahern DK, Bauer MR, et al. A randomized trial of treatments for high-utilizing somatizing patients. J Gen Intern Med. 2013;28:1396-1404. doi: 10.1007/s11606-013-2392-6
20. Newby JM, Smith J, Uppal S, et al. Internet-based cognitive behavioral therapy versus psychoeducation control for illness anxiety disorder and somatic symptom disorder: A randomized controlled trial. J Consult Clin Psychol. 2018;86:89-98. doi: 10.1037/ccp0000248
21. van Dessel N, den Boeft M, van der Wouden JC, et al. Non-pharmacological interventions for somatoform disorders and medically unexplained physical symptoms (MUPS) in adults. Cochrane Database Syst Rev. 2014(11):CD011142. doi: 10.1002/14651858.CD011142.pub2
22. Verdurmen MJ, Videler AC, Kamperman AM, et al. Cognitive behavioral therapy for somatic symptom disorders in later life: a prospective comparative explorative pilot study in two clinical populations. Neuropsychiatr Dis Treat. 2017;13:2331-2339. doi: 10.2147/NDT.S141208
23. Liu J, Gill NS, Teodorczuk A, et al. The efficacy of cognitive behavioural therapy in somatoform disorders and medically unexplained physical symptoms: a meta-analysis of randomized controlled trials. J Affect Disord. 2019;245:98-112. doi: 10.1016/j.jad.2018.10.114
24. Abbass A, Leichsenring F, Steinert C. Re: Jing et al., the efficacy of cognitive behavioural therapy in somatoform disorders and medically unexplained physical symptoms: a meta-analysis of randomized controlled trials. J Affect Disord. 2019;255:S0165-0327(18)33197-5. doi: 10.1016/j.jad.2019.02.055
THE CASE
James R* is a 30-year-old man who presented for a primary care walk-in visit due to dizziness, 2 days after he visited an emergency department (ED) for the same concern. He reported episodic symptoms lasting seconds to minutes, specifically when lying down. He said he had not fallen or experienced other physical trauma, did not have blurred vision or hearing loss, and was taking no medications. He also reported panic attacks, during which he experienced palpitations, trembling, paresthesia, and fear of dying. He stated that dizziness did not occur exclusively during panic episodes. His medical history was significant for hypertension; however, he reported significant anxiety related to medical visits. All home blood pressure readings he reported were within normal limits.
Upon examination, the patient had a blood pressure reading of 142/90 mm Hg and no evidence of nystagmus at rest. A neurologic exam was normal and a Dix-Hallpike maneuver reproduced subjective vertigo without nystagmus. Laboratory findings from the patient’s ED visit were negative for troponin and drug use, and blood oxygenation levels were within normal limits. At the time of this current visit, an electrocardiogram was unremarkable, with the exception of some tachycardia.
The presumptive diagnosis was benign paroxysmal positional vertigo (BPPV). An Epley maneuver was performed in the clinic and resulted in minimal symptom improvement. The physician taught Mr. R how to perform the Epley maneuver himself, prescribed a short course of meclizine, and referred him to the integrated mental health care service to address his panic attacks and anxiety.
Over the next few months, Mr. R continued to report significant distress about the dizzy spells, which persisted even after performing the Epley maneuver, and he reported that the meclizine was causing worsening vertigo. He received an ear-nose-and-throat consultation and cognitive behavioral therapy (CBT)–based consultation/interventions. He also reported avoiding multiple activities due to concerns about his dizziness.
●
*The patient’s name and other personally identifying information have been changed to protect his identity.
Somatic symptom disorder (SSD) is characterized by one or more physical symptoms associated with “excessive thoughts, feelings, or behaviors that result in distress and/or functional impairment.”1 Individuals with SSD are preoccupied with symptom-related severity, experience high symptom-related anxiety, or devote significant time and energy to the symptoms or heath concerns. With a diagnosis of SSD, physical symptoms experienced by the patient may or may not be medically explained. The same symptom need not be continuously present as long as the overall symptomatic presentation lasts 6 months or longer.
The specifier “with predominant pain” is used when pain dominates the presentation.1 Estimated prevalence of SSD in primary care ranges from 5% to 35%.2 The true scope of SSD is difficult to assess accurately since research tends to focus on medically unexplained symptoms, rather than excessive symptom-related concerns. Furthermore, terms such as “medically unexplained symptoms” and “functional syndromes” (including fibromyalgia and irritable bowel syndrome) are frequently used when describing SSD.3
One or more factors may contribute to unexplained symptoms: limitations of medical procedures and techniques, partial clinical information, patients’ inability to follow management recommendations, challenges in differential diagnostics, and access-to-care limitations preventing regular care and appropriate diagnostic work up.
What’s important to remember is that it’s the patient’s reaction to physical symptoms, rather than the presence of symptoms per se, that defines SSD.
Considerations in the differential diagnosis
When making a diagnosis of SSD, symptoms cannot:4
- be feigned or deliberately produced as in malingering or factitious disorder.
- result from physiologic effects of a substance (eg, intoxication, withdrawal, or adverse medication effects).
- constitute somatic delusions, as occur in psychotic disorders.
- constitute symptoms or deficits affecting voluntary motor or sensory function that are better explained by neurologic, medical, or psychiatric conditions (consider conversion disorder).
- be preoccupations with physical appearance flaws, as in body dysmorphic disorder.
- be accounted for by an anxiety disorder (eg, palpitations associated with panic attacks).
Continue to: Illness anxiety disorder...
Illness anxiety disorder is also characterized by significant health-related concerns; however, physical symptoms are either mild or absent.
Possible causes of SSD are varied and complex, including genetic and biological factors, family dynamics, behavioral modeling/learning, personality traits, difficulties with emotional regulation, and awareness.5 Patients may present with ongoing requests for symptom explanations, feelings of helplessness, fear of having concerns dismissed, and low motivation for change.3
Aids in supporting a diagnosis of SSD
It’s not appropriate to rely solely on questionnaires to make the diagnosis of SSD. However, brief screening tools are a time-efficient way to capture patients’ experiences and perceptions.6 Along with other components of clinical evaluation, brief symptom screens can both support the diagnosis and help in longitudinal symptom assessment.
Patient Health Questionnaire-15 (PHQ-15), developed for self-report screening in primary care, has desirable psychometric properties including appropriate internal reliability; convergent validity with measures of functional status, disability days, and symptom-related burden; and discriminant validity from measures of depressive symptoms.7 The PHQ-15 is an open access tool that is available in several languages. The respondent is asked to rate the extent of being bothered by a range of medical symptoms in the proceeding 4 weeks. Total scores range from 0 to 30, with higher scores indicating greater symptom aggravation. Cutoffs of 5, 10, and 15 correspond to mild, moderate, and severe symptom levels.8
Somatic Symptom Disorder - B Criteria Scale (SSD-12) aims to capture SSD symptoms in line with Diagnostic and Statistical Manual of Mental Disorders (DSM-5) diagnostic criteria. It assesses cognitive, affective, and behavioral aspects of SSD.9 The SSD-12 is copyrighted and its use requires registration and purchase. Cutoffs by age and gender are available. SSD-12 has demonstrated appropriate reliability and validity.9
Continue to: Structured Clinical Interview for DSM Disorders
Structured Clinical Interview for DSM Disorders (SCID)10,11 is perhaps the most rigorous differential diagnostic tool. However, SCID administration requires training and skill; time for administration and cost of the materials may be prohibitive in primary care.
Finally, SSD symptoms are highly associated with depression and anxiety. Ongoing elevated screening scores for anxiety and depression refractory to interventions may indicate the possibility of overlooked SSD. Furthermore, use of SSD screening tools with anxiety and depression screening tools can provide a more comprehensive picture of impairment, as well as symptom progress.
Treatment: Avoid a split approach
Diagnosing and treating SSD can be challenging for physicians who focus on biomedically based approaches in patient care. Additional tests, studies, and prescriptions are likely to fuel (rather than pacify) patients’ concerns, as such steps divert attention from the underlying psychological needs and mechanisms which maintain SSD. Avoid using a split biopsychosocial approach—ie, beginning the inquiry and treatment planning from a biomedical perspective, and then falling back on psychosocial formulation when treatment efforts have been ineffective. Such an approach leads to understandable patient dissatisfaction and can be interpreted by them as the caregiver suggesting that physical symptoms are “all in [their] head.”12
These 4 tips can help
1. Use a biopsychosocial formulation when initiating treatment. Be familiar with biopsychosocial factors in SSD and develop a narrative for discussing this formulation with patients. For example: “Mr. R, we are going to use the following [medical tests/studies/medications] to understand the cause of your symptoms and better manage them. We also need to think about the role of stress and distress in your symptoms because these can also be at play with dizziness.” This may be particularly beneficial for a functional disorder, such as chronic pain. Incorporating patient education resources is an important step toward shared understanding (see Hunter Integrated Pain Service for chronic pain educational videos; www.tga.gov.au/chronic-pain-management-video-resource-brainman13).
2. Combine education about pathophysiology with patient-centered interviewing. Significant SSD symptom improvements were noted following a single 30-minute educational session, while motivational interviewing techniques were used to probe patients’ concerns.2
Continue to: Maintain professionalism and good clinical practice
3. Maintain professionalism and good clinical practice. Consider SSD a medical matter and address it accordingly: explore concerns fully, provide evidence-based responses, communicate empathy, and employ objective management strategies.14
4. Do not overlook the value of the relationship. A recent systematic review concluded that the relationship between the patient and care provider was central to the success of the interventions for symptom reduction.15
A controversial approach. Pharmacotherapy for SSD is controversial. While several trials of antidepressants and St. John’s wort have been positive and some authors have stated that all classes of antidepressants are effective for SSD, others maintain that questions regarding dosing, treatment duration, and sustainability of improvement have not been sufficiently addressed in research.16,17
Coordination of care issues
Primary care continues to be the de facto mental health system, and specialty services may be unavailable or declined by patients.18 CBT delivered in person or online is empirically supported as a treatment approach to medically unexplained symptoms and SSD.17,19-22
A recent meta-analysis of randomized controlled trials published by Jing and colleagues23 reported that CBT was effective for SSD symptom reduction, and that treatment gains were maintained 3 to 12 months post treatment. However, concerns about the practical implementation of CBT in primary care were raised because CBT was not shown to be effective in improving social functioning or reducing the number of medical visits. Symptom improvement was maximized with longer durations of treatment (> 10 sessions) and greater session lengths (> 50 minutes). Additionally, Abbass and colleagues24 brought up several methodologic (sampling and analysis) concerns related to Jing et al’s work.
Continue to: Overally, CBT's effect sizes...
Overall, CBT’s effect sizes are small, and patients who are open to biopsychosocial explanations for their symptoms and to receiving psychological services may differ from most patients seen in primary care practices.21 Furthermore, mental health providers may hesitate to diagnose SSD because they are concerned about missing a somatic illness.3 Therefore, when coordinating care with mental health providers, it may be beneficial to discuss the treatment approach, assess familiarity with the SSD diagnosis, and closely coordinate and collaborate on the treatment plan.
While physicians cannot be expected to function as psychotherapists, an understanding of CBT and techniques for SSD treatment can be beneficial. Integrated mental health services may hold promise in addressing SSD in primary care. Onsite availability of a behavioral health provider competent in providing evidence-based care can target SSD symptoms and support both patients and physicians.
THE CASE
Mr. R’s treatment course included multiple primary care appointments (scheduled and walk in), ED visits, and specialist visits (ENT/vestibular rehabilitation). He sought care as symptoms intensified, lasted longer, or occurred in new circumstances. He reported persistent fear of the symptoms and anxiety that serious medical causes had been overlooked. He also described distress associated with vertigo and his anxiety sensitivity (anxiety about being anxious).
The behavioral health consultant (BHC; psychologist) and physician talked to the patient about the biopsychosocial antecedents of his condition and the factors that perpetuate the anxiety and stress response. The BHC described the fight/flight/freeze response to the patient and explained its role in the physiologic stress response associated with somatic symptoms and panic. Educational materials (videos and handouts) were also provided to the patient to further illustrate these concepts. The BHC also discussed the role of interoceptive and situational avoidance and active coping (eg, engaging in safe activities); taught the patient relaxation and grounding techniques; and used cognitive disputation aimed at challenging catastrophic symptom interpretations.
The BHC and the patient’s physician established joint treatment goals that included improving functioning, promoting active coping, and decreasing distress associated with symptoms. After the initial medical and BHC visits, both vertigo and anxiety symptoms appeared to abate somewhat, but symptoms have been ongoing and distress and impairment have been variable. The patient’s family physician and BHC continue to work with him to optimize the care plan and treatment goals.
CORRESPONDENCE
Nataliya Pilipenko, PhD, ABPP, Center for Family and Community Medicine, Columbia University Vagelos College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032; [email protected]
ACKNOWLEDGEMENT
The author thanks Dr. Molly Warren for her collaboration and guidance.
THE CASE
James R* is a 30-year-old man who presented for a primary care walk-in visit due to dizziness, 2 days after he visited an emergency department (ED) for the same concern. He reported episodic symptoms lasting seconds to minutes, specifically when lying down. He said he had not fallen or experienced other physical trauma, did not have blurred vision or hearing loss, and was taking no medications. He also reported panic attacks, during which he experienced palpitations, trembling, paresthesia, and fear of dying. He stated that dizziness did not occur exclusively during panic episodes. His medical history was significant for hypertension; however, he reported significant anxiety related to medical visits. All home blood pressure readings he reported were within normal limits.
Upon examination, the patient had a blood pressure reading of 142/90 mm Hg and no evidence of nystagmus at rest. A neurologic exam was normal and a Dix-Hallpike maneuver reproduced subjective vertigo without nystagmus. Laboratory findings from the patient’s ED visit were negative for troponin and drug use, and blood oxygenation levels were within normal limits. At the time of this current visit, an electrocardiogram was unremarkable, with the exception of some tachycardia.
The presumptive diagnosis was benign paroxysmal positional vertigo (BPPV). An Epley maneuver was performed in the clinic and resulted in minimal symptom improvement. The physician taught Mr. R how to perform the Epley maneuver himself, prescribed a short course of meclizine, and referred him to the integrated mental health care service to address his panic attacks and anxiety.
Over the next few months, Mr. R continued to report significant distress about the dizzy spells, which persisted even after performing the Epley maneuver, and he reported that the meclizine was causing worsening vertigo. He received an ear-nose-and-throat consultation and cognitive behavioral therapy (CBT)–based consultation/interventions. He also reported avoiding multiple activities due to concerns about his dizziness.
●
*The patient’s name and other personally identifying information have been changed to protect his identity.
Somatic symptom disorder (SSD) is characterized by one or more physical symptoms associated with “excessive thoughts, feelings, or behaviors that result in distress and/or functional impairment.”1 Individuals with SSD are preoccupied with symptom-related severity, experience high symptom-related anxiety, or devote significant time and energy to the symptoms or heath concerns. With a diagnosis of SSD, physical symptoms experienced by the patient may or may not be medically explained. The same symptom need not be continuously present as long as the overall symptomatic presentation lasts 6 months or longer.
The specifier “with predominant pain” is used when pain dominates the presentation.1 Estimated prevalence of SSD in primary care ranges from 5% to 35%.2 The true scope of SSD is difficult to assess accurately since research tends to focus on medically unexplained symptoms, rather than excessive symptom-related concerns. Furthermore, terms such as “medically unexplained symptoms” and “functional syndromes” (including fibromyalgia and irritable bowel syndrome) are frequently used when describing SSD.3
One or more factors may contribute to unexplained symptoms: limitations of medical procedures and techniques, partial clinical information, patients’ inability to follow management recommendations, challenges in differential diagnostics, and access-to-care limitations preventing regular care and appropriate diagnostic work up.
What’s important to remember is that it’s the patient’s reaction to physical symptoms, rather than the presence of symptoms per se, that defines SSD.
Considerations in the differential diagnosis
When making a diagnosis of SSD, symptoms cannot:4
- be feigned or deliberately produced as in malingering or factitious disorder.
- result from physiologic effects of a substance (eg, intoxication, withdrawal, or adverse medication effects).
- constitute somatic delusions, as occur in psychotic disorders.
- constitute symptoms or deficits affecting voluntary motor or sensory function that are better explained by neurologic, medical, or psychiatric conditions (consider conversion disorder).
- be preoccupations with physical appearance flaws, as in body dysmorphic disorder.
- be accounted for by an anxiety disorder (eg, palpitations associated with panic attacks).
Continue to: Illness anxiety disorder...
Illness anxiety disorder is also characterized by significant health-related concerns; however, physical symptoms are either mild or absent.
Possible causes of SSD are varied and complex, including genetic and biological factors, family dynamics, behavioral modeling/learning, personality traits, difficulties with emotional regulation, and awareness.5 Patients may present with ongoing requests for symptom explanations, feelings of helplessness, fear of having concerns dismissed, and low motivation for change.3
Aids in supporting a diagnosis of SSD
It’s not appropriate to rely solely on questionnaires to make the diagnosis of SSD. However, brief screening tools are a time-efficient way to capture patients’ experiences and perceptions.6 Along with other components of clinical evaluation, brief symptom screens can both support the diagnosis and help in longitudinal symptom assessment.
Patient Health Questionnaire-15 (PHQ-15), developed for self-report screening in primary care, has desirable psychometric properties including appropriate internal reliability; convergent validity with measures of functional status, disability days, and symptom-related burden; and discriminant validity from measures of depressive symptoms.7 The PHQ-15 is an open access tool that is available in several languages. The respondent is asked to rate the extent of being bothered by a range of medical symptoms in the proceeding 4 weeks. Total scores range from 0 to 30, with higher scores indicating greater symptom aggravation. Cutoffs of 5, 10, and 15 correspond to mild, moderate, and severe symptom levels.8
Somatic Symptom Disorder - B Criteria Scale (SSD-12) aims to capture SSD symptoms in line with Diagnostic and Statistical Manual of Mental Disorders (DSM-5) diagnostic criteria. It assesses cognitive, affective, and behavioral aspects of SSD.9 The SSD-12 is copyrighted and its use requires registration and purchase. Cutoffs by age and gender are available. SSD-12 has demonstrated appropriate reliability and validity.9
Continue to: Structured Clinical Interview for DSM Disorders
Structured Clinical Interview for DSM Disorders (SCID)10,11 is perhaps the most rigorous differential diagnostic tool. However, SCID administration requires training and skill; time for administration and cost of the materials may be prohibitive in primary care.
Finally, SSD symptoms are highly associated with depression and anxiety. Ongoing elevated screening scores for anxiety and depression refractory to interventions may indicate the possibility of overlooked SSD. Furthermore, use of SSD screening tools with anxiety and depression screening tools can provide a more comprehensive picture of impairment, as well as symptom progress.
Treatment: Avoid a split approach
Diagnosing and treating SSD can be challenging for physicians who focus on biomedically based approaches in patient care. Additional tests, studies, and prescriptions are likely to fuel (rather than pacify) patients’ concerns, as such steps divert attention from the underlying psychological needs and mechanisms which maintain SSD. Avoid using a split biopsychosocial approach—ie, beginning the inquiry and treatment planning from a biomedical perspective, and then falling back on psychosocial formulation when treatment efforts have been ineffective. Such an approach leads to understandable patient dissatisfaction and can be interpreted by them as the caregiver suggesting that physical symptoms are “all in [their] head.”12
These 4 tips can help
1. Use a biopsychosocial formulation when initiating treatment. Be familiar with biopsychosocial factors in SSD and develop a narrative for discussing this formulation with patients. For example: “Mr. R, we are going to use the following [medical tests/studies/medications] to understand the cause of your symptoms and better manage them. We also need to think about the role of stress and distress in your symptoms because these can also be at play with dizziness.” This may be particularly beneficial for a functional disorder, such as chronic pain. Incorporating patient education resources is an important step toward shared understanding (see Hunter Integrated Pain Service for chronic pain educational videos; www.tga.gov.au/chronic-pain-management-video-resource-brainman13).
2. Combine education about pathophysiology with patient-centered interviewing. Significant SSD symptom improvements were noted following a single 30-minute educational session, while motivational interviewing techniques were used to probe patients’ concerns.2
Continue to: Maintain professionalism and good clinical practice
3. Maintain professionalism and good clinical practice. Consider SSD a medical matter and address it accordingly: explore concerns fully, provide evidence-based responses, communicate empathy, and employ objective management strategies.14
4. Do not overlook the value of the relationship. A recent systematic review concluded that the relationship between the patient and care provider was central to the success of the interventions for symptom reduction.15
A controversial approach. Pharmacotherapy for SSD is controversial. While several trials of antidepressants and St. John’s wort have been positive and some authors have stated that all classes of antidepressants are effective for SSD, others maintain that questions regarding dosing, treatment duration, and sustainability of improvement have not been sufficiently addressed in research.16,17
Coordination of care issues
Primary care continues to be the de facto mental health system, and specialty services may be unavailable or declined by patients.18 CBT delivered in person or online is empirically supported as a treatment approach to medically unexplained symptoms and SSD.17,19-22
A recent meta-analysis of randomized controlled trials published by Jing and colleagues23 reported that CBT was effective for SSD symptom reduction, and that treatment gains were maintained 3 to 12 months post treatment. However, concerns about the practical implementation of CBT in primary care were raised because CBT was not shown to be effective in improving social functioning or reducing the number of medical visits. Symptom improvement was maximized with longer durations of treatment (> 10 sessions) and greater session lengths (> 50 minutes). Additionally, Abbass and colleagues24 brought up several methodologic (sampling and analysis) concerns related to Jing et al’s work.
Continue to: Overally, CBT's effect sizes...
Overall, CBT’s effect sizes are small, and patients who are open to biopsychosocial explanations for their symptoms and to receiving psychological services may differ from most patients seen in primary care practices.21 Furthermore, mental health providers may hesitate to diagnose SSD because they are concerned about missing a somatic illness.3 Therefore, when coordinating care with mental health providers, it may be beneficial to discuss the treatment approach, assess familiarity with the SSD diagnosis, and closely coordinate and collaborate on the treatment plan.
While physicians cannot be expected to function as psychotherapists, an understanding of CBT and techniques for SSD treatment can be beneficial. Integrated mental health services may hold promise in addressing SSD in primary care. Onsite availability of a behavioral health provider competent in providing evidence-based care can target SSD symptoms and support both patients and physicians.
THE CASE
Mr. R’s treatment course included multiple primary care appointments (scheduled and walk in), ED visits, and specialist visits (ENT/vestibular rehabilitation). He sought care as symptoms intensified, lasted longer, or occurred in new circumstances. He reported persistent fear of the symptoms and anxiety that serious medical causes had been overlooked. He also described distress associated with vertigo and his anxiety sensitivity (anxiety about being anxious).
The behavioral health consultant (BHC; psychologist) and physician talked to the patient about the biopsychosocial antecedents of his condition and the factors that perpetuate the anxiety and stress response. The BHC described the fight/flight/freeze response to the patient and explained its role in the physiologic stress response associated with somatic symptoms and panic. Educational materials (videos and handouts) were also provided to the patient to further illustrate these concepts. The BHC also discussed the role of interoceptive and situational avoidance and active coping (eg, engaging in safe activities); taught the patient relaxation and grounding techniques; and used cognitive disputation aimed at challenging catastrophic symptom interpretations.
The BHC and the patient’s physician established joint treatment goals that included improving functioning, promoting active coping, and decreasing distress associated with symptoms. After the initial medical and BHC visits, both vertigo and anxiety symptoms appeared to abate somewhat, but symptoms have been ongoing and distress and impairment have been variable. The patient’s family physician and BHC continue to work with him to optimize the care plan and treatment goals.
CORRESPONDENCE
Nataliya Pilipenko, PhD, ABPP, Center for Family and Community Medicine, Columbia University Vagelos College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032; [email protected]
ACKNOWLEDGEMENT
The author thanks Dr. Molly Warren for her collaboration and guidance.
1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th edition (DSM-5). American Psychiatric Publishing; 2013.
2. Johnson KK, Bennett C, Rochani H. Significant improvement of somatic symptom disorder with brief psychoeducational intervention by PMHNP in primary care. J Am Psychiatr Nurses Assoc. 2020;28:171-180. doi: 10.1177/1078390320960524
3. Weigel A, Maehder K, Witt M, et al. Psychotherapists’ perspective on the treatment of patients with somatic symptom disorders. J Psychosom Res. 2020;138:110228. doi: 10.1016/j.jpsychores.2020.110228
4. American Psychiatric Association. Handbook of Differential Diagnosis. American Psychiatric Publishing; 2014;234-235.
5. Mayo Clinic. Somatic symptom disorder. Accessed February 21, 2022. www.mayoclinic.org/diseases-conditions/somatic-symptom-disorder/symptoms-causes/syc-20377776?p=1
6. Toussaint A, Riedl B, Kehrer S, et al. Validity of the Somatic Symptom Disorder-B Criteria Scale (SSD-12) in primary care. Fam Pract. 2018;35:342-347. doi: 10.1093/fampra/cmx116
7. Kroenke K, Spitzer RL, Williams JB. The PHQ-15: validity of a new measure for evaluating the severity of somatic symptoms. Psychosom Med. 2002;64:258-66. doi: 10.1097/00006842-200203000-00008
8. Kroenke K, Spitzer RL, Williams JB, et al. The Patient Health Questionnaire Somatic, Anxiety, and Depressive Symptom Scales: a systematic review. Gen Hosp Psychiatry. 2010;32:345-359. doi: 10.1016/j.genhosppsych.2010.03.006
9. Toussaint A, Löwe B, Brähler E, et al. The Somatic Symptom Disorder - B Criteria Scale (SSD-12): factorial structure, validity and population-based norms. J Psychosom Res. 2017;97:9-17. doi: 10.1016/j.jpsychores.2017.03.017
10. First MB, Williams JBW, Karg RS, Spitzer RL, eds. Structured Clinical Interview for DSM-5 Disorders, Research Version. American Psychiatric Association, 2015.
11. First MB, Williams JBW, Karg RS, Spitzer RL, eds. Structured Clinical Interview for DSM-5 Disorders, Clinician Version. American Psychiatric Publishing; 2016.
12. McDaniel SH, Hepworth J, Campbell TL, et al, eds. Family Oriented Primary Care. Springer Publishing Co; 2005:1-15.
13. Hunter Integrated Pain Service (2016). Brainman videos. Hunter New England Local Health District. New South Wales, Australia. Accessed February 21, 2022. www.tga.gov.au/chronic-pain-management-video-resource-brainman
14. Murray AM, Toussaint A, Althaus A, et al. The challenge of diagnosing non-specific, functional, and somatoform disorders: a systematic review of barriers to diagnosis in primary care. J Psychosom Res. 2016;80:1-10. doi: 10.1016/j.jpsychores.2015.11.002
15. Leaviss J, Davis S, Ren S, et al. Behavioral modification interventions for medically unexplained symptoms in primary care: systematic reviews and economic evaluation. Health Technol Assess. 2020;24:1-490. doi: 10.3310/hta24460
16. Kroenke K. Efficacy of treatment for somatoform disorders: a review of randomized controlled trials. Psychosom Med. 2007;69:881-888. doi: 10.1097/PSY.0b013e31815b00c4
17. Steinbrecher N, Koerber S, Frieser D, et al. The prevalence of medically unexplained symptoms in primary care. Psychosomatics. 2011;52:263-271. doi: 10.1016/j.psym.2011.01.007
18. Kessler R, Stafford D. Primary care is the de facto mental health system. In Kessler R, Stafford D, eds. Collaborative Medicine Case Studies: Evidence in Practice. Springer Publishing Co, 2008; 9-21.
19. Barsky AJ, Ahern DK, Bauer MR, et al. A randomized trial of treatments for high-utilizing somatizing patients. J Gen Intern Med. 2013;28:1396-1404. doi: 10.1007/s11606-013-2392-6
20. Newby JM, Smith J, Uppal S, et al. Internet-based cognitive behavioral therapy versus psychoeducation control for illness anxiety disorder and somatic symptom disorder: A randomized controlled trial. J Consult Clin Psychol. 2018;86:89-98. doi: 10.1037/ccp0000248
21. van Dessel N, den Boeft M, van der Wouden JC, et al. Non-pharmacological interventions for somatoform disorders and medically unexplained physical symptoms (MUPS) in adults. Cochrane Database Syst Rev. 2014(11):CD011142. doi: 10.1002/14651858.CD011142.pub2
22. Verdurmen MJ, Videler AC, Kamperman AM, et al. Cognitive behavioral therapy for somatic symptom disorders in later life: a prospective comparative explorative pilot study in two clinical populations. Neuropsychiatr Dis Treat. 2017;13:2331-2339. doi: 10.2147/NDT.S141208
23. Liu J, Gill NS, Teodorczuk A, et al. The efficacy of cognitive behavioural therapy in somatoform disorders and medically unexplained physical symptoms: a meta-analysis of randomized controlled trials. J Affect Disord. 2019;245:98-112. doi: 10.1016/j.jad.2018.10.114
24. Abbass A, Leichsenring F, Steinert C. Re: Jing et al., the efficacy of cognitive behavioural therapy in somatoform disorders and medically unexplained physical symptoms: a meta-analysis of randomized controlled trials. J Affect Disord. 2019;255:S0165-0327(18)33197-5. doi: 10.1016/j.jad.2019.02.055
1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th edition (DSM-5). American Psychiatric Publishing; 2013.
2. Johnson KK, Bennett C, Rochani H. Significant improvement of somatic symptom disorder with brief psychoeducational intervention by PMHNP in primary care. J Am Psychiatr Nurses Assoc. 2020;28:171-180. doi: 10.1177/1078390320960524
3. Weigel A, Maehder K, Witt M, et al. Psychotherapists’ perspective on the treatment of patients with somatic symptom disorders. J Psychosom Res. 2020;138:110228. doi: 10.1016/j.jpsychores.2020.110228
4. American Psychiatric Association. Handbook of Differential Diagnosis. American Psychiatric Publishing; 2014;234-235.
5. Mayo Clinic. Somatic symptom disorder. Accessed February 21, 2022. www.mayoclinic.org/diseases-conditions/somatic-symptom-disorder/symptoms-causes/syc-20377776?p=1
6. Toussaint A, Riedl B, Kehrer S, et al. Validity of the Somatic Symptom Disorder-B Criteria Scale (SSD-12) in primary care. Fam Pract. 2018;35:342-347. doi: 10.1093/fampra/cmx116
7. Kroenke K, Spitzer RL, Williams JB. The PHQ-15: validity of a new measure for evaluating the severity of somatic symptoms. Psychosom Med. 2002;64:258-66. doi: 10.1097/00006842-200203000-00008
8. Kroenke K, Spitzer RL, Williams JB, et al. The Patient Health Questionnaire Somatic, Anxiety, and Depressive Symptom Scales: a systematic review. Gen Hosp Psychiatry. 2010;32:345-359. doi: 10.1016/j.genhosppsych.2010.03.006
9. Toussaint A, Löwe B, Brähler E, et al. The Somatic Symptom Disorder - B Criteria Scale (SSD-12): factorial structure, validity and population-based norms. J Psychosom Res. 2017;97:9-17. doi: 10.1016/j.jpsychores.2017.03.017
10. First MB, Williams JBW, Karg RS, Spitzer RL, eds. Structured Clinical Interview for DSM-5 Disorders, Research Version. American Psychiatric Association, 2015.
11. First MB, Williams JBW, Karg RS, Spitzer RL, eds. Structured Clinical Interview for DSM-5 Disorders, Clinician Version. American Psychiatric Publishing; 2016.
12. McDaniel SH, Hepworth J, Campbell TL, et al, eds. Family Oriented Primary Care. Springer Publishing Co; 2005:1-15.
13. Hunter Integrated Pain Service (2016). Brainman videos. Hunter New England Local Health District. New South Wales, Australia. Accessed February 21, 2022. www.tga.gov.au/chronic-pain-management-video-resource-brainman
14. Murray AM, Toussaint A, Althaus A, et al. The challenge of diagnosing non-specific, functional, and somatoform disorders: a systematic review of barriers to diagnosis in primary care. J Psychosom Res. 2016;80:1-10. doi: 10.1016/j.jpsychores.2015.11.002
15. Leaviss J, Davis S, Ren S, et al. Behavioral modification interventions for medically unexplained symptoms in primary care: systematic reviews and economic evaluation. Health Technol Assess. 2020;24:1-490. doi: 10.3310/hta24460
16. Kroenke K. Efficacy of treatment for somatoform disorders: a review of randomized controlled trials. Psychosom Med. 2007;69:881-888. doi: 10.1097/PSY.0b013e31815b00c4
17. Steinbrecher N, Koerber S, Frieser D, et al. The prevalence of medically unexplained symptoms in primary care. Psychosomatics. 2011;52:263-271. doi: 10.1016/j.psym.2011.01.007
18. Kessler R, Stafford D. Primary care is the de facto mental health system. In Kessler R, Stafford D, eds. Collaborative Medicine Case Studies: Evidence in Practice. Springer Publishing Co, 2008; 9-21.
19. Barsky AJ, Ahern DK, Bauer MR, et al. A randomized trial of treatments for high-utilizing somatizing patients. J Gen Intern Med. 2013;28:1396-1404. doi: 10.1007/s11606-013-2392-6
20. Newby JM, Smith J, Uppal S, et al. Internet-based cognitive behavioral therapy versus psychoeducation control for illness anxiety disorder and somatic symptom disorder: A randomized controlled trial. J Consult Clin Psychol. 2018;86:89-98. doi: 10.1037/ccp0000248
21. van Dessel N, den Boeft M, van der Wouden JC, et al. Non-pharmacological interventions for somatoform disorders and medically unexplained physical symptoms (MUPS) in adults. Cochrane Database Syst Rev. 2014(11):CD011142. doi: 10.1002/14651858.CD011142.pub2
22. Verdurmen MJ, Videler AC, Kamperman AM, et al. Cognitive behavioral therapy for somatic symptom disorders in later life: a prospective comparative explorative pilot study in two clinical populations. Neuropsychiatr Dis Treat. 2017;13:2331-2339. doi: 10.2147/NDT.S141208
23. Liu J, Gill NS, Teodorczuk A, et al. The efficacy of cognitive behavioural therapy in somatoform disorders and medically unexplained physical symptoms: a meta-analysis of randomized controlled trials. J Affect Disord. 2019;245:98-112. doi: 10.1016/j.jad.2018.10.114
24. Abbass A, Leichsenring F, Steinert C. Re: Jing et al., the efficacy of cognitive behavioural therapy in somatoform disorders and medically unexplained physical symptoms: a meta-analysis of randomized controlled trials. J Affect Disord. 2019;255:S0165-0327(18)33197-5. doi: 10.1016/j.jad.2019.02.055
Benzodiazepine and Z-hypnotic stewardship
Benzodiazepines (BZDs) and Z-hypnotics have been available for decades, yet uncertainties about their use remain. They are prescribed and overprescribed most often for anxiety and insomnia, for which they have value but also the potential for significant adverse consequences, notably physiologic dependence. Use of these agents should be limited, and planned deprescribing is a fundamental aspect of prescribing.
A brief history. BZDs are a subset of benzodiazepine receptor agonists (BZRAs), which enhance the inhibitory effect of centrally acting γ-amino butyric acid (GABA) at the GABAA receptor through allosteric modulation. In 1960, the first BZD, chlordiazepoxide, was marketed for clinical use, and as other agents in the class became available, BZDs supplanted the more toxic barbiturates, another BZRA subset (TABLE 1). By the late 1970s, BZDs had risen to the top of most prescribed medications, with one agent in particular—diazepam (Valium)—earning a reputation as “mother’s little helper,” a phrase derived from a Rolling Stones' song with that title produced in 1966.1
With recognition of the problems associated with BZDs, their popularity diminished somewhat but remained high. BZDs were listed under Schedule IV by the Drug Enforcement Administration in 1975 due to the risk for addiction, and on the American Geriatrics Society Beers Criteria list in 1991 because of significant adverse consequences in the elderly. Researchers began to question their use as early as the 1970s, and the landmark Ashton Manual, guidance for patients and clinicians alike, was published in 2002.2
Currently, there are 14 BZDs approved by the Food and Drug Administration (FDA) as well as 3 Z-hypnotics, termed such as they include the letter “z” in their generic names (TABLE 1). In recent years, BZD prescribing has risen; a 2019 study found that 1 of 8 American adults reported using a BZD in the previous year.3
Limited benefits of benzodiazepine receptor agonists
BZRAs can be of benefit in a limited range of medical conditions, including some for which they are first-line considerations. (See TABLE 2 for a list of indications for BZDs.) They are most often prescribed for anxiety and insomnia, although they are not first-line treatments for these conditions and should be prescribed only when symptoms limit a patient’s daily functioning.
BZRAs are not intended for long-term use. In recent decades, the percentage of patients prescribed BZRAs has doubled, and more than 80% of these patients indicate usage for more than 6 months.4 Evidence, however, does not support long-term daily use.
Observation periods in most studies are far shorter than the number of years over which BZDs are actually prescribed, and flawed research methodology has introduced the risk of bias. Specifically, the generalizability of reported outcomes must be qualified, since efficacy trials performed under ideal study conditions (eg, exclusion criteria to minimize confounders) differ from circumstances seen in clinical practice. Conclusions are also limited by the inherent bias of pharmaceutical industry sponsorship and unavailability of unpublished trials that may have demonstrated unfavorable results.
Continue to: Insomnia
Insomnia, a current (past 30 days) complaint in more than 40% of US adults, is associated with a variety of symptoms.5 About 20% of adults have an insomnia disorder, defined as a predominant problem for at least 1 month involving sleep initiation, maintenance, or nonrestorative sleep along with daytime function-limiting fatigue.5 Meta-analyses indicate BZRAs can reduce sleep latency (BZDs, by 4 minutes; Z-hypnotics, 22 minutes) and may increase sleep duration (BZDs, 62 minutes per limited data; Z-hypnotics, data insufficient).6,7 Definitive evidence for long-term (> 2-4 weeks) BZD benefit is lacking, and cognitive behavioral therapy for insomnia (CBT-I) is well established as first-line treatment yielding improvements that may last at least 18 months after completion of therapy. 8,9
Although CBT-I is generally provided by behavioral health specialists, elements of CBT-I and sleep hygiene measures can be effectively used by primary care clinicians.10 Data indicate other nonpharmacologic interventions are also effective,11 including acceptance and commitment therapy,12 meditation,13 and acupuncture.14
Episodic fear and anxiety are universal and essential for survival. Fear is an alarm warning of an immediate hazard. Anxiety (the emotion) paired with worry (the thought) relate to a perceived future threat. Transient (state) anxiety should not be suppressed altogether if self-management can curb its intensity and thereby allow effective problem engagement. However, when individuals are incapacitated by crisis anxiety or sporadic specific phobias such as flight anxiety, episodic BZDs do have a role.
Ongoing anxiety is a more complex treatment situation. Obsessive-compulsive disorder and posttraumatic stress disorder are no longer categorized as anxiety disorders, but they often involve anxiety. Here, BZDs have no indication aside from exceptional acute crisis presentations. Anxiety disorders are defined by a core persistent (trait) anxiety disproportionate to the actual threat, limited daily functioning, and more than 6 months’ duration. One of 3 Americans older than 13 years meet the criteria for anxiety in their lifetime; 1 of 5 meet the criteria in any single year.15
BZDs are effective in treating anxiety disorders in the short term (2-4 weeks)2,16,17; however, benefit may fade over time.18-21 For some individuals, data suggest BZDs themselves might actually generate anxiety, as evidenced by reduced symptom intensity following discontinuation.22,23 Recommended first-line medications for anxiety disorders include certain antidepressants and pregabalin, which exhibit efficacy similar to that of BZDs.24 Mindfulness and various psychotherapies have value, as well.16 Among the latter, CBT is considered first line with benefit comparable to BZDs in the short term; yet unlike BZDs, CBT gains can last 12 months or longer after the conclusion of therapy. 25,26 Because there may be a delay between the start of CBT and the onset of benefit, BZDs, which work quickly, may be used to bridge functionally impaired patients in the short term.
Continue to: Risks with benzodiazepine receptor agonists
Risks with benzodiazepine receptor agonists
Harms from BZRA use are common, tempering their utility. Sedation, dyscognition, and psychomotor impairments are often seen upon initiation of BZRA use. These adverse effects can—although not always—improve with continuous BZRA exposure, an effect known as tolerance, which is due to neuropharmacologic adaptation.
Cognitive issues include problems with memory, judgment, and decision making. These may be unrecognized or, if noted, attributed to other issues such as aging, and may become clear only when BZRAs are discontinued. Anterograde amnesia and parasomnias occur less often.
Psychomotor impairment can result in falls, fractures, and other injuries, especially in the elderly. Decrements in mood, including emergent depression and paradoxical anxiety, can occur. Some individuals experience disinhibition that is expressed through irritability, agitation, aggression, and violence.
Misuse of BZRAs is not unusual and can be related to dosing errors or attempts to ease intrusive symptoms. Nonmedical use almost always occurs in the context of an underlying use disorder, whereby BZRAs serve to amplify euphoria or ameliorate withdrawal from opioids or alcohol. Addiction per se, which entails BZRA craving and compulsive use leading to adverse consequences, is unusual.
BZRAs are associated with increased mortality, including all-cause mortality and suicide. They are respiratory depressants, although when taken alone in excess rarely result in death. They are, however, strongly implicated in opioid-related overdose fatalities, as their presence has been identified in 1 of 3 such decedents.27
Continue to: Physiologic dependence with BZRAs
Physiologic dependence with BZRAs
Among the more important adverse outcomes with ongoing BZRA exposure is physiologic dependence. This occurs primarily because of neuroadaptation of GABAA and glutaminergic receptors, but dependence probably also involves changes in the adenosine A2A, serotonergic, and peripheral benzodiazepine receptors, the latter being present on mitochondrial membranes. The hypothalamic-pituitary-adrenal axis also appears to be involved.
Physiologic dependence is expressed through BZRA tolerance and characteristic physical and psychological symptoms upon withdrawal. Tolerance refers to a reduced effect with continued substance exposure or the need for an increased dose to get the same effect. Drug withdrawal can result in manifestations distinctive to addiction-prone substances, as well as to some medications without addiction liability, such as corticosteroids and antidepressants. Tolerance and withdrawal are not applicable criteria in the diagnosis of sedative-hypnotic use disorder when BZRAs are prescribed.28
Withdrawal. Reported prevalence of BZRA physiologic dependence differs according to populations studied, criteria used, and the deprescribing process employed. Some researchers have found rates of one-third and others exceeding one-half among individuals using BZRAs for longer than a month.23,29
Deprescribing BZRAs
Because benefits are limited and adverse outcomes including physiologic dependence are common, it is recommended that clinicians urge deprescribing of BZRAs for any patient taking them consistently for more than 1 month. Published deprescribing investigations and guidance are insufficient, heterogenous, and confusing. Still, some approaches can work well, and success rates as high as 80% have been achieved among the elderly, for example.35 Brief interventions such as providing individualized advice, support, and management are effective.36,37 Abrupt discontinuation is inappropriate and can be life threatening.38 Forced cessation is also inappropriate unless significant respiratory depression is identified.
The Ashton Manual is a useful guide, readable by patients. Proceed with tapering slowly at a rate led by the patient’s response.2,39 Avoid discrediting patients’ reports of unusual withdrawal symptoms, as this can lead to misdiagnosis (eg, somatic symptom disorder) or ineffective treatment (eg, addiction recovery approaches). Adding CBT to tapering improves outcomes, and adjunctive medications may be helpful, although not without their own problems.29 Consistent support of patients by others involved in treatment (prescriber, pharmacist, behavioral health specialists, peer coach, significant others) is essential. Complex challenges generally resolve through authentic listening and response but may require referral to others with necessary skills and experience. Complete cessation may take 12 to 18 months (or longer). Even if complete cessation is not possible, the least dose necessary can be achieved.
CORRESPONDENCE
Steven Wright, MD, 1975 Ashland Mine Road, Ashland, OR 97520; [email protected]
- Chandler A, Whittaker A, Williams N, et al. Mother’s little helper? Contrasting accounts of benzodiazepine and methadone use among drug-dependent parents in the UK. Drugs (Abingdon Engl). 2014;21:470-475. doi: 10.3109/09687637.2014.930814Ash
- ton CH. Benzodiazepines: How They Work & How to Withdraw (the Ashton Manual). 2002. Accessed March 17, 2022. www.benzoinfo.com/ashtonmanual/
- Maust DT, Lin LA, Blow FC. Benzodiazepine use and misuse among adults in the United States. Psychiatr Serv. 2019;70:97-106. doi: 10.1176/appi.ps.201800321
- Kaufmann CN, Spira AP, Depp CA, et al. Long-term use of benzodiazepines and non-benzodiazepine hypnotics from 1999 to 2014: results from the National Health and Nutrition Examination Survey. Psychiatr Serv. 2018;69:235-238. doi: 10.1176/appi.ps.201700095
- Walsh JK, Coulouvrat C, Hajak G, et al. Nighttime insomnia symptoms and perceived health in the America Insomnia Survey (AIS). Sleep. 2011;34:997-1011. doi: 10.5665/SLEEP.1150
- Holbrook AM, Crowther R, Lotter A, et al. Meta-analysis of benzodiazepine use in the treatment of insomnia. CMAJ. 2000;162:225-233.
- Huedo-Medina TB, Kirsch I, Middlemass J, et al. Effectiveness of non-benzodiazepine hypnotics in treatment of adult insomnia: meta-analysis of data submitted to the Food and Drug Administration. BMJ. 2012;345:e8343. doi: 10.1136/bmj.e8343
- Curran HV, Collins R, Fletcher S, et al. Older adults and withdrawal from benzodiazepine hypnotics in general practice: effects on cognitive function, sleep, mood and quality of life. Psychol Med. 2003;33:1223-1237. doi: 10.1017/s0033291703008213
- Geiger-Brown JM, Rogers VE, Liu W, et al. Cognitive behavioral therapy in persons with comorbid insomnia: a meta-analysis. Sleep Med Rev. 2015;23:54-67. doi: 10.1016/j.smrv.2014.11.007
- Sorscher AJ. Insomnia: getting to the cause, facilitating relief. J Fam Pract. 2017;66:216-225
- Laura Hrehová L, Mezian K. Non-pharmacologic treatment of insomnia in primary care settings. Int J Clin Pract. 2021;75:e14084. doi: 10.1111/ijcp.14084.
- Daly-Eichenhardt A, Scott W, Howard-Jones M, et al. Changes in sleep problems and psychological flexibility following interdisciplinary acceptance and commitment therapy for chronic pain: an observational cohort study. Front Psychol. 2016;7:1326. doi: 10.3389/fpsyg.2016.01326
- Rusch HL, Rosario M, Levison LM, et al. The effect of mindfulness meditation on sleep quality: a systematic review and meta-analysis of randomized controlled trials. Ann N Y Acad Sci. 2019;1445:5-16. doi: 10.1111/nyas.13996
- Cao H, Pan X, Li H, et al. Acupuncture for treatment of insomnia: a systematic review of randomized controlled trials. J Altern Complement Med. 2009;15:1171-1186. doi: 10.1089/acm.2009.0041
- Kessler RC, Petukhova M, Sampson NA, et al. Twelve‐month and lifetime prevalence and lifetime morbid risk of anxiety and mood disorders in the United States. Int J Methods Psychiatr Res. 2012;21:169-184. doi: 10.1002/mpr.1359
- Bandelow B, Reitt M, Röver C, et al. Efficacy of treatments for anxiety disorders: a meta-analysis. Int Clin Psychopharmacol. 2015;30:183-192. doi: 10.1097/YIC.0000000000000078
- Lader M. Benzodiazepines revisited—will we ever learn? Addiction. 2011;106:2086-2109. doi: 10.1111/j.1360-0443.2011.03563.x
- Fava GA. Fading of therapeutic effects of alprazolam in agoraphobia. Case reports. Prog Neuropsychopharmacol Biol Psychiatry. 1988;12:109-112. doi: 10.1016/0278-5846(88)90066-8
- Fava GA, Grandi S, Belluardo P, et al. Benzodiazepines and anxiety sensitivity in panic disorder. Prog Neuropsychopharmacol Biol Psychiatry. 1994;18:1163-1168. doi: 10.1016/0278-5846(94)90118-x
- Pélissolo A, Maniere F, Boutges B, et al. Anxiety and depressive disorders in 4,425 long term benzodiazepine users in general practice. Encephale. 2007;33:32-38. doi: 10.1016/s0013-7006(07)91556-0
- Gale C, Glue P, Guaiana G, et al. Influence of covariates on heterogeneity in Hamilton Anxiety Scale ratings in placebo-controlled trials of benzodiazepines in generalized anxiety disorder: systematic review and meta-analysis. J Psychopharmacol. 2019;33:543-547. doi: 10.1177/0269881118822146
- Ashton CH. Benzodiazepine withdrawal: outcome in 50 patients. Br J Addict. 1987;82:655-671. Accessed February 22, 2022. www.benzo.org.uk/ashbzoc.htm
- Rickels K, Schweizer E, Case WG, et al. Long-term therapeutic use of benzodiazepines. I. Effects of abrupt discontinuation. Arch Gen Psychiatry. 1990;47:899-907. doi: 10.1001/archpsyc.1990.01810220015002
- Bandelow B, Sher L, Bunevicius R, et al. Guidelines for the pharmacological treatment of anxiety disorders, obsessive-compulsive disorder and posttraumatic stress disorder in primary care. Int J Psychiatry Clin Pract. 2012;16:77-84. Accessed March 17, 2022. www.wfsbp.org/fileadmin/user_upload/Treatment_Guidelines/Bandelow_et_al_01.pdf
- Imai H, Tajika A, Chen P, et al. Psychological therapies versus pharmacological interventions for panic disorder with or without agoraphobia in adults. Cochrane Database Syst Rev. 2016;10:CD011170. doi: 10.1002/14651858.CD011170.pub2
- van Dis EAM, van Veen SC, Hagenaars MA, et al. Long-term outcomes of cognitive behavioral therapy for anxiety-related disorders. A systematic review and meta-analysis. JAMA Psychiatry. 2020;77:265-273. doi:10.1001/jamapsychiatry.2019.3986
- Chen LH, Hedegaard H, Warner M. Drug-poisoning deaths Involving opioid analgesics: United States, 1999-2011. NCHS Data Brief. 2014;(166):1-8. Accessed March 17, 2022. www.cdc.gov/nchs/data/databriefs/db166.pdf
- American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th edition (DSM-5). American Psychiatric Publishing; 2013:550-555.
- Marriott S, Tyrer P. Benzodiazepine dependence: avoidance and withdrawal. Drug Safety. 1993;9:93-103. doi: 10.2165/00002018-199309020-00003
- Griffiths RR, Evans SM, Guarino JJ, et al. Intravenous flumazenil following acute and repeated exposure to lorazepam in healthy volunteers: antagonism and precipitated withdrawal. J Pharmacol Exp Ther. 1993;265:1163-1174.
- Ashton H. Benzodiazepine withdrawal: an unfinished story. Br Med J. 1984;288:1135-1140. Accessed March 17, 2022. www.ncbi.nlm.nih.gov/pmc/articles/PMC1441411/pdf/bmjcred00496-0031.pdf
- Lugoboni F, Quaglio G. Exploring the dark side of the moon: the treatment of benzodiazepine tolerance. Br J Clin Pharmacol. 2014;77:239-41. doi: 10.1111/bcp.12148
- Ashton CH. Protracted withdrawal from benzodiazepines: the post-withdrawal syndrome. Psychiatr Ann. 1995;25:174-179. Accessed March 17, 2022. https://benzo.org.uk/pha-1.htm
- Fixsen AM, Ridge D. Stories of hell and healing: internet users’ construction of benzodiazepine distress and withdrawal. Qual Health Res. 2017;27:2030-2041. doi: 10.1177/1049732317728053
- Ng BJ, Le Couteur DG, Hilmer SN. Deprescribing benzodiazepines in older patients: impact of interventions targeting physicians, pharmacists, and patients. Drugs Aging. 2018;35:493-521. doi: 10.1007/s40266-018-0544-4
- Lynch T, Ryan C, Hughes CM, et al. Brief interventions targeting long-term benzodiazepine and Z-drug use in primary care: a systematic review and meta-analysis. Addiction. 2020;115:1618-1639. doi: 10.1111/add.14981
- Darker CD, Sweeney BP, Barry JM, et al. Psychosocial interventions for benzodiazepine harmful use, abuse or dependence. Cochrane Database Syst Rev. 2015;(5):CD009652. doi: 10.1002/14651858.CD009652.pub2
- Hu X. Benzodiazepine withdrawal seizures and management. J Okla State Med Assoc. 2011;104:62-65.
- Wright SL. Benzodiazepine withdrawal: clinical aspects. In Peppin J, Raffa R, Pergolizzi J, Wright SL, eds. The Benzodiazepines Crisis: The Ramifications of an Overused Drug Class. Oxford University Press. 2020:117-148.
Benzodiazepines (BZDs) and Z-hypnotics have been available for decades, yet uncertainties about their use remain. They are prescribed and overprescribed most often for anxiety and insomnia, for which they have value but also the potential for significant adverse consequences, notably physiologic dependence. Use of these agents should be limited, and planned deprescribing is a fundamental aspect of prescribing.
A brief history. BZDs are a subset of benzodiazepine receptor agonists (BZRAs), which enhance the inhibitory effect of centrally acting γ-amino butyric acid (GABA) at the GABAA receptor through allosteric modulation. In 1960, the first BZD, chlordiazepoxide, was marketed for clinical use, and as other agents in the class became available, BZDs supplanted the more toxic barbiturates, another BZRA subset (TABLE 1). By the late 1970s, BZDs had risen to the top of most prescribed medications, with one agent in particular—diazepam (Valium)—earning a reputation as “mother’s little helper,” a phrase derived from a Rolling Stones' song with that title produced in 1966.1
With recognition of the problems associated with BZDs, their popularity diminished somewhat but remained high. BZDs were listed under Schedule IV by the Drug Enforcement Administration in 1975 due to the risk for addiction, and on the American Geriatrics Society Beers Criteria list in 1991 because of significant adverse consequences in the elderly. Researchers began to question their use as early as the 1970s, and the landmark Ashton Manual, guidance for patients and clinicians alike, was published in 2002.2
Currently, there are 14 BZDs approved by the Food and Drug Administration (FDA) as well as 3 Z-hypnotics, termed such as they include the letter “z” in their generic names (TABLE 1). In recent years, BZD prescribing has risen; a 2019 study found that 1 of 8 American adults reported using a BZD in the previous year.3
Limited benefits of benzodiazepine receptor agonists
BZRAs can be of benefit in a limited range of medical conditions, including some for which they are first-line considerations. (See TABLE 2 for a list of indications for BZDs.) They are most often prescribed for anxiety and insomnia, although they are not first-line treatments for these conditions and should be prescribed only when symptoms limit a patient’s daily functioning.
BZRAs are not intended for long-term use. In recent decades, the percentage of patients prescribed BZRAs has doubled, and more than 80% of these patients indicate usage for more than 6 months.4 Evidence, however, does not support long-term daily use.
Observation periods in most studies are far shorter than the number of years over which BZDs are actually prescribed, and flawed research methodology has introduced the risk of bias. Specifically, the generalizability of reported outcomes must be qualified, since efficacy trials performed under ideal study conditions (eg, exclusion criteria to minimize confounders) differ from circumstances seen in clinical practice. Conclusions are also limited by the inherent bias of pharmaceutical industry sponsorship and unavailability of unpublished trials that may have demonstrated unfavorable results.
Continue to: Insomnia
Insomnia, a current (past 30 days) complaint in more than 40% of US adults, is associated with a variety of symptoms.5 About 20% of adults have an insomnia disorder, defined as a predominant problem for at least 1 month involving sleep initiation, maintenance, or nonrestorative sleep along with daytime function-limiting fatigue.5 Meta-analyses indicate BZRAs can reduce sleep latency (BZDs, by 4 minutes; Z-hypnotics, 22 minutes) and may increase sleep duration (BZDs, 62 minutes per limited data; Z-hypnotics, data insufficient).6,7 Definitive evidence for long-term (> 2-4 weeks) BZD benefit is lacking, and cognitive behavioral therapy for insomnia (CBT-I) is well established as first-line treatment yielding improvements that may last at least 18 months after completion of therapy. 8,9
Although CBT-I is generally provided by behavioral health specialists, elements of CBT-I and sleep hygiene measures can be effectively used by primary care clinicians.10 Data indicate other nonpharmacologic interventions are also effective,11 including acceptance and commitment therapy,12 meditation,13 and acupuncture.14
Episodic fear and anxiety are universal and essential for survival. Fear is an alarm warning of an immediate hazard. Anxiety (the emotion) paired with worry (the thought) relate to a perceived future threat. Transient (state) anxiety should not be suppressed altogether if self-management can curb its intensity and thereby allow effective problem engagement. However, when individuals are incapacitated by crisis anxiety or sporadic specific phobias such as flight anxiety, episodic BZDs do have a role.
Ongoing anxiety is a more complex treatment situation. Obsessive-compulsive disorder and posttraumatic stress disorder are no longer categorized as anxiety disorders, but they often involve anxiety. Here, BZDs have no indication aside from exceptional acute crisis presentations. Anxiety disorders are defined by a core persistent (trait) anxiety disproportionate to the actual threat, limited daily functioning, and more than 6 months’ duration. One of 3 Americans older than 13 years meet the criteria for anxiety in their lifetime; 1 of 5 meet the criteria in any single year.15
BZDs are effective in treating anxiety disorders in the short term (2-4 weeks)2,16,17; however, benefit may fade over time.18-21 For some individuals, data suggest BZDs themselves might actually generate anxiety, as evidenced by reduced symptom intensity following discontinuation.22,23 Recommended first-line medications for anxiety disorders include certain antidepressants and pregabalin, which exhibit efficacy similar to that of BZDs.24 Mindfulness and various psychotherapies have value, as well.16 Among the latter, CBT is considered first line with benefit comparable to BZDs in the short term; yet unlike BZDs, CBT gains can last 12 months or longer after the conclusion of therapy. 25,26 Because there may be a delay between the start of CBT and the onset of benefit, BZDs, which work quickly, may be used to bridge functionally impaired patients in the short term.
Continue to: Risks with benzodiazepine receptor agonists
Risks with benzodiazepine receptor agonists
Harms from BZRA use are common, tempering their utility. Sedation, dyscognition, and psychomotor impairments are often seen upon initiation of BZRA use. These adverse effects can—although not always—improve with continuous BZRA exposure, an effect known as tolerance, which is due to neuropharmacologic adaptation.
Cognitive issues include problems with memory, judgment, and decision making. These may be unrecognized or, if noted, attributed to other issues such as aging, and may become clear only when BZRAs are discontinued. Anterograde amnesia and parasomnias occur less often.
Psychomotor impairment can result in falls, fractures, and other injuries, especially in the elderly. Decrements in mood, including emergent depression and paradoxical anxiety, can occur. Some individuals experience disinhibition that is expressed through irritability, agitation, aggression, and violence.
Misuse of BZRAs is not unusual and can be related to dosing errors or attempts to ease intrusive symptoms. Nonmedical use almost always occurs in the context of an underlying use disorder, whereby BZRAs serve to amplify euphoria or ameliorate withdrawal from opioids or alcohol. Addiction per se, which entails BZRA craving and compulsive use leading to adverse consequences, is unusual.
BZRAs are associated with increased mortality, including all-cause mortality and suicide. They are respiratory depressants, although when taken alone in excess rarely result in death. They are, however, strongly implicated in opioid-related overdose fatalities, as their presence has been identified in 1 of 3 such decedents.27
Continue to: Physiologic dependence with BZRAs
Physiologic dependence with BZRAs
Among the more important adverse outcomes with ongoing BZRA exposure is physiologic dependence. This occurs primarily because of neuroadaptation of GABAA and glutaminergic receptors, but dependence probably also involves changes in the adenosine A2A, serotonergic, and peripheral benzodiazepine receptors, the latter being present on mitochondrial membranes. The hypothalamic-pituitary-adrenal axis also appears to be involved.
Physiologic dependence is expressed through BZRA tolerance and characteristic physical and psychological symptoms upon withdrawal. Tolerance refers to a reduced effect with continued substance exposure or the need for an increased dose to get the same effect. Drug withdrawal can result in manifestations distinctive to addiction-prone substances, as well as to some medications without addiction liability, such as corticosteroids and antidepressants. Tolerance and withdrawal are not applicable criteria in the diagnosis of sedative-hypnotic use disorder when BZRAs are prescribed.28
Withdrawal. Reported prevalence of BZRA physiologic dependence differs according to populations studied, criteria used, and the deprescribing process employed. Some researchers have found rates of one-third and others exceeding one-half among individuals using BZRAs for longer than a month.23,29
Deprescribing BZRAs
Because benefits are limited and adverse outcomes including physiologic dependence are common, it is recommended that clinicians urge deprescribing of BZRAs for any patient taking them consistently for more than 1 month. Published deprescribing investigations and guidance are insufficient, heterogenous, and confusing. Still, some approaches can work well, and success rates as high as 80% have been achieved among the elderly, for example.35 Brief interventions such as providing individualized advice, support, and management are effective.36,37 Abrupt discontinuation is inappropriate and can be life threatening.38 Forced cessation is also inappropriate unless significant respiratory depression is identified.
The Ashton Manual is a useful guide, readable by patients. Proceed with tapering slowly at a rate led by the patient’s response.2,39 Avoid discrediting patients’ reports of unusual withdrawal symptoms, as this can lead to misdiagnosis (eg, somatic symptom disorder) or ineffective treatment (eg, addiction recovery approaches). Adding CBT to tapering improves outcomes, and adjunctive medications may be helpful, although not without their own problems.29 Consistent support of patients by others involved in treatment (prescriber, pharmacist, behavioral health specialists, peer coach, significant others) is essential. Complex challenges generally resolve through authentic listening and response but may require referral to others with necessary skills and experience. Complete cessation may take 12 to 18 months (or longer). Even if complete cessation is not possible, the least dose necessary can be achieved.
CORRESPONDENCE
Steven Wright, MD, 1975 Ashland Mine Road, Ashland, OR 97520; [email protected]
Benzodiazepines (BZDs) and Z-hypnotics have been available for decades, yet uncertainties about their use remain. They are prescribed and overprescribed most often for anxiety and insomnia, for which they have value but also the potential for significant adverse consequences, notably physiologic dependence. Use of these agents should be limited, and planned deprescribing is a fundamental aspect of prescribing.
A brief history. BZDs are a subset of benzodiazepine receptor agonists (BZRAs), which enhance the inhibitory effect of centrally acting γ-amino butyric acid (GABA) at the GABAA receptor through allosteric modulation. In 1960, the first BZD, chlordiazepoxide, was marketed for clinical use, and as other agents in the class became available, BZDs supplanted the more toxic barbiturates, another BZRA subset (TABLE 1). By the late 1970s, BZDs had risen to the top of most prescribed medications, with one agent in particular—diazepam (Valium)—earning a reputation as “mother’s little helper,” a phrase derived from a Rolling Stones' song with that title produced in 1966.1
With recognition of the problems associated with BZDs, their popularity diminished somewhat but remained high. BZDs were listed under Schedule IV by the Drug Enforcement Administration in 1975 due to the risk for addiction, and on the American Geriatrics Society Beers Criteria list in 1991 because of significant adverse consequences in the elderly. Researchers began to question their use as early as the 1970s, and the landmark Ashton Manual, guidance for patients and clinicians alike, was published in 2002.2
Currently, there are 14 BZDs approved by the Food and Drug Administration (FDA) as well as 3 Z-hypnotics, termed such as they include the letter “z” in their generic names (TABLE 1). In recent years, BZD prescribing has risen; a 2019 study found that 1 of 8 American adults reported using a BZD in the previous year.3
Limited benefits of benzodiazepine receptor agonists
BZRAs can be of benefit in a limited range of medical conditions, including some for which they are first-line considerations. (See TABLE 2 for a list of indications for BZDs.) They are most often prescribed for anxiety and insomnia, although they are not first-line treatments for these conditions and should be prescribed only when symptoms limit a patient’s daily functioning.
BZRAs are not intended for long-term use. In recent decades, the percentage of patients prescribed BZRAs has doubled, and more than 80% of these patients indicate usage for more than 6 months.4 Evidence, however, does not support long-term daily use.
Observation periods in most studies are far shorter than the number of years over which BZDs are actually prescribed, and flawed research methodology has introduced the risk of bias. Specifically, the generalizability of reported outcomes must be qualified, since efficacy trials performed under ideal study conditions (eg, exclusion criteria to minimize confounders) differ from circumstances seen in clinical practice. Conclusions are also limited by the inherent bias of pharmaceutical industry sponsorship and unavailability of unpublished trials that may have demonstrated unfavorable results.
Continue to: Insomnia
Insomnia, a current (past 30 days) complaint in more than 40% of US adults, is associated with a variety of symptoms.5 About 20% of adults have an insomnia disorder, defined as a predominant problem for at least 1 month involving sleep initiation, maintenance, or nonrestorative sleep along with daytime function-limiting fatigue.5 Meta-analyses indicate BZRAs can reduce sleep latency (BZDs, by 4 minutes; Z-hypnotics, 22 minutes) and may increase sleep duration (BZDs, 62 minutes per limited data; Z-hypnotics, data insufficient).6,7 Definitive evidence for long-term (> 2-4 weeks) BZD benefit is lacking, and cognitive behavioral therapy for insomnia (CBT-I) is well established as first-line treatment yielding improvements that may last at least 18 months after completion of therapy. 8,9
Although CBT-I is generally provided by behavioral health specialists, elements of CBT-I and sleep hygiene measures can be effectively used by primary care clinicians.10 Data indicate other nonpharmacologic interventions are also effective,11 including acceptance and commitment therapy,12 meditation,13 and acupuncture.14
Episodic fear and anxiety are universal and essential for survival. Fear is an alarm warning of an immediate hazard. Anxiety (the emotion) paired with worry (the thought) relate to a perceived future threat. Transient (state) anxiety should not be suppressed altogether if self-management can curb its intensity and thereby allow effective problem engagement. However, when individuals are incapacitated by crisis anxiety or sporadic specific phobias such as flight anxiety, episodic BZDs do have a role.
Ongoing anxiety is a more complex treatment situation. Obsessive-compulsive disorder and posttraumatic stress disorder are no longer categorized as anxiety disorders, but they often involve anxiety. Here, BZDs have no indication aside from exceptional acute crisis presentations. Anxiety disorders are defined by a core persistent (trait) anxiety disproportionate to the actual threat, limited daily functioning, and more than 6 months’ duration. One of 3 Americans older than 13 years meet the criteria for anxiety in their lifetime; 1 of 5 meet the criteria in any single year.15
BZDs are effective in treating anxiety disorders in the short term (2-4 weeks)2,16,17; however, benefit may fade over time.18-21 For some individuals, data suggest BZDs themselves might actually generate anxiety, as evidenced by reduced symptom intensity following discontinuation.22,23 Recommended first-line medications for anxiety disorders include certain antidepressants and pregabalin, which exhibit efficacy similar to that of BZDs.24 Mindfulness and various psychotherapies have value, as well.16 Among the latter, CBT is considered first line with benefit comparable to BZDs in the short term; yet unlike BZDs, CBT gains can last 12 months or longer after the conclusion of therapy. 25,26 Because there may be a delay between the start of CBT and the onset of benefit, BZDs, which work quickly, may be used to bridge functionally impaired patients in the short term.
Continue to: Risks with benzodiazepine receptor agonists
Risks with benzodiazepine receptor agonists
Harms from BZRA use are common, tempering their utility. Sedation, dyscognition, and psychomotor impairments are often seen upon initiation of BZRA use. These adverse effects can—although not always—improve with continuous BZRA exposure, an effect known as tolerance, which is due to neuropharmacologic adaptation.
Cognitive issues include problems with memory, judgment, and decision making. These may be unrecognized or, if noted, attributed to other issues such as aging, and may become clear only when BZRAs are discontinued. Anterograde amnesia and parasomnias occur less often.
Psychomotor impairment can result in falls, fractures, and other injuries, especially in the elderly. Decrements in mood, including emergent depression and paradoxical anxiety, can occur. Some individuals experience disinhibition that is expressed through irritability, agitation, aggression, and violence.
Misuse of BZRAs is not unusual and can be related to dosing errors or attempts to ease intrusive symptoms. Nonmedical use almost always occurs in the context of an underlying use disorder, whereby BZRAs serve to amplify euphoria or ameliorate withdrawal from opioids or alcohol. Addiction per se, which entails BZRA craving and compulsive use leading to adverse consequences, is unusual.
BZRAs are associated with increased mortality, including all-cause mortality and suicide. They are respiratory depressants, although when taken alone in excess rarely result in death. They are, however, strongly implicated in opioid-related overdose fatalities, as their presence has been identified in 1 of 3 such decedents.27
Continue to: Physiologic dependence with BZRAs
Physiologic dependence with BZRAs
Among the more important adverse outcomes with ongoing BZRA exposure is physiologic dependence. This occurs primarily because of neuroadaptation of GABAA and glutaminergic receptors, but dependence probably also involves changes in the adenosine A2A, serotonergic, and peripheral benzodiazepine receptors, the latter being present on mitochondrial membranes. The hypothalamic-pituitary-adrenal axis also appears to be involved.
Physiologic dependence is expressed through BZRA tolerance and characteristic physical and psychological symptoms upon withdrawal. Tolerance refers to a reduced effect with continued substance exposure or the need for an increased dose to get the same effect. Drug withdrawal can result in manifestations distinctive to addiction-prone substances, as well as to some medications without addiction liability, such as corticosteroids and antidepressants. Tolerance and withdrawal are not applicable criteria in the diagnosis of sedative-hypnotic use disorder when BZRAs are prescribed.28
Withdrawal. Reported prevalence of BZRA physiologic dependence differs according to populations studied, criteria used, and the deprescribing process employed. Some researchers have found rates of one-third and others exceeding one-half among individuals using BZRAs for longer than a month.23,29
Deprescribing BZRAs
Because benefits are limited and adverse outcomes including physiologic dependence are common, it is recommended that clinicians urge deprescribing of BZRAs for any patient taking them consistently for more than 1 month. Published deprescribing investigations and guidance are insufficient, heterogenous, and confusing. Still, some approaches can work well, and success rates as high as 80% have been achieved among the elderly, for example.35 Brief interventions such as providing individualized advice, support, and management are effective.36,37 Abrupt discontinuation is inappropriate and can be life threatening.38 Forced cessation is also inappropriate unless significant respiratory depression is identified.
The Ashton Manual is a useful guide, readable by patients. Proceed with tapering slowly at a rate led by the patient’s response.2,39 Avoid discrediting patients’ reports of unusual withdrawal symptoms, as this can lead to misdiagnosis (eg, somatic symptom disorder) or ineffective treatment (eg, addiction recovery approaches). Adding CBT to tapering improves outcomes, and adjunctive medications may be helpful, although not without their own problems.29 Consistent support of patients by others involved in treatment (prescriber, pharmacist, behavioral health specialists, peer coach, significant others) is essential. Complex challenges generally resolve through authentic listening and response but may require referral to others with necessary skills and experience. Complete cessation may take 12 to 18 months (or longer). Even if complete cessation is not possible, the least dose necessary can be achieved.
CORRESPONDENCE
Steven Wright, MD, 1975 Ashland Mine Road, Ashland, OR 97520; [email protected]
- Chandler A, Whittaker A, Williams N, et al. Mother’s little helper? Contrasting accounts of benzodiazepine and methadone use among drug-dependent parents in the UK. Drugs (Abingdon Engl). 2014;21:470-475. doi: 10.3109/09687637.2014.930814Ash
- ton CH. Benzodiazepines: How They Work & How to Withdraw (the Ashton Manual). 2002. Accessed March 17, 2022. www.benzoinfo.com/ashtonmanual/
- Maust DT, Lin LA, Blow FC. Benzodiazepine use and misuse among adults in the United States. Psychiatr Serv. 2019;70:97-106. doi: 10.1176/appi.ps.201800321
- Kaufmann CN, Spira AP, Depp CA, et al. Long-term use of benzodiazepines and non-benzodiazepine hypnotics from 1999 to 2014: results from the National Health and Nutrition Examination Survey. Psychiatr Serv. 2018;69:235-238. doi: 10.1176/appi.ps.201700095
- Walsh JK, Coulouvrat C, Hajak G, et al. Nighttime insomnia symptoms and perceived health in the America Insomnia Survey (AIS). Sleep. 2011;34:997-1011. doi: 10.5665/SLEEP.1150
- Holbrook AM, Crowther R, Lotter A, et al. Meta-analysis of benzodiazepine use in the treatment of insomnia. CMAJ. 2000;162:225-233.
- Huedo-Medina TB, Kirsch I, Middlemass J, et al. Effectiveness of non-benzodiazepine hypnotics in treatment of adult insomnia: meta-analysis of data submitted to the Food and Drug Administration. BMJ. 2012;345:e8343. doi: 10.1136/bmj.e8343
- Curran HV, Collins R, Fletcher S, et al. Older adults and withdrawal from benzodiazepine hypnotics in general practice: effects on cognitive function, sleep, mood and quality of life. Psychol Med. 2003;33:1223-1237. doi: 10.1017/s0033291703008213
- Geiger-Brown JM, Rogers VE, Liu W, et al. Cognitive behavioral therapy in persons with comorbid insomnia: a meta-analysis. Sleep Med Rev. 2015;23:54-67. doi: 10.1016/j.smrv.2014.11.007
- Sorscher AJ. Insomnia: getting to the cause, facilitating relief. J Fam Pract. 2017;66:216-225
- Laura Hrehová L, Mezian K. Non-pharmacologic treatment of insomnia in primary care settings. Int J Clin Pract. 2021;75:e14084. doi: 10.1111/ijcp.14084.
- Daly-Eichenhardt A, Scott W, Howard-Jones M, et al. Changes in sleep problems and psychological flexibility following interdisciplinary acceptance and commitment therapy for chronic pain: an observational cohort study. Front Psychol. 2016;7:1326. doi: 10.3389/fpsyg.2016.01326
- Rusch HL, Rosario M, Levison LM, et al. The effect of mindfulness meditation on sleep quality: a systematic review and meta-analysis of randomized controlled trials. Ann N Y Acad Sci. 2019;1445:5-16. doi: 10.1111/nyas.13996
- Cao H, Pan X, Li H, et al. Acupuncture for treatment of insomnia: a systematic review of randomized controlled trials. J Altern Complement Med. 2009;15:1171-1186. doi: 10.1089/acm.2009.0041
- Kessler RC, Petukhova M, Sampson NA, et al. Twelve‐month and lifetime prevalence and lifetime morbid risk of anxiety and mood disorders in the United States. Int J Methods Psychiatr Res. 2012;21:169-184. doi: 10.1002/mpr.1359
- Bandelow B, Reitt M, Röver C, et al. Efficacy of treatments for anxiety disorders: a meta-analysis. Int Clin Psychopharmacol. 2015;30:183-192. doi: 10.1097/YIC.0000000000000078
- Lader M. Benzodiazepines revisited—will we ever learn? Addiction. 2011;106:2086-2109. doi: 10.1111/j.1360-0443.2011.03563.x
- Fava GA. Fading of therapeutic effects of alprazolam in agoraphobia. Case reports. Prog Neuropsychopharmacol Biol Psychiatry. 1988;12:109-112. doi: 10.1016/0278-5846(88)90066-8
- Fava GA, Grandi S, Belluardo P, et al. Benzodiazepines and anxiety sensitivity in panic disorder. Prog Neuropsychopharmacol Biol Psychiatry. 1994;18:1163-1168. doi: 10.1016/0278-5846(94)90118-x
- Pélissolo A, Maniere F, Boutges B, et al. Anxiety and depressive disorders in 4,425 long term benzodiazepine users in general practice. Encephale. 2007;33:32-38. doi: 10.1016/s0013-7006(07)91556-0
- Gale C, Glue P, Guaiana G, et al. Influence of covariates on heterogeneity in Hamilton Anxiety Scale ratings in placebo-controlled trials of benzodiazepines in generalized anxiety disorder: systematic review and meta-analysis. J Psychopharmacol. 2019;33:543-547. doi: 10.1177/0269881118822146
- Ashton CH. Benzodiazepine withdrawal: outcome in 50 patients. Br J Addict. 1987;82:655-671. Accessed February 22, 2022. www.benzo.org.uk/ashbzoc.htm
- Rickels K, Schweizer E, Case WG, et al. Long-term therapeutic use of benzodiazepines. I. Effects of abrupt discontinuation. Arch Gen Psychiatry. 1990;47:899-907. doi: 10.1001/archpsyc.1990.01810220015002
- Bandelow B, Sher L, Bunevicius R, et al. Guidelines for the pharmacological treatment of anxiety disorders, obsessive-compulsive disorder and posttraumatic stress disorder in primary care. Int J Psychiatry Clin Pract. 2012;16:77-84. Accessed March 17, 2022. www.wfsbp.org/fileadmin/user_upload/Treatment_Guidelines/Bandelow_et_al_01.pdf
- Imai H, Tajika A, Chen P, et al. Psychological therapies versus pharmacological interventions for panic disorder with or without agoraphobia in adults. Cochrane Database Syst Rev. 2016;10:CD011170. doi: 10.1002/14651858.CD011170.pub2
- van Dis EAM, van Veen SC, Hagenaars MA, et al. Long-term outcomes of cognitive behavioral therapy for anxiety-related disorders. A systematic review and meta-analysis. JAMA Psychiatry. 2020;77:265-273. doi:10.1001/jamapsychiatry.2019.3986
- Chen LH, Hedegaard H, Warner M. Drug-poisoning deaths Involving opioid analgesics: United States, 1999-2011. NCHS Data Brief. 2014;(166):1-8. Accessed March 17, 2022. www.cdc.gov/nchs/data/databriefs/db166.pdf
- American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th edition (DSM-5). American Psychiatric Publishing; 2013:550-555.
- Marriott S, Tyrer P. Benzodiazepine dependence: avoidance and withdrawal. Drug Safety. 1993;9:93-103. doi: 10.2165/00002018-199309020-00003
- Griffiths RR, Evans SM, Guarino JJ, et al. Intravenous flumazenil following acute and repeated exposure to lorazepam in healthy volunteers: antagonism and precipitated withdrawal. J Pharmacol Exp Ther. 1993;265:1163-1174.
- Ashton H. Benzodiazepine withdrawal: an unfinished story. Br Med J. 1984;288:1135-1140. Accessed March 17, 2022. www.ncbi.nlm.nih.gov/pmc/articles/PMC1441411/pdf/bmjcred00496-0031.pdf
- Lugoboni F, Quaglio G. Exploring the dark side of the moon: the treatment of benzodiazepine tolerance. Br J Clin Pharmacol. 2014;77:239-41. doi: 10.1111/bcp.12148
- Ashton CH. Protracted withdrawal from benzodiazepines: the post-withdrawal syndrome. Psychiatr Ann. 1995;25:174-179. Accessed March 17, 2022. https://benzo.org.uk/pha-1.htm
- Fixsen AM, Ridge D. Stories of hell and healing: internet users’ construction of benzodiazepine distress and withdrawal. Qual Health Res. 2017;27:2030-2041. doi: 10.1177/1049732317728053
- Ng BJ, Le Couteur DG, Hilmer SN. Deprescribing benzodiazepines in older patients: impact of interventions targeting physicians, pharmacists, and patients. Drugs Aging. 2018;35:493-521. doi: 10.1007/s40266-018-0544-4
- Lynch T, Ryan C, Hughes CM, et al. Brief interventions targeting long-term benzodiazepine and Z-drug use in primary care: a systematic review and meta-analysis. Addiction. 2020;115:1618-1639. doi: 10.1111/add.14981
- Darker CD, Sweeney BP, Barry JM, et al. Psychosocial interventions for benzodiazepine harmful use, abuse or dependence. Cochrane Database Syst Rev. 2015;(5):CD009652. doi: 10.1002/14651858.CD009652.pub2
- Hu X. Benzodiazepine withdrawal seizures and management. J Okla State Med Assoc. 2011;104:62-65.
- Wright SL. Benzodiazepine withdrawal: clinical aspects. In Peppin J, Raffa R, Pergolizzi J, Wright SL, eds. The Benzodiazepines Crisis: The Ramifications of an Overused Drug Class. Oxford University Press. 2020:117-148.
- Chandler A, Whittaker A, Williams N, et al. Mother’s little helper? Contrasting accounts of benzodiazepine and methadone use among drug-dependent parents in the UK. Drugs (Abingdon Engl). 2014;21:470-475. doi: 10.3109/09687637.2014.930814Ash
- ton CH. Benzodiazepines: How They Work & How to Withdraw (the Ashton Manual). 2002. Accessed March 17, 2022. www.benzoinfo.com/ashtonmanual/
- Maust DT, Lin LA, Blow FC. Benzodiazepine use and misuse among adults in the United States. Psychiatr Serv. 2019;70:97-106. doi: 10.1176/appi.ps.201800321
- Kaufmann CN, Spira AP, Depp CA, et al. Long-term use of benzodiazepines and non-benzodiazepine hypnotics from 1999 to 2014: results from the National Health and Nutrition Examination Survey. Psychiatr Serv. 2018;69:235-238. doi: 10.1176/appi.ps.201700095
- Walsh JK, Coulouvrat C, Hajak G, et al. Nighttime insomnia symptoms and perceived health in the America Insomnia Survey (AIS). Sleep. 2011;34:997-1011. doi: 10.5665/SLEEP.1150
- Holbrook AM, Crowther R, Lotter A, et al. Meta-analysis of benzodiazepine use in the treatment of insomnia. CMAJ. 2000;162:225-233.
- Huedo-Medina TB, Kirsch I, Middlemass J, et al. Effectiveness of non-benzodiazepine hypnotics in treatment of adult insomnia: meta-analysis of data submitted to the Food and Drug Administration. BMJ. 2012;345:e8343. doi: 10.1136/bmj.e8343
- Curran HV, Collins R, Fletcher S, et al. Older adults and withdrawal from benzodiazepine hypnotics in general practice: effects on cognitive function, sleep, mood and quality of life. Psychol Med. 2003;33:1223-1237. doi: 10.1017/s0033291703008213
- Geiger-Brown JM, Rogers VE, Liu W, et al. Cognitive behavioral therapy in persons with comorbid insomnia: a meta-analysis. Sleep Med Rev. 2015;23:54-67. doi: 10.1016/j.smrv.2014.11.007
- Sorscher AJ. Insomnia: getting to the cause, facilitating relief. J Fam Pract. 2017;66:216-225
- Laura Hrehová L, Mezian K. Non-pharmacologic treatment of insomnia in primary care settings. Int J Clin Pract. 2021;75:e14084. doi: 10.1111/ijcp.14084.
- Daly-Eichenhardt A, Scott W, Howard-Jones M, et al. Changes in sleep problems and psychological flexibility following interdisciplinary acceptance and commitment therapy for chronic pain: an observational cohort study. Front Psychol. 2016;7:1326. doi: 10.3389/fpsyg.2016.01326
- Rusch HL, Rosario M, Levison LM, et al. The effect of mindfulness meditation on sleep quality: a systematic review and meta-analysis of randomized controlled trials. Ann N Y Acad Sci. 2019;1445:5-16. doi: 10.1111/nyas.13996
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PRACTICE RECOMMENDATIONS
› Recommend cognitive behavioral therapy as first-line treatment for anxiety and insomnia. A
› Limit benzodiazepine prescribing to ≤ 2 to 4 weeks for anxiety and insomnia. B
› Taper benzodiazepines slowly and flexibly. A
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
Study: Disparities shrink with aggressive depression screening
The study began soon after the U.S. Preventive Services Task Force recommended depression screening for all adults in 2016. The task force based this recommendation on evidence that people who are screened and treated experience fewer debilitating symptoms.
In the new research, the investigators analyzed electronic health record data following a rollout of a universal depression screening program at the University of California, San Francisco. The researchers found that the overall rate of depression screening doubled at six primary care practices over a little more than 2 years, reaching nearly 90%. The investigators presented the data April 9 at the Society of General Internal Medicine 2022 Annual Meeting in Orlando.
Meanwhile, screening disparities diminished for men, older individuals, racial and ethnic minorities, and people with language barriers – all groups that are undertreated for depression.
“It shows that if a health system is really invested, it can achieve really high depression screening,” primary investigator Maria Garcia, MD, MPH, co-director of UCSF’s Multiethnic Health Equity Research Center, told this news organization.
Methods for identifying depression
The health system assigned medical assistants to administer annual screening using a validated tool, the Patient Health Questionnaire-2 (PHQ-2). A “yes” response to either of its two questions triggered a longer questionnaire, the PHQ-9, used to diagnose and guide treatment.
Screening forms were available in multiple languages. Medical assistants received training on the importance of identifying depression in undertreated groups, and a banner was inserted in the electronic health record to indicate a screening was due, Dr. Garcia said.
During the rollout, a committee was assigned to monitor screening rates and adjust strategies to target disparities.
Dr. Garcia and fellow researchers calculated the likelihood of a patient being screened starting in September 2017 – when a field for depression screening status was added to the system’s electronic health record – until the rollout was completed on Dec. 31, 2019.
Screening disparities narrowed for all groups studied
The screening rate for patients who had a primary care visit increased from 40.5% to 88.8%. Early on, patients with language barriers were less likely to be screened than English-speaking White individuals (odds ratios, 0.55-0.59). Men were less likely to be screened than women (OR, 0.82; 95% confidence interval, 0.78-0.86), and the likelihood of being screened decreased as people got older. By 2019, screening disparities had narrowed for all groups and were only statistically significant for men (OR, 0.87; 95% CI, 0.81-0.93).
Ian Kronish, MD, MPH, a general internist and associate professor of medicine at Columbia University, New York, called the increases “impressive,” adding that the data show universal depression screening is possible in a system that serves a diverse population.
Dr. Kronish, who was not involved in this study, noted that other research indicates screening does not result in a significant reduction in depressive symptoms in the overall population. He found this to be the case in a trial he led, which focused on patients with recent cardiac events, for example.
“Given all the effort that is going into depression screening and the inclusion of depression screening as a quality metric, we need definitive randomized clinical trials testing whether depression screening leads to increased treatment uptake and, importantly, improved depressive symptoms and quality of life,” he said.
Dr. Garcia acknowledged that more work needs to be done to address treatment barriers, such as language and lack of insurance, and assess whether greater recognition of depressive symptoms in underserved groups can lead to effective treatment. “But this is an important step to know that universal depression screening narrowed disparities in screening over time,” she added.
Dr. Garcia and Dr. Kronish have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The study began soon after the U.S. Preventive Services Task Force recommended depression screening for all adults in 2016. The task force based this recommendation on evidence that people who are screened and treated experience fewer debilitating symptoms.
In the new research, the investigators analyzed electronic health record data following a rollout of a universal depression screening program at the University of California, San Francisco. The researchers found that the overall rate of depression screening doubled at six primary care practices over a little more than 2 years, reaching nearly 90%. The investigators presented the data April 9 at the Society of General Internal Medicine 2022 Annual Meeting in Orlando.
Meanwhile, screening disparities diminished for men, older individuals, racial and ethnic minorities, and people with language barriers – all groups that are undertreated for depression.
“It shows that if a health system is really invested, it can achieve really high depression screening,” primary investigator Maria Garcia, MD, MPH, co-director of UCSF’s Multiethnic Health Equity Research Center, told this news organization.
Methods for identifying depression
The health system assigned medical assistants to administer annual screening using a validated tool, the Patient Health Questionnaire-2 (PHQ-2). A “yes” response to either of its two questions triggered a longer questionnaire, the PHQ-9, used to diagnose and guide treatment.
Screening forms were available in multiple languages. Medical assistants received training on the importance of identifying depression in undertreated groups, and a banner was inserted in the electronic health record to indicate a screening was due, Dr. Garcia said.
During the rollout, a committee was assigned to monitor screening rates and adjust strategies to target disparities.
Dr. Garcia and fellow researchers calculated the likelihood of a patient being screened starting in September 2017 – when a field for depression screening status was added to the system’s electronic health record – until the rollout was completed on Dec. 31, 2019.
Screening disparities narrowed for all groups studied
The screening rate for patients who had a primary care visit increased from 40.5% to 88.8%. Early on, patients with language barriers were less likely to be screened than English-speaking White individuals (odds ratios, 0.55-0.59). Men were less likely to be screened than women (OR, 0.82; 95% confidence interval, 0.78-0.86), and the likelihood of being screened decreased as people got older. By 2019, screening disparities had narrowed for all groups and were only statistically significant for men (OR, 0.87; 95% CI, 0.81-0.93).
Ian Kronish, MD, MPH, a general internist and associate professor of medicine at Columbia University, New York, called the increases “impressive,” adding that the data show universal depression screening is possible in a system that serves a diverse population.
Dr. Kronish, who was not involved in this study, noted that other research indicates screening does not result in a significant reduction in depressive symptoms in the overall population. He found this to be the case in a trial he led, which focused on patients with recent cardiac events, for example.
“Given all the effort that is going into depression screening and the inclusion of depression screening as a quality metric, we need definitive randomized clinical trials testing whether depression screening leads to increased treatment uptake and, importantly, improved depressive symptoms and quality of life,” he said.
Dr. Garcia acknowledged that more work needs to be done to address treatment barriers, such as language and lack of insurance, and assess whether greater recognition of depressive symptoms in underserved groups can lead to effective treatment. “But this is an important step to know that universal depression screening narrowed disparities in screening over time,” she added.
Dr. Garcia and Dr. Kronish have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The study began soon after the U.S. Preventive Services Task Force recommended depression screening for all adults in 2016. The task force based this recommendation on evidence that people who are screened and treated experience fewer debilitating symptoms.
In the new research, the investigators analyzed electronic health record data following a rollout of a universal depression screening program at the University of California, San Francisco. The researchers found that the overall rate of depression screening doubled at six primary care practices over a little more than 2 years, reaching nearly 90%. The investigators presented the data April 9 at the Society of General Internal Medicine 2022 Annual Meeting in Orlando.
Meanwhile, screening disparities diminished for men, older individuals, racial and ethnic minorities, and people with language barriers – all groups that are undertreated for depression.
“It shows that if a health system is really invested, it can achieve really high depression screening,” primary investigator Maria Garcia, MD, MPH, co-director of UCSF’s Multiethnic Health Equity Research Center, told this news organization.
Methods for identifying depression
The health system assigned medical assistants to administer annual screening using a validated tool, the Patient Health Questionnaire-2 (PHQ-2). A “yes” response to either of its two questions triggered a longer questionnaire, the PHQ-9, used to diagnose and guide treatment.
Screening forms were available in multiple languages. Medical assistants received training on the importance of identifying depression in undertreated groups, and a banner was inserted in the electronic health record to indicate a screening was due, Dr. Garcia said.
During the rollout, a committee was assigned to monitor screening rates and adjust strategies to target disparities.
Dr. Garcia and fellow researchers calculated the likelihood of a patient being screened starting in September 2017 – when a field for depression screening status was added to the system’s electronic health record – until the rollout was completed on Dec. 31, 2019.
Screening disparities narrowed for all groups studied
The screening rate for patients who had a primary care visit increased from 40.5% to 88.8%. Early on, patients with language barriers were less likely to be screened than English-speaking White individuals (odds ratios, 0.55-0.59). Men were less likely to be screened than women (OR, 0.82; 95% confidence interval, 0.78-0.86), and the likelihood of being screened decreased as people got older. By 2019, screening disparities had narrowed for all groups and were only statistically significant for men (OR, 0.87; 95% CI, 0.81-0.93).
Ian Kronish, MD, MPH, a general internist and associate professor of medicine at Columbia University, New York, called the increases “impressive,” adding that the data show universal depression screening is possible in a system that serves a diverse population.
Dr. Kronish, who was not involved in this study, noted that other research indicates screening does not result in a significant reduction in depressive symptoms in the overall population. He found this to be the case in a trial he led, which focused on patients with recent cardiac events, for example.
“Given all the effort that is going into depression screening and the inclusion of depression screening as a quality metric, we need definitive randomized clinical trials testing whether depression screening leads to increased treatment uptake and, importantly, improved depressive symptoms and quality of life,” he said.
Dr. Garcia acknowledged that more work needs to be done to address treatment barriers, such as language and lack of insurance, and assess whether greater recognition of depressive symptoms in underserved groups can lead to effective treatment. “But this is an important step to know that universal depression screening narrowed disparities in screening over time,” she added.
Dr. Garcia and Dr. Kronish have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM SGIM 2022

