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Six healthy lifestyle habits linked to slowed memory decline
Investigators found that a healthy diet, cognitive activity, regular physical exercise, not smoking, and abstaining from alcohol were significantly linked to slowed cognitive decline irrespective of APOE4 status.
After adjusting for health and socioeconomic factors, investigators found that each individual healthy behavior was associated with a slower-than-average decline in memory over a decade. A healthy diet emerged as the strongest deterrent, followed by cognitive activity and physical exercise.
“A healthy lifestyle is associated with slower memory decline, even in the presence of the APOE4 allele,” study investigators led by Jianping Jia, MD, PhD, of the Innovation Center for Neurological Disorders and the department of neurology, Xuan Wu Hospital, Capital Medical University, Beijing, write.
“This study might offer important information to protect older adults against memory decline,” they add.
The study was published online in the BMJ.
Preventing memory decline
Memory “continuously declines as people age,” but age-related memory decline is not necessarily a prodrome of dementia and can “merely be senescent forgetfulness,” the investigators note. This can be “reversed or [can] become stable,” instead of progressing to a pathologic state.
Factors affecting memory include aging, APOE4 genotype, chronic diseases, and lifestyle patterns, with lifestyle “receiving increasing attention as a modifiable behavior.”
Nevertheless, few studies have focused on the impact of lifestyle on memory, and those that have are mostly cross-sectional and also “did not consider the interaction between a healthy lifestyle and genetic risk,” the researchers note.
To investigate, the researchers conducted a longitudinal study, known as the China Cognition and Aging Study, that considered genetic risk as well as lifestyle factors.
The study began in 2009 and concluded in 2019. Participants were evaluated and underwent neuropsychological testing in 2012, 2014, 2016, and at the study’s conclusion.
Participants (n = 29,072; mean [SD] age, 72.23 [6.61] years; 48.54% women; 20.43% APOE4 carriers) were required to have normal cognitive function at baseline. Data on those whose condition progressed to mild cognitive impairment (MCI) or dementia during the follow-up period were excluded after their diagnosis.
The Mini–Mental State Examination was used to assess global cognitive function. Memory function was assessed using the World Health Organization/University of California, Los Angeles Auditory Verbal Learning Test.
“Lifestyle” consisted of six modifiable factors: physical exercise (weekly frequency and total time), smoking (current, former, or never-smokers), alcohol consumption (never drank, drank occasionally, low to excess drinking, and heavy drinking), diet (daily intake of 12 food items: fruits, vegetables, fish, meat, dairy products, salt, oil, eggs, cereals, legumes, nuts, tea), cognitive activity (writing, reading, playing cards, mahjong, other games), and social contact (participating in meetings, attending parties, visiting friends/relatives, traveling, chatting online).
Participants’ lifestyles were scored on the basis of the number of healthy factors they engaged in.
Participants were also stratified by APOE genotype into APOE4 carriers and noncarriers.
Demographic and other items of health information, including the presence of medical illness, were used as covariates. The researchers also included the “learning effect of each participant as a covariate, due to repeated cognitive assessments.”
Important for public health
During the 10-year period, 7,164 participants died, and 3,567 stopped participating.
Participants in the favorable and average groups showed slower memory decline per increased year of age (0.007 [0.005-0.009], P < .001; and 0.002 [0 .000-0.003], P = .033 points higher, respectively), compared with those in the unfavorable group.
Healthy diet had the strongest protective effect on memory.
Memory decline occurred faster in APOE4 vesus non-APOE4 carriers (0.002 points/year [95% confidence interval, 0.001-0.003]; P = .007).
But APOE4 carriers with favorable and average lifestyles showed slower memory decline (0.027 [0.023-0.031] and 0.014 [0.010-0.019], respectively), compared with those with unfavorable lifestyles. Similar findings were obtained in non-APOE4 carriers.
Those with favorable or average lifestyle were respectively almost 90% and 30% less likely to develop dementia or MCI, compared with those with an unfavorable lifestyle.
The authors acknowledge the study’s limitations, including its observational design and the potential for measurement errors, owing to self-reporting of lifestyle factors. Additionally, some participants did not return for follow-up evaluations, leading to potential selection bias.
Nevertheless, the findings “might offer important information for public health to protect older [people] against memory decline,” they note – especially since the study “provides evidence that these effects also include individuals with the APOE4 allele.”
‘Important, encouraging’ research
In a comment, Severine Sabia, PhD, a senior researcher at the Université Paris Cité, INSERM Institut National de la Santé et de la Recherche Medicalé, France, called the findings “important and encouraging.”
However, said Dr. Sabia, who was not involved with the study, “there remain important research questions that need to be investigated in order to identify key behaviors: which combination, the cutoff of risk, and when to intervene.”
Future research on prevention “should examine a wider range of possible risk factors” and should also “identify specific exposures associated with the greatest risk, while also considering the risk threshold and age at exposure for each one.”
In an accompanying editorial, Dr. Sabia and co-author Archana Singh-Manoux, PhD, note that the risk of cognitive decline and dementia are probably determined by multiple factors.
They liken it to the “multifactorial risk paradigm introduced by the Framingham study,” which has “led to a substantial reduction in cardiovascular disease.” A similar approach could be used with dementia prevention, they suggest.
The authors received support from the Xuanwu Hospital of Capital Medical University for the submitted work. One of the authors received a grant from the French National Research Agency. The other authors have disclosed no relevant financial relationships. Dr. Sabia received grant funding from the French National Research Agency. Dr. Singh-Manoux received grants from the National Institute on Aging of the National Institutes of Health.
A version of this article first appeared on Medscape.com.
Investigators found that a healthy diet, cognitive activity, regular physical exercise, not smoking, and abstaining from alcohol were significantly linked to slowed cognitive decline irrespective of APOE4 status.
After adjusting for health and socioeconomic factors, investigators found that each individual healthy behavior was associated with a slower-than-average decline in memory over a decade. A healthy diet emerged as the strongest deterrent, followed by cognitive activity and physical exercise.
“A healthy lifestyle is associated with slower memory decline, even in the presence of the APOE4 allele,” study investigators led by Jianping Jia, MD, PhD, of the Innovation Center for Neurological Disorders and the department of neurology, Xuan Wu Hospital, Capital Medical University, Beijing, write.
“This study might offer important information to protect older adults against memory decline,” they add.
The study was published online in the BMJ.
Preventing memory decline
Memory “continuously declines as people age,” but age-related memory decline is not necessarily a prodrome of dementia and can “merely be senescent forgetfulness,” the investigators note. This can be “reversed or [can] become stable,” instead of progressing to a pathologic state.
Factors affecting memory include aging, APOE4 genotype, chronic diseases, and lifestyle patterns, with lifestyle “receiving increasing attention as a modifiable behavior.”
Nevertheless, few studies have focused on the impact of lifestyle on memory, and those that have are mostly cross-sectional and also “did not consider the interaction between a healthy lifestyle and genetic risk,” the researchers note.
To investigate, the researchers conducted a longitudinal study, known as the China Cognition and Aging Study, that considered genetic risk as well as lifestyle factors.
The study began in 2009 and concluded in 2019. Participants were evaluated and underwent neuropsychological testing in 2012, 2014, 2016, and at the study’s conclusion.
Participants (n = 29,072; mean [SD] age, 72.23 [6.61] years; 48.54% women; 20.43% APOE4 carriers) were required to have normal cognitive function at baseline. Data on those whose condition progressed to mild cognitive impairment (MCI) or dementia during the follow-up period were excluded after their diagnosis.
The Mini–Mental State Examination was used to assess global cognitive function. Memory function was assessed using the World Health Organization/University of California, Los Angeles Auditory Verbal Learning Test.
“Lifestyle” consisted of six modifiable factors: physical exercise (weekly frequency and total time), smoking (current, former, or never-smokers), alcohol consumption (never drank, drank occasionally, low to excess drinking, and heavy drinking), diet (daily intake of 12 food items: fruits, vegetables, fish, meat, dairy products, salt, oil, eggs, cereals, legumes, nuts, tea), cognitive activity (writing, reading, playing cards, mahjong, other games), and social contact (participating in meetings, attending parties, visiting friends/relatives, traveling, chatting online).
Participants’ lifestyles were scored on the basis of the number of healthy factors they engaged in.
Participants were also stratified by APOE genotype into APOE4 carriers and noncarriers.
Demographic and other items of health information, including the presence of medical illness, were used as covariates. The researchers also included the “learning effect of each participant as a covariate, due to repeated cognitive assessments.”
Important for public health
During the 10-year period, 7,164 participants died, and 3,567 stopped participating.
Participants in the favorable and average groups showed slower memory decline per increased year of age (0.007 [0.005-0.009], P < .001; and 0.002 [0 .000-0.003], P = .033 points higher, respectively), compared with those in the unfavorable group.
Healthy diet had the strongest protective effect on memory.
Memory decline occurred faster in APOE4 vesus non-APOE4 carriers (0.002 points/year [95% confidence interval, 0.001-0.003]; P = .007).
But APOE4 carriers with favorable and average lifestyles showed slower memory decline (0.027 [0.023-0.031] and 0.014 [0.010-0.019], respectively), compared with those with unfavorable lifestyles. Similar findings were obtained in non-APOE4 carriers.
Those with favorable or average lifestyle were respectively almost 90% and 30% less likely to develop dementia or MCI, compared with those with an unfavorable lifestyle.
The authors acknowledge the study’s limitations, including its observational design and the potential for measurement errors, owing to self-reporting of lifestyle factors. Additionally, some participants did not return for follow-up evaluations, leading to potential selection bias.
Nevertheless, the findings “might offer important information for public health to protect older [people] against memory decline,” they note – especially since the study “provides evidence that these effects also include individuals with the APOE4 allele.”
‘Important, encouraging’ research
In a comment, Severine Sabia, PhD, a senior researcher at the Université Paris Cité, INSERM Institut National de la Santé et de la Recherche Medicalé, France, called the findings “important and encouraging.”
However, said Dr. Sabia, who was not involved with the study, “there remain important research questions that need to be investigated in order to identify key behaviors: which combination, the cutoff of risk, and when to intervene.”
Future research on prevention “should examine a wider range of possible risk factors” and should also “identify specific exposures associated with the greatest risk, while also considering the risk threshold and age at exposure for each one.”
In an accompanying editorial, Dr. Sabia and co-author Archana Singh-Manoux, PhD, note that the risk of cognitive decline and dementia are probably determined by multiple factors.
They liken it to the “multifactorial risk paradigm introduced by the Framingham study,” which has “led to a substantial reduction in cardiovascular disease.” A similar approach could be used with dementia prevention, they suggest.
The authors received support from the Xuanwu Hospital of Capital Medical University for the submitted work. One of the authors received a grant from the French National Research Agency. The other authors have disclosed no relevant financial relationships. Dr. Sabia received grant funding from the French National Research Agency. Dr. Singh-Manoux received grants from the National Institute on Aging of the National Institutes of Health.
A version of this article first appeared on Medscape.com.
Investigators found that a healthy diet, cognitive activity, regular physical exercise, not smoking, and abstaining from alcohol were significantly linked to slowed cognitive decline irrespective of APOE4 status.
After adjusting for health and socioeconomic factors, investigators found that each individual healthy behavior was associated with a slower-than-average decline in memory over a decade. A healthy diet emerged as the strongest deterrent, followed by cognitive activity and physical exercise.
“A healthy lifestyle is associated with slower memory decline, even in the presence of the APOE4 allele,” study investigators led by Jianping Jia, MD, PhD, of the Innovation Center for Neurological Disorders and the department of neurology, Xuan Wu Hospital, Capital Medical University, Beijing, write.
“This study might offer important information to protect older adults against memory decline,” they add.
The study was published online in the BMJ.
Preventing memory decline
Memory “continuously declines as people age,” but age-related memory decline is not necessarily a prodrome of dementia and can “merely be senescent forgetfulness,” the investigators note. This can be “reversed or [can] become stable,” instead of progressing to a pathologic state.
Factors affecting memory include aging, APOE4 genotype, chronic diseases, and lifestyle patterns, with lifestyle “receiving increasing attention as a modifiable behavior.”
Nevertheless, few studies have focused on the impact of lifestyle on memory, and those that have are mostly cross-sectional and also “did not consider the interaction between a healthy lifestyle and genetic risk,” the researchers note.
To investigate, the researchers conducted a longitudinal study, known as the China Cognition and Aging Study, that considered genetic risk as well as lifestyle factors.
The study began in 2009 and concluded in 2019. Participants were evaluated and underwent neuropsychological testing in 2012, 2014, 2016, and at the study’s conclusion.
Participants (n = 29,072; mean [SD] age, 72.23 [6.61] years; 48.54% women; 20.43% APOE4 carriers) were required to have normal cognitive function at baseline. Data on those whose condition progressed to mild cognitive impairment (MCI) or dementia during the follow-up period were excluded after their diagnosis.
The Mini–Mental State Examination was used to assess global cognitive function. Memory function was assessed using the World Health Organization/University of California, Los Angeles Auditory Verbal Learning Test.
“Lifestyle” consisted of six modifiable factors: physical exercise (weekly frequency and total time), smoking (current, former, or never-smokers), alcohol consumption (never drank, drank occasionally, low to excess drinking, and heavy drinking), diet (daily intake of 12 food items: fruits, vegetables, fish, meat, dairy products, salt, oil, eggs, cereals, legumes, nuts, tea), cognitive activity (writing, reading, playing cards, mahjong, other games), and social contact (participating in meetings, attending parties, visiting friends/relatives, traveling, chatting online).
Participants’ lifestyles were scored on the basis of the number of healthy factors they engaged in.
Participants were also stratified by APOE genotype into APOE4 carriers and noncarriers.
Demographic and other items of health information, including the presence of medical illness, were used as covariates. The researchers also included the “learning effect of each participant as a covariate, due to repeated cognitive assessments.”
Important for public health
During the 10-year period, 7,164 participants died, and 3,567 stopped participating.
Participants in the favorable and average groups showed slower memory decline per increased year of age (0.007 [0.005-0.009], P < .001; and 0.002 [0 .000-0.003], P = .033 points higher, respectively), compared with those in the unfavorable group.
Healthy diet had the strongest protective effect on memory.
Memory decline occurred faster in APOE4 vesus non-APOE4 carriers (0.002 points/year [95% confidence interval, 0.001-0.003]; P = .007).
But APOE4 carriers with favorable and average lifestyles showed slower memory decline (0.027 [0.023-0.031] and 0.014 [0.010-0.019], respectively), compared with those with unfavorable lifestyles. Similar findings were obtained in non-APOE4 carriers.
Those with favorable or average lifestyle were respectively almost 90% and 30% less likely to develop dementia or MCI, compared with those with an unfavorable lifestyle.
The authors acknowledge the study’s limitations, including its observational design and the potential for measurement errors, owing to self-reporting of lifestyle factors. Additionally, some participants did not return for follow-up evaluations, leading to potential selection bias.
Nevertheless, the findings “might offer important information for public health to protect older [people] against memory decline,” they note – especially since the study “provides evidence that these effects also include individuals with the APOE4 allele.”
‘Important, encouraging’ research
In a comment, Severine Sabia, PhD, a senior researcher at the Université Paris Cité, INSERM Institut National de la Santé et de la Recherche Medicalé, France, called the findings “important and encouraging.”
However, said Dr. Sabia, who was not involved with the study, “there remain important research questions that need to be investigated in order to identify key behaviors: which combination, the cutoff of risk, and when to intervene.”
Future research on prevention “should examine a wider range of possible risk factors” and should also “identify specific exposures associated with the greatest risk, while also considering the risk threshold and age at exposure for each one.”
In an accompanying editorial, Dr. Sabia and co-author Archana Singh-Manoux, PhD, note that the risk of cognitive decline and dementia are probably determined by multiple factors.
They liken it to the “multifactorial risk paradigm introduced by the Framingham study,” which has “led to a substantial reduction in cardiovascular disease.” A similar approach could be used with dementia prevention, they suggest.
The authors received support from the Xuanwu Hospital of Capital Medical University for the submitted work. One of the authors received a grant from the French National Research Agency. The other authors have disclosed no relevant financial relationships. Dr. Sabia received grant funding from the French National Research Agency. Dr. Singh-Manoux received grants from the National Institute on Aging of the National Institutes of Health.
A version of this article first appeared on Medscape.com.
FROM THE BMJ
Even one head injury boosts all-cause mortality risk
An analysis of more than 13,000 adult participants in the Atherosclerosis Risk in Communities (ARIC) study showed a dose-response pattern in which one head injury was linked to a 66% increased risk for all-cause mortality, and two or more head injuries were associated with twice the risk in comparison with no head injuries.
These findings underscore the importance of preventing head injuries and of swift clinical intervention once a head injury occurs, lead author Holly Elser, MD, PhD, department of neurology, Hospital of the University of Pennsylvania, Philadelphia, told this news organization.
“Clinicians should counsel patients who are at risk for falls about head injuries and ensure patients are promptly evaluated in the hospital setting if they do have a fall – especially with loss of consciousness or other symptoms, such as headache or dizziness,” Dr. Elser added.
The findings were published online in JAMA Neurology.
Consistent evidence
There is “pretty consistent evidence” that mortality rates are increased in the short term after head injury, predominantly among hospitalized patients, Dr. Elser noted.
“But there’s less evidence about the long-term mortality implications of head injuries and less evidence from adults living in the community,” she added.
The analysis included 13,037 participants in the ARIC study, an ongoing study involving adults aged 45-65 years who were recruited from four geographically and racially diverse U.S. communities. The mean age at baseline (1987-1989) was 54 years; 57.7% were women; and 27.9% were Black.
Study participants are followed at routine in-person visits and semiannually via telephone.
Data on head injuries came from hospital diagnostic codes and self-reports. These reports included information on the number of injuries and whether the injury required medical care and involved loss of consciousness.
During the 27-year follow-up, 18.4% of the study sample had at least one head injury. Injuries occurred more frequently among women, which may reflect the predominance of women in the study population, said Dr. Elser.
Overall, about 56% of participants died during the study period. The estimated median amount of survival time after head injury was 4.7 years.
The most common causes of death were neoplasm, cardiovascular disease, and neurologic disorders. Regarding specific neurologic causes of death, the researchers found that 62.2% of deaths were due to neurodegenerative disease among individuals with head injury, vs. 51.4% among those without head injury.
This, said Dr. Elser, raises the possibility of reverse causality. “If you have a neurodegenerative disorder like Alzheimer’s disease dementia or Parkinson’s disease that leads to difficulty walking, you may be more likely to fall and have a head injury. The head injury in turn may lead to increased mortality,” she noted.
However, she stressed that the data on cause-specific mortality are exploratory. “Our research motivates future studies that really examine this time-dependent relationship between neurodegenerative disease and head injuries,” Dr. Elser said.
Dose-dependent response
In the unadjusted analysis, the hazard ratio of mortality among individuals with head injury was 2.21 (95% confidence interval, 2.09-2.34) compared with those who did not have head injury.
The association remained significant with adjustment for sociodemographic factors (HR, 1.99; 95% CI, 1.88-2.11) and with additional adjustment for vascular risk factors (HR, 1.92; 95% CI, 1.81-2.03).
The findings also showed a dose-response pattern in the association of head injuries with mortality. Compared with participants who did not have head injury, the HR was 1.66 (95% CI, 1.56-1.77) for those with one head injury and 2.11 (95% CI, 1.89-2.37) for those with two or more head injuries.
“It’s not as though once you’ve had one head injury, you’ve accrued all the damage you possibly can. We see pretty clearly here that recurrent head injury further increased the rate of deaths from all causes,” said Dr. Elser.
Injury severity was determined from hospital diagnostic codes using established algorithms. Results showed that mortality rates were increased with even mild head injury.
Interestingly, the association between head injury and all-cause mortality was weaker among those whose injuries were self-reported. One possibility is that these injuries were less severe, Dr. Elser noted.
“If you have head injury that’s mild enough that you don’t need to go to the hospital, it’s probably going to confer less long-term health risks than one that’s severe enough that you needed to be examined in an acute care setting,” she said.
Results were similar by race and for sex. “Even though there were more women with head injuries, the rate of mortality associated with head injury doesn’t differ from the rate among men,” Dr. Elser reported.
However, the association was stronger among those younger than 54 years at baseline (HR, 2.26) compared with older individuals (HR, 2.0) in the model that adjusted for demographics and lifestyle factors.
This may be explained by the reference group (those without a head injury) – the mortality rate was in general higher for the older participants, said Dr. Elser. It could also be that younger adults are more likely to have severe head injuries from, for example, motor vehicle accidents or violence, she added.
These new findings underscore the importance of public health measures, such as seatbelt laws, to reduce head injuries, the investigators note.
They add that clinicians with patients at risk for head injuries may recommend steps to lessen the risk of falls, such as having access to durable medical equipment, and ensuring driver safety.
Shorter life span
Commenting for this news organization, Frank Conidi, MD, director of the Florida Center for Headache and Sports Neurology in Port St. Lucie and past president of the Florida Society of Neurology, said the large number of participants “adds validity” to the finding that individuals with head injury are likely to have a shorter life span than those who do not suffer head trauma – and that this “was not purely by chance or from other causes.”
However, patients may not have accurately reported head injuries, in which case the rate of injury in the self-report subgroup would not reflect the actual incidence, noted Dr. Conidi, who was not involved with the research.
“In my practice, most patients have little knowledge as to the signs and symptoms of concussion and traumatic brain injury. Most think there needs to be some form of loss of consciousness to have a head injury, which is of course not true,” he said.
Dr. Conidi added that the finding of a higher incidence of death from neurodegenerative disorders supports the generally accepted consensus view that about 30% of patients with traumatic brain injury experience progression of symptoms and are at risk for early dementia.
The ARIC study is supported by the National Heart, Lung, and Blood Institute. Dr. Elser and Dr. Conidi have reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
An analysis of more than 13,000 adult participants in the Atherosclerosis Risk in Communities (ARIC) study showed a dose-response pattern in which one head injury was linked to a 66% increased risk for all-cause mortality, and two or more head injuries were associated with twice the risk in comparison with no head injuries.
These findings underscore the importance of preventing head injuries and of swift clinical intervention once a head injury occurs, lead author Holly Elser, MD, PhD, department of neurology, Hospital of the University of Pennsylvania, Philadelphia, told this news organization.
“Clinicians should counsel patients who are at risk for falls about head injuries and ensure patients are promptly evaluated in the hospital setting if they do have a fall – especially with loss of consciousness or other symptoms, such as headache or dizziness,” Dr. Elser added.
The findings were published online in JAMA Neurology.
Consistent evidence
There is “pretty consistent evidence” that mortality rates are increased in the short term after head injury, predominantly among hospitalized patients, Dr. Elser noted.
“But there’s less evidence about the long-term mortality implications of head injuries and less evidence from adults living in the community,” she added.
The analysis included 13,037 participants in the ARIC study, an ongoing study involving adults aged 45-65 years who were recruited from four geographically and racially diverse U.S. communities. The mean age at baseline (1987-1989) was 54 years; 57.7% were women; and 27.9% were Black.
Study participants are followed at routine in-person visits and semiannually via telephone.
Data on head injuries came from hospital diagnostic codes and self-reports. These reports included information on the number of injuries and whether the injury required medical care and involved loss of consciousness.
During the 27-year follow-up, 18.4% of the study sample had at least one head injury. Injuries occurred more frequently among women, which may reflect the predominance of women in the study population, said Dr. Elser.
Overall, about 56% of participants died during the study period. The estimated median amount of survival time after head injury was 4.7 years.
The most common causes of death were neoplasm, cardiovascular disease, and neurologic disorders. Regarding specific neurologic causes of death, the researchers found that 62.2% of deaths were due to neurodegenerative disease among individuals with head injury, vs. 51.4% among those without head injury.
This, said Dr. Elser, raises the possibility of reverse causality. “If you have a neurodegenerative disorder like Alzheimer’s disease dementia or Parkinson’s disease that leads to difficulty walking, you may be more likely to fall and have a head injury. The head injury in turn may lead to increased mortality,” she noted.
However, she stressed that the data on cause-specific mortality are exploratory. “Our research motivates future studies that really examine this time-dependent relationship between neurodegenerative disease and head injuries,” Dr. Elser said.
Dose-dependent response
In the unadjusted analysis, the hazard ratio of mortality among individuals with head injury was 2.21 (95% confidence interval, 2.09-2.34) compared with those who did not have head injury.
The association remained significant with adjustment for sociodemographic factors (HR, 1.99; 95% CI, 1.88-2.11) and with additional adjustment for vascular risk factors (HR, 1.92; 95% CI, 1.81-2.03).
The findings also showed a dose-response pattern in the association of head injuries with mortality. Compared with participants who did not have head injury, the HR was 1.66 (95% CI, 1.56-1.77) for those with one head injury and 2.11 (95% CI, 1.89-2.37) for those with two or more head injuries.
“It’s not as though once you’ve had one head injury, you’ve accrued all the damage you possibly can. We see pretty clearly here that recurrent head injury further increased the rate of deaths from all causes,” said Dr. Elser.
Injury severity was determined from hospital diagnostic codes using established algorithms. Results showed that mortality rates were increased with even mild head injury.
Interestingly, the association between head injury and all-cause mortality was weaker among those whose injuries were self-reported. One possibility is that these injuries were less severe, Dr. Elser noted.
“If you have head injury that’s mild enough that you don’t need to go to the hospital, it’s probably going to confer less long-term health risks than one that’s severe enough that you needed to be examined in an acute care setting,” she said.
Results were similar by race and for sex. “Even though there were more women with head injuries, the rate of mortality associated with head injury doesn’t differ from the rate among men,” Dr. Elser reported.
However, the association was stronger among those younger than 54 years at baseline (HR, 2.26) compared with older individuals (HR, 2.0) in the model that adjusted for demographics and lifestyle factors.
This may be explained by the reference group (those without a head injury) – the mortality rate was in general higher for the older participants, said Dr. Elser. It could also be that younger adults are more likely to have severe head injuries from, for example, motor vehicle accidents or violence, she added.
These new findings underscore the importance of public health measures, such as seatbelt laws, to reduce head injuries, the investigators note.
They add that clinicians with patients at risk for head injuries may recommend steps to lessen the risk of falls, such as having access to durable medical equipment, and ensuring driver safety.
Shorter life span
Commenting for this news organization, Frank Conidi, MD, director of the Florida Center for Headache and Sports Neurology in Port St. Lucie and past president of the Florida Society of Neurology, said the large number of participants “adds validity” to the finding that individuals with head injury are likely to have a shorter life span than those who do not suffer head trauma – and that this “was not purely by chance or from other causes.”
However, patients may not have accurately reported head injuries, in which case the rate of injury in the self-report subgroup would not reflect the actual incidence, noted Dr. Conidi, who was not involved with the research.
“In my practice, most patients have little knowledge as to the signs and symptoms of concussion and traumatic brain injury. Most think there needs to be some form of loss of consciousness to have a head injury, which is of course not true,” he said.
Dr. Conidi added that the finding of a higher incidence of death from neurodegenerative disorders supports the generally accepted consensus view that about 30% of patients with traumatic brain injury experience progression of symptoms and are at risk for early dementia.
The ARIC study is supported by the National Heart, Lung, and Blood Institute. Dr. Elser and Dr. Conidi have reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
An analysis of more than 13,000 adult participants in the Atherosclerosis Risk in Communities (ARIC) study showed a dose-response pattern in which one head injury was linked to a 66% increased risk for all-cause mortality, and two or more head injuries were associated with twice the risk in comparison with no head injuries.
These findings underscore the importance of preventing head injuries and of swift clinical intervention once a head injury occurs, lead author Holly Elser, MD, PhD, department of neurology, Hospital of the University of Pennsylvania, Philadelphia, told this news organization.
“Clinicians should counsel patients who are at risk for falls about head injuries and ensure patients are promptly evaluated in the hospital setting if they do have a fall – especially with loss of consciousness or other symptoms, such as headache or dizziness,” Dr. Elser added.
The findings were published online in JAMA Neurology.
Consistent evidence
There is “pretty consistent evidence” that mortality rates are increased in the short term after head injury, predominantly among hospitalized patients, Dr. Elser noted.
“But there’s less evidence about the long-term mortality implications of head injuries and less evidence from adults living in the community,” she added.
The analysis included 13,037 participants in the ARIC study, an ongoing study involving adults aged 45-65 years who were recruited from four geographically and racially diverse U.S. communities. The mean age at baseline (1987-1989) was 54 years; 57.7% were women; and 27.9% were Black.
Study participants are followed at routine in-person visits and semiannually via telephone.
Data on head injuries came from hospital diagnostic codes and self-reports. These reports included information on the number of injuries and whether the injury required medical care and involved loss of consciousness.
During the 27-year follow-up, 18.4% of the study sample had at least one head injury. Injuries occurred more frequently among women, which may reflect the predominance of women in the study population, said Dr. Elser.
Overall, about 56% of participants died during the study period. The estimated median amount of survival time after head injury was 4.7 years.
The most common causes of death were neoplasm, cardiovascular disease, and neurologic disorders. Regarding specific neurologic causes of death, the researchers found that 62.2% of deaths were due to neurodegenerative disease among individuals with head injury, vs. 51.4% among those without head injury.
This, said Dr. Elser, raises the possibility of reverse causality. “If you have a neurodegenerative disorder like Alzheimer’s disease dementia or Parkinson’s disease that leads to difficulty walking, you may be more likely to fall and have a head injury. The head injury in turn may lead to increased mortality,” she noted.
However, she stressed that the data on cause-specific mortality are exploratory. “Our research motivates future studies that really examine this time-dependent relationship between neurodegenerative disease and head injuries,” Dr. Elser said.
Dose-dependent response
In the unadjusted analysis, the hazard ratio of mortality among individuals with head injury was 2.21 (95% confidence interval, 2.09-2.34) compared with those who did not have head injury.
The association remained significant with adjustment for sociodemographic factors (HR, 1.99; 95% CI, 1.88-2.11) and with additional adjustment for vascular risk factors (HR, 1.92; 95% CI, 1.81-2.03).
The findings also showed a dose-response pattern in the association of head injuries with mortality. Compared with participants who did not have head injury, the HR was 1.66 (95% CI, 1.56-1.77) for those with one head injury and 2.11 (95% CI, 1.89-2.37) for those with two or more head injuries.
“It’s not as though once you’ve had one head injury, you’ve accrued all the damage you possibly can. We see pretty clearly here that recurrent head injury further increased the rate of deaths from all causes,” said Dr. Elser.
Injury severity was determined from hospital diagnostic codes using established algorithms. Results showed that mortality rates were increased with even mild head injury.
Interestingly, the association between head injury and all-cause mortality was weaker among those whose injuries were self-reported. One possibility is that these injuries were less severe, Dr. Elser noted.
“If you have head injury that’s mild enough that you don’t need to go to the hospital, it’s probably going to confer less long-term health risks than one that’s severe enough that you needed to be examined in an acute care setting,” she said.
Results were similar by race and for sex. “Even though there were more women with head injuries, the rate of mortality associated with head injury doesn’t differ from the rate among men,” Dr. Elser reported.
However, the association was stronger among those younger than 54 years at baseline (HR, 2.26) compared with older individuals (HR, 2.0) in the model that adjusted for demographics and lifestyle factors.
This may be explained by the reference group (those without a head injury) – the mortality rate was in general higher for the older participants, said Dr. Elser. It could also be that younger adults are more likely to have severe head injuries from, for example, motor vehicle accidents or violence, she added.
These new findings underscore the importance of public health measures, such as seatbelt laws, to reduce head injuries, the investigators note.
They add that clinicians with patients at risk for head injuries may recommend steps to lessen the risk of falls, such as having access to durable medical equipment, and ensuring driver safety.
Shorter life span
Commenting for this news organization, Frank Conidi, MD, director of the Florida Center for Headache and Sports Neurology in Port St. Lucie and past president of the Florida Society of Neurology, said the large number of participants “adds validity” to the finding that individuals with head injury are likely to have a shorter life span than those who do not suffer head trauma – and that this “was not purely by chance or from other causes.”
However, patients may not have accurately reported head injuries, in which case the rate of injury in the self-report subgroup would not reflect the actual incidence, noted Dr. Conidi, who was not involved with the research.
“In my practice, most patients have little knowledge as to the signs and symptoms of concussion and traumatic brain injury. Most think there needs to be some form of loss of consciousness to have a head injury, which is of course not true,” he said.
Dr. Conidi added that the finding of a higher incidence of death from neurodegenerative disorders supports the generally accepted consensus view that about 30% of patients with traumatic brain injury experience progression of symptoms and are at risk for early dementia.
The ARIC study is supported by the National Heart, Lung, and Blood Institute. Dr. Elser and Dr. Conidi have reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
FROM JAMA NEUROLOGY
Tips and tools to help you manage ADHD in children, adolescents
THE CASE
James B* is a 7-year-old Black child who presented to his primary care physician (PCP) for a well-child visit. During preventive health screening, James’ mother expressed concerns about his behavior, characterizing him as immature, aggressive, destructive, and occasionally self-loathing. She described him as physically uncoordinated, struggling to keep up with his peers in sports, and tiring after 20 minutes of activity. James slept 10 hours nightly but was often restless and snored intermittently. As a second grader, his academic achievement was not progressing, and he had become increasingly inattentive at home and at school. James’ mother offered several examples of his fighting with his siblings, noncompliance with morning routines, and avoidance of learning activities. Additionally, his mother expressed concern that James, as a Black child, might eventually be unfairly labeled as a problem child by his teachers or held back a grade level in school.
Although James did not have a family history of developmental delays or learning disorders, he had not met any milestones on time for gross or fine motor, language, cognitive, and social-emotional skills. James had a history of chronic otitis media, for which pressure equalizer tubes were inserted at age 2 years. He had not had any major physical injuries, psychological trauma, recent life transitions, or adverse childhood events. When asked, James’ mother acknowledged symptoms of maternal depression but alluded to faith-based reasons for not seeking treatment for herself.
James’ physical examination was unremarkable. His height, weight, and vitals were all within normal limits. However, he had some difficulty with verbal articulation and expression and showed signs of a possible vocal tic. Based on James’ presentation, his PCP suspected attention-deficit/hyperactivity disorder (ADHD), as well as neurodevelopmental delays.
The PCP gave James’ mother the Strengths and Difficulties Questionnaire to complete and the Vanderbilt Assessment Scales for her and James’ teacher to fill out independently and return to the clinic. The PCP also instructed James’ mother on how to use a sleep diary to maintain a 1-month log of his sleep patterns and habits. The PCP consulted the integrated behavioral health clinician (IBHC; a clinical social worker embedded in the primary care clinic) and made a warm handoff for the IBHC to further assess James’ maladaptive behaviors and interactions.
●
* The patient’s name has been changed to protect his identity.
James is one of more than 6 million children, ages 3 to 17 years, in the United States who live with ADHD.1,2 ADHD is the most common neurodevelopmental disorder among children, and it affects multiple cognitive and behavioral domains throughout the lifespan.3 Children with ADHD often initially present in primary care settings; thus, PCPs are well positioned to diagnose the disorder and provide longitudinal treatment. This Behavioral Health Consult reviews clinical assessment and practice guidelines, as well as treatment recommendations applicable across different areas of influence—individual, family, community, and systems—for PCPs and IBHCs to use in managing ADHD in children.
ADHD features can vary by age and sex
ADHD is a persistent pattern of inattention or hyperactivity and impulsivity interfering with functioning or development in childhood and functioning later in adulthood. ADHD symptoms manifest prior to age 12 years and must occur in 2 or more settings.4 Symptoms should not be better explained by another psychiatric disorder or occur exclusively during the course of another disorder (TABLE 1).4
The rate of heritability is high, with significant incidence among first-degree relatives.4 Children with ADHD show executive functioning deficits in 1 or more cognitive domains (eg, visuospatial, memory, inhibitions, decision making, and reward regulation).4,5 The prevalence of ADHD nationally is approximately 9.8% (2.2%, ages 3-5 years; 10%, ages 6-11 years; 13.2%, ages 12-17 years) in children and adolescents; worldwide prevalence is 7.2%.1,6 It persists among 2.6% to 6.8% of adults worldwide.7
Research has shown that boys ages 6 to 11 years are significantly more likely than girls to exhibit attention-getting, externalizing behaviors or conduct problems (eg, hyperactivity, impulsivity, disruption, aggression).1,6 On the other hand, girls ages 12 to 17 years tend to display internalized (eg, depressed mood, anxiety, low self-esteem) or inattentive behaviors, which clinicians and educators may assess as less severe and warranting fewer supportive measures.1
The prevalence of ADHD and its associated factors, which evolve through maturation, underscore the importance of persistent, patient-centered, and collaborative PCP and IBHC clinical management.
Continue to: Begin with a screening tool, move to a clinical interview
Begin with a screening tool, move to a clinical interview
When caregivers express concerns about their child’s behavior, focus, mood, learning, and socialization, consider initiating a multimodal evaluation for ADHD.5,8 Embarking on an ADHD assessment can require extended or multiple visits to arrive at the diagnosis, followed by still more visits to confirm a course of care and adjust medications. The integrative care approach described in the patient case and elaborated on later in this article can help facilitate assessment and treatment of ADHD.9
Signs of ADHD may be observed at initial screening using a tool such as the Ages & Stages Questionnaire (https://agesandstages.com/products-pricing/asq3/) to reveal indications of norm deviations or delays commensurate with ADHD.10 However, to substantiate the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision criteria for an accurate diagnosis,4 the American Academy of Pediatrics (AAP) clinical practice guidelines require a thorough clinical interview, administration of a standardized assessment tool, and review of objective reports in conjunction with a physical examination and psychosocial evaluation.6 Standardized measures of psychological, neurocognitive, and academic achievement reported by caregivers and collateral contacts (eg, teachers, counselors, coaches, care providers) are needed to maximize data objectivity and symptom accuracy across settings (TABLE 210-17). Additionally, periodic reassessment is recommended to validate changes in diagnostic subtype and treatment plans due to the chronic and dynamic nature of ADHD.
Consider comorbidities and alternate diagnoses
The diagnostic possibility of ADHD should also prompt consideration of other childhood disorders due to the high potential for comorbidities.4,6 In a 2016 study, approximately 64% of
Various medical disorders may manifest with similar signs or symptoms to ADHD, such as thyroid disorders, seizure disorders, adverse drug effects, anemia, genetic anomalies, and others.6,19
If there are behavioral concerns or developmental delays associated with tall stature for age or pubertal or testicular development anomalies, consult a geneticist and a developmental pediatrician for targeted testing and neurodevelopmental assessment, respectively. For example, ADHD is a common comorbidity among boys who also have XYY syndrome (Jacobs syndrome). However, due to the variability of symptoms and severity, XYY syndrome often goes undiagnosed, leaving a host of compounding pervasive and developmental problems untreated. Overall, more than two-thirds of patients with ADHD and a co-occurring condition are either inaccurately diagnosed or not referred for additional assessment and adjunct treatment.21
Continue to: Risks that arise over time
Risks that arise over time. As ADHD persists, adolescents are at greater risk for psychiatric comorbidities, suicidality, and functional impairments (eg, risky behaviors, occupational problems, truancy, delinquency, and poor self-esteem).4,8 Adolescents with internalized behaviors are more likely to experience comorbid depressive disorders with increased risk for self-harm.4,5,8 As adolescents age and their sense of autonomy increases, there is a tendency among those who have received a diagnosis of ADHD to minimize symptoms and decrease the frequency of routine clinic visits along with medication use and treatment compliance.3 Additionally, abuse, misuse, and misappropriation of stimulants among teens and young adults are commonplace.
Wide-scope, multidisciplinary evaluation and close clinical management reduce the potential for imprecise diagnoses, particularly at critical developmental junctures. AAP suggests that PCPs can treat mild and moderate cases of ADHD, but if the treating clinician does not have adequate training, experience, time, or clinical support to manage this condition, early referral is warranted.6
A guide to pharmacotherapy
Approximately 77% of children ages 2 to 17 years with a diagnosis of ADHD receive any form of treatment.2 Treatment for ADHD can include behavioral therapy and medication.2 AAP clinical practice guidelines caution against prescribing medications for children younger than 6 years, relying instead on caregiver-, teacher-, or clinician-administered behavioral strategies and parental training in behavioral modification. For children and adolescents between ages 6 and 18 years, first-line treatment includes pharmacotherapy balanced with behavioral therapy, academic modifications, and educational supports (eg, 504 Plan, individualized education plan [IEP]).6
Psychostimulants are preferred. These agents (eg, methylphenidate, amphetamine) remain the most efficacious class of medications to reduce hyperactivity and inattentiveness and to improve function. While long-acting psychostimulants are associated with better medication adherence and adverse-effect tolerance than are short-acting forms, the latter offer more flexibility in dosing. Start by titrating any stimulant to the lowest effective dose; reassess monthly until potential rebound effects stabilize.
Due to potential adverse effects of this class of medication, screen for any family history or personal risk for structural or electrical cardiac anomalies before starting pharmacotherapy. If any such risks exist, arrange for further cardiac evaluation before initiating medication.6 Adverse effects of stimulants include reduced appetite, gastrointestinal symptoms, headaches, anxiousness, parasomnia, tachycardia, and hypertension.
Continue to: Once medication is stabilized...
Once medication is stabilized, monitor treatment 2 to 3 times per year thereafter; watch for longer-term adverse effects such as weight loss, decreased growth rate, and psychiatric comorbidities including the Food and Drug Administration (FDA)’s black box warning of increased risk for suicidality.5,6,22
Other options. The optimal duration of psychostimulant use remains debatable, as existing evidence does not support its long-term use (10 years) over other interventions, such as nonstimulants and nonmedicinal therapies.22 Although backed by less evidence, additional medications indicated for the treatment of ADHD include: (1) atomoxetine, a selective norepinephrine reuptake inhibitor, and (2) the selective alpha-2 adrenergic agonists, extended-release guanfacine and extended-release clonidine (third-line agent).22
Adverse effects of these FDA-approved medications are similar to those observed in stimulant medications. Evaluation of cardiac risks is recommended before starting nonstimulant medications. The alpha-2 adrenergic agonists may also be used as adjunct therapies to stimulants. Before stopping an alpha-2 adrenergic agonist, taper the dosage slowly to avoid the risk for rebound hypertension.6,23 Given the wide variety of medication options and variability of effects, it may be necessary to try different medications as children grow and their symptoms and capacity to manage them change. Additional guidance on FDA-approved medications is available at www.ADHDMedicationGuide.com.
How multilevel care coordination can work
As with other chronic or developmental conditions, the treatment of ADHD requires an interdisciplinary perspective. Continuous, comprehensive case management can help patients overcome obstacles to wellness by balancing the resolution of problems with the development of resilience. Well-documented collaboration of subspecialists, educators, and other stakeholders engaged in ADHD care at multiple levels (individual, family, community, and health care system) increases the likelihood of meaningful, sustainable gains. Using a patient-centered medical home framework, IBHCs or other allied health professionals embedded in, or co-located with, primary care settings can be key to accessing evidence-based treatments that include: psycho-education and mindfulness-based stress reduction training for caregivers24,25; occupational,26 cognitive behavioral,27 or family therapies28,29; neuro-feedback; computer-based attention training; group- or community-based interventions; and academic and social supports.5,8
Treatment approaches that capitalize on children’s neurologic and psychological plasticity and fortify self-efficacy with developmentally appropriate tools empower them to surmount ADHD symptoms over time.23 Facilitating children’s resilience within a developmental framework and health system’s capacities with socio-culturally relevant approaches, consultation, and research can optimize outcomes and mitigate pervasiveness into adulthood. While the patient is at the center of treatment, it is important to consider the family, school, and communities in which the child lives, learns, and plays. PCPs and IBHCs together can consider a “try and track” method to follow progress, changes, and outcomes over time. With this method, the physician can employ approaches that focus on the patient, caregiver, or the caregiver–child interaction (TABLE 3).
Continue to: Assess patients' needs and the resources available
Assess patients’ needs and the resources available throughout the system of care beyond the primary care setting. Stay abreast of hospital policies, health care insurance coverage, and community- and school-based health programs, and any gaps in adequate and equitable assessment and treatment. For example, while clinical recommendations include psychiatric care, health insurance availability or limits in coverage may dissuade caregivers from seeking help or limit initial or long-term access to resources for help.30 Integrating or advocating for clinic support resources or staffing to assist patients in navigating and mitigating challenges may lessen the management burden and increase the likelihood and longevity of favorable health outcomes.
Steps to ensuring health care equity
Among children of historically marginalized and racial and ethnic minority groups or those of populations affected by health disparities, ADHD symptoms and needs are often masked by structural biases that lead to inequitable care and outcomes, as well as treatment misprioritization or delays.31 In particular, evidence has shown that recognition and diagnostic specificity of ADHD and comorbidities, not prevalence, vary more widely among minority than among nonminority populations,32 contributing to the 23% of children with ADHD who receive no treatment at all.2
Understand caregiver concerns. This diagnosis discrepancy is correlated with symptom rating sensitivities (eg, reliability, perception, accuracy) among informants and how caregivers observe, perceive, appreciate, understand, and report behaviors. This discrepancy is also related to cultural belief differences, physician–patient communication variants, and a litany of other socioeconomic determinants.2,4,31 Caregivers from some cultural, ethnic, or socioeconomic backgrounds may be doubtful of psychiatric assessment, diagnoses, treatment, or medication, and that can impact how children are engaged in clinical and educational settings from the outset.31 In the case we described, James’ mother was initially hesitant to explore psychotropic medications and was concerned about stigmatization within the school system. She also seemed to avoid psychiatric treatment for her own depressive symptoms due to cultural and religious beliefs.
Health care provider concerns. Some PCPs may hesitate to explore medications due to limited knowledge and skill in dosing and titrating based on a child’s age, stage, and symptoms, and a perceived lack of competence in managing ADHD. This, too, can indirectly perpetuate existing health disparities. Furthermore, ADHD symptoms may be deemed a secondary or tertiary concern if other complex or urgent medical or undifferentiated developmental problems manifest.
Compounding matters is the limited dissemination of empiric research articles (including randomized controlled trials with representative samples) and limited education on the effectiveness and safety of psychopharmacologic interventions across the lifespan and different cultural and ethnic groups.4 Consequently, patients who struggle with unmanaged ADHD symptoms are more likely to have chronic mental health disorders, maladaptive behaviors, and other co-occurring conditions contributing to the complexity of individual needs, health care burdens, or justice system involvement; this is particularly true for those of racial and ethnic minorities.33
Continue to: Impact of the COVID-19 pandemic
Impact of the COVID-19 pandemic. Patients—particularly those in minority or health disparity populations—who under normal circumstances might have been hesitant to seek help may have felt even more reluctant to do so during the COVID-19 pandemic. We have not yet learned the degree to which limited availability of preventive health care services, decreased routine visits, and fluctuating insurance coverage has impacted the diagnosis, management, or severity of childhood disorders during the past 2 years. Reports of national findings indicate that prolonged periods out of school and reduced daily structure were associated with increased disruptions in mood, sleep, and appetite, particularly among children with pre-existing pathologies. Evidence suggests that school-aged children experienced more anxiety, regressive behaviors, and parasomnias than they did before the pandemic, while adolescents experienced more isolation and depressive symptoms.34,35
However, there remains a paucity of large-scale or representative studies that use an intersectional lens to examine the influence of COVID-19 on children with ADHD. Therefore, PCPs and IBHCs should refocus attention on possibly undiagnosed, stagnated, or regressed ADHD cases, as well as the adults who care for them. (See “5 ways to overcome Tx barriers and promote health equity.”)
SIDEBAR
5 ways to overcome Tx barriers and promote health equitya
1. Inquire about cultural or ethnic beliefs and behaviors and socioeconomic barriers.
2. Establish trust or assuage mistrust by exploring and dispelling misinformation.
3. Offer accessible, feasible, and sustainable evidence-based interventions.
4. Encourage autonomy and selfdetermination throughout the health care process.
5. Connect caregivers and children with clinical, community, and school-based resources and coordinators.
a These recommendations are based on the authors’ combined clinical experience.
THE CASE
During a follow-up visit 1 month later, the PCP confirmed the clinical impression of ADHD combined presentation with a clinical interview and review of the Strengths and Difficulties Questionnaire completed by James’ mother and the Vanderbilt Assessment Scales completed by James’ mother and teacher. The sleep diary indicated potential problems and apneas worthy of consults for pulmonary function testing, a sleep study, and otolaryngology examination. The PCP informed James’ mother on sleep hygiene strategies and ADHD medication options. She indicated that she wanted to pursue the referrals and behavioral modifications before starting any medication trial.
The PCP referred James to a developmental pediatrician for in-depth assessment of his overall development, learning, and functioning. The developmental pediatrician ultimately confirmed the diagnosis of ADHD, as well as motor and speech delays warranting physical, occupational, and speech therapies. The developmental pediatrician also referred James for targeted genetic testing because she suspected a genetic disorder (eg, XYY syndrome).
The PCP reconnected James and his mother to the IBHC to facilitate subspecialty and school-based care coordination and to provide in-office and home-based interventions. The IBHC assessed James’ emotional dysregulation and impulsivity as adversely impacting his interpersonal relationships and planned to address these issues with behavioral and parent–child interaction therapies and skills training during the course of 6 to 12 visits. James’ mother was encouraged to engage his teacher on his academic performance and to initiate a 504 Plan or IEP for in-school accommodations and support. The IBHC aided in tracking his assessments, referrals, follow-ups, access barriers, and treatment goals.
After 6 months, James had made only modest progress, and his mother requested that he begin a trial of medication. Based on his weight, symptoms, behavior patterns, and sleep habits, the PCP prescribed extended-release dexmethylphenidate 10 mg each morning, then extended-release clonidine 0.1 mg nightly. With team-based clinical management of pharmacologic, behavioral, physical, speech, and occupational therapies, James’ behavior and sleep improved, and the signs of a vocal tic diminished.
By the next school year, James demonstrated a marked improvement in impulse control, attention, and academic functioning. He followed up with the PCP at least quarterly for reassessment of his symptoms, growth, and experience of adverse effects, and to titrate medications accordingly. James and his mother continued to work closely with the IBHC monthly to engage interventions and to monitor his progress at home and school.
CORRESPONDENCE
Sundania J. W. Wonnum, PhD, LCSW, National Institute on Minority Health and Health Disparities, 6707 Democracy Boulevard, Suite 800, Bethesda, MD 20892; sundania.wonnum@nih.gov
1. Bitsko RH, Claussen AH, Lichstein J, et al. Mental health surveillance among children—United States, 2013-2019. MMWR Suppl. 2022;71:1-42. doi: 10.15585/mmwr.su7102a1
2. Danielson ML, Holbrook JR, Blumberg SJ, et al. State-level estimates of the prevalence of parent-reported ADHD diagnosis and treatment among U.S. children and adolescents, 2016 to 2019. J Atten Disord. 2022;26:1685-1697. doi: 10.1177/10870547221099961
3. Faraone SV, Banaschewski T, Coghill D, et al. The World Federation of ADHD International Consensus Statement: 208 evidence-based conclusions about the disorder. Neurosci Biobehav Rev. 2021;128:789-818. doi: 10.1016/j.neubiorev.2021.01.022
4. American Psychiatric Association
5. Brahmbhatt K, Hilty DM, Mina H, et al. Diagnosis and treatment of attention deficit hyperactivity disorder during adolescence in the primary care setting: a concise review. J Adolesc Health. 2016;59:135-143. doi: 10.1016/j.jadohealth.2016.03.025
6. Wolraich ML, Hagan JF, Allan C, et al. AAP Subcommittee on Children and Adolescents with Attention-Deficit/Hyperactivity Disorder. Clinical Practice Guideline for the Diagnosis, Evaluation, and Treatment of Attention-Deficit/Hyperactivity Disorder in Children and Adolescents. Pediatrics. 2019;144:e20192528. doi: 10.1542/peds.2019-2528
7. Song P, Zha M, Yang Q, et al. The prevalence of adult attention-deficit hyperactivity disorder: a global systematic review and meta-analysis. J Glob Health. 2021;11:04009. doi: 10.7189/jogh.11.04009
8. Chang JG, Cimino FM, Gossa W. ADHD in children: common questions and answers. Am Fam Physician. 2020;102:592-602.
9. Asarnow JR, Rozenman M, Wiblin J, et al. Integrated medical-behavioral care compared with usual primary care for child and adolescent behavioral health: a meta-analysis. JAMA Pediatr. 2015;169:929-937. doi: 10.1001/jamapediatrics.2015.1141
10. Squires J, Bricker D. Ages & Stages Questionnaires®. 3rd ed (ASQ®-3). Paul H. Brookes Publishing Co., Inc; 2009.
11. DuPaul GJ, Barkley RA. Situational variability of attention problems: psychometric properties of the Revised Home and School Situations Questionnaires. J Clin Child Psychol. 1992;21:178-188. doi.org/10.1207/s15374424jccp2102_10
12. Merenda PF. BASC: behavior assessment system for children. Meas Eval Counsel Develop. 1996;28:229-232.
13. Conners CK. Conners, 3rd ed manual. Multi-Health Systems. 2008.
14. Achenbach TM. The Child Behavior Checklist and related instruments. In: Maruish ME, ed. The Use of Psychological Testing for Treatment Planning and Outcomes Assessment. Lawrence Erlbaum Associates Publishers; 1999:429-466.
15. Goodman R. The extended version of the Strengths and Difficulties Questionnaire as a guide to child psychiatric caseness and consequent burden. J Child Psychol Psychiatry. 1999;40:791-799.
16. Wolraich ML, Lambert W, Doffing MA, et al. Psychometric properties of the Vanderbilt ADHD Diagnostic Parent Rating Scale in a referred population. J Pediatr Psychol. 2003;28:559-567. doi: 10.1093/jpepsy/jsg046
17. Sparrow SS, Cicchetti DV. The Vineland Adaptive Behavior Scales. In: Newmark CS, ed. Major Psychological Assessment Instruments. Vol 2. Allyn & Bacon; 2003:199-231.
18. Danielson ML, Bitsko RH, Ghandour RM, et al. Prevalence of parent-reported ADHD diagnosis and associated treatment among U.S. children and adolescents, 2016. J Clin Child Adolesc Psychol. 2018;47:199-212. doi: 10.1080/15374416.2017.1417860
19. Ghriwati NA, Langberg JM, Gardner W, et al. Impact of mental health comorbidities on the community-based pediatric treatment and outcomes of children with attention deficit hyperactivity disorder. J Dev Behav Ped. 2017;38:20-28. doi: 10.1097/DBP.0000000000000359
20. Niclasen J, Obel C, Homøe P, et al. Associations between otitis media and child behavioural and learning difficulties: results from a Danish Cohort. Int J Ped Otorhinolaryngol. 2016;84:12-20. doi: 10.1016/j.ijporl.2016.02.017
21. Ross JL Roeltgen DP Kushner H, et al. Behavioral and social phenotypes in boys with 47,XYY syndrome or 47,XXY Klinefelter syndrome. doi: 10.1542/peds.2011-0719
22. Mechler K, Banaschewski T, Hohmann S, et al. Evidence-based pharmacological treatment options for ADHD in children and adolescents. Pharmacol Ther. 2022;230:107940. doi: 10.1016/j.pharmthera.2021.107940
23. Mishra J, Merzenich MM, Sagar R. Accessible online neuroplasticity-targeted training for children with ADHD. Child Adolesc Psychiatry Ment Health. 2013;7:38. doi: 10.1186/1753-2000-7-38
24. Neece CL. Mindfulness-based stress reduction for parents of young children with developmental delays: implications for parental mental health and child behavior problems. J Applied Res Intellect Disabil. 2014;27:174-186. doi: 10.1111/jar.12064
25. Petcharat M, Liehr P. Mindfulness training for parents of children with special needs: guidance for nurses in mental health practice. J Child Adolesc Psychiatr Nursing. 2017;30:35-46. doi: 10.1111/jcap.12169
26. Hahn-Markowitz J, Burger I, Manor I, et al. Efficacy of cognitive-functional (Cog-Fun) occupational therapy intervention among children with ADHD: an RCT. J Atten Disord. 2020;24:655-666. doi: 10.1177/1087054716666955
27. Young Z, Moghaddam N, Tickle A. The efficacy of cognitive behavioral therapy for adults with ADHD: a systematic review and meta-analysis of randomized controlled trials. J Atten Disord. 2020;24:875-888.
28. Carr AW, Bean RA, Nelson KF. Childhood attention-deficit hyperactivity disorder: family therapy from an attachment based perspective. Child Youth Serv Rev. 2020;119:105666.
29. Robin AL. Family therapy for adolescents with ADHD. Child Adolesc Psychiatr Clin N Am. 2014;23:747-756. doi: 10.1016/j.chc.2014.06.001
30. Cattoi B, Alpern I, Katz JS, et al. The adverse health outcomes, economic burden, and public health implications of unmanaged attention deficit hyperactivity disorder (ADHD): a call to action resulting from CHADD summit, Washington, DC, October 17, 2019. J Atten Disord. 2022;26:807-808. doi: 10.1177/10870547211036754
31. Hinojosa MS, Hinojosa R, Nguyen J. Shared decision making and treatment for minority children with ADHD. J Transcult Nurs. 2020;31:135-143. doi: 10.1177/1043659619853021
32. Slobodin O, Masalha R. Challenges in ADHD care for ethnic minority children: a review of the current literature. Transcult Psychiatry. 2020;57:468-483. doi: 10.1177/1363461520902885
33. Retz W, Ginsberg Y, Turner D, et al. Attention-deficit/hyperactivity disorder (ADHD), antisociality and delinquent behavior over the lifespan. Neurosci Biobehav Rev. 2021;120:236-248. doi: 10.1016/j.neubiorev.2020.11.025
34. Del Sol Calderon P, Izquierdo A, Garcia Moreno M. Effects of the pandemic on the mental health of children and adolescents. Review and current scientific evidence of the SARS-COV2 pandemic. Eur Psychiatry. 2021;64:S223-S224. doi: 10.1192/j.eurpsy.2021.597
35. Insa I, Alda JA. Attention deficit hyperactivity disorder (ADHD) & COVID-19: attention deficit hyperactivity disorder: consequences of the 1st wave. Eur Psychiatry. 2021;64:S660. doi: 10.1192/j.eurpsy.2021.1752
THE CASE
James B* is a 7-year-old Black child who presented to his primary care physician (PCP) for a well-child visit. During preventive health screening, James’ mother expressed concerns about his behavior, characterizing him as immature, aggressive, destructive, and occasionally self-loathing. She described him as physically uncoordinated, struggling to keep up with his peers in sports, and tiring after 20 minutes of activity. James slept 10 hours nightly but was often restless and snored intermittently. As a second grader, his academic achievement was not progressing, and he had become increasingly inattentive at home and at school. James’ mother offered several examples of his fighting with his siblings, noncompliance with morning routines, and avoidance of learning activities. Additionally, his mother expressed concern that James, as a Black child, might eventually be unfairly labeled as a problem child by his teachers or held back a grade level in school.
Although James did not have a family history of developmental delays or learning disorders, he had not met any milestones on time for gross or fine motor, language, cognitive, and social-emotional skills. James had a history of chronic otitis media, for which pressure equalizer tubes were inserted at age 2 years. He had not had any major physical injuries, psychological trauma, recent life transitions, or adverse childhood events. When asked, James’ mother acknowledged symptoms of maternal depression but alluded to faith-based reasons for not seeking treatment for herself.
James’ physical examination was unremarkable. His height, weight, and vitals were all within normal limits. However, he had some difficulty with verbal articulation and expression and showed signs of a possible vocal tic. Based on James’ presentation, his PCP suspected attention-deficit/hyperactivity disorder (ADHD), as well as neurodevelopmental delays.
The PCP gave James’ mother the Strengths and Difficulties Questionnaire to complete and the Vanderbilt Assessment Scales for her and James’ teacher to fill out independently and return to the clinic. The PCP also instructed James’ mother on how to use a sleep diary to maintain a 1-month log of his sleep patterns and habits. The PCP consulted the integrated behavioral health clinician (IBHC; a clinical social worker embedded in the primary care clinic) and made a warm handoff for the IBHC to further assess James’ maladaptive behaviors and interactions.
●
* The patient’s name has been changed to protect his identity.
James is one of more than 6 million children, ages 3 to 17 years, in the United States who live with ADHD.1,2 ADHD is the most common neurodevelopmental disorder among children, and it affects multiple cognitive and behavioral domains throughout the lifespan.3 Children with ADHD often initially present in primary care settings; thus, PCPs are well positioned to diagnose the disorder and provide longitudinal treatment. This Behavioral Health Consult reviews clinical assessment and practice guidelines, as well as treatment recommendations applicable across different areas of influence—individual, family, community, and systems—for PCPs and IBHCs to use in managing ADHD in children.
ADHD features can vary by age and sex
ADHD is a persistent pattern of inattention or hyperactivity and impulsivity interfering with functioning or development in childhood and functioning later in adulthood. ADHD symptoms manifest prior to age 12 years and must occur in 2 or more settings.4 Symptoms should not be better explained by another psychiatric disorder or occur exclusively during the course of another disorder (TABLE 1).4
The rate of heritability is high, with significant incidence among first-degree relatives.4 Children with ADHD show executive functioning deficits in 1 or more cognitive domains (eg, visuospatial, memory, inhibitions, decision making, and reward regulation).4,5 The prevalence of ADHD nationally is approximately 9.8% (2.2%, ages 3-5 years; 10%, ages 6-11 years; 13.2%, ages 12-17 years) in children and adolescents; worldwide prevalence is 7.2%.1,6 It persists among 2.6% to 6.8% of adults worldwide.7
Research has shown that boys ages 6 to 11 years are significantly more likely than girls to exhibit attention-getting, externalizing behaviors or conduct problems (eg, hyperactivity, impulsivity, disruption, aggression).1,6 On the other hand, girls ages 12 to 17 years tend to display internalized (eg, depressed mood, anxiety, low self-esteem) or inattentive behaviors, which clinicians and educators may assess as less severe and warranting fewer supportive measures.1
The prevalence of ADHD and its associated factors, which evolve through maturation, underscore the importance of persistent, patient-centered, and collaborative PCP and IBHC clinical management.
Continue to: Begin with a screening tool, move to a clinical interview
Begin with a screening tool, move to a clinical interview
When caregivers express concerns about their child’s behavior, focus, mood, learning, and socialization, consider initiating a multimodal evaluation for ADHD.5,8 Embarking on an ADHD assessment can require extended or multiple visits to arrive at the diagnosis, followed by still more visits to confirm a course of care and adjust medications. The integrative care approach described in the patient case and elaborated on later in this article can help facilitate assessment and treatment of ADHD.9
Signs of ADHD may be observed at initial screening using a tool such as the Ages & Stages Questionnaire (https://agesandstages.com/products-pricing/asq3/) to reveal indications of norm deviations or delays commensurate with ADHD.10 However, to substantiate the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision criteria for an accurate diagnosis,4 the American Academy of Pediatrics (AAP) clinical practice guidelines require a thorough clinical interview, administration of a standardized assessment tool, and review of objective reports in conjunction with a physical examination and psychosocial evaluation.6 Standardized measures of psychological, neurocognitive, and academic achievement reported by caregivers and collateral contacts (eg, teachers, counselors, coaches, care providers) are needed to maximize data objectivity and symptom accuracy across settings (TABLE 210-17). Additionally, periodic reassessment is recommended to validate changes in diagnostic subtype and treatment plans due to the chronic and dynamic nature of ADHD.
Consider comorbidities and alternate diagnoses
The diagnostic possibility of ADHD should also prompt consideration of other childhood disorders due to the high potential for comorbidities.4,6 In a 2016 study, approximately 64% of
Various medical disorders may manifest with similar signs or symptoms to ADHD, such as thyroid disorders, seizure disorders, adverse drug effects, anemia, genetic anomalies, and others.6,19
If there are behavioral concerns or developmental delays associated with tall stature for age or pubertal or testicular development anomalies, consult a geneticist and a developmental pediatrician for targeted testing and neurodevelopmental assessment, respectively. For example, ADHD is a common comorbidity among boys who also have XYY syndrome (Jacobs syndrome). However, due to the variability of symptoms and severity, XYY syndrome often goes undiagnosed, leaving a host of compounding pervasive and developmental problems untreated. Overall, more than two-thirds of patients with ADHD and a co-occurring condition are either inaccurately diagnosed or not referred for additional assessment and adjunct treatment.21
Continue to: Risks that arise over time
Risks that arise over time. As ADHD persists, adolescents are at greater risk for psychiatric comorbidities, suicidality, and functional impairments (eg, risky behaviors, occupational problems, truancy, delinquency, and poor self-esteem).4,8 Adolescents with internalized behaviors are more likely to experience comorbid depressive disorders with increased risk for self-harm.4,5,8 As adolescents age and their sense of autonomy increases, there is a tendency among those who have received a diagnosis of ADHD to minimize symptoms and decrease the frequency of routine clinic visits along with medication use and treatment compliance.3 Additionally, abuse, misuse, and misappropriation of stimulants among teens and young adults are commonplace.
Wide-scope, multidisciplinary evaluation and close clinical management reduce the potential for imprecise diagnoses, particularly at critical developmental junctures. AAP suggests that PCPs can treat mild and moderate cases of ADHD, but if the treating clinician does not have adequate training, experience, time, or clinical support to manage this condition, early referral is warranted.6
A guide to pharmacotherapy
Approximately 77% of children ages 2 to 17 years with a diagnosis of ADHD receive any form of treatment.2 Treatment for ADHD can include behavioral therapy and medication.2 AAP clinical practice guidelines caution against prescribing medications for children younger than 6 years, relying instead on caregiver-, teacher-, or clinician-administered behavioral strategies and parental training in behavioral modification. For children and adolescents between ages 6 and 18 years, first-line treatment includes pharmacotherapy balanced with behavioral therapy, academic modifications, and educational supports (eg, 504 Plan, individualized education plan [IEP]).6
Psychostimulants are preferred. These agents (eg, methylphenidate, amphetamine) remain the most efficacious class of medications to reduce hyperactivity and inattentiveness and to improve function. While long-acting psychostimulants are associated with better medication adherence and adverse-effect tolerance than are short-acting forms, the latter offer more flexibility in dosing. Start by titrating any stimulant to the lowest effective dose; reassess monthly until potential rebound effects stabilize.
Due to potential adverse effects of this class of medication, screen for any family history or personal risk for structural or electrical cardiac anomalies before starting pharmacotherapy. If any such risks exist, arrange for further cardiac evaluation before initiating medication.6 Adverse effects of stimulants include reduced appetite, gastrointestinal symptoms, headaches, anxiousness, parasomnia, tachycardia, and hypertension.
Continue to: Once medication is stabilized...
Once medication is stabilized, monitor treatment 2 to 3 times per year thereafter; watch for longer-term adverse effects such as weight loss, decreased growth rate, and psychiatric comorbidities including the Food and Drug Administration (FDA)’s black box warning of increased risk for suicidality.5,6,22
Other options. The optimal duration of psychostimulant use remains debatable, as existing evidence does not support its long-term use (10 years) over other interventions, such as nonstimulants and nonmedicinal therapies.22 Although backed by less evidence, additional medications indicated for the treatment of ADHD include: (1) atomoxetine, a selective norepinephrine reuptake inhibitor, and (2) the selective alpha-2 adrenergic agonists, extended-release guanfacine and extended-release clonidine (third-line agent).22
Adverse effects of these FDA-approved medications are similar to those observed in stimulant medications. Evaluation of cardiac risks is recommended before starting nonstimulant medications. The alpha-2 adrenergic agonists may also be used as adjunct therapies to stimulants. Before stopping an alpha-2 adrenergic agonist, taper the dosage slowly to avoid the risk for rebound hypertension.6,23 Given the wide variety of medication options and variability of effects, it may be necessary to try different medications as children grow and their symptoms and capacity to manage them change. Additional guidance on FDA-approved medications is available at www.ADHDMedicationGuide.com.
How multilevel care coordination can work
As with other chronic or developmental conditions, the treatment of ADHD requires an interdisciplinary perspective. Continuous, comprehensive case management can help patients overcome obstacles to wellness by balancing the resolution of problems with the development of resilience. Well-documented collaboration of subspecialists, educators, and other stakeholders engaged in ADHD care at multiple levels (individual, family, community, and health care system) increases the likelihood of meaningful, sustainable gains. Using a patient-centered medical home framework, IBHCs or other allied health professionals embedded in, or co-located with, primary care settings can be key to accessing evidence-based treatments that include: psycho-education and mindfulness-based stress reduction training for caregivers24,25; occupational,26 cognitive behavioral,27 or family therapies28,29; neuro-feedback; computer-based attention training; group- or community-based interventions; and academic and social supports.5,8
Treatment approaches that capitalize on children’s neurologic and psychological plasticity and fortify self-efficacy with developmentally appropriate tools empower them to surmount ADHD symptoms over time.23 Facilitating children’s resilience within a developmental framework and health system’s capacities with socio-culturally relevant approaches, consultation, and research can optimize outcomes and mitigate pervasiveness into adulthood. While the patient is at the center of treatment, it is important to consider the family, school, and communities in which the child lives, learns, and plays. PCPs and IBHCs together can consider a “try and track” method to follow progress, changes, and outcomes over time. With this method, the physician can employ approaches that focus on the patient, caregiver, or the caregiver–child interaction (TABLE 3).
Continue to: Assess patients' needs and the resources available
Assess patients’ needs and the resources available throughout the system of care beyond the primary care setting. Stay abreast of hospital policies, health care insurance coverage, and community- and school-based health programs, and any gaps in adequate and equitable assessment and treatment. For example, while clinical recommendations include psychiatric care, health insurance availability or limits in coverage may dissuade caregivers from seeking help or limit initial or long-term access to resources for help.30 Integrating or advocating for clinic support resources or staffing to assist patients in navigating and mitigating challenges may lessen the management burden and increase the likelihood and longevity of favorable health outcomes.
Steps to ensuring health care equity
Among children of historically marginalized and racial and ethnic minority groups or those of populations affected by health disparities, ADHD symptoms and needs are often masked by structural biases that lead to inequitable care and outcomes, as well as treatment misprioritization or delays.31 In particular, evidence has shown that recognition and diagnostic specificity of ADHD and comorbidities, not prevalence, vary more widely among minority than among nonminority populations,32 contributing to the 23% of children with ADHD who receive no treatment at all.2
Understand caregiver concerns. This diagnosis discrepancy is correlated with symptom rating sensitivities (eg, reliability, perception, accuracy) among informants and how caregivers observe, perceive, appreciate, understand, and report behaviors. This discrepancy is also related to cultural belief differences, physician–patient communication variants, and a litany of other socioeconomic determinants.2,4,31 Caregivers from some cultural, ethnic, or socioeconomic backgrounds may be doubtful of psychiatric assessment, diagnoses, treatment, or medication, and that can impact how children are engaged in clinical and educational settings from the outset.31 In the case we described, James’ mother was initially hesitant to explore psychotropic medications and was concerned about stigmatization within the school system. She also seemed to avoid psychiatric treatment for her own depressive symptoms due to cultural and religious beliefs.
Health care provider concerns. Some PCPs may hesitate to explore medications due to limited knowledge and skill in dosing and titrating based on a child’s age, stage, and symptoms, and a perceived lack of competence in managing ADHD. This, too, can indirectly perpetuate existing health disparities. Furthermore, ADHD symptoms may be deemed a secondary or tertiary concern if other complex or urgent medical or undifferentiated developmental problems manifest.
Compounding matters is the limited dissemination of empiric research articles (including randomized controlled trials with representative samples) and limited education on the effectiveness and safety of psychopharmacologic interventions across the lifespan and different cultural and ethnic groups.4 Consequently, patients who struggle with unmanaged ADHD symptoms are more likely to have chronic mental health disorders, maladaptive behaviors, and other co-occurring conditions contributing to the complexity of individual needs, health care burdens, or justice system involvement; this is particularly true for those of racial and ethnic minorities.33
Continue to: Impact of the COVID-19 pandemic
Impact of the COVID-19 pandemic. Patients—particularly those in minority or health disparity populations—who under normal circumstances might have been hesitant to seek help may have felt even more reluctant to do so during the COVID-19 pandemic. We have not yet learned the degree to which limited availability of preventive health care services, decreased routine visits, and fluctuating insurance coverage has impacted the diagnosis, management, or severity of childhood disorders during the past 2 years. Reports of national findings indicate that prolonged periods out of school and reduced daily structure were associated with increased disruptions in mood, sleep, and appetite, particularly among children with pre-existing pathologies. Evidence suggests that school-aged children experienced more anxiety, regressive behaviors, and parasomnias than they did before the pandemic, while adolescents experienced more isolation and depressive symptoms.34,35
However, there remains a paucity of large-scale or representative studies that use an intersectional lens to examine the influence of COVID-19 on children with ADHD. Therefore, PCPs and IBHCs should refocus attention on possibly undiagnosed, stagnated, or regressed ADHD cases, as well as the adults who care for them. (See “5 ways to overcome Tx barriers and promote health equity.”)
SIDEBAR
5 ways to overcome Tx barriers and promote health equitya
1. Inquire about cultural or ethnic beliefs and behaviors and socioeconomic barriers.
2. Establish trust or assuage mistrust by exploring and dispelling misinformation.
3. Offer accessible, feasible, and sustainable evidence-based interventions.
4. Encourage autonomy and selfdetermination throughout the health care process.
5. Connect caregivers and children with clinical, community, and school-based resources and coordinators.
a These recommendations are based on the authors’ combined clinical experience.
THE CASE
During a follow-up visit 1 month later, the PCP confirmed the clinical impression of ADHD combined presentation with a clinical interview and review of the Strengths and Difficulties Questionnaire completed by James’ mother and the Vanderbilt Assessment Scales completed by James’ mother and teacher. The sleep diary indicated potential problems and apneas worthy of consults for pulmonary function testing, a sleep study, and otolaryngology examination. The PCP informed James’ mother on sleep hygiene strategies and ADHD medication options. She indicated that she wanted to pursue the referrals and behavioral modifications before starting any medication trial.
The PCP referred James to a developmental pediatrician for in-depth assessment of his overall development, learning, and functioning. The developmental pediatrician ultimately confirmed the diagnosis of ADHD, as well as motor and speech delays warranting physical, occupational, and speech therapies. The developmental pediatrician also referred James for targeted genetic testing because she suspected a genetic disorder (eg, XYY syndrome).
The PCP reconnected James and his mother to the IBHC to facilitate subspecialty and school-based care coordination and to provide in-office and home-based interventions. The IBHC assessed James’ emotional dysregulation and impulsivity as adversely impacting his interpersonal relationships and planned to address these issues with behavioral and parent–child interaction therapies and skills training during the course of 6 to 12 visits. James’ mother was encouraged to engage his teacher on his academic performance and to initiate a 504 Plan or IEP for in-school accommodations and support. The IBHC aided in tracking his assessments, referrals, follow-ups, access barriers, and treatment goals.
After 6 months, James had made only modest progress, and his mother requested that he begin a trial of medication. Based on his weight, symptoms, behavior patterns, and sleep habits, the PCP prescribed extended-release dexmethylphenidate 10 mg each morning, then extended-release clonidine 0.1 mg nightly. With team-based clinical management of pharmacologic, behavioral, physical, speech, and occupational therapies, James’ behavior and sleep improved, and the signs of a vocal tic diminished.
By the next school year, James demonstrated a marked improvement in impulse control, attention, and academic functioning. He followed up with the PCP at least quarterly for reassessment of his symptoms, growth, and experience of adverse effects, and to titrate medications accordingly. James and his mother continued to work closely with the IBHC monthly to engage interventions and to monitor his progress at home and school.
CORRESPONDENCE
Sundania J. W. Wonnum, PhD, LCSW, National Institute on Minority Health and Health Disparities, 6707 Democracy Boulevard, Suite 800, Bethesda, MD 20892; sundania.wonnum@nih.gov
THE CASE
James B* is a 7-year-old Black child who presented to his primary care physician (PCP) for a well-child visit. During preventive health screening, James’ mother expressed concerns about his behavior, characterizing him as immature, aggressive, destructive, and occasionally self-loathing. She described him as physically uncoordinated, struggling to keep up with his peers in sports, and tiring after 20 minutes of activity. James slept 10 hours nightly but was often restless and snored intermittently. As a second grader, his academic achievement was not progressing, and he had become increasingly inattentive at home and at school. James’ mother offered several examples of his fighting with his siblings, noncompliance with morning routines, and avoidance of learning activities. Additionally, his mother expressed concern that James, as a Black child, might eventually be unfairly labeled as a problem child by his teachers or held back a grade level in school.
Although James did not have a family history of developmental delays or learning disorders, he had not met any milestones on time for gross or fine motor, language, cognitive, and social-emotional skills. James had a history of chronic otitis media, for which pressure equalizer tubes were inserted at age 2 years. He had not had any major physical injuries, psychological trauma, recent life transitions, or adverse childhood events. When asked, James’ mother acknowledged symptoms of maternal depression but alluded to faith-based reasons for not seeking treatment for herself.
James’ physical examination was unremarkable. His height, weight, and vitals were all within normal limits. However, he had some difficulty with verbal articulation and expression and showed signs of a possible vocal tic. Based on James’ presentation, his PCP suspected attention-deficit/hyperactivity disorder (ADHD), as well as neurodevelopmental delays.
The PCP gave James’ mother the Strengths and Difficulties Questionnaire to complete and the Vanderbilt Assessment Scales for her and James’ teacher to fill out independently and return to the clinic. The PCP also instructed James’ mother on how to use a sleep diary to maintain a 1-month log of his sleep patterns and habits. The PCP consulted the integrated behavioral health clinician (IBHC; a clinical social worker embedded in the primary care clinic) and made a warm handoff for the IBHC to further assess James’ maladaptive behaviors and interactions.
●
* The patient’s name has been changed to protect his identity.
James is one of more than 6 million children, ages 3 to 17 years, in the United States who live with ADHD.1,2 ADHD is the most common neurodevelopmental disorder among children, and it affects multiple cognitive and behavioral domains throughout the lifespan.3 Children with ADHD often initially present in primary care settings; thus, PCPs are well positioned to diagnose the disorder and provide longitudinal treatment. This Behavioral Health Consult reviews clinical assessment and practice guidelines, as well as treatment recommendations applicable across different areas of influence—individual, family, community, and systems—for PCPs and IBHCs to use in managing ADHD in children.
ADHD features can vary by age and sex
ADHD is a persistent pattern of inattention or hyperactivity and impulsivity interfering with functioning or development in childhood and functioning later in adulthood. ADHD symptoms manifest prior to age 12 years and must occur in 2 or more settings.4 Symptoms should not be better explained by another psychiatric disorder or occur exclusively during the course of another disorder (TABLE 1).4
The rate of heritability is high, with significant incidence among first-degree relatives.4 Children with ADHD show executive functioning deficits in 1 or more cognitive domains (eg, visuospatial, memory, inhibitions, decision making, and reward regulation).4,5 The prevalence of ADHD nationally is approximately 9.8% (2.2%, ages 3-5 years; 10%, ages 6-11 years; 13.2%, ages 12-17 years) in children and adolescents; worldwide prevalence is 7.2%.1,6 It persists among 2.6% to 6.8% of adults worldwide.7
Research has shown that boys ages 6 to 11 years are significantly more likely than girls to exhibit attention-getting, externalizing behaviors or conduct problems (eg, hyperactivity, impulsivity, disruption, aggression).1,6 On the other hand, girls ages 12 to 17 years tend to display internalized (eg, depressed mood, anxiety, low self-esteem) or inattentive behaviors, which clinicians and educators may assess as less severe and warranting fewer supportive measures.1
The prevalence of ADHD and its associated factors, which evolve through maturation, underscore the importance of persistent, patient-centered, and collaborative PCP and IBHC clinical management.
Continue to: Begin with a screening tool, move to a clinical interview
Begin with a screening tool, move to a clinical interview
When caregivers express concerns about their child’s behavior, focus, mood, learning, and socialization, consider initiating a multimodal evaluation for ADHD.5,8 Embarking on an ADHD assessment can require extended or multiple visits to arrive at the diagnosis, followed by still more visits to confirm a course of care and adjust medications. The integrative care approach described in the patient case and elaborated on later in this article can help facilitate assessment and treatment of ADHD.9
Signs of ADHD may be observed at initial screening using a tool such as the Ages & Stages Questionnaire (https://agesandstages.com/products-pricing/asq3/) to reveal indications of norm deviations or delays commensurate with ADHD.10 However, to substantiate the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision criteria for an accurate diagnosis,4 the American Academy of Pediatrics (AAP) clinical practice guidelines require a thorough clinical interview, administration of a standardized assessment tool, and review of objective reports in conjunction with a physical examination and psychosocial evaluation.6 Standardized measures of psychological, neurocognitive, and academic achievement reported by caregivers and collateral contacts (eg, teachers, counselors, coaches, care providers) are needed to maximize data objectivity and symptom accuracy across settings (TABLE 210-17). Additionally, periodic reassessment is recommended to validate changes in diagnostic subtype and treatment plans due to the chronic and dynamic nature of ADHD.
Consider comorbidities and alternate diagnoses
The diagnostic possibility of ADHD should also prompt consideration of other childhood disorders due to the high potential for comorbidities.4,6 In a 2016 study, approximately 64% of
Various medical disorders may manifest with similar signs or symptoms to ADHD, such as thyroid disorders, seizure disorders, adverse drug effects, anemia, genetic anomalies, and others.6,19
If there are behavioral concerns or developmental delays associated with tall stature for age or pubertal or testicular development anomalies, consult a geneticist and a developmental pediatrician for targeted testing and neurodevelopmental assessment, respectively. For example, ADHD is a common comorbidity among boys who also have XYY syndrome (Jacobs syndrome). However, due to the variability of symptoms and severity, XYY syndrome often goes undiagnosed, leaving a host of compounding pervasive and developmental problems untreated. Overall, more than two-thirds of patients with ADHD and a co-occurring condition are either inaccurately diagnosed or not referred for additional assessment and adjunct treatment.21
Continue to: Risks that arise over time
Risks that arise over time. As ADHD persists, adolescents are at greater risk for psychiatric comorbidities, suicidality, and functional impairments (eg, risky behaviors, occupational problems, truancy, delinquency, and poor self-esteem).4,8 Adolescents with internalized behaviors are more likely to experience comorbid depressive disorders with increased risk for self-harm.4,5,8 As adolescents age and their sense of autonomy increases, there is a tendency among those who have received a diagnosis of ADHD to minimize symptoms and decrease the frequency of routine clinic visits along with medication use and treatment compliance.3 Additionally, abuse, misuse, and misappropriation of stimulants among teens and young adults are commonplace.
Wide-scope, multidisciplinary evaluation and close clinical management reduce the potential for imprecise diagnoses, particularly at critical developmental junctures. AAP suggests that PCPs can treat mild and moderate cases of ADHD, but if the treating clinician does not have adequate training, experience, time, or clinical support to manage this condition, early referral is warranted.6
A guide to pharmacotherapy
Approximately 77% of children ages 2 to 17 years with a diagnosis of ADHD receive any form of treatment.2 Treatment for ADHD can include behavioral therapy and medication.2 AAP clinical practice guidelines caution against prescribing medications for children younger than 6 years, relying instead on caregiver-, teacher-, or clinician-administered behavioral strategies and parental training in behavioral modification. For children and adolescents between ages 6 and 18 years, first-line treatment includes pharmacotherapy balanced with behavioral therapy, academic modifications, and educational supports (eg, 504 Plan, individualized education plan [IEP]).6
Psychostimulants are preferred. These agents (eg, methylphenidate, amphetamine) remain the most efficacious class of medications to reduce hyperactivity and inattentiveness and to improve function. While long-acting psychostimulants are associated with better medication adherence and adverse-effect tolerance than are short-acting forms, the latter offer more flexibility in dosing. Start by titrating any stimulant to the lowest effective dose; reassess monthly until potential rebound effects stabilize.
Due to potential adverse effects of this class of medication, screen for any family history or personal risk for structural or electrical cardiac anomalies before starting pharmacotherapy. If any such risks exist, arrange for further cardiac evaluation before initiating medication.6 Adverse effects of stimulants include reduced appetite, gastrointestinal symptoms, headaches, anxiousness, parasomnia, tachycardia, and hypertension.
Continue to: Once medication is stabilized...
Once medication is stabilized, monitor treatment 2 to 3 times per year thereafter; watch for longer-term adverse effects such as weight loss, decreased growth rate, and psychiatric comorbidities including the Food and Drug Administration (FDA)’s black box warning of increased risk for suicidality.5,6,22
Other options. The optimal duration of psychostimulant use remains debatable, as existing evidence does not support its long-term use (10 years) over other interventions, such as nonstimulants and nonmedicinal therapies.22 Although backed by less evidence, additional medications indicated for the treatment of ADHD include: (1) atomoxetine, a selective norepinephrine reuptake inhibitor, and (2) the selective alpha-2 adrenergic agonists, extended-release guanfacine and extended-release clonidine (third-line agent).22
Adverse effects of these FDA-approved medications are similar to those observed in stimulant medications. Evaluation of cardiac risks is recommended before starting nonstimulant medications. The alpha-2 adrenergic agonists may also be used as adjunct therapies to stimulants. Before stopping an alpha-2 adrenergic agonist, taper the dosage slowly to avoid the risk for rebound hypertension.6,23 Given the wide variety of medication options and variability of effects, it may be necessary to try different medications as children grow and their symptoms and capacity to manage them change. Additional guidance on FDA-approved medications is available at www.ADHDMedicationGuide.com.
How multilevel care coordination can work
As with other chronic or developmental conditions, the treatment of ADHD requires an interdisciplinary perspective. Continuous, comprehensive case management can help patients overcome obstacles to wellness by balancing the resolution of problems with the development of resilience. Well-documented collaboration of subspecialists, educators, and other stakeholders engaged in ADHD care at multiple levels (individual, family, community, and health care system) increases the likelihood of meaningful, sustainable gains. Using a patient-centered medical home framework, IBHCs or other allied health professionals embedded in, or co-located with, primary care settings can be key to accessing evidence-based treatments that include: psycho-education and mindfulness-based stress reduction training for caregivers24,25; occupational,26 cognitive behavioral,27 or family therapies28,29; neuro-feedback; computer-based attention training; group- or community-based interventions; and academic and social supports.5,8
Treatment approaches that capitalize on children’s neurologic and psychological plasticity and fortify self-efficacy with developmentally appropriate tools empower them to surmount ADHD symptoms over time.23 Facilitating children’s resilience within a developmental framework and health system’s capacities with socio-culturally relevant approaches, consultation, and research can optimize outcomes and mitigate pervasiveness into adulthood. While the patient is at the center of treatment, it is important to consider the family, school, and communities in which the child lives, learns, and plays. PCPs and IBHCs together can consider a “try and track” method to follow progress, changes, and outcomes over time. With this method, the physician can employ approaches that focus on the patient, caregiver, or the caregiver–child interaction (TABLE 3).
Continue to: Assess patients' needs and the resources available
Assess patients’ needs and the resources available throughout the system of care beyond the primary care setting. Stay abreast of hospital policies, health care insurance coverage, and community- and school-based health programs, and any gaps in adequate and equitable assessment and treatment. For example, while clinical recommendations include psychiatric care, health insurance availability or limits in coverage may dissuade caregivers from seeking help or limit initial or long-term access to resources for help.30 Integrating or advocating for clinic support resources or staffing to assist patients in navigating and mitigating challenges may lessen the management burden and increase the likelihood and longevity of favorable health outcomes.
Steps to ensuring health care equity
Among children of historically marginalized and racial and ethnic minority groups or those of populations affected by health disparities, ADHD symptoms and needs are often masked by structural biases that lead to inequitable care and outcomes, as well as treatment misprioritization or delays.31 In particular, evidence has shown that recognition and diagnostic specificity of ADHD and comorbidities, not prevalence, vary more widely among minority than among nonminority populations,32 contributing to the 23% of children with ADHD who receive no treatment at all.2
Understand caregiver concerns. This diagnosis discrepancy is correlated with symptom rating sensitivities (eg, reliability, perception, accuracy) among informants and how caregivers observe, perceive, appreciate, understand, and report behaviors. This discrepancy is also related to cultural belief differences, physician–patient communication variants, and a litany of other socioeconomic determinants.2,4,31 Caregivers from some cultural, ethnic, or socioeconomic backgrounds may be doubtful of psychiatric assessment, diagnoses, treatment, or medication, and that can impact how children are engaged in clinical and educational settings from the outset.31 In the case we described, James’ mother was initially hesitant to explore psychotropic medications and was concerned about stigmatization within the school system. She also seemed to avoid psychiatric treatment for her own depressive symptoms due to cultural and religious beliefs.
Health care provider concerns. Some PCPs may hesitate to explore medications due to limited knowledge and skill in dosing and titrating based on a child’s age, stage, and symptoms, and a perceived lack of competence in managing ADHD. This, too, can indirectly perpetuate existing health disparities. Furthermore, ADHD symptoms may be deemed a secondary or tertiary concern if other complex or urgent medical or undifferentiated developmental problems manifest.
Compounding matters is the limited dissemination of empiric research articles (including randomized controlled trials with representative samples) and limited education on the effectiveness and safety of psychopharmacologic interventions across the lifespan and different cultural and ethnic groups.4 Consequently, patients who struggle with unmanaged ADHD symptoms are more likely to have chronic mental health disorders, maladaptive behaviors, and other co-occurring conditions contributing to the complexity of individual needs, health care burdens, or justice system involvement; this is particularly true for those of racial and ethnic minorities.33
Continue to: Impact of the COVID-19 pandemic
Impact of the COVID-19 pandemic. Patients—particularly those in minority or health disparity populations—who under normal circumstances might have been hesitant to seek help may have felt even more reluctant to do so during the COVID-19 pandemic. We have not yet learned the degree to which limited availability of preventive health care services, decreased routine visits, and fluctuating insurance coverage has impacted the diagnosis, management, or severity of childhood disorders during the past 2 years. Reports of national findings indicate that prolonged periods out of school and reduced daily structure were associated with increased disruptions in mood, sleep, and appetite, particularly among children with pre-existing pathologies. Evidence suggests that school-aged children experienced more anxiety, regressive behaviors, and parasomnias than they did before the pandemic, while adolescents experienced more isolation and depressive symptoms.34,35
However, there remains a paucity of large-scale or representative studies that use an intersectional lens to examine the influence of COVID-19 on children with ADHD. Therefore, PCPs and IBHCs should refocus attention on possibly undiagnosed, stagnated, or regressed ADHD cases, as well as the adults who care for them. (See “5 ways to overcome Tx barriers and promote health equity.”)
SIDEBAR
5 ways to overcome Tx barriers and promote health equitya
1. Inquire about cultural or ethnic beliefs and behaviors and socioeconomic barriers.
2. Establish trust or assuage mistrust by exploring and dispelling misinformation.
3. Offer accessible, feasible, and sustainable evidence-based interventions.
4. Encourage autonomy and selfdetermination throughout the health care process.
5. Connect caregivers and children with clinical, community, and school-based resources and coordinators.
a These recommendations are based on the authors’ combined clinical experience.
THE CASE
During a follow-up visit 1 month later, the PCP confirmed the clinical impression of ADHD combined presentation with a clinical interview and review of the Strengths and Difficulties Questionnaire completed by James’ mother and the Vanderbilt Assessment Scales completed by James’ mother and teacher. The sleep diary indicated potential problems and apneas worthy of consults for pulmonary function testing, a sleep study, and otolaryngology examination. The PCP informed James’ mother on sleep hygiene strategies and ADHD medication options. She indicated that she wanted to pursue the referrals and behavioral modifications before starting any medication trial.
The PCP referred James to a developmental pediatrician for in-depth assessment of his overall development, learning, and functioning. The developmental pediatrician ultimately confirmed the diagnosis of ADHD, as well as motor and speech delays warranting physical, occupational, and speech therapies. The developmental pediatrician also referred James for targeted genetic testing because she suspected a genetic disorder (eg, XYY syndrome).
The PCP reconnected James and his mother to the IBHC to facilitate subspecialty and school-based care coordination and to provide in-office and home-based interventions. The IBHC assessed James’ emotional dysregulation and impulsivity as adversely impacting his interpersonal relationships and planned to address these issues with behavioral and parent–child interaction therapies and skills training during the course of 6 to 12 visits. James’ mother was encouraged to engage his teacher on his academic performance and to initiate a 504 Plan or IEP for in-school accommodations and support. The IBHC aided in tracking his assessments, referrals, follow-ups, access barriers, and treatment goals.
After 6 months, James had made only modest progress, and his mother requested that he begin a trial of medication. Based on his weight, symptoms, behavior patterns, and sleep habits, the PCP prescribed extended-release dexmethylphenidate 10 mg each morning, then extended-release clonidine 0.1 mg nightly. With team-based clinical management of pharmacologic, behavioral, physical, speech, and occupational therapies, James’ behavior and sleep improved, and the signs of a vocal tic diminished.
By the next school year, James demonstrated a marked improvement in impulse control, attention, and academic functioning. He followed up with the PCP at least quarterly for reassessment of his symptoms, growth, and experience of adverse effects, and to titrate medications accordingly. James and his mother continued to work closely with the IBHC monthly to engage interventions and to monitor his progress at home and school.
CORRESPONDENCE
Sundania J. W. Wonnum, PhD, LCSW, National Institute on Minority Health and Health Disparities, 6707 Democracy Boulevard, Suite 800, Bethesda, MD 20892; sundania.wonnum@nih.gov
1. Bitsko RH, Claussen AH, Lichstein J, et al. Mental health surveillance among children—United States, 2013-2019. MMWR Suppl. 2022;71:1-42. doi: 10.15585/mmwr.su7102a1
2. Danielson ML, Holbrook JR, Blumberg SJ, et al. State-level estimates of the prevalence of parent-reported ADHD diagnosis and treatment among U.S. children and adolescents, 2016 to 2019. J Atten Disord. 2022;26:1685-1697. doi: 10.1177/10870547221099961
3. Faraone SV, Banaschewski T, Coghill D, et al. The World Federation of ADHD International Consensus Statement: 208 evidence-based conclusions about the disorder. Neurosci Biobehav Rev. 2021;128:789-818. doi: 10.1016/j.neubiorev.2021.01.022
4. American Psychiatric Association
5. Brahmbhatt K, Hilty DM, Mina H, et al. Diagnosis and treatment of attention deficit hyperactivity disorder during adolescence in the primary care setting: a concise review. J Adolesc Health. 2016;59:135-143. doi: 10.1016/j.jadohealth.2016.03.025
6. Wolraich ML, Hagan JF, Allan C, et al. AAP Subcommittee on Children and Adolescents with Attention-Deficit/Hyperactivity Disorder. Clinical Practice Guideline for the Diagnosis, Evaluation, and Treatment of Attention-Deficit/Hyperactivity Disorder in Children and Adolescents. Pediatrics. 2019;144:e20192528. doi: 10.1542/peds.2019-2528
7. Song P, Zha M, Yang Q, et al. The prevalence of adult attention-deficit hyperactivity disorder: a global systematic review and meta-analysis. J Glob Health. 2021;11:04009. doi: 10.7189/jogh.11.04009
8. Chang JG, Cimino FM, Gossa W. ADHD in children: common questions and answers. Am Fam Physician. 2020;102:592-602.
9. Asarnow JR, Rozenman M, Wiblin J, et al. Integrated medical-behavioral care compared with usual primary care for child and adolescent behavioral health: a meta-analysis. JAMA Pediatr. 2015;169:929-937. doi: 10.1001/jamapediatrics.2015.1141
10. Squires J, Bricker D. Ages & Stages Questionnaires®. 3rd ed (ASQ®-3). Paul H. Brookes Publishing Co., Inc; 2009.
11. DuPaul GJ, Barkley RA. Situational variability of attention problems: psychometric properties of the Revised Home and School Situations Questionnaires. J Clin Child Psychol. 1992;21:178-188. doi.org/10.1207/s15374424jccp2102_10
12. Merenda PF. BASC: behavior assessment system for children. Meas Eval Counsel Develop. 1996;28:229-232.
13. Conners CK. Conners, 3rd ed manual. Multi-Health Systems. 2008.
14. Achenbach TM. The Child Behavior Checklist and related instruments. In: Maruish ME, ed. The Use of Psychological Testing for Treatment Planning and Outcomes Assessment. Lawrence Erlbaum Associates Publishers; 1999:429-466.
15. Goodman R. The extended version of the Strengths and Difficulties Questionnaire as a guide to child psychiatric caseness and consequent burden. J Child Psychol Psychiatry. 1999;40:791-799.
16. Wolraich ML, Lambert W, Doffing MA, et al. Psychometric properties of the Vanderbilt ADHD Diagnostic Parent Rating Scale in a referred population. J Pediatr Psychol. 2003;28:559-567. doi: 10.1093/jpepsy/jsg046
17. Sparrow SS, Cicchetti DV. The Vineland Adaptive Behavior Scales. In: Newmark CS, ed. Major Psychological Assessment Instruments. Vol 2. Allyn & Bacon; 2003:199-231.
18. Danielson ML, Bitsko RH, Ghandour RM, et al. Prevalence of parent-reported ADHD diagnosis and associated treatment among U.S. children and adolescents, 2016. J Clin Child Adolesc Psychol. 2018;47:199-212. doi: 10.1080/15374416.2017.1417860
19. Ghriwati NA, Langberg JM, Gardner W, et al. Impact of mental health comorbidities on the community-based pediatric treatment and outcomes of children with attention deficit hyperactivity disorder. J Dev Behav Ped. 2017;38:20-28. doi: 10.1097/DBP.0000000000000359
20. Niclasen J, Obel C, Homøe P, et al. Associations between otitis media and child behavioural and learning difficulties: results from a Danish Cohort. Int J Ped Otorhinolaryngol. 2016;84:12-20. doi: 10.1016/j.ijporl.2016.02.017
21. Ross JL Roeltgen DP Kushner H, et al. Behavioral and social phenotypes in boys with 47,XYY syndrome or 47,XXY Klinefelter syndrome. doi: 10.1542/peds.2011-0719
22. Mechler K, Banaschewski T, Hohmann S, et al. Evidence-based pharmacological treatment options for ADHD in children and adolescents. Pharmacol Ther. 2022;230:107940. doi: 10.1016/j.pharmthera.2021.107940
23. Mishra J, Merzenich MM, Sagar R. Accessible online neuroplasticity-targeted training for children with ADHD. Child Adolesc Psychiatry Ment Health. 2013;7:38. doi: 10.1186/1753-2000-7-38
24. Neece CL. Mindfulness-based stress reduction for parents of young children with developmental delays: implications for parental mental health and child behavior problems. J Applied Res Intellect Disabil. 2014;27:174-186. doi: 10.1111/jar.12064
25. Petcharat M, Liehr P. Mindfulness training for parents of children with special needs: guidance for nurses in mental health practice. J Child Adolesc Psychiatr Nursing. 2017;30:35-46. doi: 10.1111/jcap.12169
26. Hahn-Markowitz J, Burger I, Manor I, et al. Efficacy of cognitive-functional (Cog-Fun) occupational therapy intervention among children with ADHD: an RCT. J Atten Disord. 2020;24:655-666. doi: 10.1177/1087054716666955
27. Young Z, Moghaddam N, Tickle A. The efficacy of cognitive behavioral therapy for adults with ADHD: a systematic review and meta-analysis of randomized controlled trials. J Atten Disord. 2020;24:875-888.
28. Carr AW, Bean RA, Nelson KF. Childhood attention-deficit hyperactivity disorder: family therapy from an attachment based perspective. Child Youth Serv Rev. 2020;119:105666.
29. Robin AL. Family therapy for adolescents with ADHD. Child Adolesc Psychiatr Clin N Am. 2014;23:747-756. doi: 10.1016/j.chc.2014.06.001
30. Cattoi B, Alpern I, Katz JS, et al. The adverse health outcomes, economic burden, and public health implications of unmanaged attention deficit hyperactivity disorder (ADHD): a call to action resulting from CHADD summit, Washington, DC, October 17, 2019. J Atten Disord. 2022;26:807-808. doi: 10.1177/10870547211036754
31. Hinojosa MS, Hinojosa R, Nguyen J. Shared decision making and treatment for minority children with ADHD. J Transcult Nurs. 2020;31:135-143. doi: 10.1177/1043659619853021
32. Slobodin O, Masalha R. Challenges in ADHD care for ethnic minority children: a review of the current literature. Transcult Psychiatry. 2020;57:468-483. doi: 10.1177/1363461520902885
33. Retz W, Ginsberg Y, Turner D, et al. Attention-deficit/hyperactivity disorder (ADHD), antisociality and delinquent behavior over the lifespan. Neurosci Biobehav Rev. 2021;120:236-248. doi: 10.1016/j.neubiorev.2020.11.025
34. Del Sol Calderon P, Izquierdo A, Garcia Moreno M. Effects of the pandemic on the mental health of children and adolescents. Review and current scientific evidence of the SARS-COV2 pandemic. Eur Psychiatry. 2021;64:S223-S224. doi: 10.1192/j.eurpsy.2021.597
35. Insa I, Alda JA. Attention deficit hyperactivity disorder (ADHD) & COVID-19: attention deficit hyperactivity disorder: consequences of the 1st wave. Eur Psychiatry. 2021;64:S660. doi: 10.1192/j.eurpsy.2021.1752
1. Bitsko RH, Claussen AH, Lichstein J, et al. Mental health surveillance among children—United States, 2013-2019. MMWR Suppl. 2022;71:1-42. doi: 10.15585/mmwr.su7102a1
2. Danielson ML, Holbrook JR, Blumberg SJ, et al. State-level estimates of the prevalence of parent-reported ADHD diagnosis and treatment among U.S. children and adolescents, 2016 to 2019. J Atten Disord. 2022;26:1685-1697. doi: 10.1177/10870547221099961
3. Faraone SV, Banaschewski T, Coghill D, et al. The World Federation of ADHD International Consensus Statement: 208 evidence-based conclusions about the disorder. Neurosci Biobehav Rev. 2021;128:789-818. doi: 10.1016/j.neubiorev.2021.01.022
4. American Psychiatric Association
5. Brahmbhatt K, Hilty DM, Mina H, et al. Diagnosis and treatment of attention deficit hyperactivity disorder during adolescence in the primary care setting: a concise review. J Adolesc Health. 2016;59:135-143. doi: 10.1016/j.jadohealth.2016.03.025
6. Wolraich ML, Hagan JF, Allan C, et al. AAP Subcommittee on Children and Adolescents with Attention-Deficit/Hyperactivity Disorder. Clinical Practice Guideline for the Diagnosis, Evaluation, and Treatment of Attention-Deficit/Hyperactivity Disorder in Children and Adolescents. Pediatrics. 2019;144:e20192528. doi: 10.1542/peds.2019-2528
7. Song P, Zha M, Yang Q, et al. The prevalence of adult attention-deficit hyperactivity disorder: a global systematic review and meta-analysis. J Glob Health. 2021;11:04009. doi: 10.7189/jogh.11.04009
8. Chang JG, Cimino FM, Gossa W. ADHD in children: common questions and answers. Am Fam Physician. 2020;102:592-602.
9. Asarnow JR, Rozenman M, Wiblin J, et al. Integrated medical-behavioral care compared with usual primary care for child and adolescent behavioral health: a meta-analysis. JAMA Pediatr. 2015;169:929-937. doi: 10.1001/jamapediatrics.2015.1141
10. Squires J, Bricker D. Ages & Stages Questionnaires®. 3rd ed (ASQ®-3). Paul H. Brookes Publishing Co., Inc; 2009.
11. DuPaul GJ, Barkley RA. Situational variability of attention problems: psychometric properties of the Revised Home and School Situations Questionnaires. J Clin Child Psychol. 1992;21:178-188. doi.org/10.1207/s15374424jccp2102_10
12. Merenda PF. BASC: behavior assessment system for children. Meas Eval Counsel Develop. 1996;28:229-232.
13. Conners CK. Conners, 3rd ed manual. Multi-Health Systems. 2008.
14. Achenbach TM. The Child Behavior Checklist and related instruments. In: Maruish ME, ed. The Use of Psychological Testing for Treatment Planning and Outcomes Assessment. Lawrence Erlbaum Associates Publishers; 1999:429-466.
15. Goodman R. The extended version of the Strengths and Difficulties Questionnaire as a guide to child psychiatric caseness and consequent burden. J Child Psychol Psychiatry. 1999;40:791-799.
16. Wolraich ML, Lambert W, Doffing MA, et al. Psychometric properties of the Vanderbilt ADHD Diagnostic Parent Rating Scale in a referred population. J Pediatr Psychol. 2003;28:559-567. doi: 10.1093/jpepsy/jsg046
17. Sparrow SS, Cicchetti DV. The Vineland Adaptive Behavior Scales. In: Newmark CS, ed. Major Psychological Assessment Instruments. Vol 2. Allyn & Bacon; 2003:199-231.
18. Danielson ML, Bitsko RH, Ghandour RM, et al. Prevalence of parent-reported ADHD diagnosis and associated treatment among U.S. children and adolescents, 2016. J Clin Child Adolesc Psychol. 2018;47:199-212. doi: 10.1080/15374416.2017.1417860
19. Ghriwati NA, Langberg JM, Gardner W, et al. Impact of mental health comorbidities on the community-based pediatric treatment and outcomes of children with attention deficit hyperactivity disorder. J Dev Behav Ped. 2017;38:20-28. doi: 10.1097/DBP.0000000000000359
20. Niclasen J, Obel C, Homøe P, et al. Associations between otitis media and child behavioural and learning difficulties: results from a Danish Cohort. Int J Ped Otorhinolaryngol. 2016;84:12-20. doi: 10.1016/j.ijporl.2016.02.017
21. Ross JL Roeltgen DP Kushner H, et al. Behavioral and social phenotypes in boys with 47,XYY syndrome or 47,XXY Klinefelter syndrome. doi: 10.1542/peds.2011-0719
22. Mechler K, Banaschewski T, Hohmann S, et al. Evidence-based pharmacological treatment options for ADHD in children and adolescents. Pharmacol Ther. 2022;230:107940. doi: 10.1016/j.pharmthera.2021.107940
23. Mishra J, Merzenich MM, Sagar R. Accessible online neuroplasticity-targeted training for children with ADHD. Child Adolesc Psychiatry Ment Health. 2013;7:38. doi: 10.1186/1753-2000-7-38
24. Neece CL. Mindfulness-based stress reduction for parents of young children with developmental delays: implications for parental mental health and child behavior problems. J Applied Res Intellect Disabil. 2014;27:174-186. doi: 10.1111/jar.12064
25. Petcharat M, Liehr P. Mindfulness training for parents of children with special needs: guidance for nurses in mental health practice. J Child Adolesc Psychiatr Nursing. 2017;30:35-46. doi: 10.1111/jcap.12169
26. Hahn-Markowitz J, Burger I, Manor I, et al. Efficacy of cognitive-functional (Cog-Fun) occupational therapy intervention among children with ADHD: an RCT. J Atten Disord. 2020;24:655-666. doi: 10.1177/1087054716666955
27. Young Z, Moghaddam N, Tickle A. The efficacy of cognitive behavioral therapy for adults with ADHD: a systematic review and meta-analysis of randomized controlled trials. J Atten Disord. 2020;24:875-888.
28. Carr AW, Bean RA, Nelson KF. Childhood attention-deficit hyperactivity disorder: family therapy from an attachment based perspective. Child Youth Serv Rev. 2020;119:105666.
29. Robin AL. Family therapy for adolescents with ADHD. Child Adolesc Psychiatr Clin N Am. 2014;23:747-756. doi: 10.1016/j.chc.2014.06.001
30. Cattoi B, Alpern I, Katz JS, et al. The adverse health outcomes, economic burden, and public health implications of unmanaged attention deficit hyperactivity disorder (ADHD): a call to action resulting from CHADD summit, Washington, DC, October 17, 2019. J Atten Disord. 2022;26:807-808. doi: 10.1177/10870547211036754
31. Hinojosa MS, Hinojosa R, Nguyen J. Shared decision making and treatment for minority children with ADHD. J Transcult Nurs. 2020;31:135-143. doi: 10.1177/1043659619853021
32. Slobodin O, Masalha R. Challenges in ADHD care for ethnic minority children: a review of the current literature. Transcult Psychiatry. 2020;57:468-483. doi: 10.1177/1363461520902885
33. Retz W, Ginsberg Y, Turner D, et al. Attention-deficit/hyperactivity disorder (ADHD), antisociality and delinquent behavior over the lifespan. Neurosci Biobehav Rev. 2021;120:236-248. doi: 10.1016/j.neubiorev.2020.11.025
34. Del Sol Calderon P, Izquierdo A, Garcia Moreno M. Effects of the pandemic on the mental health of children and adolescents. Review and current scientific evidence of the SARS-COV2 pandemic. Eur Psychiatry. 2021;64:S223-S224. doi: 10.1192/j.eurpsy.2021.597
35. Insa I, Alda JA. Attention deficit hyperactivity disorder (ADHD) & COVID-19: attention deficit hyperactivity disorder: consequences of the 1st wave. Eur Psychiatry. 2021;64:S660. doi: 10.1192/j.eurpsy.2021.1752
Does physical exercise reduce dementia-associated agitation?
Evidence summary
Mixed results on exercise’s effect on neuropsychiatric symptoms
A 2020 systematic review and meta-analysis of 18 RCTs investigated the effect of home-based physical activity on several markers of behavioral and psychological symptoms of dementia (BPSD). These symptoms were measured using the caregiver-completed neuropsychiatric inventory (NPI), which includes agitation. There was substantial heterogeneity between trials; however, 4 RCTs (472 patients) were included in a meta-analysis of the NPI. These RCTs were nonblinded, given the nature of the intervention.1
Interventions to enhance physical activity ranged from 12 weeks to 2 years in duration, with 2 to 8 contacts from the study team per week. The type of physical activity varied and included cardiorespiratory endurance, balance training, resistance training, and activities of daily living training.1
Exercise was associated with significantly fewer symptoms on the NPI, although the effect size was small (standard mean difference [SMD] = –0.37; 95% CI, –0.57 to –0.17). Heterogeneity in the interventions and assessments were limitations to this meta-analysis.1
A 2015 systematic review and meta-analysis of 18 RCTs compared the effect of exercise interventions against a control group for the treatment of BPSD, utilizing 10 behavioral and 2 neurovegetative components of the NPI (each scored from 0 to 5) in patients with dementia. Studies were included if they used ≥ 1 exercise intervention compared to a control or usual care group without additional exercise recommendations. Thirteen studies had a multicomponent training intervention (≥ 2 exercise types grouped together in the same training session), 2 used tai chi, 4 used walking, and 1 used dance and movement therapy. These RCTs were conducted in a variety of settings, including community-dwelling and long-term care facilities (n = 6427 patients).2
Exercise did not reduce global BPSD (N = 4441 patients), with a weighted mean difference (WMD) of −3.9 (95% CI, −9.0 to 1.2; P = .13).
A 2017 hospital-based RCT evaluated the effects of a short-term exercise program on neuropsychiatric signs and symptoms in patients with dementia in 3 specialized dementia care wards (N = 85). Patients had a diagnosis of dementia, minimum length of stay of 1 week, no delirium, and the ability to perform the Timed Up and Go Test. The intervention group included a 2-week exercise program of four 20-minute exercise sessions per day on 3 days per week, involving strengthening or endurance exercises, in addition to treatment as usual. The control group included a 2-week period of social-stimulation programs consisting of table games for 120 minutes per week, in addition to treatment as usual.3
Of 85 patients randomized, 15 (18%) were lost to follow-up (14 of whom were discharged early from the hospital). Among the 70 patients included in the final analysis, the mean age was 80 years; 47% were female and 53% male; and the mean Mini-Mental Status Examination score was 18.3 (≤ 23 indicates dementia). In both groups, most patients had moderate dementia, moderate neuropsychiatric signs and symptoms, and a low level of psychotic symptoms. Patients in the intervention group had a higher adherence rate compared with those in the control group.3
Continue to: The primary outcome...
The primary outcome was neuropsychiatric signs and symptoms as measured by the Alzheimer’s Disease Cooperative Study–Clinical Global Impression of Change (ADCS-CGIC). Compared to the control group, the intervention group experienced greater improvement on the ADCS-CGIC dimensions of emotional agitation (
A 2016 factorial cluster RCT of 16 nursing homes (with at least 60% of the population having dementia) compared the use of person-centered care vs person-centered care plus at least 1 randomly assigned additional intervention (eg, antipsychotic medication use review, social interaction interventions, and exercise over a period of 9 months) (n = 277, with 193 analyzed per protocol). Exercise was implemented at 1 hour per week or at an increase of 20% above baseline and compared with a control group with no change in exercise.4
Exercise significantly improved neuropsychiatric symptoms. The baseline NPI score of 14.54 improved by –3.59 (95% CI, –7.08 to –0.09; P < .05). However, none of the study interventions significantly improved the agitation-specific scores. The primary limitation of this study was that antipsychotic prescribing was at the discretion of the provider and not according to a protocol. In addition, the authors noted that the trial was inadequately powered to correct for testing 3 primary outcomes.4
Editor’s takeaway
Dementia and dementia with agitation are challenging conditions to treat. Disappointingly, physical exercise had inconsistent and generally minimal effect on agitation in dementia. Nevertheless, exercise had other positive effects. So, considering the benefits that exercise does provide, its low cost, and its limited adverse effects, exercise remains a small tool to address a big problem.
1. de Almeida SIL, Gomes da Silva M, de Dias Marques ASP. Home-based physical activity programs for people with dementia: systematic review and meta-analysis. Gerontologist. 2020;60:600-608. doi: 10.1093/geront/gnz176
2. de Souto Barreto P, Demougeot L, Pillard F, et al. Exercise training for managing behavioral and psychological symptoms in people with dementia: a systematic review and meta-analysis. Ageing Res Rev. 2015;24(pt B):274-285. doi: 10.1016/j.arr.2015.09.001
3. Fleiner T, Dauth H, Gersie M, et al. Structured physical exercise improves neuropsychiatric symptoms in acute dementia care: a hospital-based RCT. Alzheimers Res Ther. 2017;9:68. doi: 10.1186/s13195-017-0289-z
4. Ballard C, Orrell M, YongZhong S, et al. Impact of antipsychotic review and nonpharmacological intervention on antipsychotic use, neuropsychiatric symptoms, and mortality in people with dementia living in nursing homes: a factorial cluster-randomized controlled trial by the Well-Being and Health for People With Dementia (WHELD) Program. Am J Psychiatry. 2016;173:252-262. doi: 10.1176/appi.ajp.2015.15010130
Evidence summary
Mixed results on exercise’s effect on neuropsychiatric symptoms
A 2020 systematic review and meta-analysis of 18 RCTs investigated the effect of home-based physical activity on several markers of behavioral and psychological symptoms of dementia (BPSD). These symptoms were measured using the caregiver-completed neuropsychiatric inventory (NPI), which includes agitation. There was substantial heterogeneity between trials; however, 4 RCTs (472 patients) were included in a meta-analysis of the NPI. These RCTs were nonblinded, given the nature of the intervention.1
Interventions to enhance physical activity ranged from 12 weeks to 2 years in duration, with 2 to 8 contacts from the study team per week. The type of physical activity varied and included cardiorespiratory endurance, balance training, resistance training, and activities of daily living training.1
Exercise was associated with significantly fewer symptoms on the NPI, although the effect size was small (standard mean difference [SMD] = –0.37; 95% CI, –0.57 to –0.17). Heterogeneity in the interventions and assessments were limitations to this meta-analysis.1
A 2015 systematic review and meta-analysis of 18 RCTs compared the effect of exercise interventions against a control group for the treatment of BPSD, utilizing 10 behavioral and 2 neurovegetative components of the NPI (each scored from 0 to 5) in patients with dementia. Studies were included if they used ≥ 1 exercise intervention compared to a control or usual care group without additional exercise recommendations. Thirteen studies had a multicomponent training intervention (≥ 2 exercise types grouped together in the same training session), 2 used tai chi, 4 used walking, and 1 used dance and movement therapy. These RCTs were conducted in a variety of settings, including community-dwelling and long-term care facilities (n = 6427 patients).2
Exercise did not reduce global BPSD (N = 4441 patients), with a weighted mean difference (WMD) of −3.9 (95% CI, −9.0 to 1.2; P = .13).
A 2017 hospital-based RCT evaluated the effects of a short-term exercise program on neuropsychiatric signs and symptoms in patients with dementia in 3 specialized dementia care wards (N = 85). Patients had a diagnosis of dementia, minimum length of stay of 1 week, no delirium, and the ability to perform the Timed Up and Go Test. The intervention group included a 2-week exercise program of four 20-minute exercise sessions per day on 3 days per week, involving strengthening or endurance exercises, in addition to treatment as usual. The control group included a 2-week period of social-stimulation programs consisting of table games for 120 minutes per week, in addition to treatment as usual.3
Of 85 patients randomized, 15 (18%) were lost to follow-up (14 of whom were discharged early from the hospital). Among the 70 patients included in the final analysis, the mean age was 80 years; 47% were female and 53% male; and the mean Mini-Mental Status Examination score was 18.3 (≤ 23 indicates dementia). In both groups, most patients had moderate dementia, moderate neuropsychiatric signs and symptoms, and a low level of psychotic symptoms. Patients in the intervention group had a higher adherence rate compared with those in the control group.3
Continue to: The primary outcome...
The primary outcome was neuropsychiatric signs and symptoms as measured by the Alzheimer’s Disease Cooperative Study–Clinical Global Impression of Change (ADCS-CGIC). Compared to the control group, the intervention group experienced greater improvement on the ADCS-CGIC dimensions of emotional agitation (
A 2016 factorial cluster RCT of 16 nursing homes (with at least 60% of the population having dementia) compared the use of person-centered care vs person-centered care plus at least 1 randomly assigned additional intervention (eg, antipsychotic medication use review, social interaction interventions, and exercise over a period of 9 months) (n = 277, with 193 analyzed per protocol). Exercise was implemented at 1 hour per week or at an increase of 20% above baseline and compared with a control group with no change in exercise.4
Exercise significantly improved neuropsychiatric symptoms. The baseline NPI score of 14.54 improved by –3.59 (95% CI, –7.08 to –0.09; P < .05). However, none of the study interventions significantly improved the agitation-specific scores. The primary limitation of this study was that antipsychotic prescribing was at the discretion of the provider and not according to a protocol. In addition, the authors noted that the trial was inadequately powered to correct for testing 3 primary outcomes.4
Editor’s takeaway
Dementia and dementia with agitation are challenging conditions to treat. Disappointingly, physical exercise had inconsistent and generally minimal effect on agitation in dementia. Nevertheless, exercise had other positive effects. So, considering the benefits that exercise does provide, its low cost, and its limited adverse effects, exercise remains a small tool to address a big problem.
Evidence summary
Mixed results on exercise’s effect on neuropsychiatric symptoms
A 2020 systematic review and meta-analysis of 18 RCTs investigated the effect of home-based physical activity on several markers of behavioral and psychological symptoms of dementia (BPSD). These symptoms were measured using the caregiver-completed neuropsychiatric inventory (NPI), which includes agitation. There was substantial heterogeneity between trials; however, 4 RCTs (472 patients) were included in a meta-analysis of the NPI. These RCTs were nonblinded, given the nature of the intervention.1
Interventions to enhance physical activity ranged from 12 weeks to 2 years in duration, with 2 to 8 contacts from the study team per week. The type of physical activity varied and included cardiorespiratory endurance, balance training, resistance training, and activities of daily living training.1
Exercise was associated with significantly fewer symptoms on the NPI, although the effect size was small (standard mean difference [SMD] = –0.37; 95% CI, –0.57 to –0.17). Heterogeneity in the interventions and assessments were limitations to this meta-analysis.1
A 2015 systematic review and meta-analysis of 18 RCTs compared the effect of exercise interventions against a control group for the treatment of BPSD, utilizing 10 behavioral and 2 neurovegetative components of the NPI (each scored from 0 to 5) in patients with dementia. Studies were included if they used ≥ 1 exercise intervention compared to a control or usual care group without additional exercise recommendations. Thirteen studies had a multicomponent training intervention (≥ 2 exercise types grouped together in the same training session), 2 used tai chi, 4 used walking, and 1 used dance and movement therapy. These RCTs were conducted in a variety of settings, including community-dwelling and long-term care facilities (n = 6427 patients).2
Exercise did not reduce global BPSD (N = 4441 patients), with a weighted mean difference (WMD) of −3.9 (95% CI, −9.0 to 1.2; P = .13).
A 2017 hospital-based RCT evaluated the effects of a short-term exercise program on neuropsychiatric signs and symptoms in patients with dementia in 3 specialized dementia care wards (N = 85). Patients had a diagnosis of dementia, minimum length of stay of 1 week, no delirium, and the ability to perform the Timed Up and Go Test. The intervention group included a 2-week exercise program of four 20-minute exercise sessions per day on 3 days per week, involving strengthening or endurance exercises, in addition to treatment as usual. The control group included a 2-week period of social-stimulation programs consisting of table games for 120 minutes per week, in addition to treatment as usual.3
Of 85 patients randomized, 15 (18%) were lost to follow-up (14 of whom were discharged early from the hospital). Among the 70 patients included in the final analysis, the mean age was 80 years; 47% were female and 53% male; and the mean Mini-Mental Status Examination score was 18.3 (≤ 23 indicates dementia). In both groups, most patients had moderate dementia, moderate neuropsychiatric signs and symptoms, and a low level of psychotic symptoms. Patients in the intervention group had a higher adherence rate compared with those in the control group.3
Continue to: The primary outcome...
The primary outcome was neuropsychiatric signs and symptoms as measured by the Alzheimer’s Disease Cooperative Study–Clinical Global Impression of Change (ADCS-CGIC). Compared to the control group, the intervention group experienced greater improvement on the ADCS-CGIC dimensions of emotional agitation (
A 2016 factorial cluster RCT of 16 nursing homes (with at least 60% of the population having dementia) compared the use of person-centered care vs person-centered care plus at least 1 randomly assigned additional intervention (eg, antipsychotic medication use review, social interaction interventions, and exercise over a period of 9 months) (n = 277, with 193 analyzed per protocol). Exercise was implemented at 1 hour per week or at an increase of 20% above baseline and compared with a control group with no change in exercise.4
Exercise significantly improved neuropsychiatric symptoms. The baseline NPI score of 14.54 improved by –3.59 (95% CI, –7.08 to –0.09; P < .05). However, none of the study interventions significantly improved the agitation-specific scores. The primary limitation of this study was that antipsychotic prescribing was at the discretion of the provider and not according to a protocol. In addition, the authors noted that the trial was inadequately powered to correct for testing 3 primary outcomes.4
Editor’s takeaway
Dementia and dementia with agitation are challenging conditions to treat. Disappointingly, physical exercise had inconsistent and generally minimal effect on agitation in dementia. Nevertheless, exercise had other positive effects. So, considering the benefits that exercise does provide, its low cost, and its limited adverse effects, exercise remains a small tool to address a big problem.
1. de Almeida SIL, Gomes da Silva M, de Dias Marques ASP. Home-based physical activity programs for people with dementia: systematic review and meta-analysis. Gerontologist. 2020;60:600-608. doi: 10.1093/geront/gnz176
2. de Souto Barreto P, Demougeot L, Pillard F, et al. Exercise training for managing behavioral and psychological symptoms in people with dementia: a systematic review and meta-analysis. Ageing Res Rev. 2015;24(pt B):274-285. doi: 10.1016/j.arr.2015.09.001
3. Fleiner T, Dauth H, Gersie M, et al. Structured physical exercise improves neuropsychiatric symptoms in acute dementia care: a hospital-based RCT. Alzheimers Res Ther. 2017;9:68. doi: 10.1186/s13195-017-0289-z
4. Ballard C, Orrell M, YongZhong S, et al. Impact of antipsychotic review and nonpharmacological intervention on antipsychotic use, neuropsychiatric symptoms, and mortality in people with dementia living in nursing homes: a factorial cluster-randomized controlled trial by the Well-Being and Health for People With Dementia (WHELD) Program. Am J Psychiatry. 2016;173:252-262. doi: 10.1176/appi.ajp.2015.15010130
1. de Almeida SIL, Gomes da Silva M, de Dias Marques ASP. Home-based physical activity programs for people with dementia: systematic review and meta-analysis. Gerontologist. 2020;60:600-608. doi: 10.1093/geront/gnz176
2. de Souto Barreto P, Demougeot L, Pillard F, et al. Exercise training for managing behavioral and psychological symptoms in people with dementia: a systematic review and meta-analysis. Ageing Res Rev. 2015;24(pt B):274-285. doi: 10.1016/j.arr.2015.09.001
3. Fleiner T, Dauth H, Gersie M, et al. Structured physical exercise improves neuropsychiatric symptoms in acute dementia care: a hospital-based RCT. Alzheimers Res Ther. 2017;9:68. doi: 10.1186/s13195-017-0289-z
4. Ballard C, Orrell M, YongZhong S, et al. Impact of antipsychotic review and nonpharmacological intervention on antipsychotic use, neuropsychiatric symptoms, and mortality in people with dementia living in nursing homes: a factorial cluster-randomized controlled trial by the Well-Being and Health for People With Dementia (WHELD) Program. Am J Psychiatry. 2016;173:252-262. doi: 10.1176/appi.ajp.2015.15010130
EVIDENCE-BASED ANSWER:
Not consistently. Physical exer- cise demonstrates inconsistent benefit for neuropsychiatric symptoms, including agitation, in patients with dementia (strength of recommendation: B, inconsistent meta-analyses, 2 small randomized controlled trials [RCTs]). The care setting and the modality, frequency, and duration of exercise varied across trials; the impact of these factors is not known.
Pediatricians, specialists largely agree on ASD diagnoses
General pediatricians and a multidisciplinary team of specialists agreed most of the time on which children should be diagnosed with autism spectrum disorder (ASD), data from a new study suggest.
But when it came to ruling out ASD, the agreement rate was much lower.
The study by Melanie Penner, MSc, MD, with the Autism Research Centre at Bloorview Research Institute, Toronto, and colleagues found that 89% of the time when a physician determined a child had ASD, the multidisciplinary team agreed. But when a pediatrician thought a child did not have ASD, the multidisciplinary team agreed only 60% of the time. The study was published in JAMA Network Open.
Multidisciplinary team model can’t keep up with demand
The findings are important as many guidelines recommend multidisciplinary teams (MDTs) for all ASD diagnostic assessment. However, the resources for this model can’t meet the demand of children needing a diagnosis and can lead to long waits for ASD therapies.
In Canada, the researchers note, the average wait time from referral to receipt of ASD diagnosis has been reported as 7 months and “has likely lengthened since the COVID-19 pandemic.”
Jennifer Gerdts, PhD, an attending psychologist at the Seattle Children’s Autism Center, said in an interview that the wait there for diagnosis in children older than 4 is “multiple years,” a length of time that’s common across the United States. Meanwhile, in many states families can’t access services without a diagnosis.
Expanding capacity with diagnoses by general pediatricians may improve access, but the diagnostic accuracy is critical.
Dr. Gerdts, who was not part of the study, said this research is “hugely important in the work that is under way to build community capacity for diagnostic evaluation.”
She said this study shows that not all diagnoses need the resources of a multiple-disciplinary team and that “pediatricians can do it, too, and they can do it pretty accurately.” Dr. Gerdts evaluates children for autism and helps train pediatricians to make diagnoses.
Pediatricians, specialist team completed blinded assessments
The 17 pediatricians in the study and the specialist team independently completed blinded assessment and each recorded a decision on whether the child had ASD. The prospective diagnostic study was conducted in a specialist assessment center in Toronto and in general pediatrician practices in Ontario from June 2016 to March 2020.
Children were younger than 5.5 years, did not have an ASD diagnosis and were referred because there was a development concern. The pediatricians referred 106 children (75% boys; average age, 3.5 years). More than half (57%) of the participating children were from minority racial and ethnic groups.
The children were randomly assigned to two groups: One included children who had their MDT visits before their pediatrician assessment and the other group included those who had their MDT visits after their pediatrician assessment.
The MDT diagnosed more than two-thirds of the children (68%) with ASD.
Sensitivity and specificity of the pediatrician assessments, compared with that of the specialist team, were 0.75 (95% confidence interval, 0.67-0.83) and 0.79 (95% CI, 0.62-0.91), respectively.
A look at pediatricians’ accuracy
Pediatricians reported the decisions they would have made had the child not been in the study.
- In 69% of the true-positive cases, pediatricians would have given an ASD diagnosis.
- In 44% of true-negative cases, they would have told the family the child did not have autism; in 30% of those case, they would give alternative diagnoses (most commonly ADHD and language delay).
- The pediatrician would have diagnosed ASD in only one of the seven false-positive cases and would refer those patients to a subspecialist 71% of the time.
- In false-negative cases, the pediatrician would incorrectly tell the family the child does not have autism 44% of the time.
Regarding the false-negative cases, the authors wrote, “more caution is needed for pediatricians when definitively ruling out ASD, which might result in diagnostic delays.”
Confidence is key
Physician confidence was also correlated with accuracy.
The authors wrote: “Among true-positive cases (MDT and pediatrician agree the child has ASD), the pediatrician was certain or very certain 80% of the time (43 cases) and the MDT was certain or very certain 96% of the time (52 cases). As such, if pediatricians conferred ASD diagnoses when feeling certain or very certain, they would make 46 correct diagnoses and 2 incorrect diagnoses.”
The high accuracy of diagnosis when physicians are confident suggests “listening to that sense of certainty is important,” Dr. Gerdts said. Conversely, these numbers show when a physician is uncertain about diagnosing ASD, they should listen to that instinct, too, and refer.
The results of the study support having general pediatricians diagnose and move forward with their patients when the signs of ASD are more definitive, saving the less-certain cases for the more resource-intensive teams to diagnose. Many states are moving toward that “tiered” system, Dr. Gerdts said.
“For many, and in fact most children, general pediatricians are pretty accurate when making an autism diagnosis,” she said.
“Let’s get [general pediatricians] confident in recognizing when this is outside their skill and ability level,” she said. “If you’re not sure, it is better to refer them on than to misdiagnose them.”
The important missing piece she said is how to support them “so they don’t feel pressure to make that call,” Dr. Gerdts said.
This project was funded by a grant from the Bloorview Research Institute, a grant from the Canadian Institutes of Health Research and a grant from the Canadian Institutes of Health. Three coauthors consult for and receive grants from several pharmaceutical companies and other organizations. Dr. Gerdts declared no relevant financial relationships.
General pediatricians and a multidisciplinary team of specialists agreed most of the time on which children should be diagnosed with autism spectrum disorder (ASD), data from a new study suggest.
But when it came to ruling out ASD, the agreement rate was much lower.
The study by Melanie Penner, MSc, MD, with the Autism Research Centre at Bloorview Research Institute, Toronto, and colleagues found that 89% of the time when a physician determined a child had ASD, the multidisciplinary team agreed. But when a pediatrician thought a child did not have ASD, the multidisciplinary team agreed only 60% of the time. The study was published in JAMA Network Open.
Multidisciplinary team model can’t keep up with demand
The findings are important as many guidelines recommend multidisciplinary teams (MDTs) for all ASD diagnostic assessment. However, the resources for this model can’t meet the demand of children needing a diagnosis and can lead to long waits for ASD therapies.
In Canada, the researchers note, the average wait time from referral to receipt of ASD diagnosis has been reported as 7 months and “has likely lengthened since the COVID-19 pandemic.”
Jennifer Gerdts, PhD, an attending psychologist at the Seattle Children’s Autism Center, said in an interview that the wait there for diagnosis in children older than 4 is “multiple years,” a length of time that’s common across the United States. Meanwhile, in many states families can’t access services without a diagnosis.
Expanding capacity with diagnoses by general pediatricians may improve access, but the diagnostic accuracy is critical.
Dr. Gerdts, who was not part of the study, said this research is “hugely important in the work that is under way to build community capacity for diagnostic evaluation.”
She said this study shows that not all diagnoses need the resources of a multiple-disciplinary team and that “pediatricians can do it, too, and they can do it pretty accurately.” Dr. Gerdts evaluates children for autism and helps train pediatricians to make diagnoses.
Pediatricians, specialist team completed blinded assessments
The 17 pediatricians in the study and the specialist team independently completed blinded assessment and each recorded a decision on whether the child had ASD. The prospective diagnostic study was conducted in a specialist assessment center in Toronto and in general pediatrician practices in Ontario from June 2016 to March 2020.
Children were younger than 5.5 years, did not have an ASD diagnosis and were referred because there was a development concern. The pediatricians referred 106 children (75% boys; average age, 3.5 years). More than half (57%) of the participating children were from minority racial and ethnic groups.
The children were randomly assigned to two groups: One included children who had their MDT visits before their pediatrician assessment and the other group included those who had their MDT visits after their pediatrician assessment.
The MDT diagnosed more than two-thirds of the children (68%) with ASD.
Sensitivity and specificity of the pediatrician assessments, compared with that of the specialist team, were 0.75 (95% confidence interval, 0.67-0.83) and 0.79 (95% CI, 0.62-0.91), respectively.
A look at pediatricians’ accuracy
Pediatricians reported the decisions they would have made had the child not been in the study.
- In 69% of the true-positive cases, pediatricians would have given an ASD diagnosis.
- In 44% of true-negative cases, they would have told the family the child did not have autism; in 30% of those case, they would give alternative diagnoses (most commonly ADHD and language delay).
- The pediatrician would have diagnosed ASD in only one of the seven false-positive cases and would refer those patients to a subspecialist 71% of the time.
- In false-negative cases, the pediatrician would incorrectly tell the family the child does not have autism 44% of the time.
Regarding the false-negative cases, the authors wrote, “more caution is needed for pediatricians when definitively ruling out ASD, which might result in diagnostic delays.”
Confidence is key
Physician confidence was also correlated with accuracy.
The authors wrote: “Among true-positive cases (MDT and pediatrician agree the child has ASD), the pediatrician was certain or very certain 80% of the time (43 cases) and the MDT was certain or very certain 96% of the time (52 cases). As such, if pediatricians conferred ASD diagnoses when feeling certain or very certain, they would make 46 correct diagnoses and 2 incorrect diagnoses.”
The high accuracy of diagnosis when physicians are confident suggests “listening to that sense of certainty is important,” Dr. Gerdts said. Conversely, these numbers show when a physician is uncertain about diagnosing ASD, they should listen to that instinct, too, and refer.
The results of the study support having general pediatricians diagnose and move forward with their patients when the signs of ASD are more definitive, saving the less-certain cases for the more resource-intensive teams to diagnose. Many states are moving toward that “tiered” system, Dr. Gerdts said.
“For many, and in fact most children, general pediatricians are pretty accurate when making an autism diagnosis,” she said.
“Let’s get [general pediatricians] confident in recognizing when this is outside their skill and ability level,” she said. “If you’re not sure, it is better to refer them on than to misdiagnose them.”
The important missing piece she said is how to support them “so they don’t feel pressure to make that call,” Dr. Gerdts said.
This project was funded by a grant from the Bloorview Research Institute, a grant from the Canadian Institutes of Health Research and a grant from the Canadian Institutes of Health. Three coauthors consult for and receive grants from several pharmaceutical companies and other organizations. Dr. Gerdts declared no relevant financial relationships.
General pediatricians and a multidisciplinary team of specialists agreed most of the time on which children should be diagnosed with autism spectrum disorder (ASD), data from a new study suggest.
But when it came to ruling out ASD, the agreement rate was much lower.
The study by Melanie Penner, MSc, MD, with the Autism Research Centre at Bloorview Research Institute, Toronto, and colleagues found that 89% of the time when a physician determined a child had ASD, the multidisciplinary team agreed. But when a pediatrician thought a child did not have ASD, the multidisciplinary team agreed only 60% of the time. The study was published in JAMA Network Open.
Multidisciplinary team model can’t keep up with demand
The findings are important as many guidelines recommend multidisciplinary teams (MDTs) for all ASD diagnostic assessment. However, the resources for this model can’t meet the demand of children needing a diagnosis and can lead to long waits for ASD therapies.
In Canada, the researchers note, the average wait time from referral to receipt of ASD diagnosis has been reported as 7 months and “has likely lengthened since the COVID-19 pandemic.”
Jennifer Gerdts, PhD, an attending psychologist at the Seattle Children’s Autism Center, said in an interview that the wait there for diagnosis in children older than 4 is “multiple years,” a length of time that’s common across the United States. Meanwhile, in many states families can’t access services without a diagnosis.
Expanding capacity with diagnoses by general pediatricians may improve access, but the diagnostic accuracy is critical.
Dr. Gerdts, who was not part of the study, said this research is “hugely important in the work that is under way to build community capacity for diagnostic evaluation.”
She said this study shows that not all diagnoses need the resources of a multiple-disciplinary team and that “pediatricians can do it, too, and they can do it pretty accurately.” Dr. Gerdts evaluates children for autism and helps train pediatricians to make diagnoses.
Pediatricians, specialist team completed blinded assessments
The 17 pediatricians in the study and the specialist team independently completed blinded assessment and each recorded a decision on whether the child had ASD. The prospective diagnostic study was conducted in a specialist assessment center in Toronto and in general pediatrician practices in Ontario from June 2016 to March 2020.
Children were younger than 5.5 years, did not have an ASD diagnosis and were referred because there was a development concern. The pediatricians referred 106 children (75% boys; average age, 3.5 years). More than half (57%) of the participating children were from minority racial and ethnic groups.
The children were randomly assigned to two groups: One included children who had their MDT visits before their pediatrician assessment and the other group included those who had their MDT visits after their pediatrician assessment.
The MDT diagnosed more than two-thirds of the children (68%) with ASD.
Sensitivity and specificity of the pediatrician assessments, compared with that of the specialist team, were 0.75 (95% confidence interval, 0.67-0.83) and 0.79 (95% CI, 0.62-0.91), respectively.
A look at pediatricians’ accuracy
Pediatricians reported the decisions they would have made had the child not been in the study.
- In 69% of the true-positive cases, pediatricians would have given an ASD diagnosis.
- In 44% of true-negative cases, they would have told the family the child did not have autism; in 30% of those case, they would give alternative diagnoses (most commonly ADHD and language delay).
- The pediatrician would have diagnosed ASD in only one of the seven false-positive cases and would refer those patients to a subspecialist 71% of the time.
- In false-negative cases, the pediatrician would incorrectly tell the family the child does not have autism 44% of the time.
Regarding the false-negative cases, the authors wrote, “more caution is needed for pediatricians when definitively ruling out ASD, which might result in diagnostic delays.”
Confidence is key
Physician confidence was also correlated with accuracy.
The authors wrote: “Among true-positive cases (MDT and pediatrician agree the child has ASD), the pediatrician was certain or very certain 80% of the time (43 cases) and the MDT was certain or very certain 96% of the time (52 cases). As such, if pediatricians conferred ASD diagnoses when feeling certain or very certain, they would make 46 correct diagnoses and 2 incorrect diagnoses.”
The high accuracy of diagnosis when physicians are confident suggests “listening to that sense of certainty is important,” Dr. Gerdts said. Conversely, these numbers show when a physician is uncertain about diagnosing ASD, they should listen to that instinct, too, and refer.
The results of the study support having general pediatricians diagnose and move forward with their patients when the signs of ASD are more definitive, saving the less-certain cases for the more resource-intensive teams to diagnose. Many states are moving toward that “tiered” system, Dr. Gerdts said.
“For many, and in fact most children, general pediatricians are pretty accurate when making an autism diagnosis,” she said.
“Let’s get [general pediatricians] confident in recognizing when this is outside their skill and ability level,” she said. “If you’re not sure, it is better to refer them on than to misdiagnose them.”
The important missing piece she said is how to support them “so they don’t feel pressure to make that call,” Dr. Gerdts said.
This project was funded by a grant from the Bloorview Research Institute, a grant from the Canadian Institutes of Health Research and a grant from the Canadian Institutes of Health. Three coauthors consult for and receive grants from several pharmaceutical companies and other organizations. Dr. Gerdts declared no relevant financial relationships.
FROM JAMA NETWORK OPEN
Nine more minutes a day of vigorous exercise tied to better cognition
such as running and cycling, plays in brain health.
“Even minor differences in daily behavior appeared meaningful for cognition in this study,” researcher John J. Mitchell, MSci and PhD candidate, Medical Research Council, London, told this news organization.
The findings were published online in the Journal of Epidemiology and Community Health.
Research gap
Previous research has linked physical activity (PA) with increased cognitive reserve, which delays the onset of cognitive decline in later life. But disentangling the most important components of PA for cognition – such as intensity and volume – has not been well researched.
Previous studies didn’t capture sleep time, which typically takes up the largest component of the day. Sleep is “acutely relevant” when examining cognition, the investigators noted.
In addition, studies in this area often focus on just one or two activity components of the day, which “neglects the growing awareness” that movements “are all tightly interlinked,” said Mr. Mitchell.
The new study included 4,481 participants in the British Cohort Study who were born in 1970 across England, Scotland, and Wales. The participants were followed throughout childhood and adulthood.
The median age of the participants was 47 years, and they were predominantly White, female (52%), married (66%), and well educated. Most were occasional or nonrisky alcohol consumers, and half had never smoked.
The researchers collected biometric measurements and health, demographic, and lifestyle information. Participants wore a thigh-mounted accelerometer at least 7 consecutive hours a day for up to 7 days to track PA, sedentary behavior (SB), and sleep time.
The device used in the study could detect subtle movements as well as speed of accelerations, said Mr. Mitchell. “From this, we can distinguish MVPA from slow walking, standing, and sitting. It’s the current best practice for detecting the more subtle movements we make, such as brisk walking and stair climbing, beyond just ‘exercise,’ “ he added.
Light intensity PA (LIPA) describes movement such as walking and moving around the house or office, while MVPA includes activities such as brisk walking and running that accelerate the heart rate. SB, defined as time spent sitting or lying, is distinguished from standing by the thigh inclination.
On an average day, the cohort spent 51 minutes in MVPA; 5 hours, 42 minutes in LIPA; 9 hours, 16 minutes in SB; and 8 hours, 11 minutes sleeping.
Researchers calculated an overall global score for verbal memory and executive function.
The study used “compositional data analysis,” a statistical method that can examine the associations of cognition and PA in the context of all components of daily movement.
The analysis revealed a positive association between MVPA and cognition relative to all other behaviors, after adjustment for sociodemographic factors that included sex, age, education, and marital status. But the relationship lessened after further adjustment for health status – for example, cardiovascular disease or disability – and lifestyle factors, such as alcohol consumption and smoking status.
SB relative to all other movements remained positively associated with cognition after full adjustment. This, the authors speculated, may reflect engagement in cognitively stimulating activities such as reading.
To better understand the associations, the researchers used a statistical method to reallocate time in the cohort’s average day from one activity component to another.
“We held two of the components static but moved time between the other two and monitored the theoretical ramifications of that change for cognition,” said Mr. Mitchell.
Real cognitive change
There was a 1.31% improvement in cognition ranking compared to the sample average after replacing 9 minutes of sedentary activity with MVPA (1.31; 95% confidence interval [CI], 0.09-2.50). There was a 1.27% improvement after replacing 7 minutes of LIPA with MVPA, and a 1.2% improvement after replacing 7 minutes of sleep with MVPA.
Individuals might move up from about the 50th percentile to the 51st or 52nd percentile after just 9 minutes of more moderate to vigorous movement in place of sitting, said Mr. Mitchell. “This highlights how even very modest differences in people’s daily movement – less than 10 minutes – is linked to quite real changes in our cognitive health.”
The impact of physical activity appeared greatest on working memory and mental processes, such as planning and organization.
On the other hand, cognition declined by 1%-2% after replacing MVPA with 8 minutes of SB, 6 minutes of LIPA, or 7 minutes of sleep.
The activity tracking device couldn’t determine how well participants slept, which is “a clear limitation” of the study, said Mr. Mitchell. “We have to be cautious when trying to interpret our findings surrounding sleep.”
Another limitation is that despite a large sample size, people of color were underrepresented, limiting the generalizability of the findings. As well, other healthy pursuits – for example, reading – might have contributed to improved cognition.
Important findings
In a comment, Jennifer J. Heisz, PhD, associate professor and Canada research chair in brain health and aging, department of kinesiology, McMaster University, Hamilton, Ont., said the findings from the study are important.
“Through the statistical modelling, the authors demonstrate that swapping just 9 minutes of sedentary behavior with moderate to vigorous physical activity, such as a brisk walk or bike ride, was associated with an increase in cognition.”
She added that this seemed to be especially true for people who sit while at work.
The findings “confer with the growing consensus” that some exercise is better than none when it comes to brain health, said Dr. Heisz.
“Clinicians should encourage their patients to add a brisk, 10-minute walk to their daily routine and break up prolonged sitting with short movement breaks.”
She noted the study was cross-sectional, “so it is not possible to infer causation.”
The study received funding from the Medical Research Council and the British Heart Foundation. Mr. Mitchell and Dr. Heisz have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
such as running and cycling, plays in brain health.
“Even minor differences in daily behavior appeared meaningful for cognition in this study,” researcher John J. Mitchell, MSci and PhD candidate, Medical Research Council, London, told this news organization.
The findings were published online in the Journal of Epidemiology and Community Health.
Research gap
Previous research has linked physical activity (PA) with increased cognitive reserve, which delays the onset of cognitive decline in later life. But disentangling the most important components of PA for cognition – such as intensity and volume – has not been well researched.
Previous studies didn’t capture sleep time, which typically takes up the largest component of the day. Sleep is “acutely relevant” when examining cognition, the investigators noted.
In addition, studies in this area often focus on just one or two activity components of the day, which “neglects the growing awareness” that movements “are all tightly interlinked,” said Mr. Mitchell.
The new study included 4,481 participants in the British Cohort Study who were born in 1970 across England, Scotland, and Wales. The participants were followed throughout childhood and adulthood.
The median age of the participants was 47 years, and they were predominantly White, female (52%), married (66%), and well educated. Most were occasional or nonrisky alcohol consumers, and half had never smoked.
The researchers collected biometric measurements and health, demographic, and lifestyle information. Participants wore a thigh-mounted accelerometer at least 7 consecutive hours a day for up to 7 days to track PA, sedentary behavior (SB), and sleep time.
The device used in the study could detect subtle movements as well as speed of accelerations, said Mr. Mitchell. “From this, we can distinguish MVPA from slow walking, standing, and sitting. It’s the current best practice for detecting the more subtle movements we make, such as brisk walking and stair climbing, beyond just ‘exercise,’ “ he added.
Light intensity PA (LIPA) describes movement such as walking and moving around the house or office, while MVPA includes activities such as brisk walking and running that accelerate the heart rate. SB, defined as time spent sitting or lying, is distinguished from standing by the thigh inclination.
On an average day, the cohort spent 51 minutes in MVPA; 5 hours, 42 minutes in LIPA; 9 hours, 16 minutes in SB; and 8 hours, 11 minutes sleeping.
Researchers calculated an overall global score for verbal memory and executive function.
The study used “compositional data analysis,” a statistical method that can examine the associations of cognition and PA in the context of all components of daily movement.
The analysis revealed a positive association between MVPA and cognition relative to all other behaviors, after adjustment for sociodemographic factors that included sex, age, education, and marital status. But the relationship lessened after further adjustment for health status – for example, cardiovascular disease or disability – and lifestyle factors, such as alcohol consumption and smoking status.
SB relative to all other movements remained positively associated with cognition after full adjustment. This, the authors speculated, may reflect engagement in cognitively stimulating activities such as reading.
To better understand the associations, the researchers used a statistical method to reallocate time in the cohort’s average day from one activity component to another.
“We held two of the components static but moved time between the other two and monitored the theoretical ramifications of that change for cognition,” said Mr. Mitchell.
Real cognitive change
There was a 1.31% improvement in cognition ranking compared to the sample average after replacing 9 minutes of sedentary activity with MVPA (1.31; 95% confidence interval [CI], 0.09-2.50). There was a 1.27% improvement after replacing 7 minutes of LIPA with MVPA, and a 1.2% improvement after replacing 7 minutes of sleep with MVPA.
Individuals might move up from about the 50th percentile to the 51st or 52nd percentile after just 9 minutes of more moderate to vigorous movement in place of sitting, said Mr. Mitchell. “This highlights how even very modest differences in people’s daily movement – less than 10 minutes – is linked to quite real changes in our cognitive health.”
The impact of physical activity appeared greatest on working memory and mental processes, such as planning and organization.
On the other hand, cognition declined by 1%-2% after replacing MVPA with 8 minutes of SB, 6 minutes of LIPA, or 7 minutes of sleep.
The activity tracking device couldn’t determine how well participants slept, which is “a clear limitation” of the study, said Mr. Mitchell. “We have to be cautious when trying to interpret our findings surrounding sleep.”
Another limitation is that despite a large sample size, people of color were underrepresented, limiting the generalizability of the findings. As well, other healthy pursuits – for example, reading – might have contributed to improved cognition.
Important findings
In a comment, Jennifer J. Heisz, PhD, associate professor and Canada research chair in brain health and aging, department of kinesiology, McMaster University, Hamilton, Ont., said the findings from the study are important.
“Through the statistical modelling, the authors demonstrate that swapping just 9 minutes of sedentary behavior with moderate to vigorous physical activity, such as a brisk walk or bike ride, was associated with an increase in cognition.”
She added that this seemed to be especially true for people who sit while at work.
The findings “confer with the growing consensus” that some exercise is better than none when it comes to brain health, said Dr. Heisz.
“Clinicians should encourage their patients to add a brisk, 10-minute walk to their daily routine and break up prolonged sitting with short movement breaks.”
She noted the study was cross-sectional, “so it is not possible to infer causation.”
The study received funding from the Medical Research Council and the British Heart Foundation. Mr. Mitchell and Dr. Heisz have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
such as running and cycling, plays in brain health.
“Even minor differences in daily behavior appeared meaningful for cognition in this study,” researcher John J. Mitchell, MSci and PhD candidate, Medical Research Council, London, told this news organization.
The findings were published online in the Journal of Epidemiology and Community Health.
Research gap
Previous research has linked physical activity (PA) with increased cognitive reserve, which delays the onset of cognitive decline in later life. But disentangling the most important components of PA for cognition – such as intensity and volume – has not been well researched.
Previous studies didn’t capture sleep time, which typically takes up the largest component of the day. Sleep is “acutely relevant” when examining cognition, the investigators noted.
In addition, studies in this area often focus on just one or two activity components of the day, which “neglects the growing awareness” that movements “are all tightly interlinked,” said Mr. Mitchell.
The new study included 4,481 participants in the British Cohort Study who were born in 1970 across England, Scotland, and Wales. The participants were followed throughout childhood and adulthood.
The median age of the participants was 47 years, and they were predominantly White, female (52%), married (66%), and well educated. Most were occasional or nonrisky alcohol consumers, and half had never smoked.
The researchers collected biometric measurements and health, demographic, and lifestyle information. Participants wore a thigh-mounted accelerometer at least 7 consecutive hours a day for up to 7 days to track PA, sedentary behavior (SB), and sleep time.
The device used in the study could detect subtle movements as well as speed of accelerations, said Mr. Mitchell. “From this, we can distinguish MVPA from slow walking, standing, and sitting. It’s the current best practice for detecting the more subtle movements we make, such as brisk walking and stair climbing, beyond just ‘exercise,’ “ he added.
Light intensity PA (LIPA) describes movement such as walking and moving around the house or office, while MVPA includes activities such as brisk walking and running that accelerate the heart rate. SB, defined as time spent sitting or lying, is distinguished from standing by the thigh inclination.
On an average day, the cohort spent 51 minutes in MVPA; 5 hours, 42 minutes in LIPA; 9 hours, 16 minutes in SB; and 8 hours, 11 minutes sleeping.
Researchers calculated an overall global score for verbal memory and executive function.
The study used “compositional data analysis,” a statistical method that can examine the associations of cognition and PA in the context of all components of daily movement.
The analysis revealed a positive association between MVPA and cognition relative to all other behaviors, after adjustment for sociodemographic factors that included sex, age, education, and marital status. But the relationship lessened after further adjustment for health status – for example, cardiovascular disease or disability – and lifestyle factors, such as alcohol consumption and smoking status.
SB relative to all other movements remained positively associated with cognition after full adjustment. This, the authors speculated, may reflect engagement in cognitively stimulating activities such as reading.
To better understand the associations, the researchers used a statistical method to reallocate time in the cohort’s average day from one activity component to another.
“We held two of the components static but moved time between the other two and monitored the theoretical ramifications of that change for cognition,” said Mr. Mitchell.
Real cognitive change
There was a 1.31% improvement in cognition ranking compared to the sample average after replacing 9 minutes of sedentary activity with MVPA (1.31; 95% confidence interval [CI], 0.09-2.50). There was a 1.27% improvement after replacing 7 minutes of LIPA with MVPA, and a 1.2% improvement after replacing 7 minutes of sleep with MVPA.
Individuals might move up from about the 50th percentile to the 51st or 52nd percentile after just 9 minutes of more moderate to vigorous movement in place of sitting, said Mr. Mitchell. “This highlights how even very modest differences in people’s daily movement – less than 10 minutes – is linked to quite real changes in our cognitive health.”
The impact of physical activity appeared greatest on working memory and mental processes, such as planning and organization.
On the other hand, cognition declined by 1%-2% after replacing MVPA with 8 minutes of SB, 6 minutes of LIPA, or 7 minutes of sleep.
The activity tracking device couldn’t determine how well participants slept, which is “a clear limitation” of the study, said Mr. Mitchell. “We have to be cautious when trying to interpret our findings surrounding sleep.”
Another limitation is that despite a large sample size, people of color were underrepresented, limiting the generalizability of the findings. As well, other healthy pursuits – for example, reading – might have contributed to improved cognition.
Important findings
In a comment, Jennifer J. Heisz, PhD, associate professor and Canada research chair in brain health and aging, department of kinesiology, McMaster University, Hamilton, Ont., said the findings from the study are important.
“Through the statistical modelling, the authors demonstrate that swapping just 9 minutes of sedentary behavior with moderate to vigorous physical activity, such as a brisk walk or bike ride, was associated with an increase in cognition.”
She added that this seemed to be especially true for people who sit while at work.
The findings “confer with the growing consensus” that some exercise is better than none when it comes to brain health, said Dr. Heisz.
“Clinicians should encourage their patients to add a brisk, 10-minute walk to their daily routine and break up prolonged sitting with short movement breaks.”
She noted the study was cross-sectional, “so it is not possible to infer causation.”
The study received funding from the Medical Research Council and the British Heart Foundation. Mr. Mitchell and Dr. Heisz have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH
Flu, other common viruses linked to neurologic disease
People hospitalized with viral infections like the flu are more likely to have disorders that degrade the nervous system, like Alzheimer’s or Parkinson’s, later in life, a new analysis shows.
The viruses included influenza, encephalitis, herpes, hepatitis, pneumonia, meningitis, and shingles. Those viruses were linked to one or more of these conditions: Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS), dementia, and multiple sclerosis.
The authors of the study, which was published this month in the journal Neuron, cautioned that their findings stopped short of saying the viruses caused the disorders.
“Neurodegenerative disorders are a collection of diseases for which there are very few effective treatments and many risk factors,” study author and National Institutes of Health researcher Andrew B. Singleton, PhD, said in a news release from the NIH. “Our results support the idea that viral infections and related inflammation in the nervous system may be common – and possibly avoidable – risk factors for these types of disorders.”
For the study, two data sets were analyzed with a combined 800,000 medical records for people in Finland and the United Kingdom. People who were hospitalized with COVID-19 were excluded from the study.
Generalized dementia was the condition linked to the most viruses. People exposed to viral encephalitis, which causes brain inflammation, were 20 times more likely to be diagnosed with Alzheimer’s, compared with those who were not diagnosed with that virus.
Both influenza and pneumonia were also associated with all of the neurodegenerative disorder diagnoses studied, with the exception of multiple sclerosis. The researchers found that severe flu cases were linked to the most risks.
“Keep in mind that the individuals we studied did not have the common cold. Their infections made them so sick that they had to go to the hospital,” said study author and NIH researcher Michael Nalls, PhD. “Nevertheless, the fact that commonly used vaccines reduce the risk or severity of many of the viral illnesses observed in this study raises the possibility that the risks of neurodegenerative disorders might also be mitigated.”
The researchers examined the time from when someone was infected with a virus to the time when they were diagnosed with one of the neurodegenerative disorders. They found that most had a high risk within 1 year of infection. But in six scenarios, there were significant links that showed up after 5-15 years.
The authors wrote that vaccines that are available for some of the viruses studied may be a way to reduce the risk of getting diseases that degrade the nervous system.
A version of this article first appeared on WebMD.com.
People hospitalized with viral infections like the flu are more likely to have disorders that degrade the nervous system, like Alzheimer’s or Parkinson’s, later in life, a new analysis shows.
The viruses included influenza, encephalitis, herpes, hepatitis, pneumonia, meningitis, and shingles. Those viruses were linked to one or more of these conditions: Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS), dementia, and multiple sclerosis.
The authors of the study, which was published this month in the journal Neuron, cautioned that their findings stopped short of saying the viruses caused the disorders.
“Neurodegenerative disorders are a collection of diseases for which there are very few effective treatments and many risk factors,” study author and National Institutes of Health researcher Andrew B. Singleton, PhD, said in a news release from the NIH. “Our results support the idea that viral infections and related inflammation in the nervous system may be common – and possibly avoidable – risk factors for these types of disorders.”
For the study, two data sets were analyzed with a combined 800,000 medical records for people in Finland and the United Kingdom. People who were hospitalized with COVID-19 were excluded from the study.
Generalized dementia was the condition linked to the most viruses. People exposed to viral encephalitis, which causes brain inflammation, were 20 times more likely to be diagnosed with Alzheimer’s, compared with those who were not diagnosed with that virus.
Both influenza and pneumonia were also associated with all of the neurodegenerative disorder diagnoses studied, with the exception of multiple sclerosis. The researchers found that severe flu cases were linked to the most risks.
“Keep in mind that the individuals we studied did not have the common cold. Their infections made them so sick that they had to go to the hospital,” said study author and NIH researcher Michael Nalls, PhD. “Nevertheless, the fact that commonly used vaccines reduce the risk or severity of many of the viral illnesses observed in this study raises the possibility that the risks of neurodegenerative disorders might also be mitigated.”
The researchers examined the time from when someone was infected with a virus to the time when they were diagnosed with one of the neurodegenerative disorders. They found that most had a high risk within 1 year of infection. But in six scenarios, there were significant links that showed up after 5-15 years.
The authors wrote that vaccines that are available for some of the viruses studied may be a way to reduce the risk of getting diseases that degrade the nervous system.
A version of this article first appeared on WebMD.com.
People hospitalized with viral infections like the flu are more likely to have disorders that degrade the nervous system, like Alzheimer’s or Parkinson’s, later in life, a new analysis shows.
The viruses included influenza, encephalitis, herpes, hepatitis, pneumonia, meningitis, and shingles. Those viruses were linked to one or more of these conditions: Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS), dementia, and multiple sclerosis.
The authors of the study, which was published this month in the journal Neuron, cautioned that their findings stopped short of saying the viruses caused the disorders.
“Neurodegenerative disorders are a collection of diseases for which there are very few effective treatments and many risk factors,” study author and National Institutes of Health researcher Andrew B. Singleton, PhD, said in a news release from the NIH. “Our results support the idea that viral infections and related inflammation in the nervous system may be common – and possibly avoidable – risk factors for these types of disorders.”
For the study, two data sets were analyzed with a combined 800,000 medical records for people in Finland and the United Kingdom. People who were hospitalized with COVID-19 were excluded from the study.
Generalized dementia was the condition linked to the most viruses. People exposed to viral encephalitis, which causes brain inflammation, were 20 times more likely to be diagnosed with Alzheimer’s, compared with those who were not diagnosed with that virus.
Both influenza and pneumonia were also associated with all of the neurodegenerative disorder diagnoses studied, with the exception of multiple sclerosis. The researchers found that severe flu cases were linked to the most risks.
“Keep in mind that the individuals we studied did not have the common cold. Their infections made them so sick that they had to go to the hospital,” said study author and NIH researcher Michael Nalls, PhD. “Nevertheless, the fact that commonly used vaccines reduce the risk or severity of many of the viral illnesses observed in this study raises the possibility that the risks of neurodegenerative disorders might also be mitigated.”
The researchers examined the time from when someone was infected with a virus to the time when they were diagnosed with one of the neurodegenerative disorders. They found that most had a high risk within 1 year of infection. But in six scenarios, there were significant links that showed up after 5-15 years.
The authors wrote that vaccines that are available for some of the viruses studied may be a way to reduce the risk of getting diseases that degrade the nervous system.
A version of this article first appeared on WebMD.com.
FROM NEURON
Children with autism but no intellectual disability may be falling through the cracks
Approximately two out of three children with autism spectrum disorder (ASD) do not have concurrent intellectual disability, according to a population study of ASD trends.
Intellectual functioning remains the best predictor of functional outcomes in kids with ASD, and missing those with no cognitive impairment (ASD-N) can prevent intervention and affect future achievement.
Furthermore, while the study found that ASD-N increased among all demographic subgroups from 2000 to 2016, it also observed widespread health disparities in identifying ASD-N, especially in Black, Hispanic, and underprivileged children.
“ASD is a major public health concern and prevalence estimates are likely to continue to rise as disparities are reduced and ASD identification is improved,” wrote researchers led by Josephine Shenouda, DrPH, MS, of Rutgers School of Public Health in Piscataway, N.J., in Pediatrics .
The study period saw a surprising 500% increase in the prevalence of ASD-N and a 200% increase in the prevalence of cognitive impairment–associated ASD-I , with higher rates across all sex, race, ethnicity, and socioeconomic subgroups. The five- and twofold respective increases are consistent with previous research.
“To a large degree, the rise in autism estimates has been driven by individuals without intellectual disability,” Dr. Shenouda said in an interview. “The best way to address increasing autism and to affect disparities in autism identification is through universal autism screening during the toddler period. And different metrics of functional outcomes need to be developed to understand the expression of autism better.”
Her group had previously seen autism estimates of approximately 1% in 2000 rise to 3% by 2016 but had noted variations, with some communities exceeding 5% for autism estimates. “That led to the question of why, and we saw that in areas with high estimates, we are identifying more children with autism without intellectual disability,” she said. “We wanted to know if the increase over time was equally distributed among children with autism with and without intellectual disability.”
A study in disparities
The cross-sectional study examined data from active ASD surveillance by the CDC’s Autism and Developmental Disabilities Monitoring Network in 8-year-olds residing in the New York/New Jersey Metropolitan Area. Overall, 4,661 children were identified with ASD, with ASD-I affecting 1,505 (32.3%), and ASD-N affecting 2,764 (59.3%). Non-Hispanic Black children who were affected numbered 946 (20.3%), while 1,230 (26.4%) were Hispanic, and 2,114 (45.4%) were non-Hispanic White.
Notably, Black children were 30% less likely to be identified with ASD-N compared with White children, and children residing in affluent areas were 80% more likely to be identified with ASD-N versus those in underserved areas. Furthermore, a greater proportion of children with ASD-I resided in vulnerable areas compared with their counterparts with ASD-N.
While males had a higher prevalence compared with females regardless of intellectual disability status, male-to-female ratios were slightly lower among ASD-I compared with ASD-N cases.
Commenting on the study but not involved in it, Barbara J. Howard, MD, an assistant professor of medicine at Johns Hopkins University, Baltimore, said the increasing gap in identifying ASD-N according to race, ethnicity, and socioeconomic status measures probably reflects greater parental awareness of ASD and access to diagnostic services in White families and those of higher socioeconomic status. “There were no racial, ethnicity, or socioeconomic status differences in the prevalence of the more obvious and impairing ASD-I in the sample, but its prevalence was also increasing over this period,” she said.
Although the greater recognition of the less impairing ASD-N is important for optimal outcomes through intervention, the increasing discrepancies mean that more children generally and more marginalized children specifically are not being diagnosed or served. “There should be no differences in prevalence by these characteristics,” Dr. Howard said. “The striking inequity for non-White children and those of lower socioeconomic status in being diagnosed with ASD-N and thus qualifying for intervention that could improve their long-term functioning is likely also compounded by service, educational, and social disadvantages they may experience.”
In light of these disparities, an accompanying editorial by Emily Hotez, PhD, of the University of California, Los Angeles, and Lindsay Shea, DrPH, of the A.J. Drexel Autism Institute at Drexel University, Philadelphia, argues that social determinants of health (SDOH) should be prioritized in the public health surveillance of autism since these factors potentially contribute to the general underdiagnosis of autism in minority groups and merit more attention from pediatricians. While SDOH affects many nonautistic conditions, it may be even more important for families dealing with the stressors and isolation associated with autism, the commentators said. “Our commentary speaks to the utility of increasing SDOH surveillance in improving our understanding of autistic individuals’ needs, experiences, and priorities on a population level,” Dr. Hotez said in an interview. She added that integrating SDOH surveillance into pediatricians’ workflows will lead to improvements in clinical practice and patient care in the long term.
“Specifically, increased uptake of universal SDOH screening and referral practices will allow pediatricians to more proactively link autistic children and families, particularly those from marginalized groups, with much-needed health-promoting services and supports.” She cautioned, however, that while most providers believe universal SDOH screening is important, fewer report that screening is feasible or feel prepared to address families’ social needs when they are identified.
This study was supported by the Centers for Disease Control and Prevention and the National Institutes of Health/National Institute of Environmental Health Sciences. The authors had no conflicts of interest to disclose. The commentators had no potential conflicts of interest to disclose. Dr. Howard disclosed no competing interests relevant to her comments.
Approximately two out of three children with autism spectrum disorder (ASD) do not have concurrent intellectual disability, according to a population study of ASD trends.
Intellectual functioning remains the best predictor of functional outcomes in kids with ASD, and missing those with no cognitive impairment (ASD-N) can prevent intervention and affect future achievement.
Furthermore, while the study found that ASD-N increased among all demographic subgroups from 2000 to 2016, it also observed widespread health disparities in identifying ASD-N, especially in Black, Hispanic, and underprivileged children.
“ASD is a major public health concern and prevalence estimates are likely to continue to rise as disparities are reduced and ASD identification is improved,” wrote researchers led by Josephine Shenouda, DrPH, MS, of Rutgers School of Public Health in Piscataway, N.J., in Pediatrics .
The study period saw a surprising 500% increase in the prevalence of ASD-N and a 200% increase in the prevalence of cognitive impairment–associated ASD-I , with higher rates across all sex, race, ethnicity, and socioeconomic subgroups. The five- and twofold respective increases are consistent with previous research.
“To a large degree, the rise in autism estimates has been driven by individuals without intellectual disability,” Dr. Shenouda said in an interview. “The best way to address increasing autism and to affect disparities in autism identification is through universal autism screening during the toddler period. And different metrics of functional outcomes need to be developed to understand the expression of autism better.”
Her group had previously seen autism estimates of approximately 1% in 2000 rise to 3% by 2016 but had noted variations, with some communities exceeding 5% for autism estimates. “That led to the question of why, and we saw that in areas with high estimates, we are identifying more children with autism without intellectual disability,” she said. “We wanted to know if the increase over time was equally distributed among children with autism with and without intellectual disability.”
A study in disparities
The cross-sectional study examined data from active ASD surveillance by the CDC’s Autism and Developmental Disabilities Monitoring Network in 8-year-olds residing in the New York/New Jersey Metropolitan Area. Overall, 4,661 children were identified with ASD, with ASD-I affecting 1,505 (32.3%), and ASD-N affecting 2,764 (59.3%). Non-Hispanic Black children who were affected numbered 946 (20.3%), while 1,230 (26.4%) were Hispanic, and 2,114 (45.4%) were non-Hispanic White.
Notably, Black children were 30% less likely to be identified with ASD-N compared with White children, and children residing in affluent areas were 80% more likely to be identified with ASD-N versus those in underserved areas. Furthermore, a greater proportion of children with ASD-I resided in vulnerable areas compared with their counterparts with ASD-N.
While males had a higher prevalence compared with females regardless of intellectual disability status, male-to-female ratios were slightly lower among ASD-I compared with ASD-N cases.
Commenting on the study but not involved in it, Barbara J. Howard, MD, an assistant professor of medicine at Johns Hopkins University, Baltimore, said the increasing gap in identifying ASD-N according to race, ethnicity, and socioeconomic status measures probably reflects greater parental awareness of ASD and access to diagnostic services in White families and those of higher socioeconomic status. “There were no racial, ethnicity, or socioeconomic status differences in the prevalence of the more obvious and impairing ASD-I in the sample, but its prevalence was also increasing over this period,” she said.
Although the greater recognition of the less impairing ASD-N is important for optimal outcomes through intervention, the increasing discrepancies mean that more children generally and more marginalized children specifically are not being diagnosed or served. “There should be no differences in prevalence by these characteristics,” Dr. Howard said. “The striking inequity for non-White children and those of lower socioeconomic status in being diagnosed with ASD-N and thus qualifying for intervention that could improve their long-term functioning is likely also compounded by service, educational, and social disadvantages they may experience.”
In light of these disparities, an accompanying editorial by Emily Hotez, PhD, of the University of California, Los Angeles, and Lindsay Shea, DrPH, of the A.J. Drexel Autism Institute at Drexel University, Philadelphia, argues that social determinants of health (SDOH) should be prioritized in the public health surveillance of autism since these factors potentially contribute to the general underdiagnosis of autism in minority groups and merit more attention from pediatricians. While SDOH affects many nonautistic conditions, it may be even more important for families dealing with the stressors and isolation associated with autism, the commentators said. “Our commentary speaks to the utility of increasing SDOH surveillance in improving our understanding of autistic individuals’ needs, experiences, and priorities on a population level,” Dr. Hotez said in an interview. She added that integrating SDOH surveillance into pediatricians’ workflows will lead to improvements in clinical practice and patient care in the long term.
“Specifically, increased uptake of universal SDOH screening and referral practices will allow pediatricians to more proactively link autistic children and families, particularly those from marginalized groups, with much-needed health-promoting services and supports.” She cautioned, however, that while most providers believe universal SDOH screening is important, fewer report that screening is feasible or feel prepared to address families’ social needs when they are identified.
This study was supported by the Centers for Disease Control and Prevention and the National Institutes of Health/National Institute of Environmental Health Sciences. The authors had no conflicts of interest to disclose. The commentators had no potential conflicts of interest to disclose. Dr. Howard disclosed no competing interests relevant to her comments.
Approximately two out of three children with autism spectrum disorder (ASD) do not have concurrent intellectual disability, according to a population study of ASD trends.
Intellectual functioning remains the best predictor of functional outcomes in kids with ASD, and missing those with no cognitive impairment (ASD-N) can prevent intervention and affect future achievement.
Furthermore, while the study found that ASD-N increased among all demographic subgroups from 2000 to 2016, it also observed widespread health disparities in identifying ASD-N, especially in Black, Hispanic, and underprivileged children.
“ASD is a major public health concern and prevalence estimates are likely to continue to rise as disparities are reduced and ASD identification is improved,” wrote researchers led by Josephine Shenouda, DrPH, MS, of Rutgers School of Public Health in Piscataway, N.J., in Pediatrics .
The study period saw a surprising 500% increase in the prevalence of ASD-N and a 200% increase in the prevalence of cognitive impairment–associated ASD-I , with higher rates across all sex, race, ethnicity, and socioeconomic subgroups. The five- and twofold respective increases are consistent with previous research.
“To a large degree, the rise in autism estimates has been driven by individuals without intellectual disability,” Dr. Shenouda said in an interview. “The best way to address increasing autism and to affect disparities in autism identification is through universal autism screening during the toddler period. And different metrics of functional outcomes need to be developed to understand the expression of autism better.”
Her group had previously seen autism estimates of approximately 1% in 2000 rise to 3% by 2016 but had noted variations, with some communities exceeding 5% for autism estimates. “That led to the question of why, and we saw that in areas with high estimates, we are identifying more children with autism without intellectual disability,” she said. “We wanted to know if the increase over time was equally distributed among children with autism with and without intellectual disability.”
A study in disparities
The cross-sectional study examined data from active ASD surveillance by the CDC’s Autism and Developmental Disabilities Monitoring Network in 8-year-olds residing in the New York/New Jersey Metropolitan Area. Overall, 4,661 children were identified with ASD, with ASD-I affecting 1,505 (32.3%), and ASD-N affecting 2,764 (59.3%). Non-Hispanic Black children who were affected numbered 946 (20.3%), while 1,230 (26.4%) were Hispanic, and 2,114 (45.4%) were non-Hispanic White.
Notably, Black children were 30% less likely to be identified with ASD-N compared with White children, and children residing in affluent areas were 80% more likely to be identified with ASD-N versus those in underserved areas. Furthermore, a greater proportion of children with ASD-I resided in vulnerable areas compared with their counterparts with ASD-N.
While males had a higher prevalence compared with females regardless of intellectual disability status, male-to-female ratios were slightly lower among ASD-I compared with ASD-N cases.
Commenting on the study but not involved in it, Barbara J. Howard, MD, an assistant professor of medicine at Johns Hopkins University, Baltimore, said the increasing gap in identifying ASD-N according to race, ethnicity, and socioeconomic status measures probably reflects greater parental awareness of ASD and access to diagnostic services in White families and those of higher socioeconomic status. “There were no racial, ethnicity, or socioeconomic status differences in the prevalence of the more obvious and impairing ASD-I in the sample, but its prevalence was also increasing over this period,” she said.
Although the greater recognition of the less impairing ASD-N is important for optimal outcomes through intervention, the increasing discrepancies mean that more children generally and more marginalized children specifically are not being diagnosed or served. “There should be no differences in prevalence by these characteristics,” Dr. Howard said. “The striking inequity for non-White children and those of lower socioeconomic status in being diagnosed with ASD-N and thus qualifying for intervention that could improve their long-term functioning is likely also compounded by service, educational, and social disadvantages they may experience.”
In light of these disparities, an accompanying editorial by Emily Hotez, PhD, of the University of California, Los Angeles, and Lindsay Shea, DrPH, of the A.J. Drexel Autism Institute at Drexel University, Philadelphia, argues that social determinants of health (SDOH) should be prioritized in the public health surveillance of autism since these factors potentially contribute to the general underdiagnosis of autism in minority groups and merit more attention from pediatricians. While SDOH affects many nonautistic conditions, it may be even more important for families dealing with the stressors and isolation associated with autism, the commentators said. “Our commentary speaks to the utility of increasing SDOH surveillance in improving our understanding of autistic individuals’ needs, experiences, and priorities on a population level,” Dr. Hotez said in an interview. She added that integrating SDOH surveillance into pediatricians’ workflows will lead to improvements in clinical practice and patient care in the long term.
“Specifically, increased uptake of universal SDOH screening and referral practices will allow pediatricians to more proactively link autistic children and families, particularly those from marginalized groups, with much-needed health-promoting services and supports.” She cautioned, however, that while most providers believe universal SDOH screening is important, fewer report that screening is feasible or feel prepared to address families’ social needs when they are identified.
This study was supported by the Centers for Disease Control and Prevention and the National Institutes of Health/National Institute of Environmental Health Sciences. The authors had no conflicts of interest to disclose. The commentators had no potential conflicts of interest to disclose. Dr. Howard disclosed no competing interests relevant to her comments.
FROM PEDIATRICS
Put down the electronics after a concussion?
ILLUSTRATIVE CASE
A 17-year-old high school football player presents to the emergency department (ED) after a helmet-to-helmet tackle in a game earlier that day. After the tackle, he experienced immediate confusion. Once he returned to his feet, he felt dizzy and nauseated and began to develop a headache. When his symptoms failed to resolve within a few hours, his mother brought him to the hospital for an evaluation. In the ED, he receives a diagnosis of concussion, and his mother asks for recommendations on how he can recover as quickly as possible.
Traumatic brain injuries account for an estimated 2.5 million ED visits annually in the United States.2 Concussions are the most common form of traumatic brain injury, with adolescents contributing to the highest incidence of concussions.3,4 An estimated 1.6 to 3.8 million people experience a sports-related concussion annually.5
Time to recovery is a clinical endpoint that matters greatly to our young, physically active patients, who are often eager to return to their daily activities as soon as possible. Guidelines frequently recommend cognitive and physical rest for 24 to 48 hours immediately following a concussion, but the use of screens during this cognitive rest period remains uncertain.6,7 International guidelines and the Centers for Disease Control and Prevention recommend symptom-limited activities—including screen time—during the initial period of a concussion.6,7 Although this gradual approach is standard of care, it has been unclear if abstaining completely from certain activities during the initial days of a concussion has any impact on recovery time.
Recent studies have examined physical activity to clarify the optimal timing of physical rest after a concussion. Among adolescents with concussions, strict rest for 5 days does not appear to improve symptoms compared with rest for 1 to 2 days.8 Additionally, physical activity within 7 days of acute head injury may help reduce symptoms and prevent postconcussive symptoms.9,10
This same level of clarity has been lacking for cognitive rest and screen time. The use of screens is a part of most patients’ daily activities, particularly among adolescents and young adults. One report found that students ages 8 to 18 years engage in approximately 7 hours of daily screen time, excluding that related to
STUDY SUMMARY
Symptom duration was significantly reduced by cutting screen time
This single-site, parallel-design, randomized clinical trial examined the effectiveness of limiting screen time exposure within the first 48 hours after a concussion in reducing the time to resolution of concussive symptoms in 125 patients. 1 Patients were included if they were 12 to 25 years old (mean age, 17 years) and presented within 24 hours of sustaining a concussion (as defined on the Acute Concussion Evaluation–Emergency Department tool) to the pediatric or adult ED at a US tertiary medical center.
Patients were randomized to either engage in screen time as tolerated or to abstain from screen time for 48 hours following their injury. Screen modalities included television, phones, video games, and computers/tablets. The Post-Concussive Symptom Scale (PCSS; 0-132) was used to characterize 22 symptoms from 0 (absent) to 6 (severe) daily for 10 days. Patients also self-reported the amount of screen time they engaged in during Days 1 to 3 of the study period and completed an activity survey on Days 4 to 10. Among the participants, 76% completed the PCSS form until symptom resolution or until Day 10 (the end of the study period).
Continue to: The primary outcome...
The primary outcome was days to resolution of concussive symptoms, defined as a PCSS score ≤ 3. The median baseline PCSS score was 21 in the screen time–permitted group and 24.5 in the screen time–abstinent group. The screen time–permitted group reported a median screen time of 630 minutes during the intervention period, compared with 130 minutes in the screen time–abstinent group, and was less likely to recover during the study period than the screen time–abstinent group (hazard ratio = 0.51; 95% CI, 0.29-0.90). The screen time–permitted group had a significantly longer median recovery time compared with the screen time–abstinent group (8.0 vs 3.5 days; P = .03).
WHAT'S NEW?
Exploring the role of screen time during the cognitive rest period
This study provides evidence supporting the recommendation that adolescent and young adult patients abstain from screen time in the first 48 hours following a concussion to decrease time to symptom resolution, thus shortening the timeline to return to their usual daily activities.
CAVEATS
Self-reporting of data may introduce bias
This study used a self-reporting method to collect data, which could have resulted in underreporting or overreporting of screen time and potentially introduced recall and reporting bias. The screen time–abstinent group did not completely abstain from all screen time, with a self-reported average of 5 to 10 minutes of daily screen time to complete the required research surveys, so it is not immediately clear what extent of abstinence vs significant screen time reduction led to the clinical endpoints observed. Furthermore, this study did not ask patients to differentiate between active screen time (eg, texting and gaming) and passive screen time (eg, watching videos), which may differentially impact symptom resolution.
CHALLENGES TO IMPLEMENTATION
Turning off the ever-present screen may present obstacles
This intervention is easy to recommend, with few barriers to implementation. It’s worth noting that screens are often used in a patient’s school or job, and 48 hours of abstinence from these activities is a difficult ask when much of our society’s education, entertainment, and productivity revolve around the use of technology. When appropriate, a shared decision-making discussion between patient and physician should center on the idea that 48 hours of screen time abstinence could be well worth the increased likelihood of total recovery at Day 10, as opposed to the risk for persistent and prolonged symptoms that interfere with the patient’s lifestyle.
1. Macnow T, Curran T, Tolliday C, et al. Effect of screen time on recovery from concussion: a randomized clinical trial. JAMA Pediatr. 2021;175:1124-1131. doi: 10.1001/jamapediat rics.2021.2782
2. Taylor CA, Bell JM, Breiding MJ, et al. Traumatic brain injury–related emergency department visits, hospitalizations, and deaths—United States, 2007 and 2013. MMWR Surveill Summ. 2017;66:1-16. doi: 10.15585/mmwr.ss6609a1
3. Vos PE, Battistin L, Birbamer G, et al; European Federation of Neurological Societies. EFNS guideline on mild traumatic brain injury: report of an EFNS task force. Eur J Neurol. 2002;9:207-219. doi: 10.1046/j.1468-1331.2002.00407.x
4. Zhang AL, Sing DC, Rugg CM, et al. The rise of concussions in the adolescent population. Orthop J Sports Med. 2016;4:2325967116662458. doi: 10.1177/2325967116662458
5. McKee AC, Cantu RC, Nowinski CJ, et al. Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury. J Neuropathol Exp Neurol. 2009;68:709-735. doi: 10.1097/NEN.0b013e3181a9d503
6. McCrory P, Meeuwisse W, Dvorák J, et al. Consensus statement on concussion in sport—the 5th international conference on concussion in sport held in Berlin, October 2016. Br J Sports Med. 2017;51:838-847. doi: 10.1136/bjsports-2017-097699
7. Lumba-Brown A, Yeates KO, Sarmiento K, et al. Centers for Disease Control and Prevention guideline on the diagnosis and management of mild traumatic brain injury among children. JAMA Pediatr. 2018;172:e182853. doi: 10.1001/jamapediat rics.2018.2853
8. Thomas DG, Apps JN, Hoffmann RG, et al. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics. 2015;135:213-223. doi: 10.1542/peds.2014-0966
9. Grool AM, Aglipay M, Momoli F, et al; Pediatric Emergency Research Canada (PERC) Concussion Team. Association between early participation in physical activity following acute concussion and persistent postconcussive symptoms in children and adolescents. JAMA. 2016;316:2504-2514. doi: 10.1001/jama.2016.17396
10. Lal A, Kolakowsky-Hayner SA, Ghajar J, et al. The effect of physical exercise after a concussion: a systematic review and meta-analysis. Am J Sports Med. 2018;46:743-752. doi: 10.1177/0363546517706137
11. Rideout V, Peebles A, Mann S, et al. The Common Sense Census: Media Use by Tweens and Teens, 2021. Common Sense Media; 2022. Accessed December 28, 2022. www.commonsensemedia.org/sites/default/files/research/report/8-18-census-integrated-report-final-web_0.pdf
ILLUSTRATIVE CASE
A 17-year-old high school football player presents to the emergency department (ED) after a helmet-to-helmet tackle in a game earlier that day. After the tackle, he experienced immediate confusion. Once he returned to his feet, he felt dizzy and nauseated and began to develop a headache. When his symptoms failed to resolve within a few hours, his mother brought him to the hospital for an evaluation. In the ED, he receives a diagnosis of concussion, and his mother asks for recommendations on how he can recover as quickly as possible.
Traumatic brain injuries account for an estimated 2.5 million ED visits annually in the United States.2 Concussions are the most common form of traumatic brain injury, with adolescents contributing to the highest incidence of concussions.3,4 An estimated 1.6 to 3.8 million people experience a sports-related concussion annually.5
Time to recovery is a clinical endpoint that matters greatly to our young, physically active patients, who are often eager to return to their daily activities as soon as possible. Guidelines frequently recommend cognitive and physical rest for 24 to 48 hours immediately following a concussion, but the use of screens during this cognitive rest period remains uncertain.6,7 International guidelines and the Centers for Disease Control and Prevention recommend symptom-limited activities—including screen time—during the initial period of a concussion.6,7 Although this gradual approach is standard of care, it has been unclear if abstaining completely from certain activities during the initial days of a concussion has any impact on recovery time.
Recent studies have examined physical activity to clarify the optimal timing of physical rest after a concussion. Among adolescents with concussions, strict rest for 5 days does not appear to improve symptoms compared with rest for 1 to 2 days.8 Additionally, physical activity within 7 days of acute head injury may help reduce symptoms and prevent postconcussive symptoms.9,10
This same level of clarity has been lacking for cognitive rest and screen time. The use of screens is a part of most patients’ daily activities, particularly among adolescents and young adults. One report found that students ages 8 to 18 years engage in approximately 7 hours of daily screen time, excluding that related to
STUDY SUMMARY
Symptom duration was significantly reduced by cutting screen time
This single-site, parallel-design, randomized clinical trial examined the effectiveness of limiting screen time exposure within the first 48 hours after a concussion in reducing the time to resolution of concussive symptoms in 125 patients. 1 Patients were included if they were 12 to 25 years old (mean age, 17 years) and presented within 24 hours of sustaining a concussion (as defined on the Acute Concussion Evaluation–Emergency Department tool) to the pediatric or adult ED at a US tertiary medical center.
Patients were randomized to either engage in screen time as tolerated or to abstain from screen time for 48 hours following their injury. Screen modalities included television, phones, video games, and computers/tablets. The Post-Concussive Symptom Scale (PCSS; 0-132) was used to characterize 22 symptoms from 0 (absent) to 6 (severe) daily for 10 days. Patients also self-reported the amount of screen time they engaged in during Days 1 to 3 of the study period and completed an activity survey on Days 4 to 10. Among the participants, 76% completed the PCSS form until symptom resolution or until Day 10 (the end of the study period).
Continue to: The primary outcome...
The primary outcome was days to resolution of concussive symptoms, defined as a PCSS score ≤ 3. The median baseline PCSS score was 21 in the screen time–permitted group and 24.5 in the screen time–abstinent group. The screen time–permitted group reported a median screen time of 630 minutes during the intervention period, compared with 130 minutes in the screen time–abstinent group, and was less likely to recover during the study period than the screen time–abstinent group (hazard ratio = 0.51; 95% CI, 0.29-0.90). The screen time–permitted group had a significantly longer median recovery time compared with the screen time–abstinent group (8.0 vs 3.5 days; P = .03).
WHAT'S NEW?
Exploring the role of screen time during the cognitive rest period
This study provides evidence supporting the recommendation that adolescent and young adult patients abstain from screen time in the first 48 hours following a concussion to decrease time to symptom resolution, thus shortening the timeline to return to their usual daily activities.
CAVEATS
Self-reporting of data may introduce bias
This study used a self-reporting method to collect data, which could have resulted in underreporting or overreporting of screen time and potentially introduced recall and reporting bias. The screen time–abstinent group did not completely abstain from all screen time, with a self-reported average of 5 to 10 minutes of daily screen time to complete the required research surveys, so it is not immediately clear what extent of abstinence vs significant screen time reduction led to the clinical endpoints observed. Furthermore, this study did not ask patients to differentiate between active screen time (eg, texting and gaming) and passive screen time (eg, watching videos), which may differentially impact symptom resolution.
CHALLENGES TO IMPLEMENTATION
Turning off the ever-present screen may present obstacles
This intervention is easy to recommend, with few barriers to implementation. It’s worth noting that screens are often used in a patient’s school or job, and 48 hours of abstinence from these activities is a difficult ask when much of our society’s education, entertainment, and productivity revolve around the use of technology. When appropriate, a shared decision-making discussion between patient and physician should center on the idea that 48 hours of screen time abstinence could be well worth the increased likelihood of total recovery at Day 10, as opposed to the risk for persistent and prolonged symptoms that interfere with the patient’s lifestyle.
ILLUSTRATIVE CASE
A 17-year-old high school football player presents to the emergency department (ED) after a helmet-to-helmet tackle in a game earlier that day. After the tackle, he experienced immediate confusion. Once he returned to his feet, he felt dizzy and nauseated and began to develop a headache. When his symptoms failed to resolve within a few hours, his mother brought him to the hospital for an evaluation. In the ED, he receives a diagnosis of concussion, and his mother asks for recommendations on how he can recover as quickly as possible.
Traumatic brain injuries account for an estimated 2.5 million ED visits annually in the United States.2 Concussions are the most common form of traumatic brain injury, with adolescents contributing to the highest incidence of concussions.3,4 An estimated 1.6 to 3.8 million people experience a sports-related concussion annually.5
Time to recovery is a clinical endpoint that matters greatly to our young, physically active patients, who are often eager to return to their daily activities as soon as possible. Guidelines frequently recommend cognitive and physical rest for 24 to 48 hours immediately following a concussion, but the use of screens during this cognitive rest period remains uncertain.6,7 International guidelines and the Centers for Disease Control and Prevention recommend symptom-limited activities—including screen time—during the initial period of a concussion.6,7 Although this gradual approach is standard of care, it has been unclear if abstaining completely from certain activities during the initial days of a concussion has any impact on recovery time.
Recent studies have examined physical activity to clarify the optimal timing of physical rest after a concussion. Among adolescents with concussions, strict rest for 5 days does not appear to improve symptoms compared with rest for 1 to 2 days.8 Additionally, physical activity within 7 days of acute head injury may help reduce symptoms and prevent postconcussive symptoms.9,10
This same level of clarity has been lacking for cognitive rest and screen time. The use of screens is a part of most patients’ daily activities, particularly among adolescents and young adults. One report found that students ages 8 to 18 years engage in approximately 7 hours of daily screen time, excluding that related to
STUDY SUMMARY
Symptom duration was significantly reduced by cutting screen time
This single-site, parallel-design, randomized clinical trial examined the effectiveness of limiting screen time exposure within the first 48 hours after a concussion in reducing the time to resolution of concussive symptoms in 125 patients. 1 Patients were included if they were 12 to 25 years old (mean age, 17 years) and presented within 24 hours of sustaining a concussion (as defined on the Acute Concussion Evaluation–Emergency Department tool) to the pediatric or adult ED at a US tertiary medical center.
Patients were randomized to either engage in screen time as tolerated or to abstain from screen time for 48 hours following their injury. Screen modalities included television, phones, video games, and computers/tablets. The Post-Concussive Symptom Scale (PCSS; 0-132) was used to characterize 22 symptoms from 0 (absent) to 6 (severe) daily for 10 days. Patients also self-reported the amount of screen time they engaged in during Days 1 to 3 of the study period and completed an activity survey on Days 4 to 10. Among the participants, 76% completed the PCSS form until symptom resolution or until Day 10 (the end of the study period).
Continue to: The primary outcome...
The primary outcome was days to resolution of concussive symptoms, defined as a PCSS score ≤ 3. The median baseline PCSS score was 21 in the screen time–permitted group and 24.5 in the screen time–abstinent group. The screen time–permitted group reported a median screen time of 630 minutes during the intervention period, compared with 130 minutes in the screen time–abstinent group, and was less likely to recover during the study period than the screen time–abstinent group (hazard ratio = 0.51; 95% CI, 0.29-0.90). The screen time–permitted group had a significantly longer median recovery time compared with the screen time–abstinent group (8.0 vs 3.5 days; P = .03).
WHAT'S NEW?
Exploring the role of screen time during the cognitive rest period
This study provides evidence supporting the recommendation that adolescent and young adult patients abstain from screen time in the first 48 hours following a concussion to decrease time to symptom resolution, thus shortening the timeline to return to their usual daily activities.
CAVEATS
Self-reporting of data may introduce bias
This study used a self-reporting method to collect data, which could have resulted in underreporting or overreporting of screen time and potentially introduced recall and reporting bias. The screen time–abstinent group did not completely abstain from all screen time, with a self-reported average of 5 to 10 minutes of daily screen time to complete the required research surveys, so it is not immediately clear what extent of abstinence vs significant screen time reduction led to the clinical endpoints observed. Furthermore, this study did not ask patients to differentiate between active screen time (eg, texting and gaming) and passive screen time (eg, watching videos), which may differentially impact symptom resolution.
CHALLENGES TO IMPLEMENTATION
Turning off the ever-present screen may present obstacles
This intervention is easy to recommend, with few barriers to implementation. It’s worth noting that screens are often used in a patient’s school or job, and 48 hours of abstinence from these activities is a difficult ask when much of our society’s education, entertainment, and productivity revolve around the use of technology. When appropriate, a shared decision-making discussion between patient and physician should center on the idea that 48 hours of screen time abstinence could be well worth the increased likelihood of total recovery at Day 10, as opposed to the risk for persistent and prolonged symptoms that interfere with the patient’s lifestyle.
1. Macnow T, Curran T, Tolliday C, et al. Effect of screen time on recovery from concussion: a randomized clinical trial. JAMA Pediatr. 2021;175:1124-1131. doi: 10.1001/jamapediat rics.2021.2782
2. Taylor CA, Bell JM, Breiding MJ, et al. Traumatic brain injury–related emergency department visits, hospitalizations, and deaths—United States, 2007 and 2013. MMWR Surveill Summ. 2017;66:1-16. doi: 10.15585/mmwr.ss6609a1
3. Vos PE, Battistin L, Birbamer G, et al; European Federation of Neurological Societies. EFNS guideline on mild traumatic brain injury: report of an EFNS task force. Eur J Neurol. 2002;9:207-219. doi: 10.1046/j.1468-1331.2002.00407.x
4. Zhang AL, Sing DC, Rugg CM, et al. The rise of concussions in the adolescent population. Orthop J Sports Med. 2016;4:2325967116662458. doi: 10.1177/2325967116662458
5. McKee AC, Cantu RC, Nowinski CJ, et al. Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury. J Neuropathol Exp Neurol. 2009;68:709-735. doi: 10.1097/NEN.0b013e3181a9d503
6. McCrory P, Meeuwisse W, Dvorák J, et al. Consensus statement on concussion in sport—the 5th international conference on concussion in sport held in Berlin, October 2016. Br J Sports Med. 2017;51:838-847. doi: 10.1136/bjsports-2017-097699
7. Lumba-Brown A, Yeates KO, Sarmiento K, et al. Centers for Disease Control and Prevention guideline on the diagnosis and management of mild traumatic brain injury among children. JAMA Pediatr. 2018;172:e182853. doi: 10.1001/jamapediat rics.2018.2853
8. Thomas DG, Apps JN, Hoffmann RG, et al. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics. 2015;135:213-223. doi: 10.1542/peds.2014-0966
9. Grool AM, Aglipay M, Momoli F, et al; Pediatric Emergency Research Canada (PERC) Concussion Team. Association between early participation in physical activity following acute concussion and persistent postconcussive symptoms in children and adolescents. JAMA. 2016;316:2504-2514. doi: 10.1001/jama.2016.17396
10. Lal A, Kolakowsky-Hayner SA, Ghajar J, et al. The effect of physical exercise after a concussion: a systematic review and meta-analysis. Am J Sports Med. 2018;46:743-752. doi: 10.1177/0363546517706137
11. Rideout V, Peebles A, Mann S, et al. The Common Sense Census: Media Use by Tweens and Teens, 2021. Common Sense Media; 2022. Accessed December 28, 2022. www.commonsensemedia.org/sites/default/files/research/report/8-18-census-integrated-report-final-web_0.pdf
1. Macnow T, Curran T, Tolliday C, et al. Effect of screen time on recovery from concussion: a randomized clinical trial. JAMA Pediatr. 2021;175:1124-1131. doi: 10.1001/jamapediat rics.2021.2782
2. Taylor CA, Bell JM, Breiding MJ, et al. Traumatic brain injury–related emergency department visits, hospitalizations, and deaths—United States, 2007 and 2013. MMWR Surveill Summ. 2017;66:1-16. doi: 10.15585/mmwr.ss6609a1
3. Vos PE, Battistin L, Birbamer G, et al; European Federation of Neurological Societies. EFNS guideline on mild traumatic brain injury: report of an EFNS task force. Eur J Neurol. 2002;9:207-219. doi: 10.1046/j.1468-1331.2002.00407.x
4. Zhang AL, Sing DC, Rugg CM, et al. The rise of concussions in the adolescent population. Orthop J Sports Med. 2016;4:2325967116662458. doi: 10.1177/2325967116662458
5. McKee AC, Cantu RC, Nowinski CJ, et al. Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury. J Neuropathol Exp Neurol. 2009;68:709-735. doi: 10.1097/NEN.0b013e3181a9d503
6. McCrory P, Meeuwisse W, Dvorák J, et al. Consensus statement on concussion in sport—the 5th international conference on concussion in sport held in Berlin, October 2016. Br J Sports Med. 2017;51:838-847. doi: 10.1136/bjsports-2017-097699
7. Lumba-Brown A, Yeates KO, Sarmiento K, et al. Centers for Disease Control and Prevention guideline on the diagnosis and management of mild traumatic brain injury among children. JAMA Pediatr. 2018;172:e182853. doi: 10.1001/jamapediat rics.2018.2853
8. Thomas DG, Apps JN, Hoffmann RG, et al. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics. 2015;135:213-223. doi: 10.1542/peds.2014-0966
9. Grool AM, Aglipay M, Momoli F, et al; Pediatric Emergency Research Canada (PERC) Concussion Team. Association between early participation in physical activity following acute concussion and persistent postconcussive symptoms in children and adolescents. JAMA. 2016;316:2504-2514. doi: 10.1001/jama.2016.17396
10. Lal A, Kolakowsky-Hayner SA, Ghajar J, et al. The effect of physical exercise after a concussion: a systematic review and meta-analysis. Am J Sports Med. 2018;46:743-752. doi: 10.1177/0363546517706137
11. Rideout V, Peebles A, Mann S, et al. The Common Sense Census: Media Use by Tweens and Teens, 2021. Common Sense Media; 2022. Accessed December 28, 2022. www.commonsensemedia.org/sites/default/files/research/report/8-18-census-integrated-report-final-web_0.pdf
PRACTICE CHANGER
Advise your teenaged and young adult patients with concussion to avoid electronic screens in the first 48 hours after a concussion to minimize time to symptom resolution.
STRENGTH OF RECOMMENDATION
B: Based on a single randomized clinical trial.1
Macnow T, Curran T, Tolliday C, et al. Effect of screen time on recovery from concussion: a randomized clinical trial. JAMA Pediatr. 2021;175:1124-1131. doi: 10.1001/jamapediatrics.2021.2782
Outdoor play may mitigate screen time’s risk to brain development
Watching a screen more than an hour a day as a toddler is directly linked with poorer communication and daily living skills at age 4, but outdoor play may lessen some of the effects, new research suggests.
The results point to outdoor play as a potential targeted intervention to counter suboptimal brain development in young children who are watching screens at increasingly younger ages.
The findings were published online in JAMA Pediatrics.
The researchers first investigated whether higher screen time (more than 1 hour a day on a device or watching television) at age 2 years is associated with neurodevelopmental outcomes at age 4.
They found the 885 children in the sample from the Japanese Hamamatsu Birth Cohort Study for Mothers and Children who had more screen time had lower scores on communication and daily living skills than children who watched less than an hour a day.
Scores were based on the Vineland Adaptive Behavior Scale according to parent responses to questions. The children included were born between December 2007 and March 2012 and were followed from 18 months to 4 years.
After finding the connection between screen time and lower scores, the researchers investigated whether outdoor play (at least 30 minutes a day) introduced at a 2 years and 8 months made a difference. They considered 6 or 7 days per week frequent outdoor play.
Outdoor play mitigated poorer daily living scores
The researchers found that the outdoor play intervention mitigated 18% of the association between high screen time and lower daily living scores but did not mitigate the lower communication scores.
They also found that more screen time at age 2 was significantly linked with infrequent outdoor play at age 32 months (odds ratio, 2.03; 95% confidence interval, 1.48-2.76).
The associations were consistent after taking into account factors including a child’s sex, parental education, and any autism spectrum disorder symptoms at age 18 months.
The authors noted that neurodevelopment concerns with screen use are particularly troubling as the age for use is getting younger.
A recent meta-analysis found that 75% of children younger than 2 use or watch screens, even though guidelines recommend against any screen time before 2.
In addition, the “COVID-19 pandemic led to children having more screen time, less outdoor play, and less physical activity, putting them at potentially greater risk for neurodevelopmental problems,” the authors noted.
“What is concerning is that data show screen time has not decreased after seclusion measures were lifted,” they added.
Proven benefits for outdoor play
Jennifer Cross, MD,* assistant professor and section chief for developmental pediatrics at Weill Cornell Medicine, New York, who was not part of the study, said the mitigation properties of outdoor play were something she hadn’t seen before but the concept makes sense.
“The overwhelming evidence is that screen time is not helpful for young children under the age of 2,” she said.
Outdoor play, on the other hand, has proven benefits.
“Physical activity has been shown to be good for physical and mental health so there’s no reason to believe it wouldn’t be good for 2-and-a-half-year olds,” Dr. Cross said. “It’s also good for developmental health. You want them to be engaged in imaginative play and be interactive.”
“[Outdoor play] gets them away from screens and gives them an opportunity to experience another environment and work on their motor skills and motor planning,” she added. “Exercise will change, briefly, the way our brains process information.”
Dr. Cross added that a lot of motor skills are involved in daily living skills, such as feeding, dressing, and toileting.
Screen time is increasing
The authors acknowledged that screen time may be underestimated by parents. They also noted that they did not have access to what children were watching on the screens.
“This should have been collected because the effect of high screen time differs depending on the type of program,” the authors wrote.
They added that children born in the 2020s may have been exposed to more screen time than the children reared in the early 2010s in this study.
Dr. Cross said screen use in the 2020s may be higher than estimated here and higher in certain populations globally, so it’s not easy to tell if the intervention in this study would have the same mitigating effect on a real-world population.
However, she said, the effect of outdoor play is always going to be helpful for brain development and there’s no downside.
“Exercise is just as important for little kids as it is for grown-ups,” she said.
The authors reported no relevant financial disclosures. Dr. Cross reported no relevant financial disclosures.
*Dr. Jennifer Cross is the correct name, not Dr. Jennifer Frost. The correction was made on Jan. 27, 2023.
Watching a screen more than an hour a day as a toddler is directly linked with poorer communication and daily living skills at age 4, but outdoor play may lessen some of the effects, new research suggests.
The results point to outdoor play as a potential targeted intervention to counter suboptimal brain development in young children who are watching screens at increasingly younger ages.
The findings were published online in JAMA Pediatrics.
The researchers first investigated whether higher screen time (more than 1 hour a day on a device or watching television) at age 2 years is associated with neurodevelopmental outcomes at age 4.
They found the 885 children in the sample from the Japanese Hamamatsu Birth Cohort Study for Mothers and Children who had more screen time had lower scores on communication and daily living skills than children who watched less than an hour a day.
Scores were based on the Vineland Adaptive Behavior Scale according to parent responses to questions. The children included were born between December 2007 and March 2012 and were followed from 18 months to 4 years.
After finding the connection between screen time and lower scores, the researchers investigated whether outdoor play (at least 30 minutes a day) introduced at a 2 years and 8 months made a difference. They considered 6 or 7 days per week frequent outdoor play.
Outdoor play mitigated poorer daily living scores
The researchers found that the outdoor play intervention mitigated 18% of the association between high screen time and lower daily living scores but did not mitigate the lower communication scores.
They also found that more screen time at age 2 was significantly linked with infrequent outdoor play at age 32 months (odds ratio, 2.03; 95% confidence interval, 1.48-2.76).
The associations were consistent after taking into account factors including a child’s sex, parental education, and any autism spectrum disorder symptoms at age 18 months.
The authors noted that neurodevelopment concerns with screen use are particularly troubling as the age for use is getting younger.
A recent meta-analysis found that 75% of children younger than 2 use or watch screens, even though guidelines recommend against any screen time before 2.
In addition, the “COVID-19 pandemic led to children having more screen time, less outdoor play, and less physical activity, putting them at potentially greater risk for neurodevelopmental problems,” the authors noted.
“What is concerning is that data show screen time has not decreased after seclusion measures were lifted,” they added.
Proven benefits for outdoor play
Jennifer Cross, MD,* assistant professor and section chief for developmental pediatrics at Weill Cornell Medicine, New York, who was not part of the study, said the mitigation properties of outdoor play were something she hadn’t seen before but the concept makes sense.
“The overwhelming evidence is that screen time is not helpful for young children under the age of 2,” she said.
Outdoor play, on the other hand, has proven benefits.
“Physical activity has been shown to be good for physical and mental health so there’s no reason to believe it wouldn’t be good for 2-and-a-half-year olds,” Dr. Cross said. “It’s also good for developmental health. You want them to be engaged in imaginative play and be interactive.”
“[Outdoor play] gets them away from screens and gives them an opportunity to experience another environment and work on their motor skills and motor planning,” she added. “Exercise will change, briefly, the way our brains process information.”
Dr. Cross added that a lot of motor skills are involved in daily living skills, such as feeding, dressing, and toileting.
Screen time is increasing
The authors acknowledged that screen time may be underestimated by parents. They also noted that they did not have access to what children were watching on the screens.
“This should have been collected because the effect of high screen time differs depending on the type of program,” the authors wrote.
They added that children born in the 2020s may have been exposed to more screen time than the children reared in the early 2010s in this study.
Dr. Cross said screen use in the 2020s may be higher than estimated here and higher in certain populations globally, so it’s not easy to tell if the intervention in this study would have the same mitigating effect on a real-world population.
However, she said, the effect of outdoor play is always going to be helpful for brain development and there’s no downside.
“Exercise is just as important for little kids as it is for grown-ups,” she said.
The authors reported no relevant financial disclosures. Dr. Cross reported no relevant financial disclosures.
*Dr. Jennifer Cross is the correct name, not Dr. Jennifer Frost. The correction was made on Jan. 27, 2023.
Watching a screen more than an hour a day as a toddler is directly linked with poorer communication and daily living skills at age 4, but outdoor play may lessen some of the effects, new research suggests.
The results point to outdoor play as a potential targeted intervention to counter suboptimal brain development in young children who are watching screens at increasingly younger ages.
The findings were published online in JAMA Pediatrics.
The researchers first investigated whether higher screen time (more than 1 hour a day on a device or watching television) at age 2 years is associated with neurodevelopmental outcomes at age 4.
They found the 885 children in the sample from the Japanese Hamamatsu Birth Cohort Study for Mothers and Children who had more screen time had lower scores on communication and daily living skills than children who watched less than an hour a day.
Scores were based on the Vineland Adaptive Behavior Scale according to parent responses to questions. The children included were born between December 2007 and March 2012 and were followed from 18 months to 4 years.
After finding the connection between screen time and lower scores, the researchers investigated whether outdoor play (at least 30 minutes a day) introduced at a 2 years and 8 months made a difference. They considered 6 or 7 days per week frequent outdoor play.
Outdoor play mitigated poorer daily living scores
The researchers found that the outdoor play intervention mitigated 18% of the association between high screen time and lower daily living scores but did not mitigate the lower communication scores.
They also found that more screen time at age 2 was significantly linked with infrequent outdoor play at age 32 months (odds ratio, 2.03; 95% confidence interval, 1.48-2.76).
The associations were consistent after taking into account factors including a child’s sex, parental education, and any autism spectrum disorder symptoms at age 18 months.
The authors noted that neurodevelopment concerns with screen use are particularly troubling as the age for use is getting younger.
A recent meta-analysis found that 75% of children younger than 2 use or watch screens, even though guidelines recommend against any screen time before 2.
In addition, the “COVID-19 pandemic led to children having more screen time, less outdoor play, and less physical activity, putting them at potentially greater risk for neurodevelopmental problems,” the authors noted.
“What is concerning is that data show screen time has not decreased after seclusion measures were lifted,” they added.
Proven benefits for outdoor play
Jennifer Cross, MD,* assistant professor and section chief for developmental pediatrics at Weill Cornell Medicine, New York, who was not part of the study, said the mitigation properties of outdoor play were something she hadn’t seen before but the concept makes sense.
“The overwhelming evidence is that screen time is not helpful for young children under the age of 2,” she said.
Outdoor play, on the other hand, has proven benefits.
“Physical activity has been shown to be good for physical and mental health so there’s no reason to believe it wouldn’t be good for 2-and-a-half-year olds,” Dr. Cross said. “It’s also good for developmental health. You want them to be engaged in imaginative play and be interactive.”
“[Outdoor play] gets them away from screens and gives them an opportunity to experience another environment and work on their motor skills and motor planning,” she added. “Exercise will change, briefly, the way our brains process information.”
Dr. Cross added that a lot of motor skills are involved in daily living skills, such as feeding, dressing, and toileting.
Screen time is increasing
The authors acknowledged that screen time may be underestimated by parents. They also noted that they did not have access to what children were watching on the screens.
“This should have been collected because the effect of high screen time differs depending on the type of program,” the authors wrote.
They added that children born in the 2020s may have been exposed to more screen time than the children reared in the early 2010s in this study.
Dr. Cross said screen use in the 2020s may be higher than estimated here and higher in certain populations globally, so it’s not easy to tell if the intervention in this study would have the same mitigating effect on a real-world population.
However, she said, the effect of outdoor play is always going to be helpful for brain development and there’s no downside.
“Exercise is just as important for little kids as it is for grown-ups,” she said.
The authors reported no relevant financial disclosures. Dr. Cross reported no relevant financial disclosures.
*Dr. Jennifer Cross is the correct name, not Dr. Jennifer Frost. The correction was made on Jan. 27, 2023.
FROM JAMA PEDIATRICS