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Stabilizing circadian rhythm tied to lower suicide risk in bipolar disorder
Social rhythm therapy (SRT), which uses behavioral strategies to support healthy sleep and other routines, is linked to improved mood and reduced suicide risk in young people with bipolar disorder (BD), early research suggests.
The small study also showed SRT is both feasible and acceptable in this patient population.
Results showed SRT, which was primarily delivered via telehealth sessions, began to show efficacy approximately 6 weeks into the 12-week therapeutic program, the researchers noted.
“Improving the regularity of daily rhythms like sleep, physical activity, and social activities can be really robust in improving mental health and even reducing suicide risk,” study investigator Hilary P. Blumberg, MD, the John and Hope Furth Professor of Psychiatric Neuroscience and director of the mood disorders research program at Yale University, New Haven, Conn., said in an interview.
The findings are published in the American Journal of Psychotherapy.
Trigger for depression, mania
Previous research shows unstable circadian rhythms may trigger depressive and manic symptoms – and are risk factors for suicidal thoughts and behaviors. Although interpersonal and social rhythm therapy has shown promise in patients with mood disorders, there is little research focusing only on the social rhythm aspect of the therapy.
The researchers only examined SRT, modified to create a therapeutic program aimed at adolescents and young adults.
The study included 13 participants (mean age, 20.5 years) with BD and a score of 15 or more on the 29-item Hamilton Depression Rating Scale (HDRS-29) and/or a score of 12 or more on the Young Mania Rating Scale (YMRS).
Participants were enrolled in the National Institute of Mental Health Brain Emotion Circuitry Targeted Self-Monitoring and Regulation Therapy (BE-SMART) program, which requires MRI sessions at three in-person visits to assess brain changes with the therapy. All but one participant was taking mood-stabilizing medications.
“We didn’t ask them to come off medications because we didn’t want to exacerbate things,” said Dr. Blumberg. She added the therapeutic approach “could be adjunctive to further improve symptoms and reduce risk.”
The majority occurred on a secure video platform. Three were conducted in person.
Working with a therapist, participants were taught how to follow a daily routine. Dr. Blumberg noted this is not just a matter of going to sleep and getting up at the same time every day, but thoroughly reviewing details of all daily activities and routines, including who participants eat with and when, their exercise schedule, and social engagements.
Each week, participants completed the five-item version of the Social Rhythm Metric. At the end of the intervention, they also completed the Client Satisfaction Questionnaire (CSQ). Scores on the CSQ range from 8 to 32, with scores of 26-32 indicating “excellent” satisfaction.
In addition, participants and therapists completed the Working Alliance Inventory, which assesses the client-therapist relationship by asking about such things as degree of comfort and respect.
Before and after the intervention, participants reported the regularity of their social rhythms using the Brief Social Rhythm Scale (BSRS) and risk for suicidal behavior using a subscale of the Concise Health Risk Tracking (CHRT) scale.
High retention, ‘excellent satisfaction’
Results showed 10 of the 13 participants (9 females) completed all study procedures, for a retention rate of 77%. Treatment satisfaction was excellent (mean CSQ, 29.4).
Both therapists and participants had high scores on all aspects of the Working Alliance Inventory scale.
“High treatment retention, excellent client satisfaction, and strong working alliance scores support the feasibility and acceptability of this intervention for adolescents and young adults with bipolar disorder,” the investigators wrote.
Participants showed significant improvement in social rhythm regularity and reductions in depression and manic symptoms as well as suicide propensity (P = .016 for BSRS; .024 for HDRS-29; .028 for YMRS; and .028 for CHRT suicide propensity). Effect sizes were in the moderate to high range.
By the midpoint of the therapy, there were significant improvements in social rhythm regularity and suicide propensity and trend-level reductions in depression, suggesting the potential for early benefits.
Dr. Blumberg noted it is difficult to find a therapy that helps with both depressive and mania symptoms. “An antidepressant may reduce depression, but sometimes can worsen manic symptoms.”
Impact on emotional brain circuitry?
The association between improved regularity of social rhythms and reduced suicide propensity persisted even after controlling for mood symptom changes.
“Suicide risk was reduced not just because subjects were less depressed. There’s something about regularizing rhythms that can reduce suicide risk,” said Dr. Blumberg.
The reviewers noted that SRT administered remotely improves accessibility; and this intervention “is well suited to the future of psychotherapy delivery, which will undoubtedly include remote treatment delivery.”
The absence of a comparator condition was cited as a study limitation. The investigators noted the small sample size means the findings should be interpreted cautiously and verified in an adequately powered randomized controlled trial.
The researchers now have early results from the brain scanning component of the study. “Preliminary findings suggest the intervention seems to benefit emotional brain circuitry,” Dr. Blumberg said.
The researchers are about to embark on a new study funded by a grant from the American Foundation of Suicide Prevention. It will investigate SRT in preventing suicide in adolescents and adults to age 29 years with depression or BD.
In addition, the researchers have secured support from the Klingenstein Third Generation Foundation to research prevention in youth at risk for BD – and from Women’s Health Access Matters to examine the therapy in women 50 and older with depression, a population possibly at increased risk for dementia.
‘Promising’ results
Commenting on the findings, Michael Thase, MD, professor of psychiatry, University of Pennsylvania, and research psychiatrist at the Corporal Michael J. Crescenz Veterans Affairs Medical Center, both in Philadelphia, praised the study.
“It’s a very, very promising initial study because even though there’s no control group, it does show that participants liked the program, most finished it, and on average, people got quite a bit better,” said Dr. Thase, who was not involved with the research.
The treatment may be especially beneficial for young patients with bipolar disorder who, just by their very age, experience lifestyle disruptions, Dr. Thase noted. Results from a previous study of the therapeutic approach in adults showed “probably half of the adults didn’t take to it.”
However, not everyone in this new study benefited either, as some dropped out, which Dr. Thase noted is not atypical.
“No form of intervention is suitable for everyone,” he said.
The study was supported by grants from the National Institute of Mental Health, AIM Youth Mental Health Foundation, Klingenstein Third Generation Foundation, American Foundation for Suicide Prevention, International Bipolar Foundation, MQ Brighter Futures Program, For the Love of Travis Foundation, and the John and Hope Furth Endowment. Dr. Blumberg and Dr. Thase reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Social rhythm therapy (SRT), which uses behavioral strategies to support healthy sleep and other routines, is linked to improved mood and reduced suicide risk in young people with bipolar disorder (BD), early research suggests.
The small study also showed SRT is both feasible and acceptable in this patient population.
Results showed SRT, which was primarily delivered via telehealth sessions, began to show efficacy approximately 6 weeks into the 12-week therapeutic program, the researchers noted.
“Improving the regularity of daily rhythms like sleep, physical activity, and social activities can be really robust in improving mental health and even reducing suicide risk,” study investigator Hilary P. Blumberg, MD, the John and Hope Furth Professor of Psychiatric Neuroscience and director of the mood disorders research program at Yale University, New Haven, Conn., said in an interview.
The findings are published in the American Journal of Psychotherapy.
Trigger for depression, mania
Previous research shows unstable circadian rhythms may trigger depressive and manic symptoms – and are risk factors for suicidal thoughts and behaviors. Although interpersonal and social rhythm therapy has shown promise in patients with mood disorders, there is little research focusing only on the social rhythm aspect of the therapy.
The researchers only examined SRT, modified to create a therapeutic program aimed at adolescents and young adults.
The study included 13 participants (mean age, 20.5 years) with BD and a score of 15 or more on the 29-item Hamilton Depression Rating Scale (HDRS-29) and/or a score of 12 or more on the Young Mania Rating Scale (YMRS).
Participants were enrolled in the National Institute of Mental Health Brain Emotion Circuitry Targeted Self-Monitoring and Regulation Therapy (BE-SMART) program, which requires MRI sessions at three in-person visits to assess brain changes with the therapy. All but one participant was taking mood-stabilizing medications.
“We didn’t ask them to come off medications because we didn’t want to exacerbate things,” said Dr. Blumberg. She added the therapeutic approach “could be adjunctive to further improve symptoms and reduce risk.”
The majority occurred on a secure video platform. Three were conducted in person.
Working with a therapist, participants were taught how to follow a daily routine. Dr. Blumberg noted this is not just a matter of going to sleep and getting up at the same time every day, but thoroughly reviewing details of all daily activities and routines, including who participants eat with and when, their exercise schedule, and social engagements.
Each week, participants completed the five-item version of the Social Rhythm Metric. At the end of the intervention, they also completed the Client Satisfaction Questionnaire (CSQ). Scores on the CSQ range from 8 to 32, with scores of 26-32 indicating “excellent” satisfaction.
In addition, participants and therapists completed the Working Alliance Inventory, which assesses the client-therapist relationship by asking about such things as degree of comfort and respect.
Before and after the intervention, participants reported the regularity of their social rhythms using the Brief Social Rhythm Scale (BSRS) and risk for suicidal behavior using a subscale of the Concise Health Risk Tracking (CHRT) scale.
High retention, ‘excellent satisfaction’
Results showed 10 of the 13 participants (9 females) completed all study procedures, for a retention rate of 77%. Treatment satisfaction was excellent (mean CSQ, 29.4).
Both therapists and participants had high scores on all aspects of the Working Alliance Inventory scale.
“High treatment retention, excellent client satisfaction, and strong working alliance scores support the feasibility and acceptability of this intervention for adolescents and young adults with bipolar disorder,” the investigators wrote.
Participants showed significant improvement in social rhythm regularity and reductions in depression and manic symptoms as well as suicide propensity (P = .016 for BSRS; .024 for HDRS-29; .028 for YMRS; and .028 for CHRT suicide propensity). Effect sizes were in the moderate to high range.
By the midpoint of the therapy, there were significant improvements in social rhythm regularity and suicide propensity and trend-level reductions in depression, suggesting the potential for early benefits.
Dr. Blumberg noted it is difficult to find a therapy that helps with both depressive and mania symptoms. “An antidepressant may reduce depression, but sometimes can worsen manic symptoms.”
Impact on emotional brain circuitry?
The association between improved regularity of social rhythms and reduced suicide propensity persisted even after controlling for mood symptom changes.
“Suicide risk was reduced not just because subjects were less depressed. There’s something about regularizing rhythms that can reduce suicide risk,” said Dr. Blumberg.
The reviewers noted that SRT administered remotely improves accessibility; and this intervention “is well suited to the future of psychotherapy delivery, which will undoubtedly include remote treatment delivery.”
The absence of a comparator condition was cited as a study limitation. The investigators noted the small sample size means the findings should be interpreted cautiously and verified in an adequately powered randomized controlled trial.
The researchers now have early results from the brain scanning component of the study. “Preliminary findings suggest the intervention seems to benefit emotional brain circuitry,” Dr. Blumberg said.
The researchers are about to embark on a new study funded by a grant from the American Foundation of Suicide Prevention. It will investigate SRT in preventing suicide in adolescents and adults to age 29 years with depression or BD.
In addition, the researchers have secured support from the Klingenstein Third Generation Foundation to research prevention in youth at risk for BD – and from Women’s Health Access Matters to examine the therapy in women 50 and older with depression, a population possibly at increased risk for dementia.
‘Promising’ results
Commenting on the findings, Michael Thase, MD, professor of psychiatry, University of Pennsylvania, and research psychiatrist at the Corporal Michael J. Crescenz Veterans Affairs Medical Center, both in Philadelphia, praised the study.
“It’s a very, very promising initial study because even though there’s no control group, it does show that participants liked the program, most finished it, and on average, people got quite a bit better,” said Dr. Thase, who was not involved with the research.
The treatment may be especially beneficial for young patients with bipolar disorder who, just by their very age, experience lifestyle disruptions, Dr. Thase noted. Results from a previous study of the therapeutic approach in adults showed “probably half of the adults didn’t take to it.”
However, not everyone in this new study benefited either, as some dropped out, which Dr. Thase noted is not atypical.
“No form of intervention is suitable for everyone,” he said.
The study was supported by grants from the National Institute of Mental Health, AIM Youth Mental Health Foundation, Klingenstein Third Generation Foundation, American Foundation for Suicide Prevention, International Bipolar Foundation, MQ Brighter Futures Program, For the Love of Travis Foundation, and the John and Hope Furth Endowment. Dr. Blumberg and Dr. Thase reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Social rhythm therapy (SRT), which uses behavioral strategies to support healthy sleep and other routines, is linked to improved mood and reduced suicide risk in young people with bipolar disorder (BD), early research suggests.
The small study also showed SRT is both feasible and acceptable in this patient population.
Results showed SRT, which was primarily delivered via telehealth sessions, began to show efficacy approximately 6 weeks into the 12-week therapeutic program, the researchers noted.
“Improving the regularity of daily rhythms like sleep, physical activity, and social activities can be really robust in improving mental health and even reducing suicide risk,” study investigator Hilary P. Blumberg, MD, the John and Hope Furth Professor of Psychiatric Neuroscience and director of the mood disorders research program at Yale University, New Haven, Conn., said in an interview.
The findings are published in the American Journal of Psychotherapy.
Trigger for depression, mania
Previous research shows unstable circadian rhythms may trigger depressive and manic symptoms – and are risk factors for suicidal thoughts and behaviors. Although interpersonal and social rhythm therapy has shown promise in patients with mood disorders, there is little research focusing only on the social rhythm aspect of the therapy.
The researchers only examined SRT, modified to create a therapeutic program aimed at adolescents and young adults.
The study included 13 participants (mean age, 20.5 years) with BD and a score of 15 or more on the 29-item Hamilton Depression Rating Scale (HDRS-29) and/or a score of 12 or more on the Young Mania Rating Scale (YMRS).
Participants were enrolled in the National Institute of Mental Health Brain Emotion Circuitry Targeted Self-Monitoring and Regulation Therapy (BE-SMART) program, which requires MRI sessions at three in-person visits to assess brain changes with the therapy. All but one participant was taking mood-stabilizing medications.
“We didn’t ask them to come off medications because we didn’t want to exacerbate things,” said Dr. Blumberg. She added the therapeutic approach “could be adjunctive to further improve symptoms and reduce risk.”
The majority occurred on a secure video platform. Three were conducted in person.
Working with a therapist, participants were taught how to follow a daily routine. Dr. Blumberg noted this is not just a matter of going to sleep and getting up at the same time every day, but thoroughly reviewing details of all daily activities and routines, including who participants eat with and when, their exercise schedule, and social engagements.
Each week, participants completed the five-item version of the Social Rhythm Metric. At the end of the intervention, they also completed the Client Satisfaction Questionnaire (CSQ). Scores on the CSQ range from 8 to 32, with scores of 26-32 indicating “excellent” satisfaction.
In addition, participants and therapists completed the Working Alliance Inventory, which assesses the client-therapist relationship by asking about such things as degree of comfort and respect.
Before and after the intervention, participants reported the regularity of their social rhythms using the Brief Social Rhythm Scale (BSRS) and risk for suicidal behavior using a subscale of the Concise Health Risk Tracking (CHRT) scale.
High retention, ‘excellent satisfaction’
Results showed 10 of the 13 participants (9 females) completed all study procedures, for a retention rate of 77%. Treatment satisfaction was excellent (mean CSQ, 29.4).
Both therapists and participants had high scores on all aspects of the Working Alliance Inventory scale.
“High treatment retention, excellent client satisfaction, and strong working alliance scores support the feasibility and acceptability of this intervention for adolescents and young adults with bipolar disorder,” the investigators wrote.
Participants showed significant improvement in social rhythm regularity and reductions in depression and manic symptoms as well as suicide propensity (P = .016 for BSRS; .024 for HDRS-29; .028 for YMRS; and .028 for CHRT suicide propensity). Effect sizes were in the moderate to high range.
By the midpoint of the therapy, there were significant improvements in social rhythm regularity and suicide propensity and trend-level reductions in depression, suggesting the potential for early benefits.
Dr. Blumberg noted it is difficult to find a therapy that helps with both depressive and mania symptoms. “An antidepressant may reduce depression, but sometimes can worsen manic symptoms.”
Impact on emotional brain circuitry?
The association between improved regularity of social rhythms and reduced suicide propensity persisted even after controlling for mood symptom changes.
“Suicide risk was reduced not just because subjects were less depressed. There’s something about regularizing rhythms that can reduce suicide risk,” said Dr. Blumberg.
The reviewers noted that SRT administered remotely improves accessibility; and this intervention “is well suited to the future of psychotherapy delivery, which will undoubtedly include remote treatment delivery.”
The absence of a comparator condition was cited as a study limitation. The investigators noted the small sample size means the findings should be interpreted cautiously and verified in an adequately powered randomized controlled trial.
The researchers now have early results from the brain scanning component of the study. “Preliminary findings suggest the intervention seems to benefit emotional brain circuitry,” Dr. Blumberg said.
The researchers are about to embark on a new study funded by a grant from the American Foundation of Suicide Prevention. It will investigate SRT in preventing suicide in adolescents and adults to age 29 years with depression or BD.
In addition, the researchers have secured support from the Klingenstein Third Generation Foundation to research prevention in youth at risk for BD – and from Women’s Health Access Matters to examine the therapy in women 50 and older with depression, a population possibly at increased risk for dementia.
‘Promising’ results
Commenting on the findings, Michael Thase, MD, professor of psychiatry, University of Pennsylvania, and research psychiatrist at the Corporal Michael J. Crescenz Veterans Affairs Medical Center, both in Philadelphia, praised the study.
“It’s a very, very promising initial study because even though there’s no control group, it does show that participants liked the program, most finished it, and on average, people got quite a bit better,” said Dr. Thase, who was not involved with the research.
The treatment may be especially beneficial for young patients with bipolar disorder who, just by their very age, experience lifestyle disruptions, Dr. Thase noted. Results from a previous study of the therapeutic approach in adults showed “probably half of the adults didn’t take to it.”
However, not everyone in this new study benefited either, as some dropped out, which Dr. Thase noted is not atypical.
“No form of intervention is suitable for everyone,” he said.
The study was supported by grants from the National Institute of Mental Health, AIM Youth Mental Health Foundation, Klingenstein Third Generation Foundation, American Foundation for Suicide Prevention, International Bipolar Foundation, MQ Brighter Futures Program, For the Love of Travis Foundation, and the John and Hope Furth Endowment. Dr. Blumberg and Dr. Thase reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE AMERICAN JOURNAL OF PSYCHOTHERAPY
Reducing night-time checks is safe and helps patients sleep
Routine checks of vital signs during the night often prevent hospitalized patients from getting sufficient recuperative sleep. But patients who are judged to be clinically stable by an algorithm that uses real-time data can be safely spared these checks, according to a recent study published in JAMA Internal Medicine.
In their study,
“Sleep is crucial to health,” writes Hyung J. Cho, MD, from the New York University Grossman School of Medicine, in an accompanying editorial. “Ironically, hospitals, where people go to recover from illness, are among the most difficult places to sleep.”
Noise from the surrounding area, night-time examinations, multibed rooms, an unfamiliar environment, early morning blood sample collections, and frequent vital sign checks often prevent patients from sleeping through the night.
The goal of the study was to see if the elimination of one of these disrupting factors – the frequent checks of vital signs – would improve sleep and lead to a reduction in delirium, the primary endpoint.
To do this, the researchers incorporated a predictive algorithm they developed “to identify patients who are at low risk for abnormal night-time vital signs” into the hospitals electronic health records system. Attending physicians received a notification, based on real-time patient data, if it was predicted with a high degree of probability that a patient’s night-time vital signs would be within the normal range. Each physician was free to decide whether they would forgo night-time checks of the vital signs or whether they would turn off the notifications for a specific period.
The randomized clinical trial was conducted at a tertiary care academic teaching hospital from March to November 2019. Half the 1,930 patients were randomized to the algorithm group and half to standard care. None of the patients were receiving intensive care.
Number of night-time checks successfully reduced
The mean number of night-time checks was significantly lower in the algorithm group than in the standard-care group (0.97 vs. 1.41; P < .001).
The reduction in night-time checks had no effect on patient safety. There was no increase in transfers to the intensive care unit in the algorithm or standard-care groups (5% vs 5%; P = .92), and no difference between the number of heart alarms (0.2% vs. 0.9%; P = .07).
However, the reduction also had no effect on the incidence of episodes of delirium in the algorithm or standard-care groups (11% vs. 13%; P = .32).
“The reduction in vital signs checking, although statistically significant, was relatively small,” Dr. Cho explains. But the primary endpoint might have been different had the adherence to intervention been better, he notes.
In fact, the analysis confirmed that changes to routine daily practice in a hospital are not always easy to implement. In 35% of cases, the patients’ vital signs were checked at night, despite the physician’s order to the contrary.
“Busy patient-care assistants and nurses may check vital signs out of habit without noticing that the order has changed for some of the patients,” Dr. Najafi and his coauthors write. Many hospitals are used to thinking that regular measurements of the vital signs are part of good practice.
Include nursing staff
Future projects should use an interdisciplinary approach that includes nursing staff, Dr. Cho recommends. More user-friendly displays and optimized alerts in the electronic patient records could also encourage better implementation of the orders.
Less frequent checks of the vital signs would be welcomed by frontline staff because it would lighten their already heavy workload, he adds.
Although the study didn’t meet its primary endpoint, patients subjected to fewer night-time checks because of the algorithm were able to get a good night’s sleep. Other aspects of hospital care that are based on the patient’s stability, such as cardiac monitoring, could also potentially benefit from this type of intervention, Dr. Najafi and his colleagues suggest.
A version of this article first appeared on Medscape.com.
Routine checks of vital signs during the night often prevent hospitalized patients from getting sufficient recuperative sleep. But patients who are judged to be clinically stable by an algorithm that uses real-time data can be safely spared these checks, according to a recent study published in JAMA Internal Medicine.
In their study,
“Sleep is crucial to health,” writes Hyung J. Cho, MD, from the New York University Grossman School of Medicine, in an accompanying editorial. “Ironically, hospitals, where people go to recover from illness, are among the most difficult places to sleep.”
Noise from the surrounding area, night-time examinations, multibed rooms, an unfamiliar environment, early morning blood sample collections, and frequent vital sign checks often prevent patients from sleeping through the night.
The goal of the study was to see if the elimination of one of these disrupting factors – the frequent checks of vital signs – would improve sleep and lead to a reduction in delirium, the primary endpoint.
To do this, the researchers incorporated a predictive algorithm they developed “to identify patients who are at low risk for abnormal night-time vital signs” into the hospitals electronic health records system. Attending physicians received a notification, based on real-time patient data, if it was predicted with a high degree of probability that a patient’s night-time vital signs would be within the normal range. Each physician was free to decide whether they would forgo night-time checks of the vital signs or whether they would turn off the notifications for a specific period.
The randomized clinical trial was conducted at a tertiary care academic teaching hospital from March to November 2019. Half the 1,930 patients were randomized to the algorithm group and half to standard care. None of the patients were receiving intensive care.
Number of night-time checks successfully reduced
The mean number of night-time checks was significantly lower in the algorithm group than in the standard-care group (0.97 vs. 1.41; P < .001).
The reduction in night-time checks had no effect on patient safety. There was no increase in transfers to the intensive care unit in the algorithm or standard-care groups (5% vs 5%; P = .92), and no difference between the number of heart alarms (0.2% vs. 0.9%; P = .07).
However, the reduction also had no effect on the incidence of episodes of delirium in the algorithm or standard-care groups (11% vs. 13%; P = .32).
“The reduction in vital signs checking, although statistically significant, was relatively small,” Dr. Cho explains. But the primary endpoint might have been different had the adherence to intervention been better, he notes.
In fact, the analysis confirmed that changes to routine daily practice in a hospital are not always easy to implement. In 35% of cases, the patients’ vital signs were checked at night, despite the physician’s order to the contrary.
“Busy patient-care assistants and nurses may check vital signs out of habit without noticing that the order has changed for some of the patients,” Dr. Najafi and his coauthors write. Many hospitals are used to thinking that regular measurements of the vital signs are part of good practice.
Include nursing staff
Future projects should use an interdisciplinary approach that includes nursing staff, Dr. Cho recommends. More user-friendly displays and optimized alerts in the electronic patient records could also encourage better implementation of the orders.
Less frequent checks of the vital signs would be welcomed by frontline staff because it would lighten their already heavy workload, he adds.
Although the study didn’t meet its primary endpoint, patients subjected to fewer night-time checks because of the algorithm were able to get a good night’s sleep. Other aspects of hospital care that are based on the patient’s stability, such as cardiac monitoring, could also potentially benefit from this type of intervention, Dr. Najafi and his colleagues suggest.
A version of this article first appeared on Medscape.com.
Routine checks of vital signs during the night often prevent hospitalized patients from getting sufficient recuperative sleep. But patients who are judged to be clinically stable by an algorithm that uses real-time data can be safely spared these checks, according to a recent study published in JAMA Internal Medicine.
In their study,
“Sleep is crucial to health,” writes Hyung J. Cho, MD, from the New York University Grossman School of Medicine, in an accompanying editorial. “Ironically, hospitals, where people go to recover from illness, are among the most difficult places to sleep.”
Noise from the surrounding area, night-time examinations, multibed rooms, an unfamiliar environment, early morning blood sample collections, and frequent vital sign checks often prevent patients from sleeping through the night.
The goal of the study was to see if the elimination of one of these disrupting factors – the frequent checks of vital signs – would improve sleep and lead to a reduction in delirium, the primary endpoint.
To do this, the researchers incorporated a predictive algorithm they developed “to identify patients who are at low risk for abnormal night-time vital signs” into the hospitals electronic health records system. Attending physicians received a notification, based on real-time patient data, if it was predicted with a high degree of probability that a patient’s night-time vital signs would be within the normal range. Each physician was free to decide whether they would forgo night-time checks of the vital signs or whether they would turn off the notifications for a specific period.
The randomized clinical trial was conducted at a tertiary care academic teaching hospital from March to November 2019. Half the 1,930 patients were randomized to the algorithm group and half to standard care. None of the patients were receiving intensive care.
Number of night-time checks successfully reduced
The mean number of night-time checks was significantly lower in the algorithm group than in the standard-care group (0.97 vs. 1.41; P < .001).
The reduction in night-time checks had no effect on patient safety. There was no increase in transfers to the intensive care unit in the algorithm or standard-care groups (5% vs 5%; P = .92), and no difference between the number of heart alarms (0.2% vs. 0.9%; P = .07).
However, the reduction also had no effect on the incidence of episodes of delirium in the algorithm or standard-care groups (11% vs. 13%; P = .32).
“The reduction in vital signs checking, although statistically significant, was relatively small,” Dr. Cho explains. But the primary endpoint might have been different had the adherence to intervention been better, he notes.
In fact, the analysis confirmed that changes to routine daily practice in a hospital are not always easy to implement. In 35% of cases, the patients’ vital signs were checked at night, despite the physician’s order to the contrary.
“Busy patient-care assistants and nurses may check vital signs out of habit without noticing that the order has changed for some of the patients,” Dr. Najafi and his coauthors write. Many hospitals are used to thinking that regular measurements of the vital signs are part of good practice.
Include nursing staff
Future projects should use an interdisciplinary approach that includes nursing staff, Dr. Cho recommends. More user-friendly displays and optimized alerts in the electronic patient records could also encourage better implementation of the orders.
Less frequent checks of the vital signs would be welcomed by frontline staff because it would lighten their already heavy workload, he adds.
Although the study didn’t meet its primary endpoint, patients subjected to fewer night-time checks because of the algorithm were able to get a good night’s sleep. Other aspects of hospital care that are based on the patient’s stability, such as cardiac monitoring, could also potentially benefit from this type of intervention, Dr. Najafi and his colleagues suggest.
A version of this article first appeared on Medscape.com.
Sorting out sleep complaints in children with AD can be complex
according to Stephen H. Sheldon, DO.
“They wake up frequently,” Dr. Sheldon, professor of pediatrics and neurology at Northwestern University, Chicago, said during the Revolutionizing Atopic Dermatitis symposium. “They may not stay up for long periods of time, but they move about often. There’s a loss of about 50 minutes of sleep per night in children with AD. This loss can result in significant sleep debt the following day. They have difficulty settling at night. Once they get into bed, they have difficulty falling asleep, and many of them have difficulty staying asleep.”
At the sleep medicine center at Lurie Children’s Hospital of Chicago, he and his colleagues have observed that some children with AD complain of difficulty with limb movements. “Part of the issue has been that they have been diagnosed with different sleep-related disorders, such as period limb movement disorder, restless leg syndrome, and growing pain,” Dr. Sheldon said. “Often, they do not know how to describe the manifestations of their leg discomfort in restless leg syndrome and period limb movement disorder and limb movements of sleep.”
Children who complain of growing pains say that their legs hurt, he continued. Sometimes they’ll say that they feel like spiders are crawling on their legs, or that their legs itch, but they often say they have pain in their legs that wakes them up and keeps them from keeping their legs still.
According to the American Academy of Sleep Medicine, periodic limb movement disorder of sleep is characterized by frequent limb movements that last at least 0.5 seconds and are separated by no more than 90 seconds. “They’re four movements in a row that are at least 5 seconds apart,” Dr. Sheldon said.
Interestingly, he added, children who have limb movement disorder have symptoms during the day, similar to adults. “But we see many children with periodic limb movements of sleep whose arms and legs are moving all night, and they don’t have many symptoms during the day.” These children may have difficulty falling or staying asleep, but do not fulfill all of the American Academy of Sleep Medicine criteria for diagnosis of periodic limb movement disorder, he added.
In 2018, Lourdes M. DelRosso, MD, EdD, of Seattle Children’s Hospital, and colleagues described a new sleep problem they termed restless sleep disorder: those who do not fit the criteria for any other sleep disorder but have daytime impairment.
“On video they have very frequent movements – more than five movements an hour of major body activity,” Dr. Sheldon explained. “They’ll move their trunk, their legs, and reposition themselves. We have found that there are many children who presented to the sleep disorder center with restless sleep, limb movement disorder, periodic limb movements of sleep, and daytime symptoms that would fulfill the criteria of periodic limb movement disorder but also have atopic dermatitis.”
Recently, Dr. Sheldon and his colleagues used polysomnographic variables to study children who presented to Lurie Children’s Hospital with AD and symptoms such as difficulty maintaining sleep and snoring with allergic rhinitis. They found that there were increased periods of being awake after the onset of sleep, “meaning the children fell asleep fairly easily in the beginning of the night but they had significant wake after they fell asleep,” he said. “They would wake up in the middle of the night and stay awake for long periods of time – either one long session or multiple shorter sessions throughout the night. They had increased total limb movements per hour of sleep. This means that their limb movements were greater than five events per hour of sleep and it resulted in restless sleep and limb movements that would fulfill the criteria of periodic limb movement disorder.”
Most of these children had mild to moderate AD, he continued. “We feel that the sensory afferent loop in these youngsters doesn’t really turn off completely when they’re asleep. This is ripe for further study, but it makes intuitive sense that if the sensory afferent loop continues during sleep, it may affect the arousal system significantly.”
Dr. Sheldon recommended that any child who presents with a diagnosis of periodic limb movement disorder, periodic limb movements of sleep, or restless sleep disorder should be evaluated for AD. “The treatment then, would first require differentiation between periodic limb movement disorder of sleep and AD. Both should be addressed at the same time in order to solve the child’s daytime AD problem as well as the sleep-related issues that occur with an AD diagnosis.”
He reported having no financial disclosures.
according to Stephen H. Sheldon, DO.
“They wake up frequently,” Dr. Sheldon, professor of pediatrics and neurology at Northwestern University, Chicago, said during the Revolutionizing Atopic Dermatitis symposium. “They may not stay up for long periods of time, but they move about often. There’s a loss of about 50 minutes of sleep per night in children with AD. This loss can result in significant sleep debt the following day. They have difficulty settling at night. Once they get into bed, they have difficulty falling asleep, and many of them have difficulty staying asleep.”
At the sleep medicine center at Lurie Children’s Hospital of Chicago, he and his colleagues have observed that some children with AD complain of difficulty with limb movements. “Part of the issue has been that they have been diagnosed with different sleep-related disorders, such as period limb movement disorder, restless leg syndrome, and growing pain,” Dr. Sheldon said. “Often, they do not know how to describe the manifestations of their leg discomfort in restless leg syndrome and period limb movement disorder and limb movements of sleep.”
Children who complain of growing pains say that their legs hurt, he continued. Sometimes they’ll say that they feel like spiders are crawling on their legs, or that their legs itch, but they often say they have pain in their legs that wakes them up and keeps them from keeping their legs still.
According to the American Academy of Sleep Medicine, periodic limb movement disorder of sleep is characterized by frequent limb movements that last at least 0.5 seconds and are separated by no more than 90 seconds. “They’re four movements in a row that are at least 5 seconds apart,” Dr. Sheldon said.
Interestingly, he added, children who have limb movement disorder have symptoms during the day, similar to adults. “But we see many children with periodic limb movements of sleep whose arms and legs are moving all night, and they don’t have many symptoms during the day.” These children may have difficulty falling or staying asleep, but do not fulfill all of the American Academy of Sleep Medicine criteria for diagnosis of periodic limb movement disorder, he added.
In 2018, Lourdes M. DelRosso, MD, EdD, of Seattle Children’s Hospital, and colleagues described a new sleep problem they termed restless sleep disorder: those who do not fit the criteria for any other sleep disorder but have daytime impairment.
“On video they have very frequent movements – more than five movements an hour of major body activity,” Dr. Sheldon explained. “They’ll move their trunk, their legs, and reposition themselves. We have found that there are many children who presented to the sleep disorder center with restless sleep, limb movement disorder, periodic limb movements of sleep, and daytime symptoms that would fulfill the criteria of periodic limb movement disorder but also have atopic dermatitis.”
Recently, Dr. Sheldon and his colleagues used polysomnographic variables to study children who presented to Lurie Children’s Hospital with AD and symptoms such as difficulty maintaining sleep and snoring with allergic rhinitis. They found that there were increased periods of being awake after the onset of sleep, “meaning the children fell asleep fairly easily in the beginning of the night but they had significant wake after they fell asleep,” he said. “They would wake up in the middle of the night and stay awake for long periods of time – either one long session or multiple shorter sessions throughout the night. They had increased total limb movements per hour of sleep. This means that their limb movements were greater than five events per hour of sleep and it resulted in restless sleep and limb movements that would fulfill the criteria of periodic limb movement disorder.”
Most of these children had mild to moderate AD, he continued. “We feel that the sensory afferent loop in these youngsters doesn’t really turn off completely when they’re asleep. This is ripe for further study, but it makes intuitive sense that if the sensory afferent loop continues during sleep, it may affect the arousal system significantly.”
Dr. Sheldon recommended that any child who presents with a diagnosis of periodic limb movement disorder, periodic limb movements of sleep, or restless sleep disorder should be evaluated for AD. “The treatment then, would first require differentiation between periodic limb movement disorder of sleep and AD. Both should be addressed at the same time in order to solve the child’s daytime AD problem as well as the sleep-related issues that occur with an AD diagnosis.”
He reported having no financial disclosures.
according to Stephen H. Sheldon, DO.
“They wake up frequently,” Dr. Sheldon, professor of pediatrics and neurology at Northwestern University, Chicago, said during the Revolutionizing Atopic Dermatitis symposium. “They may not stay up for long periods of time, but they move about often. There’s a loss of about 50 minutes of sleep per night in children with AD. This loss can result in significant sleep debt the following day. They have difficulty settling at night. Once they get into bed, they have difficulty falling asleep, and many of them have difficulty staying asleep.”
At the sleep medicine center at Lurie Children’s Hospital of Chicago, he and his colleagues have observed that some children with AD complain of difficulty with limb movements. “Part of the issue has been that they have been diagnosed with different sleep-related disorders, such as period limb movement disorder, restless leg syndrome, and growing pain,” Dr. Sheldon said. “Often, they do not know how to describe the manifestations of their leg discomfort in restless leg syndrome and period limb movement disorder and limb movements of sleep.”
Children who complain of growing pains say that their legs hurt, he continued. Sometimes they’ll say that they feel like spiders are crawling on their legs, or that their legs itch, but they often say they have pain in their legs that wakes them up and keeps them from keeping their legs still.
According to the American Academy of Sleep Medicine, periodic limb movement disorder of sleep is characterized by frequent limb movements that last at least 0.5 seconds and are separated by no more than 90 seconds. “They’re four movements in a row that are at least 5 seconds apart,” Dr. Sheldon said.
Interestingly, he added, children who have limb movement disorder have symptoms during the day, similar to adults. “But we see many children with periodic limb movements of sleep whose arms and legs are moving all night, and they don’t have many symptoms during the day.” These children may have difficulty falling or staying asleep, but do not fulfill all of the American Academy of Sleep Medicine criteria for diagnosis of periodic limb movement disorder, he added.
In 2018, Lourdes M. DelRosso, MD, EdD, of Seattle Children’s Hospital, and colleagues described a new sleep problem they termed restless sleep disorder: those who do not fit the criteria for any other sleep disorder but have daytime impairment.
“On video they have very frequent movements – more than five movements an hour of major body activity,” Dr. Sheldon explained. “They’ll move their trunk, their legs, and reposition themselves. We have found that there are many children who presented to the sleep disorder center with restless sleep, limb movement disorder, periodic limb movements of sleep, and daytime symptoms that would fulfill the criteria of periodic limb movement disorder but also have atopic dermatitis.”
Recently, Dr. Sheldon and his colleagues used polysomnographic variables to study children who presented to Lurie Children’s Hospital with AD and symptoms such as difficulty maintaining sleep and snoring with allergic rhinitis. They found that there were increased periods of being awake after the onset of sleep, “meaning the children fell asleep fairly easily in the beginning of the night but they had significant wake after they fell asleep,” he said. “They would wake up in the middle of the night and stay awake for long periods of time – either one long session or multiple shorter sessions throughout the night. They had increased total limb movements per hour of sleep. This means that their limb movements were greater than five events per hour of sleep and it resulted in restless sleep and limb movements that would fulfill the criteria of periodic limb movement disorder.”
Most of these children had mild to moderate AD, he continued. “We feel that the sensory afferent loop in these youngsters doesn’t really turn off completely when they’re asleep. This is ripe for further study, but it makes intuitive sense that if the sensory afferent loop continues during sleep, it may affect the arousal system significantly.”
Dr. Sheldon recommended that any child who presents with a diagnosis of periodic limb movement disorder, periodic limb movements of sleep, or restless sleep disorder should be evaluated for AD. “The treatment then, would first require differentiation between periodic limb movement disorder of sleep and AD. Both should be addressed at the same time in order to solve the child’s daytime AD problem as well as the sleep-related issues that occur with an AD diagnosis.”
He reported having no financial disclosures.
FROM RAD 2021
Heavy snoring in early pregnancy linked to increased insulin resistance
Severe maternal sleep-disordered breathing (SDB) is a known risk factor for gestational diabetes, which is commonly diagnosed in the second or third trimester of pregnancy.
Now, a new study suggests that increases in insulin resistance, a precursor for gestational diabetes, may take place as early as the first trimester of pregnancy in women with risk factors for obstructive sleep apnea (OSA), such as overweight and habitual snoring.
This finding could potentially provide physicians with a window of opportunity to improve outcomes by screening at-risk women early in pregnancy or even prior to conception, Laura Sanapo, MD, assistant professor of medicine (research) at Brown University, Providence, R.I., and colleagues wrote in Sleep.
“Further studies are needed to investigate the association and its impact on the development of gestational diabetes, and to establish whether early-gestation or pregestational treatment of SDB would improve glucose metabolic outcomes in pregnancy,” they wrote.
”What this paper demonstrates is that the changes that predate gestational diabetes are seen much earlier in pregnancy,” senior study author Ghada Bourjeily, MD, professor of medicine at Brown University, said in an interview. Women should be screened for SDB rather than insulin resistance in early pregnancy since continuous positive airway pressure therapy (CPAP) is a highly effective intervention.
Waiting until midpregnancy to screen for OSA “is too late to make significant changes in the care of these women,” said Dr. Bourjeily, who is also director of research and training at the Women’s Medicine Collaborative at The Miriam Hospital in Providence, R.I. “By the time you diagnose gestational diabetes, the cat is out of the bag.”
For the study, women with early singleton pregnancies and risk factors for OSA such as habitual snoring and a median body mass index (BMI) of at least 27 kg/m2 were recruited from two prospective clinical trial studies enriched for OSA positivity. Women with a history of pregestational diabetes and those using CPAP or receiving chronic steroid therapy were excluded from the current study.
A total of 192 study participants underwent in-home sleep study (HSAT) and homeostatic model assessment (HOMA) between 11 and 15 gestational weeks, respectively. The association between continuous measures of SDB as a respiratory-event index as well as oxygen-desaturation index and glucose metabolism parameters such as insulin resistance (HOMA-IR) were analyzed after adjusting for gestational age, maternal age, BMI, ethnicity, race, and parity.
In all, 61 women (32%) were diagnosed with OSA based on respiratory event index values greater than or equal to five events per hour. These participants were more likely to be older, to have a high BMI, and to be multipara, compared with women who didn’t have a diagnosis of OSA. Women with a diagnosis of OSA exhibited higher glucose and C-peptide values and a higher degree of insulin resistance, compared with women without OSA, the researchers found. An increase of 0.3 in HOMA-IR related to maternal SDB in early pregnancy may significantly affect glucose metabolism.
Although the findings of the current study cannot be extrapolated to women who don’t have overweight or obesity, some women with normal-range BMI (18.5-24.9) are also at increased risk of glucose metabolism changes, Dr. Bourjeily pointed out. This includes those of Southeast Asian descent. “We found that the association of SDB parameters with insulin resistance was actually happening independently of BMI and other factors.”
Ideally, screening for SDB would begin prior to pregnancy, Dr. Bourjeily said. A BMI greater than 25 should be taken into account and patients asked if they snore and if so, whether it’s loud enough to wake their partner. They should also be asked about experiencing daytime sleepiness.
“Based on these answers, especially in women screened prior to pregnancy, there will be time to make the diagnosis of sleep apnea and get the patient on CPAP,” Dr. Bourjeily said.
“This is an interesting study and one of the rare ones looking at early pregnancy and some of the mechanisms that could possibly be contributing to gestational diabetes,” commented Grenye O’Malley, MD, assistant professor in the division of endocrinology, diabetes, and bone disease at the Icahn School of Medicine at Mount Sinai, New York. Dr. O’Malley was not involved in the study.
“It confirms our suspicions that there’s probably a lot of things happening earlier in pregnancy before a diagnosis of gestational diabetes. It also confirms that some of the mechanisms are probably very similar to those involved in the association between disordered sleep and the development of type 2 diabetes.”
However, it’s too early to determine whether screening for SDB and the use of CPAP will prevent glycemic changes, Dr. O’Malley said in an interview. “Whenever we screen, we ask whether we have an intervention that changes outcomes and we don’t know that yet.”
Some of the symptoms of SDB are also common in early pregnancy, such as a BMI greater than 25 and daytime sleepiness, Dr. O’Malley pointed out. It was unclear whether the study participants had a propensity to develop type 2 diabetes or whether they were at risk of gestational diabetes.
This study was funded by the National Heart, Lung, and Blood Institute; the National Institute for Child Health; and the National Institute of General Medical Sciences. Dr. Bourjeily and colleagues, as well as Dr. O’Malley, reported having no potential financial conflicts of interest.
Severe maternal sleep-disordered breathing (SDB) is a known risk factor for gestational diabetes, which is commonly diagnosed in the second or third trimester of pregnancy.
Now, a new study suggests that increases in insulin resistance, a precursor for gestational diabetes, may take place as early as the first trimester of pregnancy in women with risk factors for obstructive sleep apnea (OSA), such as overweight and habitual snoring.
This finding could potentially provide physicians with a window of opportunity to improve outcomes by screening at-risk women early in pregnancy or even prior to conception, Laura Sanapo, MD, assistant professor of medicine (research) at Brown University, Providence, R.I., and colleagues wrote in Sleep.
“Further studies are needed to investigate the association and its impact on the development of gestational diabetes, and to establish whether early-gestation or pregestational treatment of SDB would improve glucose metabolic outcomes in pregnancy,” they wrote.
”What this paper demonstrates is that the changes that predate gestational diabetes are seen much earlier in pregnancy,” senior study author Ghada Bourjeily, MD, professor of medicine at Brown University, said in an interview. Women should be screened for SDB rather than insulin resistance in early pregnancy since continuous positive airway pressure therapy (CPAP) is a highly effective intervention.
Waiting until midpregnancy to screen for OSA “is too late to make significant changes in the care of these women,” said Dr. Bourjeily, who is also director of research and training at the Women’s Medicine Collaborative at The Miriam Hospital in Providence, R.I. “By the time you diagnose gestational diabetes, the cat is out of the bag.”
For the study, women with early singleton pregnancies and risk factors for OSA such as habitual snoring and a median body mass index (BMI) of at least 27 kg/m2 were recruited from two prospective clinical trial studies enriched for OSA positivity. Women with a history of pregestational diabetes and those using CPAP or receiving chronic steroid therapy were excluded from the current study.
A total of 192 study participants underwent in-home sleep study (HSAT) and homeostatic model assessment (HOMA) between 11 and 15 gestational weeks, respectively. The association between continuous measures of SDB as a respiratory-event index as well as oxygen-desaturation index and glucose metabolism parameters such as insulin resistance (HOMA-IR) were analyzed after adjusting for gestational age, maternal age, BMI, ethnicity, race, and parity.
In all, 61 women (32%) were diagnosed with OSA based on respiratory event index values greater than or equal to five events per hour. These participants were more likely to be older, to have a high BMI, and to be multipara, compared with women who didn’t have a diagnosis of OSA. Women with a diagnosis of OSA exhibited higher glucose and C-peptide values and a higher degree of insulin resistance, compared with women without OSA, the researchers found. An increase of 0.3 in HOMA-IR related to maternal SDB in early pregnancy may significantly affect glucose metabolism.
Although the findings of the current study cannot be extrapolated to women who don’t have overweight or obesity, some women with normal-range BMI (18.5-24.9) are also at increased risk of glucose metabolism changes, Dr. Bourjeily pointed out. This includes those of Southeast Asian descent. “We found that the association of SDB parameters with insulin resistance was actually happening independently of BMI and other factors.”
Ideally, screening for SDB would begin prior to pregnancy, Dr. Bourjeily said. A BMI greater than 25 should be taken into account and patients asked if they snore and if so, whether it’s loud enough to wake their partner. They should also be asked about experiencing daytime sleepiness.
“Based on these answers, especially in women screened prior to pregnancy, there will be time to make the diagnosis of sleep apnea and get the patient on CPAP,” Dr. Bourjeily said.
“This is an interesting study and one of the rare ones looking at early pregnancy and some of the mechanisms that could possibly be contributing to gestational diabetes,” commented Grenye O’Malley, MD, assistant professor in the division of endocrinology, diabetes, and bone disease at the Icahn School of Medicine at Mount Sinai, New York. Dr. O’Malley was not involved in the study.
“It confirms our suspicions that there’s probably a lot of things happening earlier in pregnancy before a diagnosis of gestational diabetes. It also confirms that some of the mechanisms are probably very similar to those involved in the association between disordered sleep and the development of type 2 diabetes.”
However, it’s too early to determine whether screening for SDB and the use of CPAP will prevent glycemic changes, Dr. O’Malley said in an interview. “Whenever we screen, we ask whether we have an intervention that changes outcomes and we don’t know that yet.”
Some of the symptoms of SDB are also common in early pregnancy, such as a BMI greater than 25 and daytime sleepiness, Dr. O’Malley pointed out. It was unclear whether the study participants had a propensity to develop type 2 diabetes or whether they were at risk of gestational diabetes.
This study was funded by the National Heart, Lung, and Blood Institute; the National Institute for Child Health; and the National Institute of General Medical Sciences. Dr. Bourjeily and colleagues, as well as Dr. O’Malley, reported having no potential financial conflicts of interest.
Severe maternal sleep-disordered breathing (SDB) is a known risk factor for gestational diabetes, which is commonly diagnosed in the second or third trimester of pregnancy.
Now, a new study suggests that increases in insulin resistance, a precursor for gestational diabetes, may take place as early as the first trimester of pregnancy in women with risk factors for obstructive sleep apnea (OSA), such as overweight and habitual snoring.
This finding could potentially provide physicians with a window of opportunity to improve outcomes by screening at-risk women early in pregnancy or even prior to conception, Laura Sanapo, MD, assistant professor of medicine (research) at Brown University, Providence, R.I., and colleagues wrote in Sleep.
“Further studies are needed to investigate the association and its impact on the development of gestational diabetes, and to establish whether early-gestation or pregestational treatment of SDB would improve glucose metabolic outcomes in pregnancy,” they wrote.
”What this paper demonstrates is that the changes that predate gestational diabetes are seen much earlier in pregnancy,” senior study author Ghada Bourjeily, MD, professor of medicine at Brown University, said in an interview. Women should be screened for SDB rather than insulin resistance in early pregnancy since continuous positive airway pressure therapy (CPAP) is a highly effective intervention.
Waiting until midpregnancy to screen for OSA “is too late to make significant changes in the care of these women,” said Dr. Bourjeily, who is also director of research and training at the Women’s Medicine Collaborative at The Miriam Hospital in Providence, R.I. “By the time you diagnose gestational diabetes, the cat is out of the bag.”
For the study, women with early singleton pregnancies and risk factors for OSA such as habitual snoring and a median body mass index (BMI) of at least 27 kg/m2 were recruited from two prospective clinical trial studies enriched for OSA positivity. Women with a history of pregestational diabetes and those using CPAP or receiving chronic steroid therapy were excluded from the current study.
A total of 192 study participants underwent in-home sleep study (HSAT) and homeostatic model assessment (HOMA) between 11 and 15 gestational weeks, respectively. The association between continuous measures of SDB as a respiratory-event index as well as oxygen-desaturation index and glucose metabolism parameters such as insulin resistance (HOMA-IR) were analyzed after adjusting for gestational age, maternal age, BMI, ethnicity, race, and parity.
In all, 61 women (32%) were diagnosed with OSA based on respiratory event index values greater than or equal to five events per hour. These participants were more likely to be older, to have a high BMI, and to be multipara, compared with women who didn’t have a diagnosis of OSA. Women with a diagnosis of OSA exhibited higher glucose and C-peptide values and a higher degree of insulin resistance, compared with women without OSA, the researchers found. An increase of 0.3 in HOMA-IR related to maternal SDB in early pregnancy may significantly affect glucose metabolism.
Although the findings of the current study cannot be extrapolated to women who don’t have overweight or obesity, some women with normal-range BMI (18.5-24.9) are also at increased risk of glucose metabolism changes, Dr. Bourjeily pointed out. This includes those of Southeast Asian descent. “We found that the association of SDB parameters with insulin resistance was actually happening independently of BMI and other factors.”
Ideally, screening for SDB would begin prior to pregnancy, Dr. Bourjeily said. A BMI greater than 25 should be taken into account and patients asked if they snore and if so, whether it’s loud enough to wake their partner. They should also be asked about experiencing daytime sleepiness.
“Based on these answers, especially in women screened prior to pregnancy, there will be time to make the diagnosis of sleep apnea and get the patient on CPAP,” Dr. Bourjeily said.
“This is an interesting study and one of the rare ones looking at early pregnancy and some of the mechanisms that could possibly be contributing to gestational diabetes,” commented Grenye O’Malley, MD, assistant professor in the division of endocrinology, diabetes, and bone disease at the Icahn School of Medicine at Mount Sinai, New York. Dr. O’Malley was not involved in the study.
“It confirms our suspicions that there’s probably a lot of things happening earlier in pregnancy before a diagnosis of gestational diabetes. It also confirms that some of the mechanisms are probably very similar to those involved in the association between disordered sleep and the development of type 2 diabetes.”
However, it’s too early to determine whether screening for SDB and the use of CPAP will prevent glycemic changes, Dr. O’Malley said in an interview. “Whenever we screen, we ask whether we have an intervention that changes outcomes and we don’t know that yet.”
Some of the symptoms of SDB are also common in early pregnancy, such as a BMI greater than 25 and daytime sleepiness, Dr. O’Malley pointed out. It was unclear whether the study participants had a propensity to develop type 2 diabetes or whether they were at risk of gestational diabetes.
This study was funded by the National Heart, Lung, and Blood Institute; the National Institute for Child Health; and the National Institute of General Medical Sciences. Dr. Bourjeily and colleagues, as well as Dr. O’Malley, reported having no potential financial conflicts of interest.
FROM SLEEP
FDA OKs new adult insomnia med
The Food and Drug Administration has approved the dual orexin receptor antagonist daridorexant (Quviviq) for the treatment of insomnia in adults, the drug’s manufacturer, Idorsia, has announced.
The FDA’s decision was based partly on a phase 3 trial of adults with moderate to severe insomnia who were randomly assigned to receive 25 or 50 mg of daridorexant or matching placebo. Daridorexant was associated with dose-dependent improvements in wake after sleep onset, total sleep time, and latency to persistent sleep.
Whereas the overall results are very positive, the improvements in daytime functioning are especially “exciting,” Thomas Roth, PhD, director of the Sleep Disorders and Research Center at Henry Ford Hospital in Detroit, said in an interview.
“That’s sort of a big deal. For me, that’s the biggest deal there is,” said Dr. Roth, who was a consultant on the design of the phase 3 trial and on the interpretation of the data.
The drug will be available in doses of 25 mg and 50 mg, and the FDA has recommended that it be classified as a controlled substance. After it is scheduled by the Drug Enforcement Administration, daridorexant is expected to be made available in May.
Favorable safety profile
Insomnia is a common disorder characterized by difficulty falling asleep or staying asleep and by early-morning awakenings. Patients with insomnia often report fatigue, irritability, and difficulty with concentration. The condition can also result in significant problems with work and social activities, thus contributing to anxiety or depression.
As with other dual orexin receptor antagonists, daridorexant competitively binds with both orexin receptors in the lateral hypothalamus to block the activity of orexin in a reversible way. This approach decreases the downstream action of the wake-promoting neurotransmitters that are overactive in patients with insomnia.
The phase 3 trial measured daytime functioning using the new Insomnia Daytime Symptoms and Impacts Questionnaire (IDSIQ), a patient-reported outcome instrument. Daridorexant was associated with significant improvements in daytime function, particularly in sleepiness and mood.
Previous trials of other dual orexin receptor antagonists did not use the IDSIQ as an outcome, so it is not possible to compare daridorexant with those drugs in this respect, Dr. Roth noted. Researchers also have not conducted head-to-head trials of the drug with other dual orexin receptor antagonists.
Daridorexant also had a favorable safety profile and was not associated with rebound insomnia or withdrawal effects. The most common adverse events were headache and somnolence or fatigue.
“They had no effect on sleep stage distribution [and] they had no significant effects on sleep and breathing in people with mild to moderate sleep apnea,” said Dr. Roth, who presented the phase 3 findings at SLEEP 2020.
In addition to serving as a consultant for Idorsia on the trial design and interpretation of results, Dr. Roth has also served as a consultant for other companies that develop sleep agents.
A version of this article first appeared on Medscape.com.
The Food and Drug Administration has approved the dual orexin receptor antagonist daridorexant (Quviviq) for the treatment of insomnia in adults, the drug’s manufacturer, Idorsia, has announced.
The FDA’s decision was based partly on a phase 3 trial of adults with moderate to severe insomnia who were randomly assigned to receive 25 or 50 mg of daridorexant or matching placebo. Daridorexant was associated with dose-dependent improvements in wake after sleep onset, total sleep time, and latency to persistent sleep.
Whereas the overall results are very positive, the improvements in daytime functioning are especially “exciting,” Thomas Roth, PhD, director of the Sleep Disorders and Research Center at Henry Ford Hospital in Detroit, said in an interview.
“That’s sort of a big deal. For me, that’s the biggest deal there is,” said Dr. Roth, who was a consultant on the design of the phase 3 trial and on the interpretation of the data.
The drug will be available in doses of 25 mg and 50 mg, and the FDA has recommended that it be classified as a controlled substance. After it is scheduled by the Drug Enforcement Administration, daridorexant is expected to be made available in May.
Favorable safety profile
Insomnia is a common disorder characterized by difficulty falling asleep or staying asleep and by early-morning awakenings. Patients with insomnia often report fatigue, irritability, and difficulty with concentration. The condition can also result in significant problems with work and social activities, thus contributing to anxiety or depression.
As with other dual orexin receptor antagonists, daridorexant competitively binds with both orexin receptors in the lateral hypothalamus to block the activity of orexin in a reversible way. This approach decreases the downstream action of the wake-promoting neurotransmitters that are overactive in patients with insomnia.
The phase 3 trial measured daytime functioning using the new Insomnia Daytime Symptoms and Impacts Questionnaire (IDSIQ), a patient-reported outcome instrument. Daridorexant was associated with significant improvements in daytime function, particularly in sleepiness and mood.
Previous trials of other dual orexin receptor antagonists did not use the IDSIQ as an outcome, so it is not possible to compare daridorexant with those drugs in this respect, Dr. Roth noted. Researchers also have not conducted head-to-head trials of the drug with other dual orexin receptor antagonists.
Daridorexant also had a favorable safety profile and was not associated with rebound insomnia or withdrawal effects. The most common adverse events were headache and somnolence or fatigue.
“They had no effect on sleep stage distribution [and] they had no significant effects on sleep and breathing in people with mild to moderate sleep apnea,” said Dr. Roth, who presented the phase 3 findings at SLEEP 2020.
In addition to serving as a consultant for Idorsia on the trial design and interpretation of results, Dr. Roth has also served as a consultant for other companies that develop sleep agents.
A version of this article first appeared on Medscape.com.
The Food and Drug Administration has approved the dual orexin receptor antagonist daridorexant (Quviviq) for the treatment of insomnia in adults, the drug’s manufacturer, Idorsia, has announced.
The FDA’s decision was based partly on a phase 3 trial of adults with moderate to severe insomnia who were randomly assigned to receive 25 or 50 mg of daridorexant or matching placebo. Daridorexant was associated with dose-dependent improvements in wake after sleep onset, total sleep time, and latency to persistent sleep.
Whereas the overall results are very positive, the improvements in daytime functioning are especially “exciting,” Thomas Roth, PhD, director of the Sleep Disorders and Research Center at Henry Ford Hospital in Detroit, said in an interview.
“That’s sort of a big deal. For me, that’s the biggest deal there is,” said Dr. Roth, who was a consultant on the design of the phase 3 trial and on the interpretation of the data.
The drug will be available in doses of 25 mg and 50 mg, and the FDA has recommended that it be classified as a controlled substance. After it is scheduled by the Drug Enforcement Administration, daridorexant is expected to be made available in May.
Favorable safety profile
Insomnia is a common disorder characterized by difficulty falling asleep or staying asleep and by early-morning awakenings. Patients with insomnia often report fatigue, irritability, and difficulty with concentration. The condition can also result in significant problems with work and social activities, thus contributing to anxiety or depression.
As with other dual orexin receptor antagonists, daridorexant competitively binds with both orexin receptors in the lateral hypothalamus to block the activity of orexin in a reversible way. This approach decreases the downstream action of the wake-promoting neurotransmitters that are overactive in patients with insomnia.
The phase 3 trial measured daytime functioning using the new Insomnia Daytime Symptoms and Impacts Questionnaire (IDSIQ), a patient-reported outcome instrument. Daridorexant was associated with significant improvements in daytime function, particularly in sleepiness and mood.
Previous trials of other dual orexin receptor antagonists did not use the IDSIQ as an outcome, so it is not possible to compare daridorexant with those drugs in this respect, Dr. Roth noted. Researchers also have not conducted head-to-head trials of the drug with other dual orexin receptor antagonists.
Daridorexant also had a favorable safety profile and was not associated with rebound insomnia or withdrawal effects. The most common adverse events were headache and somnolence or fatigue.
“They had no effect on sleep stage distribution [and] they had no significant effects on sleep and breathing in people with mild to moderate sleep apnea,” said Dr. Roth, who presented the phase 3 findings at SLEEP 2020.
In addition to serving as a consultant for Idorsia on the trial design and interpretation of results, Dr. Roth has also served as a consultant for other companies that develop sleep agents.
A version of this article first appeared on Medscape.com.
Key questions to ask atopic dermatitis patients with sleep complaints
If you don’t think it’s important to assess for sleep disorders in your patients with atopic dermatitis (AD), think again.
According to Sabra M. Abbott, MD, PhD, professor of neurology at Northwestern University, Chicago, as well as increased night kicks and nocturnal leg cramps, and a more than twofold increased risk for insomnia.
During the Revolutionizing Atopic Dermatitis symposium, she offered key questions to ask AD patients who present with sleep complaints:
When do you go to bed? “This does not refer to when you get into bed, but when do you actually go to bed with an intention to go to sleep, outside of watching television or answering emails?” Dr. Abbott said.
How long does it take for you to fall asleep?
Do you wake up in the middle of the night, and for how long? What do you do if you wake up?
When do you wake up in the morning? Is it on your own, or with an alarm clock?
Does this schedule change on nonworkdays?
Do you have daytime impairment? Meaning, do your sleep complaints impact how you function during the daytime?
Do you snore? Meaning, is there concern for sleep apnea?
Do you have uncomfortable sensations in your legs? Are they worse in the evening and improve with movement? These are signs of possible restless legs syndrome.
The Epworth Sleepiness Scale is one self-administered questionnaire to consider using for AD patients with sleep complaints. “This provides patients with several examples of typical scenarios they might encounter during the day and queries whether or not they feel that they could deal with any of those scenarios,” Dr. Abbott said. “A score of greater than 10 indicates that they are sleepy; it’s not just an overall sense of fatigue and decreased energy.”
Other brief self-assessment tools she recommended are the Insomnia Severity Index and the STOP-Bang questionnaire.
Dr. Abbott reported having no financial disclosures.
If you don’t think it’s important to assess for sleep disorders in your patients with atopic dermatitis (AD), think again.
According to Sabra M. Abbott, MD, PhD, professor of neurology at Northwestern University, Chicago, as well as increased night kicks and nocturnal leg cramps, and a more than twofold increased risk for insomnia.
During the Revolutionizing Atopic Dermatitis symposium, she offered key questions to ask AD patients who present with sleep complaints:
When do you go to bed? “This does not refer to when you get into bed, but when do you actually go to bed with an intention to go to sleep, outside of watching television or answering emails?” Dr. Abbott said.
How long does it take for you to fall asleep?
Do you wake up in the middle of the night, and for how long? What do you do if you wake up?
When do you wake up in the morning? Is it on your own, or with an alarm clock?
Does this schedule change on nonworkdays?
Do you have daytime impairment? Meaning, do your sleep complaints impact how you function during the daytime?
Do you snore? Meaning, is there concern for sleep apnea?
Do you have uncomfortable sensations in your legs? Are they worse in the evening and improve with movement? These are signs of possible restless legs syndrome.
The Epworth Sleepiness Scale is one self-administered questionnaire to consider using for AD patients with sleep complaints. “This provides patients with several examples of typical scenarios they might encounter during the day and queries whether or not they feel that they could deal with any of those scenarios,” Dr. Abbott said. “A score of greater than 10 indicates that they are sleepy; it’s not just an overall sense of fatigue and decreased energy.”
Other brief self-assessment tools she recommended are the Insomnia Severity Index and the STOP-Bang questionnaire.
Dr. Abbott reported having no financial disclosures.
If you don’t think it’s important to assess for sleep disorders in your patients with atopic dermatitis (AD), think again.
According to Sabra M. Abbott, MD, PhD, professor of neurology at Northwestern University, Chicago, as well as increased night kicks and nocturnal leg cramps, and a more than twofold increased risk for insomnia.
During the Revolutionizing Atopic Dermatitis symposium, she offered key questions to ask AD patients who present with sleep complaints:
When do you go to bed? “This does not refer to when you get into bed, but when do you actually go to bed with an intention to go to sleep, outside of watching television or answering emails?” Dr. Abbott said.
How long does it take for you to fall asleep?
Do you wake up in the middle of the night, and for how long? What do you do if you wake up?
When do you wake up in the morning? Is it on your own, or with an alarm clock?
Does this schedule change on nonworkdays?
Do you have daytime impairment? Meaning, do your sleep complaints impact how you function during the daytime?
Do you snore? Meaning, is there concern for sleep apnea?
Do you have uncomfortable sensations in your legs? Are they worse in the evening and improve with movement? These are signs of possible restless legs syndrome.
The Epworth Sleepiness Scale is one self-administered questionnaire to consider using for AD patients with sleep complaints. “This provides patients with several examples of typical scenarios they might encounter during the day and queries whether or not they feel that they could deal with any of those scenarios,” Dr. Abbott said. “A score of greater than 10 indicates that they are sleepy; it’s not just an overall sense of fatigue and decreased energy.”
Other brief self-assessment tools she recommended are the Insomnia Severity Index and the STOP-Bang questionnaire.
Dr. Abbott reported having no financial disclosures.
FROM REVOLUTIONIZING AD 2021
Pediatric insomnia: Treatment
Children and adolescents who do not receive sufficient sleep can experience worsening inattention, daytime fatigue, and cognitive and behavioral difficulties. Assessment and treatment of insomnia and other sleep difficulties in young patients is critical as poor sleep increases their risk for depression, self-harm, and suicide.
In Part 1 of this article (Pediatric insomnia: Assessment and diagnosis,
Psychotherapeutic interventions
Regardless of the source of a child’s insomnia or co-occurring disorders, healthy sleep practices are the first line behavioral treatment, including for youth with attention-deficit/hyperactivity disorder (ADHD), anxiety disorders, obsessive-compulsive disorder, and depressive disorders.
Healthy sleep practices/sleep hygiene
Developmentally appropriate bedtimes and routines (Table). Helping children establish a regular, consistent bedtime is key in promoting healthy sleep. Ideally, the bedtime routine involves 3 to 4 activities each night in the same order, and these activities should be relaxing and soothing (eg, taking a bath, putting on pajamas, reading books). Setting age-appropriate bedtimes also is important. If an older child is asked to go to bed at 8 pm but cannot fall asleep for an hour, they may not have insomnia but instead a developmentally inappropriate bedtime. Several studies found that children younger than age 10 should go to bed no later than 9 pm. Bedtimes later than 9 pm for young children are correlated with shorter sleep duration.1
Consistent sleep schedules. Another important aspect of healthy sleep is working with parents to enforce a consistent bedtime and wake-up time, including weekdays and weekends. Ideally, bedtime on weekdays and weekends should not vary by more than 1 hour. Helping children wake up at the same time each day helps to set and regulate their circadian rhythm. Keeping these schedules consistent on vacations and school holidays also is helpful. For adolescents, the weekday/weekend bedtimes can vary by up to 2 hours because adolescents have a delayed circadian rhythm and wake-up times for high school can be early.
Environmental factors. An important piece of parental education is stimulus control and the ingredients of healthy sleep. Healthy sleep ingredients include a dark, quiet, consistent, and cool bedroom; a comfortable bed, the child feeling safe, and limited environmental stimuli.
Continue to: Cognitive-behavioral therapy for insomnia...
Cognitive-behavioral therapy for insomnia
Relaxation. Pediatric patients can be taught relaxation, mindfulness, meditation, and progressive muscle relaxation techniques to help lower overall stress. This can be especially helpful for youth with sleep disorders or anxiety. Guided relaxation apps are popular among children and teens, and various apps offer soothing sounds, deep breathing, progressive muscle relaxation, and guided imagery. This can be taught in psychotherapy sessions and used at home to promote gains in between sessions.
Stimulus control. Stimulus control involves using the bed exclusively for sleep and avoiding nonsleep activities in bed (eg, reading, watching television, using a computer, worrying). These activities promote wakefulness and insomnia. This may mean the child does not get into bed until they cannot keep their eyes open, even if that delays bedtime. If the child is still awake within 15 to 20 minutes, they should be encouraged to get out of bed and engage in a nonstimulating activity such as meditation, reading, or sitting quietly in the dark or low light. This recommendation can run counter to parents’ intuition that children with sleep problems should go to bed earlier. Using the bed only for sleep conditions the child to falling asleep or being asleep when in bed.
Sleep restriction. Sleep restriction involves restricting sleep to a set number of hours in order to increase their sleep efficiency (time slept in bed divided by total time spent in bed x 100). Restricting sleep to 6 to 7 hours increases sleep efficiency, consolidates sleep, and extinguishes the association of being awake in bed. For older adolescents, sleep restriction may help to limit their time in bed to either falling asleep or being asleep. This is intended to be used as a short-term strategy and only after other sleep hygiene measures (bedtime routine, environmental factors, etc) have been put into place for several weeks. While this strategy sounds unappealing to most individuals with insomnia, it can lead to lasting change due to the use of behavioral conditioning in bed. Because sleep restriction can lead to significant daytime sleepiness and impairment during the day, sleep should not be restricted to <6 hours a day for children and adolescents. Once the adolescent is sleeping more consistently and sleep efficiency reaches 85% or higher, time in bed for sleep is increased.2
Cognitive restructuring. Some children and adolescents develop maladaptive thoughts about sleep that further promote insomnia. These thoughts might include “I will never get to sleep,” “I am going to have a terrible day if I cannot fall asleep,” or “I will fail my test tomorrow if I am unable to sleep.” Such maladaptive thoughts are often untrue but promote wakefulness in the early or middle part of the night. Cognitive restructuring involves helping the child identify each problematic thought, challenge how accurate each thought is with evidence, and replace the problematic thought with a more helpful thought. For instance, an adolescent can recognize that even if they have a sleepless night, their catastrophic outcome (eg, “I will not be able to function”) is likely untrue. A psychologist can help review evidence for this, including previous times when the adolescent has not slept well and managed to get through the next day.
When is pharmacologic treatment needed?
Pharmacologic treatment may be indicated if a child does not show significant improvement following behavioral intervention (Figure). However, it is critical to exclude other primary causes of dyssomnia (eg, obstructive sleep apnea, iron deficiency anemia) before pursuing pharmacotherapy, because pharmacotherapy could mask an underlying disorder. Moreover, while there is relatively limited evidence for psychopharmacologic interventions for sleep difficulties in children and adolescents, a large survey of child and adolescent psychiatrists (N = 1,273) suggested that medications were considered for one-quarter of pediatric patients with insomnia.3 Further, patients with specific comorbidities such as neurodevelopmental disorders may be more likely to be prescribed soporifics.4
Continue to: What is the evidence for pharmacotherapy?...
What is the evidence for pharmacotherapy?
Antihistamines. Histamine antagonists—which promote sleep by blocking the wakefulness-promoting and circadian-related effects of histamine—are the most commonly used medications to treat pediatric insomnia, despite a dearth of data from prospective trials.5,6 In 1 small study, Russo et al7 found diphenhydramine, 1 mg/kg at bedtime, reduced sleep latency and nighttime awakenings, and increased sleep duration in patients ages 2 to 12; similar effects have been observed in pediatric burn patients.8 There are some limited data for other H1 antagonists (eg, hydroxyzine) in pediatric insomnia.9-11
Alpha-2 agonists increase rapid eye movement sleep via dose-dependent downregulation of noradrenergic signaling12 and thus have been commonly prescribed for insomnia in children and adolescents. In fact, the nonselective alpha-2 agonist clonidine is among the most prescribed medications for youth with insomnia, and may be efficacious in youth with neurodevelopmental disorders and ADHD.13 In small retrospective studies, clonidine decreased sleep latency and nighttime awakenings in addition to increasing sleep duration.14 Also, clonidine was well tolerated but associated with daytime somnolence. Guanfacine—a selective alpha-2 agonist—is also commonly prescribed for insomnia in youth, although results of trials have been equivocal.15 Given the more rapid absorption and shorter Tmax of clonidine relative to guanfacine, the former may be preferred as a soporific.
Melatonin and melatonin agonists. The primary regulator of the sleep-wake cycle is melatonin, an endogenous hormone produced by the pineal gland in response to changes in retinal light perception. Exogenous melatonin supplementation may be the preferred initial pharmacotherapy for sleep-onset insomnia due to its chronobiotic properties.16 In clinical studies, both immediate-release17,18 and extended-release19 melatonin reduced sleep-onset latency and increased total sleep duration in pediatric patients, although the increase in total duration of sleep was greater with extended-release preparations. Additionally, tolerability data for melatonin in pediatric patients are encouraging. A 2-year randomized trial of prolonged-release melatonin for insomnia in pediatric patients found no adverse effects with regard to growth, body mass index, or pubertal development.20 Additionally, significant improvements in sleep quality, sleep patterns, and caregiver satisfaction were maintained throughout the trial, and no withdrawal symptoms were observed upon discontinuation.
Melatonin may have a particularly important role in circadian rhythm sleep disorders. In this regard, low-dose melatonin (0.5 mg), when timed relative to the endogenous dim light melatonin onset (DLMO), is more effective in shifting sleep phase than higher doses, which suggests that timing may have greater impact than dosage.21 Data regarding melatonin administration with respect to DLMO suggest that the optimal administration time is 4 to 6 hours before a child’s preferred bedtime, and doses of 0.5 to 1 mg have been effective when given in this window.22 Variation across studies has contributed to a lack of consensus regarding pediatric melatonin dosing. For example, .05 mg/kg may be a minimal effective dose when given 1 to 2 hours before bedtime18; however, in surveys doses vary considerably, with typical doses of 2.5 to 3 mg for prepubertal children and 5 mg for adolescents.5 Of note, in patients with decreased cytochrome P450 (CYP) 1A2 activity, lack of diurnal variation in melatonin serum concentration may decrease the effectiveness of melatonin.16Ramelteon is a potent agonist of the melatonin MT1 and MT2 receptors, with a significantly higher binding affinity than melatonin in vitro. In case reports, ramelteon was well-tolerated, improved delayed sleep onset, and decreased nighttime awakenings.23
Zolpidem, eszopiclone and zaleplon. Studies of selective GABAergic modulators and benzodiazepines have not produced positive results in prospective trials of youth with insomnia. Zolpidem was studied in children and adolescents (N = 201) with ADHD; although sleep latency did not differ between zolpidem and placebo, some significant improvements were observed in adolescents.24 Zolpidem was generally well tolerated, with approximately 10% of youth discontinuing due to adverse effects. Additionally, eszopiclone—which has a longer duration of action compared with zolpidem—has been studied in children and adolescents with ADHD (N = 486) who were also evaluated with a sleep study. No differences were observed between placebo and eszopiclone in terms of sleep latency and approximately 10% of patients discontinued treatment as a result of adverse events.25 We were unable to locate any prospective trials of zaleplon or benzodiazepine receptor agonists for insomnia in youth, although some reports suggest that clonazepam may have a possible role for specific parasomnias.26,27Dual orexin receptor antagonists. Suvorexant, an antagonist of the wakefulness-promoting neuropeptide orexin, improved subjective sleep quality in a prospective trial of adolescents with insomnia (N = 30), although dropout was high (44%).28 Of those patients, reasons for discontinuation included loss to follow-up, lack of effectiveness, and abnormal dreams. We were unable to locate any trials of lemborexant in pediatric patients.
Atypical antidepressants. Trazodone is commonly prescribed for insomnia in pediatric patients with comorbid mood or anxiety disorders. In open-label studies of children and toddlers, trazodone may be well-tolerated and improve sleep.29 Additionally, development of a physiologically based pharmacokinetic model to inform trazodone dosing for youth with insomnia is underway.30 Some studies in adolescents with depression suggest that caution should be used when combining trazodone with medications that inhibit CYP2D6. In the Treatment of SSRI-Resistant Depression in Adolescents study, none of the patients who were treated with trazodone (vs other soporifics) improved.31 This may relate to CYP2D6 interactions and accumulation of methyl-chloro-piperazine (mCPP), a trazodone metabolite that is associated with dysphoria, irritability, and depression.31 This finding has been replicated in a separate cohort of depressed adolescents.32
Because of its antihistaminergic effects, mirtazapine has been used to treat insomnia in adults. One open-label study of mirtazapine in children and young adults ages 3 to 23 with neurodevelopmental disorders suggested that mirtazapine improved behavioral symptoms and insomnia, and was associated with few treatment-limiting adverse effects.33
Tricyclic antidepressants. In a retrospective study of youth with insomnia who failed behavioral interventions and melatonin (N = 29), doxepin, a potent H1 antagonist, improved subjective sleep in one-half of patients.34
Continue to: Consultation with pediatric sleep medicine specialists...
Consultation with pediatric sleep medicine specialists
It often will behoove the psychiatric clinician to review their concerns with a behavioral sleep medicine specialist or a psychologist with specific expertise in the psychotherapeutic treatment of sleep who can provide important guidance regarding the key aspects of treatment. When discussing a particular patient’s presentation with the pediatric behavioral sleep psychologist/specialist, consider the following questions:
- Is the child’s sleep disorder the primary problem, or is the child’s insomnia secondary to another diagnosis (psychiatric or nonpsychiatric)?
- What are the primary sleep-related problems the child/family presents with? How long have the symptoms been present?
- Is the sleep disorder interfering with the child’s functioning, either academically or socially? Does the child’s sleep problem interfere with other family members’ sleep?
- Does the child have a comorbid psychological conditions such as ADHD, depression, or anxiety, and/or is undergoing treatment for these disorders, which may play a role in the sleep problem?
- Is a sleep study warranted?
A sleep study, also known as polysomnography (PSG), is a diagnostic test in which physiologic parameters are continuously recorded during a period of sleep via electroencephalography, electromyography, electrooculogram, electrocardiogram, airflow sensors, pulse oximeter, body position monitors, and video. In 2012, the American Academy of Sleep Medicine published evidenced-based practice parameters for respiratory and nonrespiratory indications for PSG.35 It is most commonly indicated to rule out obstructive sleep apnea in pediatric patients who exhibit snoring, gasping, irregular breathing, witnessed apneic events, unusual head positioning, or other signs of obstructive breathing during sleep. Nonrespiratory indications for PSG include children suspected of having periodic limb movement disorder and suspected narcolepsy. Children with frequent parasomnias, epilepsy, or nocturnal enuresis should be clinically screened for presence of comorbid sleep disorders, and PSG would be indicated if there are concerns about a possible sleep-disordered breathing disorder. PSG is also recommended for children with hypersomnia, to differentiate a parasomnia from sleep-related epilepsy, and for children suspected of having restless leg syndrome.36 PSG is not typically indicated in the initial evaluation of insomnia (unless there is evidence of a comorbid sleep disorder), circadian rhythm disorders (ie, delayed sleep phase syndrome), or for evaluation of children with sleep-related bruxism.3 Special considerations for PSG in children include ensuring a parent or guardian is always with the child, providing developmentally appropriate sleeping arrangements, arranging family tours of the sleep lab prior to the study, and accommodating for earlier bedtimes.37
Bottom Line
Techniques to promote healthy sleep in pediatric patients include behavioral interventions such as setting a developmentally appropriate bedtime and a consistent wake time, establishing bedtime routines, and encouraging relaxation/ wind-down period before bed. Cognitive-behavioral therapy for insomnia (CBT-I) may include cognitive restructuring of anxious thoughts, relaxation training, stimulus control, and sleep restriction. Use of medications may be indicated for children and teens who have not responded to CBT-I or soporific dosing of melatonin.
1. Mindell JA, Li AM, Sadeh A, et al. Bedtime routines for young children: a dose-dependent association with sleep outcomes. Sleep. 2015;38(5):717-722.
2. Kansagra S. Sleep disorders in adolescents. Pediatrics. 2020;145(Suppl 2):S204-S209.
3. Owens JA, Mindell JA. Pediatric insomnia. Pediatr Clin North Am. 2011;58(3):555-569.
4. Bruni O, Angriman M, Melegari MG, et al. Pharmacotherapeutic management of sleep disorders in children with neurodevelopmental disorders. Expert Opin Pharmacother. 2019;20(18):2257-2271.
5. Owens JA, Rosen CL, Mindell JA, et al. Use of pharmacotherapy for insomnia in child psychiatry practice: a national survey. Sleep Med. 2010;11(7):692-700.
6. Schnoes CJ, Kuhn BR, Workman EF, et al. Pediatric prescribing practices for clonidine and other pharmacologic agents for children with sleep disturbance. Clin Pediatr (Phila). 2006;45(3):229-238.
7. Russo RM, Gururaj VJ, Allen JE. The effectiveness of diphenhydramine HCI in pediatric sleep disorders. J Clin Pharmacol. 1976;16(5-6):284-288.
8. Yangzom N, Gottschlich MM, Ossege J, et al. The effect of diphenhydramine on sleep in pediatric burn patients: a secondary analysis. J Burn Care Res. 2015;36(2):266-271.
9. Ghanizadeh A, Zare S. A preliminary randomised double-blind placebo-controlled clinical trial of hydroxyzine for treating sleep bruxism in children. J Oral Rehabil. 2013;40(6):413-417.
10. Bektas O, Arıca B, Teber S, et al. Chloral hydrate and/or hydroxyzine for sedation in pediatric EEG recording. Brain Dev. 2014;36(2):130-136.
11. Ottaviano S, Giannotti F, Cortesi F. The effect of niaprazine on some common sleep disorders in children. A double-blind clinical trial by means of continuous home-videorecorded sleep. Childs Nerv Syst. 1991;7(6):332-335.
12. Nguyen M, Tharani S, Rahmani M, et al. A review of the use of clonidine as a sleep aid in the child and adolescent population. Clin Pediatr (Phila). 2014;53(3):211-216.
13. Prince JB, Wilens TE, Biederman J, et al. Clonidine for sleep disturbances associated with attention-deficit hyperactivity disorder: a systematic chart review of 62 cases. J Am Acad Child Adolesc Psychiatry. 1996;35(5):599-605.

14. Ingrassia A, Turk J. The use of clonidine for severe and intractable sleep problems in children with neurodevelopmental disorders--a case series. Eur Child Adolesc Psychiatry. 2005;14(1):34-40.
15. Politte LC, Scahill L, Figueroa J, et al. A randomized, placebo-controlled trial of extended-release guanfacine in children with autism spectrum disorder and ADHD symptoms: an analysis of secondary outcome measures. Neuropsychopharmacology. 2018;43(8):1772-1778.
16. Bruni O, Alonso-Alconada D, Besag F, et al. Current role of melatonin in pediatric neurology: clinical recommendations. Eur J Paediatr Neurol. 2015;19(2):122-1233.
17. Jain SV, Horn PS, Simakajornboon N, et al. Melatonin improves sleep in children with epilepsy: a randomized, double-blind, crossover study. Sleep Med. 2015;16(5):637-644.
18. van Geijlswijk IM, van der Heijden KB, Egberts AC, et al. Dose finding of melatonin for chronic idiopathic childhood sleep onset insomnia: an RCT. Psychopharmacology (Berl). 2010;212(3):379-391.
19. Gringras P, Nir T, Breddy J, et al. Efficacy and safety of pediatric prolonged-release melatonin for insomnia in children with autism spectrum disorder. J Am Acad Child Adolesc Psychiatry. 2017;56(11):948-957.e4.
20. Malow BA, Findling RL, Schroder CM, et al. Sleep, growth, and puberty after two years of prolonged-release melatonin in children with autism spectrum disorder. J Am Acad Child Adolesc Psychiatry. 2021;60(2):252-261.e3.
21. Burgess HJ, Emens JS. Drugs used in circadian sleep-wake rhythm disturbances. Sleep Med Clin. 2020;15(2):301-310.
22. Arns M, Kooij JJS, Coogan AN. Review: identification and management of circadian rhythm sleep disorders as a transdiagnostic feature in child and adolescent psychiatry. J Am Acad Child Adolesc Psychiatry. 2021;60(9):1085-1095.
23. Kawabe K, Horiuchi F, Oka Y, et al. The melatonin receptor agonist ramelteon effectively treats insomnia and behavioral symptoms in autistic disorder. Case Rep Psychiatry. 2014;2014:561071.
24. Blumer JL, Findling RL, Shih WJ, et al. Controlled clinical trial of zolpidem for the treatment of insomnia associated with attention-deficit/hyperactivity disorder in children 6 to 17 years of age. Pediatrics. 2009;123(5):e770-e776.
25. Sangal RB, Blumer JL, Lankford DA, et al. Eszopiclone for insomnia associated with attention-deficit/hyperactivity disorder. Pediatrics. 2014;134(4):e1095-e1103.
26. Arens R, Wright B, Elliott J, et al. Periodic limb movement in sleep in children with Williams syndrome. J Pediatr. 1998;133(5):670-674.
27. Thirumalai SS, Shubin RA, Robinson R. Rapid eye movement sleep behavior disorder in children with autism. J Child Neurol. 2002;17(3):173-178.
28. Kawabe K, Horiuchi F, Ochi M, et al. Suvorexant for the treatment of insomnia in adolescents. J Child Adolesc Psychopharmacol. 2017;27(9):792-795.
29. Pranzatelli MR, Tate ED, Dukart WS, et al. Sleep disturbance and rage attacks in opsoclonus-myoclonus syndrome: Response to trazodone. J Pediatr. 2005;147(3):372-378.
30. Oggianu L, Ke AB, Chetty M, et al. Estimation of an appropriate dose of trazodone for pediatric insomnia and the potential for a trazodone-atomoxetine interaction. CPT Pharmacometrics Syst Pharmacol. 2020;9(2):77-86.
31. Shamseddeen W, Clarke G, Keller MB, et al. Adjunctive sleep medications and depression outcome in the treatment of serotonin-selective reuptake inhibitor resistant depression in adolescents study. J Child Adolesc Psychopharmacol. 2012;22(1):29-36.
32. Sultan MA, Courtney DB. Adjunctive trazodone and depression outcome in adolescents treated with serotonin re-uptake inhibitors. J Can Acad Child Adolesc Psychiatry. 2017;26(3):233-240.
33. Posey DJ, Guenin KD, Kohn AE, et al. A naturalistic open-label study of mirtazapine in autistic and other pervasive developmental disorders. J Child Adolesc Psychopharmacol. 2001;11(3):267-277.
34. Shah YD, Stringel V, Pavkovic I, et al. Doxepin in children and adolescents with symptoms of insomnia: a single-center experience. J Clin Sleep Med. 2020;16(5):743-747.
35. Aurora RN, Lamm CI, Zak RS, et al. Practice parameters for the non-respiratory indications for polysomnography and multiple sleep latency testing for children. Sleep. 2012;35(11):1467-1473.
36. de Zambotti M, Goldstone A, Colrain IM, et al. Insomnia disorder in adolescence: diagnosis, impact, and treatment. Sleep Med Rev. 2018;39:12-24.
37. Beck SE, Marcus CL. Pediatric polysomnography. Sleep Med Clin. 2009;4(3):393-406.
Children and adolescents who do not receive sufficient sleep can experience worsening inattention, daytime fatigue, and cognitive and behavioral difficulties. Assessment and treatment of insomnia and other sleep difficulties in young patients is critical as poor sleep increases their risk for depression, self-harm, and suicide.
In Part 1 of this article (Pediatric insomnia: Assessment and diagnosis,
Psychotherapeutic interventions
Regardless of the source of a child’s insomnia or co-occurring disorders, healthy sleep practices are the first line behavioral treatment, including for youth with attention-deficit/hyperactivity disorder (ADHD), anxiety disorders, obsessive-compulsive disorder, and depressive disorders.
Healthy sleep practices/sleep hygiene
Developmentally appropriate bedtimes and routines (Table). Helping children establish a regular, consistent bedtime is key in promoting healthy sleep. Ideally, the bedtime routine involves 3 to 4 activities each night in the same order, and these activities should be relaxing and soothing (eg, taking a bath, putting on pajamas, reading books). Setting age-appropriate bedtimes also is important. If an older child is asked to go to bed at 8 pm but cannot fall asleep for an hour, they may not have insomnia but instead a developmentally inappropriate bedtime. Several studies found that children younger than age 10 should go to bed no later than 9 pm. Bedtimes later than 9 pm for young children are correlated with shorter sleep duration.1
Consistent sleep schedules. Another important aspect of healthy sleep is working with parents to enforce a consistent bedtime and wake-up time, including weekdays and weekends. Ideally, bedtime on weekdays and weekends should not vary by more than 1 hour. Helping children wake up at the same time each day helps to set and regulate their circadian rhythm. Keeping these schedules consistent on vacations and school holidays also is helpful. For adolescents, the weekday/weekend bedtimes can vary by up to 2 hours because adolescents have a delayed circadian rhythm and wake-up times for high school can be early.
Environmental factors. An important piece of parental education is stimulus control and the ingredients of healthy sleep. Healthy sleep ingredients include a dark, quiet, consistent, and cool bedroom; a comfortable bed, the child feeling safe, and limited environmental stimuli.
Continue to: Cognitive-behavioral therapy for insomnia...
Cognitive-behavioral therapy for insomnia
Relaxation. Pediatric patients can be taught relaxation, mindfulness, meditation, and progressive muscle relaxation techniques to help lower overall stress. This can be especially helpful for youth with sleep disorders or anxiety. Guided relaxation apps are popular among children and teens, and various apps offer soothing sounds, deep breathing, progressive muscle relaxation, and guided imagery. This can be taught in psychotherapy sessions and used at home to promote gains in between sessions.
Stimulus control. Stimulus control involves using the bed exclusively for sleep and avoiding nonsleep activities in bed (eg, reading, watching television, using a computer, worrying). These activities promote wakefulness and insomnia. This may mean the child does not get into bed until they cannot keep their eyes open, even if that delays bedtime. If the child is still awake within 15 to 20 minutes, they should be encouraged to get out of bed and engage in a nonstimulating activity such as meditation, reading, or sitting quietly in the dark or low light. This recommendation can run counter to parents’ intuition that children with sleep problems should go to bed earlier. Using the bed only for sleep conditions the child to falling asleep or being asleep when in bed.
Sleep restriction. Sleep restriction involves restricting sleep to a set number of hours in order to increase their sleep efficiency (time slept in bed divided by total time spent in bed x 100). Restricting sleep to 6 to 7 hours increases sleep efficiency, consolidates sleep, and extinguishes the association of being awake in bed. For older adolescents, sleep restriction may help to limit their time in bed to either falling asleep or being asleep. This is intended to be used as a short-term strategy and only after other sleep hygiene measures (bedtime routine, environmental factors, etc) have been put into place for several weeks. While this strategy sounds unappealing to most individuals with insomnia, it can lead to lasting change due to the use of behavioral conditioning in bed. Because sleep restriction can lead to significant daytime sleepiness and impairment during the day, sleep should not be restricted to <6 hours a day for children and adolescents. Once the adolescent is sleeping more consistently and sleep efficiency reaches 85% or higher, time in bed for sleep is increased.2
Cognitive restructuring. Some children and adolescents develop maladaptive thoughts about sleep that further promote insomnia. These thoughts might include “I will never get to sleep,” “I am going to have a terrible day if I cannot fall asleep,” or “I will fail my test tomorrow if I am unable to sleep.” Such maladaptive thoughts are often untrue but promote wakefulness in the early or middle part of the night. Cognitive restructuring involves helping the child identify each problematic thought, challenge how accurate each thought is with evidence, and replace the problematic thought with a more helpful thought. For instance, an adolescent can recognize that even if they have a sleepless night, their catastrophic outcome (eg, “I will not be able to function”) is likely untrue. A psychologist can help review evidence for this, including previous times when the adolescent has not slept well and managed to get through the next day.
When is pharmacologic treatment needed?
Pharmacologic treatment may be indicated if a child does not show significant improvement following behavioral intervention (Figure). However, it is critical to exclude other primary causes of dyssomnia (eg, obstructive sleep apnea, iron deficiency anemia) before pursuing pharmacotherapy, because pharmacotherapy could mask an underlying disorder. Moreover, while there is relatively limited evidence for psychopharmacologic interventions for sleep difficulties in children and adolescents, a large survey of child and adolescent psychiatrists (N = 1,273) suggested that medications were considered for one-quarter of pediatric patients with insomnia.3 Further, patients with specific comorbidities such as neurodevelopmental disorders may be more likely to be prescribed soporifics.4
Continue to: What is the evidence for pharmacotherapy?...
What is the evidence for pharmacotherapy?
Antihistamines. Histamine antagonists—which promote sleep by blocking the wakefulness-promoting and circadian-related effects of histamine—are the most commonly used medications to treat pediatric insomnia, despite a dearth of data from prospective trials.5,6 In 1 small study, Russo et al7 found diphenhydramine, 1 mg/kg at bedtime, reduced sleep latency and nighttime awakenings, and increased sleep duration in patients ages 2 to 12; similar effects have been observed in pediatric burn patients.8 There are some limited data for other H1 antagonists (eg, hydroxyzine) in pediatric insomnia.9-11
Alpha-2 agonists increase rapid eye movement sleep via dose-dependent downregulation of noradrenergic signaling12 and thus have been commonly prescribed for insomnia in children and adolescents. In fact, the nonselective alpha-2 agonist clonidine is among the most prescribed medications for youth with insomnia, and may be efficacious in youth with neurodevelopmental disorders and ADHD.13 In small retrospective studies, clonidine decreased sleep latency and nighttime awakenings in addition to increasing sleep duration.14 Also, clonidine was well tolerated but associated with daytime somnolence. Guanfacine—a selective alpha-2 agonist—is also commonly prescribed for insomnia in youth, although results of trials have been equivocal.15 Given the more rapid absorption and shorter Tmax of clonidine relative to guanfacine, the former may be preferred as a soporific.
Melatonin and melatonin agonists. The primary regulator of the sleep-wake cycle is melatonin, an endogenous hormone produced by the pineal gland in response to changes in retinal light perception. Exogenous melatonin supplementation may be the preferred initial pharmacotherapy for sleep-onset insomnia due to its chronobiotic properties.16 In clinical studies, both immediate-release17,18 and extended-release19 melatonin reduced sleep-onset latency and increased total sleep duration in pediatric patients, although the increase in total duration of sleep was greater with extended-release preparations. Additionally, tolerability data for melatonin in pediatric patients are encouraging. A 2-year randomized trial of prolonged-release melatonin for insomnia in pediatric patients found no adverse effects with regard to growth, body mass index, or pubertal development.20 Additionally, significant improvements in sleep quality, sleep patterns, and caregiver satisfaction were maintained throughout the trial, and no withdrawal symptoms were observed upon discontinuation.
Melatonin may have a particularly important role in circadian rhythm sleep disorders. In this regard, low-dose melatonin (0.5 mg), when timed relative to the endogenous dim light melatonin onset (DLMO), is more effective in shifting sleep phase than higher doses, which suggests that timing may have greater impact than dosage.21 Data regarding melatonin administration with respect to DLMO suggest that the optimal administration time is 4 to 6 hours before a child’s preferred bedtime, and doses of 0.5 to 1 mg have been effective when given in this window.22 Variation across studies has contributed to a lack of consensus regarding pediatric melatonin dosing. For example, .05 mg/kg may be a minimal effective dose when given 1 to 2 hours before bedtime18; however, in surveys doses vary considerably, with typical doses of 2.5 to 3 mg for prepubertal children and 5 mg for adolescents.5 Of note, in patients with decreased cytochrome P450 (CYP) 1A2 activity, lack of diurnal variation in melatonin serum concentration may decrease the effectiveness of melatonin.16Ramelteon is a potent agonist of the melatonin MT1 and MT2 receptors, with a significantly higher binding affinity than melatonin in vitro. In case reports, ramelteon was well-tolerated, improved delayed sleep onset, and decreased nighttime awakenings.23
Zolpidem, eszopiclone and zaleplon. Studies of selective GABAergic modulators and benzodiazepines have not produced positive results in prospective trials of youth with insomnia. Zolpidem was studied in children and adolescents (N = 201) with ADHD; although sleep latency did not differ between zolpidem and placebo, some significant improvements were observed in adolescents.24 Zolpidem was generally well tolerated, with approximately 10% of youth discontinuing due to adverse effects. Additionally, eszopiclone—which has a longer duration of action compared with zolpidem—has been studied in children and adolescents with ADHD (N = 486) who were also evaluated with a sleep study. No differences were observed between placebo and eszopiclone in terms of sleep latency and approximately 10% of patients discontinued treatment as a result of adverse events.25 We were unable to locate any prospective trials of zaleplon or benzodiazepine receptor agonists for insomnia in youth, although some reports suggest that clonazepam may have a possible role for specific parasomnias.26,27Dual orexin receptor antagonists. Suvorexant, an antagonist of the wakefulness-promoting neuropeptide orexin, improved subjective sleep quality in a prospective trial of adolescents with insomnia (N = 30), although dropout was high (44%).28 Of those patients, reasons for discontinuation included loss to follow-up, lack of effectiveness, and abnormal dreams. We were unable to locate any trials of lemborexant in pediatric patients.
Atypical antidepressants. Trazodone is commonly prescribed for insomnia in pediatric patients with comorbid mood or anxiety disorders. In open-label studies of children and toddlers, trazodone may be well-tolerated and improve sleep.29 Additionally, development of a physiologically based pharmacokinetic model to inform trazodone dosing for youth with insomnia is underway.30 Some studies in adolescents with depression suggest that caution should be used when combining trazodone with medications that inhibit CYP2D6. In the Treatment of SSRI-Resistant Depression in Adolescents study, none of the patients who were treated with trazodone (vs other soporifics) improved.31 This may relate to CYP2D6 interactions and accumulation of methyl-chloro-piperazine (mCPP), a trazodone metabolite that is associated with dysphoria, irritability, and depression.31 This finding has been replicated in a separate cohort of depressed adolescents.32
Because of its antihistaminergic effects, mirtazapine has been used to treat insomnia in adults. One open-label study of mirtazapine in children and young adults ages 3 to 23 with neurodevelopmental disorders suggested that mirtazapine improved behavioral symptoms and insomnia, and was associated with few treatment-limiting adverse effects.33
Tricyclic antidepressants. In a retrospective study of youth with insomnia who failed behavioral interventions and melatonin (N = 29), doxepin, a potent H1 antagonist, improved subjective sleep in one-half of patients.34
Continue to: Consultation with pediatric sleep medicine specialists...
Consultation with pediatric sleep medicine specialists
It often will behoove the psychiatric clinician to review their concerns with a behavioral sleep medicine specialist or a psychologist with specific expertise in the psychotherapeutic treatment of sleep who can provide important guidance regarding the key aspects of treatment. When discussing a particular patient’s presentation with the pediatric behavioral sleep psychologist/specialist, consider the following questions:
- Is the child’s sleep disorder the primary problem, or is the child’s insomnia secondary to another diagnosis (psychiatric or nonpsychiatric)?
- What are the primary sleep-related problems the child/family presents with? How long have the symptoms been present?
- Is the sleep disorder interfering with the child’s functioning, either academically or socially? Does the child’s sleep problem interfere with other family members’ sleep?
- Does the child have a comorbid psychological conditions such as ADHD, depression, or anxiety, and/or is undergoing treatment for these disorders, which may play a role in the sleep problem?
- Is a sleep study warranted?
A sleep study, also known as polysomnography (PSG), is a diagnostic test in which physiologic parameters are continuously recorded during a period of sleep via electroencephalography, electromyography, electrooculogram, electrocardiogram, airflow sensors, pulse oximeter, body position monitors, and video. In 2012, the American Academy of Sleep Medicine published evidenced-based practice parameters for respiratory and nonrespiratory indications for PSG.35 It is most commonly indicated to rule out obstructive sleep apnea in pediatric patients who exhibit snoring, gasping, irregular breathing, witnessed apneic events, unusual head positioning, or other signs of obstructive breathing during sleep. Nonrespiratory indications for PSG include children suspected of having periodic limb movement disorder and suspected narcolepsy. Children with frequent parasomnias, epilepsy, or nocturnal enuresis should be clinically screened for presence of comorbid sleep disorders, and PSG would be indicated if there are concerns about a possible sleep-disordered breathing disorder. PSG is also recommended for children with hypersomnia, to differentiate a parasomnia from sleep-related epilepsy, and for children suspected of having restless leg syndrome.36 PSG is not typically indicated in the initial evaluation of insomnia (unless there is evidence of a comorbid sleep disorder), circadian rhythm disorders (ie, delayed sleep phase syndrome), or for evaluation of children with sleep-related bruxism.3 Special considerations for PSG in children include ensuring a parent or guardian is always with the child, providing developmentally appropriate sleeping arrangements, arranging family tours of the sleep lab prior to the study, and accommodating for earlier bedtimes.37
Bottom Line
Techniques to promote healthy sleep in pediatric patients include behavioral interventions such as setting a developmentally appropriate bedtime and a consistent wake time, establishing bedtime routines, and encouraging relaxation/ wind-down period before bed. Cognitive-behavioral therapy for insomnia (CBT-I) may include cognitive restructuring of anxious thoughts, relaxation training, stimulus control, and sleep restriction. Use of medications may be indicated for children and teens who have not responded to CBT-I or soporific dosing of melatonin.
Children and adolescents who do not receive sufficient sleep can experience worsening inattention, daytime fatigue, and cognitive and behavioral difficulties. Assessment and treatment of insomnia and other sleep difficulties in young patients is critical as poor sleep increases their risk for depression, self-harm, and suicide.
In Part 1 of this article (Pediatric insomnia: Assessment and diagnosis,
Psychotherapeutic interventions
Regardless of the source of a child’s insomnia or co-occurring disorders, healthy sleep practices are the first line behavioral treatment, including for youth with attention-deficit/hyperactivity disorder (ADHD), anxiety disorders, obsessive-compulsive disorder, and depressive disorders.
Healthy sleep practices/sleep hygiene
Developmentally appropriate bedtimes and routines (Table). Helping children establish a regular, consistent bedtime is key in promoting healthy sleep. Ideally, the bedtime routine involves 3 to 4 activities each night in the same order, and these activities should be relaxing and soothing (eg, taking a bath, putting on pajamas, reading books). Setting age-appropriate bedtimes also is important. If an older child is asked to go to bed at 8 pm but cannot fall asleep for an hour, they may not have insomnia but instead a developmentally inappropriate bedtime. Several studies found that children younger than age 10 should go to bed no later than 9 pm. Bedtimes later than 9 pm for young children are correlated with shorter sleep duration.1
Consistent sleep schedules. Another important aspect of healthy sleep is working with parents to enforce a consistent bedtime and wake-up time, including weekdays and weekends. Ideally, bedtime on weekdays and weekends should not vary by more than 1 hour. Helping children wake up at the same time each day helps to set and regulate their circadian rhythm. Keeping these schedules consistent on vacations and school holidays also is helpful. For adolescents, the weekday/weekend bedtimes can vary by up to 2 hours because adolescents have a delayed circadian rhythm and wake-up times for high school can be early.
Environmental factors. An important piece of parental education is stimulus control and the ingredients of healthy sleep. Healthy sleep ingredients include a dark, quiet, consistent, and cool bedroom; a comfortable bed, the child feeling safe, and limited environmental stimuli.
Continue to: Cognitive-behavioral therapy for insomnia...
Cognitive-behavioral therapy for insomnia
Relaxation. Pediatric patients can be taught relaxation, mindfulness, meditation, and progressive muscle relaxation techniques to help lower overall stress. This can be especially helpful for youth with sleep disorders or anxiety. Guided relaxation apps are popular among children and teens, and various apps offer soothing sounds, deep breathing, progressive muscle relaxation, and guided imagery. This can be taught in psychotherapy sessions and used at home to promote gains in between sessions.
Stimulus control. Stimulus control involves using the bed exclusively for sleep and avoiding nonsleep activities in bed (eg, reading, watching television, using a computer, worrying). These activities promote wakefulness and insomnia. This may mean the child does not get into bed until they cannot keep their eyes open, even if that delays bedtime. If the child is still awake within 15 to 20 minutes, they should be encouraged to get out of bed and engage in a nonstimulating activity such as meditation, reading, or sitting quietly in the dark or low light. This recommendation can run counter to parents’ intuition that children with sleep problems should go to bed earlier. Using the bed only for sleep conditions the child to falling asleep or being asleep when in bed.
Sleep restriction. Sleep restriction involves restricting sleep to a set number of hours in order to increase their sleep efficiency (time slept in bed divided by total time spent in bed x 100). Restricting sleep to 6 to 7 hours increases sleep efficiency, consolidates sleep, and extinguishes the association of being awake in bed. For older adolescents, sleep restriction may help to limit their time in bed to either falling asleep or being asleep. This is intended to be used as a short-term strategy and only after other sleep hygiene measures (bedtime routine, environmental factors, etc) have been put into place for several weeks. While this strategy sounds unappealing to most individuals with insomnia, it can lead to lasting change due to the use of behavioral conditioning in bed. Because sleep restriction can lead to significant daytime sleepiness and impairment during the day, sleep should not be restricted to <6 hours a day for children and adolescents. Once the adolescent is sleeping more consistently and sleep efficiency reaches 85% or higher, time in bed for sleep is increased.2
Cognitive restructuring. Some children and adolescents develop maladaptive thoughts about sleep that further promote insomnia. These thoughts might include “I will never get to sleep,” “I am going to have a terrible day if I cannot fall asleep,” or “I will fail my test tomorrow if I am unable to sleep.” Such maladaptive thoughts are often untrue but promote wakefulness in the early or middle part of the night. Cognitive restructuring involves helping the child identify each problematic thought, challenge how accurate each thought is with evidence, and replace the problematic thought with a more helpful thought. For instance, an adolescent can recognize that even if they have a sleepless night, their catastrophic outcome (eg, “I will not be able to function”) is likely untrue. A psychologist can help review evidence for this, including previous times when the adolescent has not slept well and managed to get through the next day.
When is pharmacologic treatment needed?
Pharmacologic treatment may be indicated if a child does not show significant improvement following behavioral intervention (Figure). However, it is critical to exclude other primary causes of dyssomnia (eg, obstructive sleep apnea, iron deficiency anemia) before pursuing pharmacotherapy, because pharmacotherapy could mask an underlying disorder. Moreover, while there is relatively limited evidence for psychopharmacologic interventions for sleep difficulties in children and adolescents, a large survey of child and adolescent psychiatrists (N = 1,273) suggested that medications were considered for one-quarter of pediatric patients with insomnia.3 Further, patients with specific comorbidities such as neurodevelopmental disorders may be more likely to be prescribed soporifics.4
Continue to: What is the evidence for pharmacotherapy?...
What is the evidence for pharmacotherapy?
Antihistamines. Histamine antagonists—which promote sleep by blocking the wakefulness-promoting and circadian-related effects of histamine—are the most commonly used medications to treat pediatric insomnia, despite a dearth of data from prospective trials.5,6 In 1 small study, Russo et al7 found diphenhydramine, 1 mg/kg at bedtime, reduced sleep latency and nighttime awakenings, and increased sleep duration in patients ages 2 to 12; similar effects have been observed in pediatric burn patients.8 There are some limited data for other H1 antagonists (eg, hydroxyzine) in pediatric insomnia.9-11
Alpha-2 agonists increase rapid eye movement sleep via dose-dependent downregulation of noradrenergic signaling12 and thus have been commonly prescribed for insomnia in children and adolescents. In fact, the nonselective alpha-2 agonist clonidine is among the most prescribed medications for youth with insomnia, and may be efficacious in youth with neurodevelopmental disorders and ADHD.13 In small retrospective studies, clonidine decreased sleep latency and nighttime awakenings in addition to increasing sleep duration.14 Also, clonidine was well tolerated but associated with daytime somnolence. Guanfacine—a selective alpha-2 agonist—is also commonly prescribed for insomnia in youth, although results of trials have been equivocal.15 Given the more rapid absorption and shorter Tmax of clonidine relative to guanfacine, the former may be preferred as a soporific.
Melatonin and melatonin agonists. The primary regulator of the sleep-wake cycle is melatonin, an endogenous hormone produced by the pineal gland in response to changes in retinal light perception. Exogenous melatonin supplementation may be the preferred initial pharmacotherapy for sleep-onset insomnia due to its chronobiotic properties.16 In clinical studies, both immediate-release17,18 and extended-release19 melatonin reduced sleep-onset latency and increased total sleep duration in pediatric patients, although the increase in total duration of sleep was greater with extended-release preparations. Additionally, tolerability data for melatonin in pediatric patients are encouraging. A 2-year randomized trial of prolonged-release melatonin for insomnia in pediatric patients found no adverse effects with regard to growth, body mass index, or pubertal development.20 Additionally, significant improvements in sleep quality, sleep patterns, and caregiver satisfaction were maintained throughout the trial, and no withdrawal symptoms were observed upon discontinuation.
Melatonin may have a particularly important role in circadian rhythm sleep disorders. In this regard, low-dose melatonin (0.5 mg), when timed relative to the endogenous dim light melatonin onset (DLMO), is more effective in shifting sleep phase than higher doses, which suggests that timing may have greater impact than dosage.21 Data regarding melatonin administration with respect to DLMO suggest that the optimal administration time is 4 to 6 hours before a child’s preferred bedtime, and doses of 0.5 to 1 mg have been effective when given in this window.22 Variation across studies has contributed to a lack of consensus regarding pediatric melatonin dosing. For example, .05 mg/kg may be a minimal effective dose when given 1 to 2 hours before bedtime18; however, in surveys doses vary considerably, with typical doses of 2.5 to 3 mg for prepubertal children and 5 mg for adolescents.5 Of note, in patients with decreased cytochrome P450 (CYP) 1A2 activity, lack of diurnal variation in melatonin serum concentration may decrease the effectiveness of melatonin.16Ramelteon is a potent agonist of the melatonin MT1 and MT2 receptors, with a significantly higher binding affinity than melatonin in vitro. In case reports, ramelteon was well-tolerated, improved delayed sleep onset, and decreased nighttime awakenings.23
Zolpidem, eszopiclone and zaleplon. Studies of selective GABAergic modulators and benzodiazepines have not produced positive results in prospective trials of youth with insomnia. Zolpidem was studied in children and adolescents (N = 201) with ADHD; although sleep latency did not differ between zolpidem and placebo, some significant improvements were observed in adolescents.24 Zolpidem was generally well tolerated, with approximately 10% of youth discontinuing due to adverse effects. Additionally, eszopiclone—which has a longer duration of action compared with zolpidem—has been studied in children and adolescents with ADHD (N = 486) who were also evaluated with a sleep study. No differences were observed between placebo and eszopiclone in terms of sleep latency and approximately 10% of patients discontinued treatment as a result of adverse events.25 We were unable to locate any prospective trials of zaleplon or benzodiazepine receptor agonists for insomnia in youth, although some reports suggest that clonazepam may have a possible role for specific parasomnias.26,27Dual orexin receptor antagonists. Suvorexant, an antagonist of the wakefulness-promoting neuropeptide orexin, improved subjective sleep quality in a prospective trial of adolescents with insomnia (N = 30), although dropout was high (44%).28 Of those patients, reasons for discontinuation included loss to follow-up, lack of effectiveness, and abnormal dreams. We were unable to locate any trials of lemborexant in pediatric patients.
Atypical antidepressants. Trazodone is commonly prescribed for insomnia in pediatric patients with comorbid mood or anxiety disorders. In open-label studies of children and toddlers, trazodone may be well-tolerated and improve sleep.29 Additionally, development of a physiologically based pharmacokinetic model to inform trazodone dosing for youth with insomnia is underway.30 Some studies in adolescents with depression suggest that caution should be used when combining trazodone with medications that inhibit CYP2D6. In the Treatment of SSRI-Resistant Depression in Adolescents study, none of the patients who were treated with trazodone (vs other soporifics) improved.31 This may relate to CYP2D6 interactions and accumulation of methyl-chloro-piperazine (mCPP), a trazodone metabolite that is associated with dysphoria, irritability, and depression.31 This finding has been replicated in a separate cohort of depressed adolescents.32
Because of its antihistaminergic effects, mirtazapine has been used to treat insomnia in adults. One open-label study of mirtazapine in children and young adults ages 3 to 23 with neurodevelopmental disorders suggested that mirtazapine improved behavioral symptoms and insomnia, and was associated with few treatment-limiting adverse effects.33
Tricyclic antidepressants. In a retrospective study of youth with insomnia who failed behavioral interventions and melatonin (N = 29), doxepin, a potent H1 antagonist, improved subjective sleep in one-half of patients.34
Continue to: Consultation with pediatric sleep medicine specialists...
Consultation with pediatric sleep medicine specialists
It often will behoove the psychiatric clinician to review their concerns with a behavioral sleep medicine specialist or a psychologist with specific expertise in the psychotherapeutic treatment of sleep who can provide important guidance regarding the key aspects of treatment. When discussing a particular patient’s presentation with the pediatric behavioral sleep psychologist/specialist, consider the following questions:
- Is the child’s sleep disorder the primary problem, or is the child’s insomnia secondary to another diagnosis (psychiatric or nonpsychiatric)?
- What are the primary sleep-related problems the child/family presents with? How long have the symptoms been present?
- Is the sleep disorder interfering with the child’s functioning, either academically or socially? Does the child’s sleep problem interfere with other family members’ sleep?
- Does the child have a comorbid psychological conditions such as ADHD, depression, or anxiety, and/or is undergoing treatment for these disorders, which may play a role in the sleep problem?
- Is a sleep study warranted?
A sleep study, also known as polysomnography (PSG), is a diagnostic test in which physiologic parameters are continuously recorded during a period of sleep via electroencephalography, electromyography, electrooculogram, electrocardiogram, airflow sensors, pulse oximeter, body position monitors, and video. In 2012, the American Academy of Sleep Medicine published evidenced-based practice parameters for respiratory and nonrespiratory indications for PSG.35 It is most commonly indicated to rule out obstructive sleep apnea in pediatric patients who exhibit snoring, gasping, irregular breathing, witnessed apneic events, unusual head positioning, or other signs of obstructive breathing during sleep. Nonrespiratory indications for PSG include children suspected of having periodic limb movement disorder and suspected narcolepsy. Children with frequent parasomnias, epilepsy, or nocturnal enuresis should be clinically screened for presence of comorbid sleep disorders, and PSG would be indicated if there are concerns about a possible sleep-disordered breathing disorder. PSG is also recommended for children with hypersomnia, to differentiate a parasomnia from sleep-related epilepsy, and for children suspected of having restless leg syndrome.36 PSG is not typically indicated in the initial evaluation of insomnia (unless there is evidence of a comorbid sleep disorder), circadian rhythm disorders (ie, delayed sleep phase syndrome), or for evaluation of children with sleep-related bruxism.3 Special considerations for PSG in children include ensuring a parent or guardian is always with the child, providing developmentally appropriate sleeping arrangements, arranging family tours of the sleep lab prior to the study, and accommodating for earlier bedtimes.37
Bottom Line
Techniques to promote healthy sleep in pediatric patients include behavioral interventions such as setting a developmentally appropriate bedtime and a consistent wake time, establishing bedtime routines, and encouraging relaxation/ wind-down period before bed. Cognitive-behavioral therapy for insomnia (CBT-I) may include cognitive restructuring of anxious thoughts, relaxation training, stimulus control, and sleep restriction. Use of medications may be indicated for children and teens who have not responded to CBT-I or soporific dosing of melatonin.
1. Mindell JA, Li AM, Sadeh A, et al. Bedtime routines for young children: a dose-dependent association with sleep outcomes. Sleep. 2015;38(5):717-722.
2. Kansagra S. Sleep disorders in adolescents. Pediatrics. 2020;145(Suppl 2):S204-S209.
3. Owens JA, Mindell JA. Pediatric insomnia. Pediatr Clin North Am. 2011;58(3):555-569.
4. Bruni O, Angriman M, Melegari MG, et al. Pharmacotherapeutic management of sleep disorders in children with neurodevelopmental disorders. Expert Opin Pharmacother. 2019;20(18):2257-2271.
5. Owens JA, Rosen CL, Mindell JA, et al. Use of pharmacotherapy for insomnia in child psychiatry practice: a national survey. Sleep Med. 2010;11(7):692-700.
6. Schnoes CJ, Kuhn BR, Workman EF, et al. Pediatric prescribing practices for clonidine and other pharmacologic agents for children with sleep disturbance. Clin Pediatr (Phila). 2006;45(3):229-238.
7. Russo RM, Gururaj VJ, Allen JE. The effectiveness of diphenhydramine HCI in pediatric sleep disorders. J Clin Pharmacol. 1976;16(5-6):284-288.
8. Yangzom N, Gottschlich MM, Ossege J, et al. The effect of diphenhydramine on sleep in pediatric burn patients: a secondary analysis. J Burn Care Res. 2015;36(2):266-271.
9. Ghanizadeh A, Zare S. A preliminary randomised double-blind placebo-controlled clinical trial of hydroxyzine for treating sleep bruxism in children. J Oral Rehabil. 2013;40(6):413-417.
10. Bektas O, Arıca B, Teber S, et al. Chloral hydrate and/or hydroxyzine for sedation in pediatric EEG recording. Brain Dev. 2014;36(2):130-136.
11. Ottaviano S, Giannotti F, Cortesi F. The effect of niaprazine on some common sleep disorders in children. A double-blind clinical trial by means of continuous home-videorecorded sleep. Childs Nerv Syst. 1991;7(6):332-335.
12. Nguyen M, Tharani S, Rahmani M, et al. A review of the use of clonidine as a sleep aid in the child and adolescent population. Clin Pediatr (Phila). 2014;53(3):211-216.
13. Prince JB, Wilens TE, Biederman J, et al. Clonidine for sleep disturbances associated with attention-deficit hyperactivity disorder: a systematic chart review of 62 cases. J Am Acad Child Adolesc Psychiatry. 1996;35(5):599-605.

14. Ingrassia A, Turk J. The use of clonidine for severe and intractable sleep problems in children with neurodevelopmental disorders--a case series. Eur Child Adolesc Psychiatry. 2005;14(1):34-40.
15. Politte LC, Scahill L, Figueroa J, et al. A randomized, placebo-controlled trial of extended-release guanfacine in children with autism spectrum disorder and ADHD symptoms: an analysis of secondary outcome measures. Neuropsychopharmacology. 2018;43(8):1772-1778.
16. Bruni O, Alonso-Alconada D, Besag F, et al. Current role of melatonin in pediatric neurology: clinical recommendations. Eur J Paediatr Neurol. 2015;19(2):122-1233.
17. Jain SV, Horn PS, Simakajornboon N, et al. Melatonin improves sleep in children with epilepsy: a randomized, double-blind, crossover study. Sleep Med. 2015;16(5):637-644.
18. van Geijlswijk IM, van der Heijden KB, Egberts AC, et al. Dose finding of melatonin for chronic idiopathic childhood sleep onset insomnia: an RCT. Psychopharmacology (Berl). 2010;212(3):379-391.
19. Gringras P, Nir T, Breddy J, et al. Efficacy and safety of pediatric prolonged-release melatonin for insomnia in children with autism spectrum disorder. J Am Acad Child Adolesc Psychiatry. 2017;56(11):948-957.e4.
20. Malow BA, Findling RL, Schroder CM, et al. Sleep, growth, and puberty after two years of prolonged-release melatonin in children with autism spectrum disorder. J Am Acad Child Adolesc Psychiatry. 2021;60(2):252-261.e3.
21. Burgess HJ, Emens JS. Drugs used in circadian sleep-wake rhythm disturbances. Sleep Med Clin. 2020;15(2):301-310.
22. Arns M, Kooij JJS, Coogan AN. Review: identification and management of circadian rhythm sleep disorders as a transdiagnostic feature in child and adolescent psychiatry. J Am Acad Child Adolesc Psychiatry. 2021;60(9):1085-1095.
23. Kawabe K, Horiuchi F, Oka Y, et al. The melatonin receptor agonist ramelteon effectively treats insomnia and behavioral symptoms in autistic disorder. Case Rep Psychiatry. 2014;2014:561071.
24. Blumer JL, Findling RL, Shih WJ, et al. Controlled clinical trial of zolpidem for the treatment of insomnia associated with attention-deficit/hyperactivity disorder in children 6 to 17 years of age. Pediatrics. 2009;123(5):e770-e776.
25. Sangal RB, Blumer JL, Lankford DA, et al. Eszopiclone for insomnia associated with attention-deficit/hyperactivity disorder. Pediatrics. 2014;134(4):e1095-e1103.
26. Arens R, Wright B, Elliott J, et al. Periodic limb movement in sleep in children with Williams syndrome. J Pediatr. 1998;133(5):670-674.
27. Thirumalai SS, Shubin RA, Robinson R. Rapid eye movement sleep behavior disorder in children with autism. J Child Neurol. 2002;17(3):173-178.
28. Kawabe K, Horiuchi F, Ochi M, et al. Suvorexant for the treatment of insomnia in adolescents. J Child Adolesc Psychopharmacol. 2017;27(9):792-795.
29. Pranzatelli MR, Tate ED, Dukart WS, et al. Sleep disturbance and rage attacks in opsoclonus-myoclonus syndrome: Response to trazodone. J Pediatr. 2005;147(3):372-378.
30. Oggianu L, Ke AB, Chetty M, et al. Estimation of an appropriate dose of trazodone for pediatric insomnia and the potential for a trazodone-atomoxetine interaction. CPT Pharmacometrics Syst Pharmacol. 2020;9(2):77-86.
31. Shamseddeen W, Clarke G, Keller MB, et al. Adjunctive sleep medications and depression outcome in the treatment of serotonin-selective reuptake inhibitor resistant depression in adolescents study. J Child Adolesc Psychopharmacol. 2012;22(1):29-36.
32. Sultan MA, Courtney DB. Adjunctive trazodone and depression outcome in adolescents treated with serotonin re-uptake inhibitors. J Can Acad Child Adolesc Psychiatry. 2017;26(3):233-240.
33. Posey DJ, Guenin KD, Kohn AE, et al. A naturalistic open-label study of mirtazapine in autistic and other pervasive developmental disorders. J Child Adolesc Psychopharmacol. 2001;11(3):267-277.
34. Shah YD, Stringel V, Pavkovic I, et al. Doxepin in children and adolescents with symptoms of insomnia: a single-center experience. J Clin Sleep Med. 2020;16(5):743-747.
35. Aurora RN, Lamm CI, Zak RS, et al. Practice parameters for the non-respiratory indications for polysomnography and multiple sleep latency testing for children. Sleep. 2012;35(11):1467-1473.
36. de Zambotti M, Goldstone A, Colrain IM, et al. Insomnia disorder in adolescence: diagnosis, impact, and treatment. Sleep Med Rev. 2018;39:12-24.
37. Beck SE, Marcus CL. Pediatric polysomnography. Sleep Med Clin. 2009;4(3):393-406.
1. Mindell JA, Li AM, Sadeh A, et al. Bedtime routines for young children: a dose-dependent association with sleep outcomes. Sleep. 2015;38(5):717-722.
2. Kansagra S. Sleep disorders in adolescents. Pediatrics. 2020;145(Suppl 2):S204-S209.
3. Owens JA, Mindell JA. Pediatric insomnia. Pediatr Clin North Am. 2011;58(3):555-569.
4. Bruni O, Angriman M, Melegari MG, et al. Pharmacotherapeutic management of sleep disorders in children with neurodevelopmental disorders. Expert Opin Pharmacother. 2019;20(18):2257-2271.
5. Owens JA, Rosen CL, Mindell JA, et al. Use of pharmacotherapy for insomnia in child psychiatry practice: a national survey. Sleep Med. 2010;11(7):692-700.
6. Schnoes CJ, Kuhn BR, Workman EF, et al. Pediatric prescribing practices for clonidine and other pharmacologic agents for children with sleep disturbance. Clin Pediatr (Phila). 2006;45(3):229-238.
7. Russo RM, Gururaj VJ, Allen JE. The effectiveness of diphenhydramine HCI in pediatric sleep disorders. J Clin Pharmacol. 1976;16(5-6):284-288.
8. Yangzom N, Gottschlich MM, Ossege J, et al. The effect of diphenhydramine on sleep in pediatric burn patients: a secondary analysis. J Burn Care Res. 2015;36(2):266-271.
9. Ghanizadeh A, Zare S. A preliminary randomised double-blind placebo-controlled clinical trial of hydroxyzine for treating sleep bruxism in children. J Oral Rehabil. 2013;40(6):413-417.
10. Bektas O, Arıca B, Teber S, et al. Chloral hydrate and/or hydroxyzine for sedation in pediatric EEG recording. Brain Dev. 2014;36(2):130-136.
11. Ottaviano S, Giannotti F, Cortesi F. The effect of niaprazine on some common sleep disorders in children. A double-blind clinical trial by means of continuous home-videorecorded sleep. Childs Nerv Syst. 1991;7(6):332-335.
12. Nguyen M, Tharani S, Rahmani M, et al. A review of the use of clonidine as a sleep aid in the child and adolescent population. Clin Pediatr (Phila). 2014;53(3):211-216.
13. Prince JB, Wilens TE, Biederman J, et al. Clonidine for sleep disturbances associated with attention-deficit hyperactivity disorder: a systematic chart review of 62 cases. J Am Acad Child Adolesc Psychiatry. 1996;35(5):599-605.

14. Ingrassia A, Turk J. The use of clonidine for severe and intractable sleep problems in children with neurodevelopmental disorders--a case series. Eur Child Adolesc Psychiatry. 2005;14(1):34-40.
15. Politte LC, Scahill L, Figueroa J, et al. A randomized, placebo-controlled trial of extended-release guanfacine in children with autism spectrum disorder and ADHD symptoms: an analysis of secondary outcome measures. Neuropsychopharmacology. 2018;43(8):1772-1778.
16. Bruni O, Alonso-Alconada D, Besag F, et al. Current role of melatonin in pediatric neurology: clinical recommendations. Eur J Paediatr Neurol. 2015;19(2):122-1233.
17. Jain SV, Horn PS, Simakajornboon N, et al. Melatonin improves sleep in children with epilepsy: a randomized, double-blind, crossover study. Sleep Med. 2015;16(5):637-644.
18. van Geijlswijk IM, van der Heijden KB, Egberts AC, et al. Dose finding of melatonin for chronic idiopathic childhood sleep onset insomnia: an RCT. Psychopharmacology (Berl). 2010;212(3):379-391.
19. Gringras P, Nir T, Breddy J, et al. Efficacy and safety of pediatric prolonged-release melatonin for insomnia in children with autism spectrum disorder. J Am Acad Child Adolesc Psychiatry. 2017;56(11):948-957.e4.
20. Malow BA, Findling RL, Schroder CM, et al. Sleep, growth, and puberty after two years of prolonged-release melatonin in children with autism spectrum disorder. J Am Acad Child Adolesc Psychiatry. 2021;60(2):252-261.e3.
21. Burgess HJ, Emens JS. Drugs used in circadian sleep-wake rhythm disturbances. Sleep Med Clin. 2020;15(2):301-310.
22. Arns M, Kooij JJS, Coogan AN. Review: identification and management of circadian rhythm sleep disorders as a transdiagnostic feature in child and adolescent psychiatry. J Am Acad Child Adolesc Psychiatry. 2021;60(9):1085-1095.
23. Kawabe K, Horiuchi F, Oka Y, et al. The melatonin receptor agonist ramelteon effectively treats insomnia and behavioral symptoms in autistic disorder. Case Rep Psychiatry. 2014;2014:561071.
24. Blumer JL, Findling RL, Shih WJ, et al. Controlled clinical trial of zolpidem for the treatment of insomnia associated with attention-deficit/hyperactivity disorder in children 6 to 17 years of age. Pediatrics. 2009;123(5):e770-e776.
25. Sangal RB, Blumer JL, Lankford DA, et al. Eszopiclone for insomnia associated with attention-deficit/hyperactivity disorder. Pediatrics. 2014;134(4):e1095-e1103.
26. Arens R, Wright B, Elliott J, et al. Periodic limb movement in sleep in children with Williams syndrome. J Pediatr. 1998;133(5):670-674.
27. Thirumalai SS, Shubin RA, Robinson R. Rapid eye movement sleep behavior disorder in children with autism. J Child Neurol. 2002;17(3):173-178.
28. Kawabe K, Horiuchi F, Ochi M, et al. Suvorexant for the treatment of insomnia in adolescents. J Child Adolesc Psychopharmacol. 2017;27(9):792-795.
29. Pranzatelli MR, Tate ED, Dukart WS, et al. Sleep disturbance and rage attacks in opsoclonus-myoclonus syndrome: Response to trazodone. J Pediatr. 2005;147(3):372-378.
30. Oggianu L, Ke AB, Chetty M, et al. Estimation of an appropriate dose of trazodone for pediatric insomnia and the potential for a trazodone-atomoxetine interaction. CPT Pharmacometrics Syst Pharmacol. 2020;9(2):77-86.
31. Shamseddeen W, Clarke G, Keller MB, et al. Adjunctive sleep medications and depression outcome in the treatment of serotonin-selective reuptake inhibitor resistant depression in adolescents study. J Child Adolesc Psychopharmacol. 2012;22(1):29-36.
32. Sultan MA, Courtney DB. Adjunctive trazodone and depression outcome in adolescents treated with serotonin re-uptake inhibitors. J Can Acad Child Adolesc Psychiatry. 2017;26(3):233-240.
33. Posey DJ, Guenin KD, Kohn AE, et al. A naturalistic open-label study of mirtazapine in autistic and other pervasive developmental disorders. J Child Adolesc Psychopharmacol. 2001;11(3):267-277.
34. Shah YD, Stringel V, Pavkovic I, et al. Doxepin in children and adolescents with symptoms of insomnia: a single-center experience. J Clin Sleep Med. 2020;16(5):743-747.
35. Aurora RN, Lamm CI, Zak RS, et al. Practice parameters for the non-respiratory indications for polysomnography and multiple sleep latency testing for children. Sleep. 2012;35(11):1467-1473.
36. de Zambotti M, Goldstone A, Colrain IM, et al. Insomnia disorder in adolescence: diagnosis, impact, and treatment. Sleep Med Rev. 2018;39:12-24.
37. Beck SE, Marcus CL. Pediatric polysomnography. Sleep Med Clin. 2009;4(3):393-406.
Omega-3 supplementation improves sleep, mood in breast cancer patients on hormone therapy
After 4 weeks of treatment, patients who received omega-3 reported better sleep, depression, and mood outcomes than those who received placebo.
Estrogen-receptor inhibitors are used to treat breast cancer with positive hormone receptors in combination with other therapies. However, the drugs can lead to long-term side effects, including hot flashes, night sweats, and changes to mood and sleep.
These side effects are often treated with selective serotonin reuptake inhibitors and some anticonvulsant drugs. Omega-3 supplements contain various polyunsaturated fatty acids, which influence cell signaling and contribute to the production of bioactive fat mediators that counter inflammation. They are widely used in cardiovascular disease, breast cancer, rheumatoid arthritis, depression, and other cognitive disorders. They also appear to amplify the antitumor efficacy of tamoxifen through the inhibition of proliferative and antiapoptotic pathways that that are influenced by estrogen-receptor signaling.
“This study showed that omega-3 supplementation can improve mood and sleep disorder in women suffering from breast cancer while they (are) managing with antihormone drugs. … this supplement can be proposed for the treatment of these patients,” wrote researchers led by Azadeh Moghaddas, MD, PhD, who is an associate professor of clinical pharmacy and pharmacy practice at Isfahan (Iran) University of Medical Sciences.
The study was made available as a preprint on ResearchSquare and has not yet been peer reviewed. It included 60 patients who were screened for baseline mood disorders using the hospital anxiety and depression scale (HADS), then randomized to 2 mg omega-3 per day for 4 weeks, or placebo.
Studies have shown that omega-3 supplementation improves menopause and mood symptoms in postmenopausal women without cancer.
Omega-3 supplementation has neuroprotective effects and improved brain function and mood in rats, and a 2019 review suggested that the evidence is strong enough to warrant clinical studies.
To determine if the supplement was also safe and effective in women with breast cancer undergoing hormone therapy, the researchers analyzed data from 32 patients in the intervention group and 28 patients in the placebo group.
At 4 weeks of follow-up, patients in the intervention group had significantly lower values on the Center for Epidemiological Studies-Depression scale (mean, 22.8 vs. 30.8; P < .001), Profile of Mood State (mean, 30.8 versus 39.5; P<.001), and Pittsburgh Sleep Quality Index (mean, 4.6 vs. 5.9; P = .04). There were no statistically significant changes in these values in the placebo group.
At 4 weeks, paired samples t-test comparisons between the intervention and the placebo groups revealed lower scores in the intervention group for mean scores in the PSQI subscales subjective sleep quality (0.8 vs. 1.4; P = .002), delay in falling asleep (1.1 vs. 1.6; P = .02), and sleep disturbances (0.8 vs. 1.1; P = .005).
There were no significant adverse reactions in either group.
The study is limited by its small sample size and the short follow-up period.
The study was funded by Isfahan University of Medical Sciences. The authors declare no other conflicts of interest.
After 4 weeks of treatment, patients who received omega-3 reported better sleep, depression, and mood outcomes than those who received placebo.
Estrogen-receptor inhibitors are used to treat breast cancer with positive hormone receptors in combination with other therapies. However, the drugs can lead to long-term side effects, including hot flashes, night sweats, and changes to mood and sleep.
These side effects are often treated with selective serotonin reuptake inhibitors and some anticonvulsant drugs. Omega-3 supplements contain various polyunsaturated fatty acids, which influence cell signaling and contribute to the production of bioactive fat mediators that counter inflammation. They are widely used in cardiovascular disease, breast cancer, rheumatoid arthritis, depression, and other cognitive disorders. They also appear to amplify the antitumor efficacy of tamoxifen through the inhibition of proliferative and antiapoptotic pathways that that are influenced by estrogen-receptor signaling.
“This study showed that omega-3 supplementation can improve mood and sleep disorder in women suffering from breast cancer while they (are) managing with antihormone drugs. … this supplement can be proposed for the treatment of these patients,” wrote researchers led by Azadeh Moghaddas, MD, PhD, who is an associate professor of clinical pharmacy and pharmacy practice at Isfahan (Iran) University of Medical Sciences.
The study was made available as a preprint on ResearchSquare and has not yet been peer reviewed. It included 60 patients who were screened for baseline mood disorders using the hospital anxiety and depression scale (HADS), then randomized to 2 mg omega-3 per day for 4 weeks, or placebo.
Studies have shown that omega-3 supplementation improves menopause and mood symptoms in postmenopausal women without cancer.
Omega-3 supplementation has neuroprotective effects and improved brain function and mood in rats, and a 2019 review suggested that the evidence is strong enough to warrant clinical studies.
To determine if the supplement was also safe and effective in women with breast cancer undergoing hormone therapy, the researchers analyzed data from 32 patients in the intervention group and 28 patients in the placebo group.
At 4 weeks of follow-up, patients in the intervention group had significantly lower values on the Center for Epidemiological Studies-Depression scale (mean, 22.8 vs. 30.8; P < .001), Profile of Mood State (mean, 30.8 versus 39.5; P<.001), and Pittsburgh Sleep Quality Index (mean, 4.6 vs. 5.9; P = .04). There were no statistically significant changes in these values in the placebo group.
At 4 weeks, paired samples t-test comparisons between the intervention and the placebo groups revealed lower scores in the intervention group for mean scores in the PSQI subscales subjective sleep quality (0.8 vs. 1.4; P = .002), delay in falling asleep (1.1 vs. 1.6; P = .02), and sleep disturbances (0.8 vs. 1.1; P = .005).
There were no significant adverse reactions in either group.
The study is limited by its small sample size and the short follow-up period.
The study was funded by Isfahan University of Medical Sciences. The authors declare no other conflicts of interest.
After 4 weeks of treatment, patients who received omega-3 reported better sleep, depression, and mood outcomes than those who received placebo.
Estrogen-receptor inhibitors are used to treat breast cancer with positive hormone receptors in combination with other therapies. However, the drugs can lead to long-term side effects, including hot flashes, night sweats, and changes to mood and sleep.
These side effects are often treated with selective serotonin reuptake inhibitors and some anticonvulsant drugs. Omega-3 supplements contain various polyunsaturated fatty acids, which influence cell signaling and contribute to the production of bioactive fat mediators that counter inflammation. They are widely used in cardiovascular disease, breast cancer, rheumatoid arthritis, depression, and other cognitive disorders. They also appear to amplify the antitumor efficacy of tamoxifen through the inhibition of proliferative and antiapoptotic pathways that that are influenced by estrogen-receptor signaling.
“This study showed that omega-3 supplementation can improve mood and sleep disorder in women suffering from breast cancer while they (are) managing with antihormone drugs. … this supplement can be proposed for the treatment of these patients,” wrote researchers led by Azadeh Moghaddas, MD, PhD, who is an associate professor of clinical pharmacy and pharmacy practice at Isfahan (Iran) University of Medical Sciences.
The study was made available as a preprint on ResearchSquare and has not yet been peer reviewed. It included 60 patients who were screened for baseline mood disorders using the hospital anxiety and depression scale (HADS), then randomized to 2 mg omega-3 per day for 4 weeks, or placebo.
Studies have shown that omega-3 supplementation improves menopause and mood symptoms in postmenopausal women without cancer.
Omega-3 supplementation has neuroprotective effects and improved brain function and mood in rats, and a 2019 review suggested that the evidence is strong enough to warrant clinical studies.
To determine if the supplement was also safe and effective in women with breast cancer undergoing hormone therapy, the researchers analyzed data from 32 patients in the intervention group and 28 patients in the placebo group.
At 4 weeks of follow-up, patients in the intervention group had significantly lower values on the Center for Epidemiological Studies-Depression scale (mean, 22.8 vs. 30.8; P < .001), Profile of Mood State (mean, 30.8 versus 39.5; P<.001), and Pittsburgh Sleep Quality Index (mean, 4.6 vs. 5.9; P = .04). There were no statistically significant changes in these values in the placebo group.
At 4 weeks, paired samples t-test comparisons between the intervention and the placebo groups revealed lower scores in the intervention group for mean scores in the PSQI subscales subjective sleep quality (0.8 vs. 1.4; P = .002), delay in falling asleep (1.1 vs. 1.6; P = .02), and sleep disturbances (0.8 vs. 1.1; P = .005).
There were no significant adverse reactions in either group.
The study is limited by its small sample size and the short follow-up period.
The study was funded by Isfahan University of Medical Sciences. The authors declare no other conflicts of interest.
FROM RESEARCHSQUARE
Sleep disturbances more profound in older adults with atopic dermatitis
especially trouble staying asleep.
Those are key findings from a cross-sectional study that Jaya Manjunath, BS, and Jonathan I. Silverberg, MD, PhD, MPH, presented during a poster session at the Revolutionizing Atopic Dermatitis symposium.
“Atopic dermatitis is a chronic, pruritic skin disease associated with sleep disturbance and fatigue affecting adults of all ages,” they wrote. “When caring for geriatric patients, several factors such as sleep disturbance, polypharmacy, cognition, social support, and mobility should be considered. However, little is known about the characteristics of atopic dermatitis in the geriatric population.”
Ms. Manjunath, a student at George Washington University, Washington, and Dr. Silverberg, director of clinical research in the department of dermatology at GWU, recruited patients with AD aged 18 years and older diagnosed by Hanifin-Rajka criteria who were evaluated at an academic medical center between 2014 and 2019. They underwent full body skin exams and completed electronic questionnaires. AD severity was assessed with the Eczema Area and Severity Index (EASI), Scoring Atopic Dermatitis (SCORAD) total and itch subscores, Investigator’s Global Assessment (IGA), patient-reported Global Assessment of AD severity, and the Patient-Oriented Eczema Measure (POEM).
The researchers also assessed the frequency of sleep disturbances, including difficulty falling asleep and staying asleep, and used multivariable logistic regression models to evaluate associations of age (65 and older vs. 18-64 years) with AD severity, sleep disturbance or fatigue, controlling for total POEM score, sex, and race.
Using adjusted odds ratios, Ms. Manjunath and Dr. Silverberg found that being 65 or older was not associated with AD severity on the EASI (adjusted odds ratio, 1.47); total SCORAD (aOR, 1.10), and itch subscore (aOR, 1.00); IGA (aOR, 1.87); patient-reported Global Assessment of AD severity (aOR, 0.80), or the patient-oriented eczema measure (aOR, 0.55), associations that were not statistically significant.
However, the researchers found that older adult age was associated with an increased number of nights of sleep disturbance from AD in the past week (aOR, 2.14; P = .0142), as well as increased fatigue in the past 7 days (aOR, 1.81; P = .0313), trouble sleeping in the past 7 days (aOR, 1.98; P = .0118), and trouble staying asleep in the past 7 days (aOR, 2.26; P = .0030), but not with difficulty falling asleep in the last 7 days (aOR, 1.16; P = .5996).
“Future studies are needed to determine why geriatric AD patients have increased sleep disturbance and optimal interventions to address their sleep disturbance,” the researchers concluded.
The study was supported by the Agency for Healthcare Research and Quality, the Dermatology Foundation, and by an unrestricted grant from Galderma. Ms. Manjunath disclosed no relevant financial relationships. Dr. Silverberg reported that he is a consultant to and/or an advisory board member for several pharmaceutical companies. He is also a speaker for Regeneron and Sanofi and has received a grant from Galderma.
A version of this article first appeared on Medscape.com.
especially trouble staying asleep.
Those are key findings from a cross-sectional study that Jaya Manjunath, BS, and Jonathan I. Silverberg, MD, PhD, MPH, presented during a poster session at the Revolutionizing Atopic Dermatitis symposium.
“Atopic dermatitis is a chronic, pruritic skin disease associated with sleep disturbance and fatigue affecting adults of all ages,” they wrote. “When caring for geriatric patients, several factors such as sleep disturbance, polypharmacy, cognition, social support, and mobility should be considered. However, little is known about the characteristics of atopic dermatitis in the geriatric population.”
Ms. Manjunath, a student at George Washington University, Washington, and Dr. Silverberg, director of clinical research in the department of dermatology at GWU, recruited patients with AD aged 18 years and older diagnosed by Hanifin-Rajka criteria who were evaluated at an academic medical center between 2014 and 2019. They underwent full body skin exams and completed electronic questionnaires. AD severity was assessed with the Eczema Area and Severity Index (EASI), Scoring Atopic Dermatitis (SCORAD) total and itch subscores, Investigator’s Global Assessment (IGA), patient-reported Global Assessment of AD severity, and the Patient-Oriented Eczema Measure (POEM).
The researchers also assessed the frequency of sleep disturbances, including difficulty falling asleep and staying asleep, and used multivariable logistic regression models to evaluate associations of age (65 and older vs. 18-64 years) with AD severity, sleep disturbance or fatigue, controlling for total POEM score, sex, and race.
Using adjusted odds ratios, Ms. Manjunath and Dr. Silverberg found that being 65 or older was not associated with AD severity on the EASI (adjusted odds ratio, 1.47); total SCORAD (aOR, 1.10), and itch subscore (aOR, 1.00); IGA (aOR, 1.87); patient-reported Global Assessment of AD severity (aOR, 0.80), or the patient-oriented eczema measure (aOR, 0.55), associations that were not statistically significant.
However, the researchers found that older adult age was associated with an increased number of nights of sleep disturbance from AD in the past week (aOR, 2.14; P = .0142), as well as increased fatigue in the past 7 days (aOR, 1.81; P = .0313), trouble sleeping in the past 7 days (aOR, 1.98; P = .0118), and trouble staying asleep in the past 7 days (aOR, 2.26; P = .0030), but not with difficulty falling asleep in the last 7 days (aOR, 1.16; P = .5996).
“Future studies are needed to determine why geriatric AD patients have increased sleep disturbance and optimal interventions to address their sleep disturbance,” the researchers concluded.
The study was supported by the Agency for Healthcare Research and Quality, the Dermatology Foundation, and by an unrestricted grant from Galderma. Ms. Manjunath disclosed no relevant financial relationships. Dr. Silverberg reported that he is a consultant to and/or an advisory board member for several pharmaceutical companies. He is also a speaker for Regeneron and Sanofi and has received a grant from Galderma.
A version of this article first appeared on Medscape.com.
especially trouble staying asleep.
Those are key findings from a cross-sectional study that Jaya Manjunath, BS, and Jonathan I. Silverberg, MD, PhD, MPH, presented during a poster session at the Revolutionizing Atopic Dermatitis symposium.
“Atopic dermatitis is a chronic, pruritic skin disease associated with sleep disturbance and fatigue affecting adults of all ages,” they wrote. “When caring for geriatric patients, several factors such as sleep disturbance, polypharmacy, cognition, social support, and mobility should be considered. However, little is known about the characteristics of atopic dermatitis in the geriatric population.”
Ms. Manjunath, a student at George Washington University, Washington, and Dr. Silverberg, director of clinical research in the department of dermatology at GWU, recruited patients with AD aged 18 years and older diagnosed by Hanifin-Rajka criteria who were evaluated at an academic medical center between 2014 and 2019. They underwent full body skin exams and completed electronic questionnaires. AD severity was assessed with the Eczema Area and Severity Index (EASI), Scoring Atopic Dermatitis (SCORAD) total and itch subscores, Investigator’s Global Assessment (IGA), patient-reported Global Assessment of AD severity, and the Patient-Oriented Eczema Measure (POEM).
The researchers also assessed the frequency of sleep disturbances, including difficulty falling asleep and staying asleep, and used multivariable logistic regression models to evaluate associations of age (65 and older vs. 18-64 years) with AD severity, sleep disturbance or fatigue, controlling for total POEM score, sex, and race.
Using adjusted odds ratios, Ms. Manjunath and Dr. Silverberg found that being 65 or older was not associated with AD severity on the EASI (adjusted odds ratio, 1.47); total SCORAD (aOR, 1.10), and itch subscore (aOR, 1.00); IGA (aOR, 1.87); patient-reported Global Assessment of AD severity (aOR, 0.80), or the patient-oriented eczema measure (aOR, 0.55), associations that were not statistically significant.
However, the researchers found that older adult age was associated with an increased number of nights of sleep disturbance from AD in the past week (aOR, 2.14; P = .0142), as well as increased fatigue in the past 7 days (aOR, 1.81; P = .0313), trouble sleeping in the past 7 days (aOR, 1.98; P = .0118), and trouble staying asleep in the past 7 days (aOR, 2.26; P = .0030), but not with difficulty falling asleep in the last 7 days (aOR, 1.16; P = .5996).
“Future studies are needed to determine why geriatric AD patients have increased sleep disturbance and optimal interventions to address their sleep disturbance,” the researchers concluded.
The study was supported by the Agency for Healthcare Research and Quality, the Dermatology Foundation, and by an unrestricted grant from Galderma. Ms. Manjunath disclosed no relevant financial relationships. Dr. Silverberg reported that he is a consultant to and/or an advisory board member for several pharmaceutical companies. He is also a speaker for Regeneron and Sanofi and has received a grant from Galderma.
A version of this article first appeared on Medscape.com.
FROM REVOLUTIONIZING AD 2021
A very strange place to find a tooth
A nose for the tooth
Have you ever had a stuffy nose that just wouldn’t go away? Those irritating head colds have nothing on the stuffy nose a man in New York recently had to go through. A stuffy nose to top all stuffy noses. One stuffy nose to rule them all, as it were.
This man went to a Mount Sinai clinic with difficulty breathing through his right nostril, a problem that had been going on for years. Let us repeat that: A stuffy nose that lasted for years. The exam revealed a white mass jutting through the back of the septum and a CT scan confirmed the diagnosis. Perhaps you’ve already guessed, since the headline does give things away. Yes, this man had a tooth growing into his nose.
The problem was a half-inch-long ectopic tooth. Ectopic teeth are rare, occurring in less than 1% of people, but an ectopic tooth growing backward into the nasal cavity? Well, that’s so uncommon that this man got a case report in the New England Journal of Medicine.
This story does have a happy ending. Not all ectopic teeth need to be treated, but this one really did have to go. The offending tooth was surgically removed and, at a 3-month follow-up, the stuffy nose issue was completely resolved. So our friend gets the best of both worlds: His issue gets cured and he gets a case report in a major medical publication. If that’s not living the dream, we don’t know what is, and that’s the tooth.
Lettuce recommend you a sleep aid
Lettuce is great for many things. The star in a salad? Of course. The fresh element in a BLT? Yep. A sleep aid? According to a TikTok hack with almost 5 million views, the pinch hitter in a sandwich is switching leagues to be used like a tea for faster sleep. But, does it really work? Researchers say yes and no, according to a recent report at Tyla.com.
Studies conducted in 2013 and 2017 pointed toward a compound called lactucin, which is found in the plant’s n-butanol fraction. In the 2013 study, mice that received n-butanol fraction fell asleep faster and stayed asleep longer. In 2017, researchers found that lettuce made mice sleep longer and helped protect against cell inflammation and damage.
OK, so it works on mice. But what about humans? In the TikTok video, user Shapla Hoque pours hot water on a few lettuce leaves in a mug with a peppermint tea bag (for flavor). After 10 minutes, when the leaves are soaked and soggy, she removes them and drinks the lettuce tea. By the end of the video she’s visibly drowsy and ready to crash. Does this hold water?
Here’s the no. Dr. Charlotte Norton of the Slimming Clinic told Tyla.com that yeah, there are some properties in lettuce that will help you fall asleep, such as lactucarium, which is prominent in romaine. But you would need a massive amount of lettuce to get any effect. The TikTok video, she said, is an example of the placebo effect.
Brains get a rise out of Viagra
A lot of medications are used off label. Antidepressants for COVID have taken the cake recently, but here’s a new one: Viagra for Alzheimer’s disease.
Although there’s no definite link yet between the two, neuron models derived from induced pluripotent stem cells from patients with Alzheimer’s suggest that sildenafil increases neurite growth and decreases phospho-tau expression, Jiansong Fang, PhD, of the Cleveland Clinic, and associates said in Nature Aging.
Their research is an attempt to find untapped sources of new treatments among existing drugs. They began the search with 1,600 approved drugs and focused on those that target the buildup of beta amyloid and tau proteins in the brain, according to the Daily Beast.
Since sildenafil is obviously for men, more research will need to be done on how this drug affects women. Don’t start stocking up just yet.
Omicron is not a social-distancing robot
COVID, safe to say, has not been your typical, run-of-the-mill pandemic. People have protested social distancing. People have protested lockdowns. People have protested mask mandates. People have protested vaccine mandates. People have protested people protesting vaccine mandates.
Someone used a fake arm to get a COVID vaccine card. People have tried to reverse their COVID vaccinations. People had COVID contamination parties.
The common denominator? People. Humans. Maybe what we need is a nonhuman intervention. To fight COVID, we need a hero. A robotic hero.
And where can we find such a hero? The University of Maryland, of course, where computer scientists and engineers are working on an autonomous mobile robot to enforce indoor social-distancing rules.
Their robot can detect lapses in social distancing using cameras, both thermal and visual, along with a LiDAR (Light Detection and Ranging) sensor. It then sorts the offenders into various groups depending on whether they are standing still or moving and predicts their future movement using a state-of-the-art hybrid collision avoidance method known as Frozone, Adarsh Jagan Sathyamoorthy and associates explained in PLOS One.
“Once it reaches the breach, the robot encourages people to move apart via text that appears on a mounted display,” ScienceDaily said.
Maybe you were expecting a Terminator-type robot coming to enforce social distancing requirements rather than a simple text message. Let’s just hope that all COVID guidelines are followed, including social distancing, so the pandemic will finally end and won’t “be back.”
A nose for the tooth
Have you ever had a stuffy nose that just wouldn’t go away? Those irritating head colds have nothing on the stuffy nose a man in New York recently had to go through. A stuffy nose to top all stuffy noses. One stuffy nose to rule them all, as it were.
This man went to a Mount Sinai clinic with difficulty breathing through his right nostril, a problem that had been going on for years. Let us repeat that: A stuffy nose that lasted for years. The exam revealed a white mass jutting through the back of the septum and a CT scan confirmed the diagnosis. Perhaps you’ve already guessed, since the headline does give things away. Yes, this man had a tooth growing into his nose.
The problem was a half-inch-long ectopic tooth. Ectopic teeth are rare, occurring in less than 1% of people, but an ectopic tooth growing backward into the nasal cavity? Well, that’s so uncommon that this man got a case report in the New England Journal of Medicine.
This story does have a happy ending. Not all ectopic teeth need to be treated, but this one really did have to go. The offending tooth was surgically removed and, at a 3-month follow-up, the stuffy nose issue was completely resolved. So our friend gets the best of both worlds: His issue gets cured and he gets a case report in a major medical publication. If that’s not living the dream, we don’t know what is, and that’s the tooth.
Lettuce recommend you a sleep aid
Lettuce is great for many things. The star in a salad? Of course. The fresh element in a BLT? Yep. A sleep aid? According to a TikTok hack with almost 5 million views, the pinch hitter in a sandwich is switching leagues to be used like a tea for faster sleep. But, does it really work? Researchers say yes and no, according to a recent report at Tyla.com.
Studies conducted in 2013 and 2017 pointed toward a compound called lactucin, which is found in the plant’s n-butanol fraction. In the 2013 study, mice that received n-butanol fraction fell asleep faster and stayed asleep longer. In 2017, researchers found that lettuce made mice sleep longer and helped protect against cell inflammation and damage.
OK, so it works on mice. But what about humans? In the TikTok video, user Shapla Hoque pours hot water on a few lettuce leaves in a mug with a peppermint tea bag (for flavor). After 10 minutes, when the leaves are soaked and soggy, she removes them and drinks the lettuce tea. By the end of the video she’s visibly drowsy and ready to crash. Does this hold water?
Here’s the no. Dr. Charlotte Norton of the Slimming Clinic told Tyla.com that yeah, there are some properties in lettuce that will help you fall asleep, such as lactucarium, which is prominent in romaine. But you would need a massive amount of lettuce to get any effect. The TikTok video, she said, is an example of the placebo effect.
Brains get a rise out of Viagra
A lot of medications are used off label. Antidepressants for COVID have taken the cake recently, but here’s a new one: Viagra for Alzheimer’s disease.
Although there’s no definite link yet between the two, neuron models derived from induced pluripotent stem cells from patients with Alzheimer’s suggest that sildenafil increases neurite growth and decreases phospho-tau expression, Jiansong Fang, PhD, of the Cleveland Clinic, and associates said in Nature Aging.
Their research is an attempt to find untapped sources of new treatments among existing drugs. They began the search with 1,600 approved drugs and focused on those that target the buildup of beta amyloid and tau proteins in the brain, according to the Daily Beast.
Since sildenafil is obviously for men, more research will need to be done on how this drug affects women. Don’t start stocking up just yet.
Omicron is not a social-distancing robot
COVID, safe to say, has not been your typical, run-of-the-mill pandemic. People have protested social distancing. People have protested lockdowns. People have protested mask mandates. People have protested vaccine mandates. People have protested people protesting vaccine mandates.
Someone used a fake arm to get a COVID vaccine card. People have tried to reverse their COVID vaccinations. People had COVID contamination parties.
The common denominator? People. Humans. Maybe what we need is a nonhuman intervention. To fight COVID, we need a hero. A robotic hero.
And where can we find such a hero? The University of Maryland, of course, where computer scientists and engineers are working on an autonomous mobile robot to enforce indoor social-distancing rules.
Their robot can detect lapses in social distancing using cameras, both thermal and visual, along with a LiDAR (Light Detection and Ranging) sensor. It then sorts the offenders into various groups depending on whether they are standing still or moving and predicts their future movement using a state-of-the-art hybrid collision avoidance method known as Frozone, Adarsh Jagan Sathyamoorthy and associates explained in PLOS One.
“Once it reaches the breach, the robot encourages people to move apart via text that appears on a mounted display,” ScienceDaily said.
Maybe you were expecting a Terminator-type robot coming to enforce social distancing requirements rather than a simple text message. Let’s just hope that all COVID guidelines are followed, including social distancing, so the pandemic will finally end and won’t “be back.”
A nose for the tooth
Have you ever had a stuffy nose that just wouldn’t go away? Those irritating head colds have nothing on the stuffy nose a man in New York recently had to go through. A stuffy nose to top all stuffy noses. One stuffy nose to rule them all, as it were.
This man went to a Mount Sinai clinic with difficulty breathing through his right nostril, a problem that had been going on for years. Let us repeat that: A stuffy nose that lasted for years. The exam revealed a white mass jutting through the back of the septum and a CT scan confirmed the diagnosis. Perhaps you’ve already guessed, since the headline does give things away. Yes, this man had a tooth growing into his nose.
The problem was a half-inch-long ectopic tooth. Ectopic teeth are rare, occurring in less than 1% of people, but an ectopic tooth growing backward into the nasal cavity? Well, that’s so uncommon that this man got a case report in the New England Journal of Medicine.
This story does have a happy ending. Not all ectopic teeth need to be treated, but this one really did have to go. The offending tooth was surgically removed and, at a 3-month follow-up, the stuffy nose issue was completely resolved. So our friend gets the best of both worlds: His issue gets cured and he gets a case report in a major medical publication. If that’s not living the dream, we don’t know what is, and that’s the tooth.
Lettuce recommend you a sleep aid
Lettuce is great for many things. The star in a salad? Of course. The fresh element in a BLT? Yep. A sleep aid? According to a TikTok hack with almost 5 million views, the pinch hitter in a sandwich is switching leagues to be used like a tea for faster sleep. But, does it really work? Researchers say yes and no, according to a recent report at Tyla.com.
Studies conducted in 2013 and 2017 pointed toward a compound called lactucin, which is found in the plant’s n-butanol fraction. In the 2013 study, mice that received n-butanol fraction fell asleep faster and stayed asleep longer. In 2017, researchers found that lettuce made mice sleep longer and helped protect against cell inflammation and damage.
OK, so it works on mice. But what about humans? In the TikTok video, user Shapla Hoque pours hot water on a few lettuce leaves in a mug with a peppermint tea bag (for flavor). After 10 minutes, when the leaves are soaked and soggy, she removes them and drinks the lettuce tea. By the end of the video she’s visibly drowsy and ready to crash. Does this hold water?
Here’s the no. Dr. Charlotte Norton of the Slimming Clinic told Tyla.com that yeah, there are some properties in lettuce that will help you fall asleep, such as lactucarium, which is prominent in romaine. But you would need a massive amount of lettuce to get any effect. The TikTok video, she said, is an example of the placebo effect.
Brains get a rise out of Viagra
A lot of medications are used off label. Antidepressants for COVID have taken the cake recently, but here’s a new one: Viagra for Alzheimer’s disease.
Although there’s no definite link yet between the two, neuron models derived from induced pluripotent stem cells from patients with Alzheimer’s suggest that sildenafil increases neurite growth and decreases phospho-tau expression, Jiansong Fang, PhD, of the Cleveland Clinic, and associates said in Nature Aging.
Their research is an attempt to find untapped sources of new treatments among existing drugs. They began the search with 1,600 approved drugs and focused on those that target the buildup of beta amyloid and tau proteins in the brain, according to the Daily Beast.
Since sildenafil is obviously for men, more research will need to be done on how this drug affects women. Don’t start stocking up just yet.
Omicron is not a social-distancing robot
COVID, safe to say, has not been your typical, run-of-the-mill pandemic. People have protested social distancing. People have protested lockdowns. People have protested mask mandates. People have protested vaccine mandates. People have protested people protesting vaccine mandates.
Someone used a fake arm to get a COVID vaccine card. People have tried to reverse their COVID vaccinations. People had COVID contamination parties.
The common denominator? People. Humans. Maybe what we need is a nonhuman intervention. To fight COVID, we need a hero. A robotic hero.
And where can we find such a hero? The University of Maryland, of course, where computer scientists and engineers are working on an autonomous mobile robot to enforce indoor social-distancing rules.
Their robot can detect lapses in social distancing using cameras, both thermal and visual, along with a LiDAR (Light Detection and Ranging) sensor. It then sorts the offenders into various groups depending on whether they are standing still or moving and predicts their future movement using a state-of-the-art hybrid collision avoidance method known as Frozone, Adarsh Jagan Sathyamoorthy and associates explained in PLOS One.
“Once it reaches the breach, the robot encourages people to move apart via text that appears on a mounted display,” ScienceDaily said.
Maybe you were expecting a Terminator-type robot coming to enforce social distancing requirements rather than a simple text message. Let’s just hope that all COVID guidelines are followed, including social distancing, so the pandemic will finally end and won’t “be back.”