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Self-harm
Nonsuicidal self-injury (NSSI) has become more prevalent in youth over recent years and has many inherent risks. In the Diagnostic and Statistical Manual, Fifth Edition (DSM-5), NSSI is a diagnosis suggested for further study, and criteria include engaging in self-injury for 5 or more days without suicidal intent as well as self-injury associated with at least 1 of the following: obtaining relief from negative thoughts or feelings, resolving interpersonal challenges, inducing positive feelings. It is associated with interpersonal difficulties or negative thoughts/feelings. The behavior causes significant impairment in functioning and is not better explained by another condition.1
Estimates of lifetime prevalence in community-based samples of youth range from 15% to 20%. Individuals often start during early adolescence. It can pose many risks including infection, permanent scarring or disfigurement, decreased self-esteem, interpersonal conflict, severe injury, or death. Reasons for engaging in self-harm can vary and include attempts to regulate negative affect, to manage feelings of emptiness/numbness, regain a sense of control over body, feelings, etc., or to provide a consequence for perceived faults. Youth often may start to engage in self-harm covertly, and it may first become apparent in emergency or primary care settings. However, upon discovery, the response given also may affect future behavior.
Efforts also have been underway to distinguish between youth who engage in self-harm with and without suicidal ideation. Girls are more likely than are boys to report NSSI, although male NSSI may present differently. In addition to cutting or more stereotypical self-injury, they may punch walls or engage in fights or other risky behaviors as a proxy for self-harm. Risk factors for boys with regard to suicide attempts include hopelessness and history of sexual abuse. Maladaptive eating patterns and hopelessness were the two most significant factors for girls.4
With regard to issues of confidentiality, it will be important to carefully gauge level of safety and to clearly communicate with the patient (and family) limits of confidentiality. This may result in working within shades of gray to help maintain the therapeutic relationship and the patient’s comfort in being able to disclose potentially sensitive information.
Families can struggle with how to manage this, and it can generate fear as well as other strong emotions.
Tips for parents and guardians
- Validate the underlying emotions while not validating the behavior. Self-injury is a coping strategy. Focus on the driving forces for the actions rather than the actions themselves.
- Approach your child from a nonjudgmental stance.
- Recognize that change may not happen overnight, and that there may be periods of regression.
- Acknowledge successes when they occur.
- Make yourself available for open communication. Open-ended questions may facilitate more dialogue.
- Take care of yourself as well. Ensure you use your supports and are engaging in healthy self-care.
- Take the behavior seriously. While this behavior is relatively common, do not assume it is “just a phase.”
- While remaining supportive, it is important to maintain a parental role and to keep expectations rather than “walking on eggshells.”
- Involve the child in identifying what can be of support.
- Become aware of local crisis resources in your community. National resources include Call 1-800-273-TALK for the national suicide hotline or Text 741741 to connect with a crisis counselor.
Things to avoid
- Avoid taking a punitive stance. While the behavior can be provocative, most likely the primary purpose is not for attention.
- Avoid engaging in power struggles.
- Avoid creating increased isolation for the child. This can be a delicate balance with regard to peer groups, but encouraging healthy social interactions and activities is a way to help build resilience.
- Avoid taking the behavior personally.5
In working with youth who engage in self-harm, it is important to work within a team, which may include family, primary care, mental health support, school, and potentially other community supports. Treatment evidence is relatively limited, but there is some evidence to support use of cognitive behavioral therapy, dialectical behavior therapy, and mentalization-based therapy. Regardless, work will likely be long term and at times intensive in addressing the problems leading to self-harm behavior.6
Dr. Strange is an assistant professor in the department of psychiatry at the University of Vermont Medical Center and University of Vermont Robert Larner College of Medicine, both in Burlington. She works with children and adolescents. She has no relevant financial disclosures.
References
1. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Arlington, Va.: American Psychiatric Association Publishing, 2013)
2. J Adolesc. 2014 Dec;37(8):1335-44.
3. Behav Ther. 2017 May; 48(3):366-79.
4. Acad Pediatr. 2012 May-Jun;12(3):205-13.
5. “Information for parents: What you need to know about self-injury.” The Fact Sheet Series, Cornell Research Program on Self-Injury and Recovery. 2009.
6. Clin Pediatr. 2016 Sep 13;55(11):1012-9.
Nonsuicidal self-injury (NSSI) has become more prevalent in youth over recent years and has many inherent risks. In the Diagnostic and Statistical Manual, Fifth Edition (DSM-5), NSSI is a diagnosis suggested for further study, and criteria include engaging in self-injury for 5 or more days without suicidal intent as well as self-injury associated with at least 1 of the following: obtaining relief from negative thoughts or feelings, resolving interpersonal challenges, inducing positive feelings. It is associated with interpersonal difficulties or negative thoughts/feelings. The behavior causes significant impairment in functioning and is not better explained by another condition.1
Estimates of lifetime prevalence in community-based samples of youth range from 15% to 20%. Individuals often start during early adolescence. It can pose many risks including infection, permanent scarring or disfigurement, decreased self-esteem, interpersonal conflict, severe injury, or death. Reasons for engaging in self-harm can vary and include attempts to regulate negative affect, to manage feelings of emptiness/numbness, regain a sense of control over body, feelings, etc., or to provide a consequence for perceived faults. Youth often may start to engage in self-harm covertly, and it may first become apparent in emergency or primary care settings. However, upon discovery, the response given also may affect future behavior.
Efforts also have been underway to distinguish between youth who engage in self-harm with and without suicidal ideation. Girls are more likely than are boys to report NSSI, although male NSSI may present differently. In addition to cutting or more stereotypical self-injury, they may punch walls or engage in fights or other risky behaviors as a proxy for self-harm. Risk factors for boys with regard to suicide attempts include hopelessness and history of sexual abuse. Maladaptive eating patterns and hopelessness were the two most significant factors for girls.4
With regard to issues of confidentiality, it will be important to carefully gauge level of safety and to clearly communicate with the patient (and family) limits of confidentiality. This may result in working within shades of gray to help maintain the therapeutic relationship and the patient’s comfort in being able to disclose potentially sensitive information.
Families can struggle with how to manage this, and it can generate fear as well as other strong emotions.
Tips for parents and guardians
- Validate the underlying emotions while not validating the behavior. Self-injury is a coping strategy. Focus on the driving forces for the actions rather than the actions themselves.
- Approach your child from a nonjudgmental stance.
- Recognize that change may not happen overnight, and that there may be periods of regression.
- Acknowledge successes when they occur.
- Make yourself available for open communication. Open-ended questions may facilitate more dialogue.
- Take care of yourself as well. Ensure you use your supports and are engaging in healthy self-care.
- Take the behavior seriously. While this behavior is relatively common, do not assume it is “just a phase.”
- While remaining supportive, it is important to maintain a parental role and to keep expectations rather than “walking on eggshells.”
- Involve the child in identifying what can be of support.
- Become aware of local crisis resources in your community. National resources include Call 1-800-273-TALK for the national suicide hotline or Text 741741 to connect with a crisis counselor.
Things to avoid
- Avoid taking a punitive stance. While the behavior can be provocative, most likely the primary purpose is not for attention.
- Avoid engaging in power struggles.
- Avoid creating increased isolation for the child. This can be a delicate balance with regard to peer groups, but encouraging healthy social interactions and activities is a way to help build resilience.
- Avoid taking the behavior personally.5
In working with youth who engage in self-harm, it is important to work within a team, which may include family, primary care, mental health support, school, and potentially other community supports. Treatment evidence is relatively limited, but there is some evidence to support use of cognitive behavioral therapy, dialectical behavior therapy, and mentalization-based therapy. Regardless, work will likely be long term and at times intensive in addressing the problems leading to self-harm behavior.6
Dr. Strange is an assistant professor in the department of psychiatry at the University of Vermont Medical Center and University of Vermont Robert Larner College of Medicine, both in Burlington. She works with children and adolescents. She has no relevant financial disclosures.
References
1. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Arlington, Va.: American Psychiatric Association Publishing, 2013)
2. J Adolesc. 2014 Dec;37(8):1335-44.
3. Behav Ther. 2017 May; 48(3):366-79.
4. Acad Pediatr. 2012 May-Jun;12(3):205-13.
5. “Information for parents: What you need to know about self-injury.” The Fact Sheet Series, Cornell Research Program on Self-Injury and Recovery. 2009.
6. Clin Pediatr. 2016 Sep 13;55(11):1012-9.
Nonsuicidal self-injury (NSSI) has become more prevalent in youth over recent years and has many inherent risks. In the Diagnostic and Statistical Manual, Fifth Edition (DSM-5), NSSI is a diagnosis suggested for further study, and criteria include engaging in self-injury for 5 or more days without suicidal intent as well as self-injury associated with at least 1 of the following: obtaining relief from negative thoughts or feelings, resolving interpersonal challenges, inducing positive feelings. It is associated with interpersonal difficulties or negative thoughts/feelings. The behavior causes significant impairment in functioning and is not better explained by another condition.1
Estimates of lifetime prevalence in community-based samples of youth range from 15% to 20%. Individuals often start during early adolescence. It can pose many risks including infection, permanent scarring or disfigurement, decreased self-esteem, interpersonal conflict, severe injury, or death. Reasons for engaging in self-harm can vary and include attempts to regulate negative affect, to manage feelings of emptiness/numbness, regain a sense of control over body, feelings, etc., or to provide a consequence for perceived faults. Youth often may start to engage in self-harm covertly, and it may first become apparent in emergency or primary care settings. However, upon discovery, the response given also may affect future behavior.
Efforts also have been underway to distinguish between youth who engage in self-harm with and without suicidal ideation. Girls are more likely than are boys to report NSSI, although male NSSI may present differently. In addition to cutting or more stereotypical self-injury, they may punch walls or engage in fights or other risky behaviors as a proxy for self-harm. Risk factors for boys with regard to suicide attempts include hopelessness and history of sexual abuse. Maladaptive eating patterns and hopelessness were the two most significant factors for girls.4
With regard to issues of confidentiality, it will be important to carefully gauge level of safety and to clearly communicate with the patient (and family) limits of confidentiality. This may result in working within shades of gray to help maintain the therapeutic relationship and the patient’s comfort in being able to disclose potentially sensitive information.
Families can struggle with how to manage this, and it can generate fear as well as other strong emotions.
Tips for parents and guardians
- Validate the underlying emotions while not validating the behavior. Self-injury is a coping strategy. Focus on the driving forces for the actions rather than the actions themselves.
- Approach your child from a nonjudgmental stance.
- Recognize that change may not happen overnight, and that there may be periods of regression.
- Acknowledge successes when they occur.
- Make yourself available for open communication. Open-ended questions may facilitate more dialogue.
- Take care of yourself as well. Ensure you use your supports and are engaging in healthy self-care.
- Take the behavior seriously. While this behavior is relatively common, do not assume it is “just a phase.”
- While remaining supportive, it is important to maintain a parental role and to keep expectations rather than “walking on eggshells.”
- Involve the child in identifying what can be of support.
- Become aware of local crisis resources in your community. National resources include Call 1-800-273-TALK for the national suicide hotline or Text 741741 to connect with a crisis counselor.
Things to avoid
- Avoid taking a punitive stance. While the behavior can be provocative, most likely the primary purpose is not for attention.
- Avoid engaging in power struggles.
- Avoid creating increased isolation for the child. This can be a delicate balance with regard to peer groups, but encouraging healthy social interactions and activities is a way to help build resilience.
- Avoid taking the behavior personally.5
In working with youth who engage in self-harm, it is important to work within a team, which may include family, primary care, mental health support, school, and potentially other community supports. Treatment evidence is relatively limited, but there is some evidence to support use of cognitive behavioral therapy, dialectical behavior therapy, and mentalization-based therapy. Regardless, work will likely be long term and at times intensive in addressing the problems leading to self-harm behavior.6
Dr. Strange is an assistant professor in the department of psychiatry at the University of Vermont Medical Center and University of Vermont Robert Larner College of Medicine, both in Burlington. She works with children and adolescents. She has no relevant financial disclosures.
References
1. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Arlington, Va.: American Psychiatric Association Publishing, 2013)
2. J Adolesc. 2014 Dec;37(8):1335-44.
3. Behav Ther. 2017 May; 48(3):366-79.
4. Acad Pediatr. 2012 May-Jun;12(3):205-13.
5. “Information for parents: What you need to know about self-injury.” The Fact Sheet Series, Cornell Research Program on Self-Injury and Recovery. 2009.
6. Clin Pediatr. 2016 Sep 13;55(11):1012-9.
Insomnia – going beyond sleep hygiene
Difficulties with sleep are prevalent and significant across the developmental spectrum. Not only does poor sleep affect daytime functioning in relation to mood, focus, appetite, and emotional regulation, but ineffective bedtime routines can cause significant distress for youth and caregivers, as well. The American Academy of Sleep Medicine describes insomnia as “repeated difficulty with sleep initiation, duration, consolidation, or quality that occurs despite age-appropriate time and opportunity for sleep and results in daytime functional impairment for the child and/or family.’’1
Pediatric providers likely are familiar already with initial steps in the evaluation and treatment of insomnia. The emphasis here is assessment and intervention approaches beyond the foundational use of sleep hygiene recommendations.
In working with a patient such as Katie who comes laden with diagnoses and medications, stepping back to reconsider the assessment is an important starting point. Problems related to sleep are rife in psychiatric conditions, from depression, anxiety, and PTSD to bipolar disorder, ADHD, and autism.2
Next is see if there are external factors engendering insomnia. Sleep hygiene focuses on these, but sometimes recent stressors or familial conflict are overlooked, which may be linchpins to improving sleep patterns. Commonly prescribed medications (steroids, bupropion, and stimulants) and intoxication or withdrawal symptoms from substance use can contribute to wakefulness and deserve consideration. It can be useful to track sleep for a while to identify contributing factors, impediments to sleep, and ineffective patterns (see tools at sleepfoundation.org or the free app CBT-I Coach).
After assessment, the bulk of the evidence for pediatric insomnia is for behavioral treatments, mostly for infants and young children. This may be familiar territory, and it offers a good time to assess the level of motivation. Are the patient and family aware of how insomnia affects their lives on a day-to-day basis and is this problem a priority?
For adolescents who are convinced of the life-changing properties of a good night’s sleep, cognitive-behavioral therapy for insomnia (CBT-i) is developing a strong evidence base for insomnia in adolescents.3 CBT-i adds to the usual interventions for addressing insomnia in infants and young children by additionally training adolescents relaxation techniques, by addressing cognitive distortions about sleep, and by actually restricting sleep. This last technique involves initially reducing the amount of sleep in order to build a tight association between sleep and the bedroom, improve sleep efficiency, and increase sleep drive.
In general, medications are considered when other appropriate interventions have proven inadequate. There is very little evidence for using pharmacologic interventions for pediatric insomnia, so even if a medication is selected, behavioral approaches should remain a mainstay.4 Patients and caregivers should agree to specific short-term goals ahead of time when using sleep medicine, given the limited effectiveness and recommended short duration of use. Many medications change sleep architecture, and none have been clearly shown to sustainably improve sleep quality or quantity or reduce daytime symptoms of insomnia.
Prescribing guidelines for insomnia suggest selecting an agent matched to the symptoms and relevant to any comorbidities. Melatonin may be most helpful in shifting the sleep phase rather than for direct hypnotic effects; thus adolescents or patients with ADHD whose sleep schedule has naturally shifted later may benefit from a small dose of melatonin (1-3 mg) several hours before bedtime to prime their system. Beware that melatonin is not regulated by the Food and Drug Administration and animal studies have shown significant alterations of the gonadal hormone axis, although this has not been examined in human trials. Alpha-2 agonists – such as clonidine and guanfacine – may be helpful for sleep initiation, especially in populations with comorbid ADHD, aggression, or tics, where these medications might be otherwise indicated. Prazosin, an alpha-1 antagonist, has some limited evidence as a treatment for nightmares and PTSD symptoms, so it may be a good choice for children with trauma-related hypervigilance.
In patients with depression, low doses of trazodone (12.5-50 mg) or mirtazapine (7.5-15 mg) may be effective. Although short-acting benzodiazepines may be useful in the short-term, particularly for sleep-onset difficulties, they generally are not recommended because of the risks of abuse, diversion, withdrawal, cognitive side effects, disinhibition, development of tolerance, and contraindication with such comorbidities as sleep apnea. However, the benzodiazepine receptor agonists such as zaleplon, zolpidem, and eszopiclone, while lacking evidence in the pediatric population, may be worthwhile considerations as their varying half-lives allow for specificity in treating sleep-onset vs. sleep-maintenance problems. Caregivers should be warned about the potential for sleepwalking or other complex sleep-related behaviors with this class of medicines.
Avoid tricyclic antidepressants because of the potential for anticholinergic effects and cardiotoxicity. Atypical antipsychotics generally are not worth the risk of serious and rapid side effects associated with this class of medications, which include metabolic syndrome.
The assessment and treatment of pediatric insomnia may require several visits to complete. But, given growing knowledge of how much sleep contributes to learning, longevity, and well-being, and the consequences of sleep deprivation with regard to safety, irritability, poor concentration, disordered metabolism and appetite, etc., the potential benefits seem well worth the time.
Dr. Rosenfeld is assistant professor of psychiatry at Vermont Center for Children, Youth & Families, at the University of Vermont Medical Center, and the University of Vermont, Burlington. He has received honorarium from Oakstone Publishing for contributing board review course content on human development.
References
1. International Classification of Sleep Disorders: Diagnostic & Coding Manual. 2nd edition. (Westchester: American Academy of Sleep Medicine, 2005).
2. Child Adolesc Psychiatr Clin N Am. 2009 Oct;18(4):979-1000
3. J Child Psychol Psychiatry. 2017, Oct 20. doi: 10.1111/jcpp.12834.
4. Child Adolesc Psychiatric Clin N Am. 2009, Oct;18(4):1001-16.
Difficulties with sleep are prevalent and significant across the developmental spectrum. Not only does poor sleep affect daytime functioning in relation to mood, focus, appetite, and emotional regulation, but ineffective bedtime routines can cause significant distress for youth and caregivers, as well. The American Academy of Sleep Medicine describes insomnia as “repeated difficulty with sleep initiation, duration, consolidation, or quality that occurs despite age-appropriate time and opportunity for sleep and results in daytime functional impairment for the child and/or family.’’1
Pediatric providers likely are familiar already with initial steps in the evaluation and treatment of insomnia. The emphasis here is assessment and intervention approaches beyond the foundational use of sleep hygiene recommendations.
In working with a patient such as Katie who comes laden with diagnoses and medications, stepping back to reconsider the assessment is an important starting point. Problems related to sleep are rife in psychiatric conditions, from depression, anxiety, and PTSD to bipolar disorder, ADHD, and autism.2
Next is see if there are external factors engendering insomnia. Sleep hygiene focuses on these, but sometimes recent stressors or familial conflict are overlooked, which may be linchpins to improving sleep patterns. Commonly prescribed medications (steroids, bupropion, and stimulants) and intoxication or withdrawal symptoms from substance use can contribute to wakefulness and deserve consideration. It can be useful to track sleep for a while to identify contributing factors, impediments to sleep, and ineffective patterns (see tools at sleepfoundation.org or the free app CBT-I Coach).
After assessment, the bulk of the evidence for pediatric insomnia is for behavioral treatments, mostly for infants and young children. This may be familiar territory, and it offers a good time to assess the level of motivation. Are the patient and family aware of how insomnia affects their lives on a day-to-day basis and is this problem a priority?
For adolescents who are convinced of the life-changing properties of a good night’s sleep, cognitive-behavioral therapy for insomnia (CBT-i) is developing a strong evidence base for insomnia in adolescents.3 CBT-i adds to the usual interventions for addressing insomnia in infants and young children by additionally training adolescents relaxation techniques, by addressing cognitive distortions about sleep, and by actually restricting sleep. This last technique involves initially reducing the amount of sleep in order to build a tight association between sleep and the bedroom, improve sleep efficiency, and increase sleep drive.
In general, medications are considered when other appropriate interventions have proven inadequate. There is very little evidence for using pharmacologic interventions for pediatric insomnia, so even if a medication is selected, behavioral approaches should remain a mainstay.4 Patients and caregivers should agree to specific short-term goals ahead of time when using sleep medicine, given the limited effectiveness and recommended short duration of use. Many medications change sleep architecture, and none have been clearly shown to sustainably improve sleep quality or quantity or reduce daytime symptoms of insomnia.
Prescribing guidelines for insomnia suggest selecting an agent matched to the symptoms and relevant to any comorbidities. Melatonin may be most helpful in shifting the sleep phase rather than for direct hypnotic effects; thus adolescents or patients with ADHD whose sleep schedule has naturally shifted later may benefit from a small dose of melatonin (1-3 mg) several hours before bedtime to prime their system. Beware that melatonin is not regulated by the Food and Drug Administration and animal studies have shown significant alterations of the gonadal hormone axis, although this has not been examined in human trials. Alpha-2 agonists – such as clonidine and guanfacine – may be helpful for sleep initiation, especially in populations with comorbid ADHD, aggression, or tics, where these medications might be otherwise indicated. Prazosin, an alpha-1 antagonist, has some limited evidence as a treatment for nightmares and PTSD symptoms, so it may be a good choice for children with trauma-related hypervigilance.
In patients with depression, low doses of trazodone (12.5-50 mg) or mirtazapine (7.5-15 mg) may be effective. Although short-acting benzodiazepines may be useful in the short-term, particularly for sleep-onset difficulties, they generally are not recommended because of the risks of abuse, diversion, withdrawal, cognitive side effects, disinhibition, development of tolerance, and contraindication with such comorbidities as sleep apnea. However, the benzodiazepine receptor agonists such as zaleplon, zolpidem, and eszopiclone, while lacking evidence in the pediatric population, may be worthwhile considerations as their varying half-lives allow for specificity in treating sleep-onset vs. sleep-maintenance problems. Caregivers should be warned about the potential for sleepwalking or other complex sleep-related behaviors with this class of medicines.
Avoid tricyclic antidepressants because of the potential for anticholinergic effects and cardiotoxicity. Atypical antipsychotics generally are not worth the risk of serious and rapid side effects associated with this class of medications, which include metabolic syndrome.
The assessment and treatment of pediatric insomnia may require several visits to complete. But, given growing knowledge of how much sleep contributes to learning, longevity, and well-being, and the consequences of sleep deprivation with regard to safety, irritability, poor concentration, disordered metabolism and appetite, etc., the potential benefits seem well worth the time.
Dr. Rosenfeld is assistant professor of psychiatry at Vermont Center for Children, Youth & Families, at the University of Vermont Medical Center, and the University of Vermont, Burlington. He has received honorarium from Oakstone Publishing for contributing board review course content on human development.
References
1. International Classification of Sleep Disorders: Diagnostic & Coding Manual. 2nd edition. (Westchester: American Academy of Sleep Medicine, 2005).
2. Child Adolesc Psychiatr Clin N Am. 2009 Oct;18(4):979-1000
3. J Child Psychol Psychiatry. 2017, Oct 20. doi: 10.1111/jcpp.12834.
4. Child Adolesc Psychiatric Clin N Am. 2009, Oct;18(4):1001-16.
Difficulties with sleep are prevalent and significant across the developmental spectrum. Not only does poor sleep affect daytime functioning in relation to mood, focus, appetite, and emotional regulation, but ineffective bedtime routines can cause significant distress for youth and caregivers, as well. The American Academy of Sleep Medicine describes insomnia as “repeated difficulty with sleep initiation, duration, consolidation, or quality that occurs despite age-appropriate time and opportunity for sleep and results in daytime functional impairment for the child and/or family.’’1
Pediatric providers likely are familiar already with initial steps in the evaluation and treatment of insomnia. The emphasis here is assessment and intervention approaches beyond the foundational use of sleep hygiene recommendations.
In working with a patient such as Katie who comes laden with diagnoses and medications, stepping back to reconsider the assessment is an important starting point. Problems related to sleep are rife in psychiatric conditions, from depression, anxiety, and PTSD to bipolar disorder, ADHD, and autism.2
Next is see if there are external factors engendering insomnia. Sleep hygiene focuses on these, but sometimes recent stressors or familial conflict are overlooked, which may be linchpins to improving sleep patterns. Commonly prescribed medications (steroids, bupropion, and stimulants) and intoxication or withdrawal symptoms from substance use can contribute to wakefulness and deserve consideration. It can be useful to track sleep for a while to identify contributing factors, impediments to sleep, and ineffective patterns (see tools at sleepfoundation.org or the free app CBT-I Coach).
After assessment, the bulk of the evidence for pediatric insomnia is for behavioral treatments, mostly for infants and young children. This may be familiar territory, and it offers a good time to assess the level of motivation. Are the patient and family aware of how insomnia affects their lives on a day-to-day basis and is this problem a priority?
For adolescents who are convinced of the life-changing properties of a good night’s sleep, cognitive-behavioral therapy for insomnia (CBT-i) is developing a strong evidence base for insomnia in adolescents.3 CBT-i adds to the usual interventions for addressing insomnia in infants and young children by additionally training adolescents relaxation techniques, by addressing cognitive distortions about sleep, and by actually restricting sleep. This last technique involves initially reducing the amount of sleep in order to build a tight association between sleep and the bedroom, improve sleep efficiency, and increase sleep drive.
In general, medications are considered when other appropriate interventions have proven inadequate. There is very little evidence for using pharmacologic interventions for pediatric insomnia, so even if a medication is selected, behavioral approaches should remain a mainstay.4 Patients and caregivers should agree to specific short-term goals ahead of time when using sleep medicine, given the limited effectiveness and recommended short duration of use. Many medications change sleep architecture, and none have been clearly shown to sustainably improve sleep quality or quantity or reduce daytime symptoms of insomnia.
Prescribing guidelines for insomnia suggest selecting an agent matched to the symptoms and relevant to any comorbidities. Melatonin may be most helpful in shifting the sleep phase rather than for direct hypnotic effects; thus adolescents or patients with ADHD whose sleep schedule has naturally shifted later may benefit from a small dose of melatonin (1-3 mg) several hours before bedtime to prime their system. Beware that melatonin is not regulated by the Food and Drug Administration and animal studies have shown significant alterations of the gonadal hormone axis, although this has not been examined in human trials. Alpha-2 agonists – such as clonidine and guanfacine – may be helpful for sleep initiation, especially in populations with comorbid ADHD, aggression, or tics, where these medications might be otherwise indicated. Prazosin, an alpha-1 antagonist, has some limited evidence as a treatment for nightmares and PTSD symptoms, so it may be a good choice for children with trauma-related hypervigilance.
In patients with depression, low doses of trazodone (12.5-50 mg) or mirtazapine (7.5-15 mg) may be effective. Although short-acting benzodiazepines may be useful in the short-term, particularly for sleep-onset difficulties, they generally are not recommended because of the risks of abuse, diversion, withdrawal, cognitive side effects, disinhibition, development of tolerance, and contraindication with such comorbidities as sleep apnea. However, the benzodiazepine receptor agonists such as zaleplon, zolpidem, and eszopiclone, while lacking evidence in the pediatric population, may be worthwhile considerations as their varying half-lives allow for specificity in treating sleep-onset vs. sleep-maintenance problems. Caregivers should be warned about the potential for sleepwalking or other complex sleep-related behaviors with this class of medicines.
Avoid tricyclic antidepressants because of the potential for anticholinergic effects and cardiotoxicity. Atypical antipsychotics generally are not worth the risk of serious and rapid side effects associated with this class of medications, which include metabolic syndrome.
The assessment and treatment of pediatric insomnia may require several visits to complete. But, given growing knowledge of how much sleep contributes to learning, longevity, and well-being, and the consequences of sleep deprivation with regard to safety, irritability, poor concentration, disordered metabolism and appetite, etc., the potential benefits seem well worth the time.
Dr. Rosenfeld is assistant professor of psychiatry at Vermont Center for Children, Youth & Families, at the University of Vermont Medical Center, and the University of Vermont, Burlington. He has received honorarium from Oakstone Publishing for contributing board review course content on human development.
References
1. International Classification of Sleep Disorders: Diagnostic & Coding Manual. 2nd edition. (Westchester: American Academy of Sleep Medicine, 2005).
2. Child Adolesc Psychiatr Clin N Am. 2009 Oct;18(4):979-1000
3. J Child Psychol Psychiatry. 2017, Oct 20. doi: 10.1111/jcpp.12834.
4. Child Adolesc Psychiatric Clin N Am. 2009, Oct;18(4):1001-16.
How to integrate mental health care into primary care
During my training as a child and adolescent psychiatry fellow, I “lived” down the hall from 10 other people just like me who had similar offices and training. Our pace was tailored to pediatric psychiatry. Appointments were 30 minutes or more. Our goal was to provide the most comprehensive mental health care for the families whom we grew to know and love.
The impetus to create an integrated mental health care approach has been well elucidated by the American Academy of Child and Adolescent Psychiatry (AACAP) in its report, Collaborative mental health care in pediatric primary care. It is based on some telling statistics: Fifty percent of all cases of mental illness begin before age 14 years and 75% begin by age 24. Half of all pediatric office visits involve behavioral, psychosocial, or educational concerns. The American Academy of Pediatrics’ Task Force on Mental Health similarly has stated that primary care clinicians can and should be able to provide mental health services to children and adolescents in a primary care setting.
Integrative psychiatry and primary care treatment comes in three forms: classic consultation, in which a specialist sees a patient and refers back to the PCP with recommendations; colocation, in which mental health specialists practice in the same office but essentially are “ships crossing in the night” with PCPs; and the most-lauded form, collaborative/integrative care, in which back-and-forth consultation and discussions of a case occur between mental health specialists and PCPs, with in-person follow-up as needed.
Several institutions offer programs to address the AACAP and AAP imperatives, most prominently the University of Washington, Seattle, and the University of Massachusetts, Worcester. Both offer resources on how to create an integrated care model (University of Washington AIMS Resource Center; The University of Massachusetts Center for Integrated Care).
What can one do in a busy pediatric primary care practice to address mental health imperatives on the individual provider level? Often PCPs can, as I do, offer families some resources by having a set of mental health handouts and resources. I have gathered useful handouts for families throughout my residency to use as shortcuts and visual aids to promote mental health. I use the AACAP Facts for Families for handouts on mental health diagnoses and topics. I use the National Sleep Foundation for its sleep hygiene tips. I also offer some low-cost mindfulness resources to help kids and parents with their anxiety, such as the Calm app and Headspace app. If parents have difficulty with access to parent management training (the first-line treatment to manage aggression in children), I often recommend “The Defiant Child: A Parent’s Guide to Oppositional Defiant Disorder” (Lanham, Md.: Taylor Trade Publishing, 1997), which shows how to create a rewards system in the home to promote positive behavior. “How to Talk So Kids Will Listen & Listen So Kids Will Talk” (New York: Scribner, 2012 ) is a beloved book for parents (and there is a teenager version) that I recommend when parents launch into questions about how to talk to kids and teens about difficult topics so that, ultimately, they can improve their relationship.
Dr. Pawlowski is an adult, adolescent, and child psychiatrist at the University of Vermont Medical Center and an assistant professor of psychiatry at UVM, both in Burlington. Email her at [email protected].
Resources
The AACAP website has materials to help clinicians develop a collaborative mental health care model in the primary care setting: Search for “collaboration with primary care.”
The journal Pediatrics also has a useful resource: Improving mental health services in primary care: Reducing administrative and financial barriers to access and collaboration. (2009;123;1248-51).
During my training as a child and adolescent psychiatry fellow, I “lived” down the hall from 10 other people just like me who had similar offices and training. Our pace was tailored to pediatric psychiatry. Appointments were 30 minutes or more. Our goal was to provide the most comprehensive mental health care for the families whom we grew to know and love.
The impetus to create an integrated mental health care approach has been well elucidated by the American Academy of Child and Adolescent Psychiatry (AACAP) in its report, Collaborative mental health care in pediatric primary care. It is based on some telling statistics: Fifty percent of all cases of mental illness begin before age 14 years and 75% begin by age 24. Half of all pediatric office visits involve behavioral, psychosocial, or educational concerns. The American Academy of Pediatrics’ Task Force on Mental Health similarly has stated that primary care clinicians can and should be able to provide mental health services to children and adolescents in a primary care setting.
Integrative psychiatry and primary care treatment comes in three forms: classic consultation, in which a specialist sees a patient and refers back to the PCP with recommendations; colocation, in which mental health specialists practice in the same office but essentially are “ships crossing in the night” with PCPs; and the most-lauded form, collaborative/integrative care, in which back-and-forth consultation and discussions of a case occur between mental health specialists and PCPs, with in-person follow-up as needed.
Several institutions offer programs to address the AACAP and AAP imperatives, most prominently the University of Washington, Seattle, and the University of Massachusetts, Worcester. Both offer resources on how to create an integrated care model (University of Washington AIMS Resource Center; The University of Massachusetts Center for Integrated Care).
What can one do in a busy pediatric primary care practice to address mental health imperatives on the individual provider level? Often PCPs can, as I do, offer families some resources by having a set of mental health handouts and resources. I have gathered useful handouts for families throughout my residency to use as shortcuts and visual aids to promote mental health. I use the AACAP Facts for Families for handouts on mental health diagnoses and topics. I use the National Sleep Foundation for its sleep hygiene tips. I also offer some low-cost mindfulness resources to help kids and parents with their anxiety, such as the Calm app and Headspace app. If parents have difficulty with access to parent management training (the first-line treatment to manage aggression in children), I often recommend “The Defiant Child: A Parent’s Guide to Oppositional Defiant Disorder” (Lanham, Md.: Taylor Trade Publishing, 1997), which shows how to create a rewards system in the home to promote positive behavior. “How to Talk So Kids Will Listen & Listen So Kids Will Talk” (New York: Scribner, 2012 ) is a beloved book for parents (and there is a teenager version) that I recommend when parents launch into questions about how to talk to kids and teens about difficult topics so that, ultimately, they can improve their relationship.
Dr. Pawlowski is an adult, adolescent, and child psychiatrist at the University of Vermont Medical Center and an assistant professor of psychiatry at UVM, both in Burlington. Email her at [email protected].
Resources
The AACAP website has materials to help clinicians develop a collaborative mental health care model in the primary care setting: Search for “collaboration with primary care.”
The journal Pediatrics also has a useful resource: Improving mental health services in primary care: Reducing administrative and financial barriers to access and collaboration. (2009;123;1248-51).
During my training as a child and adolescent psychiatry fellow, I “lived” down the hall from 10 other people just like me who had similar offices and training. Our pace was tailored to pediatric psychiatry. Appointments were 30 minutes or more. Our goal was to provide the most comprehensive mental health care for the families whom we grew to know and love.
The impetus to create an integrated mental health care approach has been well elucidated by the American Academy of Child and Adolescent Psychiatry (AACAP) in its report, Collaborative mental health care in pediatric primary care. It is based on some telling statistics: Fifty percent of all cases of mental illness begin before age 14 years and 75% begin by age 24. Half of all pediatric office visits involve behavioral, psychosocial, or educational concerns. The American Academy of Pediatrics’ Task Force on Mental Health similarly has stated that primary care clinicians can and should be able to provide mental health services to children and adolescents in a primary care setting.
Integrative psychiatry and primary care treatment comes in three forms: classic consultation, in which a specialist sees a patient and refers back to the PCP with recommendations; colocation, in which mental health specialists practice in the same office but essentially are “ships crossing in the night” with PCPs; and the most-lauded form, collaborative/integrative care, in which back-and-forth consultation and discussions of a case occur between mental health specialists and PCPs, with in-person follow-up as needed.
Several institutions offer programs to address the AACAP and AAP imperatives, most prominently the University of Washington, Seattle, and the University of Massachusetts, Worcester. Both offer resources on how to create an integrated care model (University of Washington AIMS Resource Center; The University of Massachusetts Center for Integrated Care).
What can one do in a busy pediatric primary care practice to address mental health imperatives on the individual provider level? Often PCPs can, as I do, offer families some resources by having a set of mental health handouts and resources. I have gathered useful handouts for families throughout my residency to use as shortcuts and visual aids to promote mental health. I use the AACAP Facts for Families for handouts on mental health diagnoses and topics. I use the National Sleep Foundation for its sleep hygiene tips. I also offer some low-cost mindfulness resources to help kids and parents with their anxiety, such as the Calm app and Headspace app. If parents have difficulty with access to parent management training (the first-line treatment to manage aggression in children), I often recommend “The Defiant Child: A Parent’s Guide to Oppositional Defiant Disorder” (Lanham, Md.: Taylor Trade Publishing, 1997), which shows how to create a rewards system in the home to promote positive behavior. “How to Talk So Kids Will Listen & Listen So Kids Will Talk” (New York: Scribner, 2012 ) is a beloved book for parents (and there is a teenager version) that I recommend when parents launch into questions about how to talk to kids and teens about difficult topics so that, ultimately, they can improve their relationship.
Dr. Pawlowski is an adult, adolescent, and child psychiatrist at the University of Vermont Medical Center and an assistant professor of psychiatry at UVM, both in Burlington. Email her at [email protected].
Resources
The AACAP website has materials to help clinicians develop a collaborative mental health care model in the primary care setting: Search for “collaboration with primary care.”
The journal Pediatrics also has a useful resource: Improving mental health services in primary care: Reducing administrative and financial barriers to access and collaboration. (2009;123;1248-51).
Anxiety disorders: Psychopharmacologic treatment update
Anxiety disorders, including separation anxiety disorder, social anxiety disorder, and generalized anxiety disorder, are some of the most common psychiatric conditions of childhood and adolescence, affecting up to 20% of youth.1 Patients commonly present with a mix of symptoms that often span multiple anxiety disorder diagnoses. While this pattern can present somewhat of a diagnostic conundrum, it can be reassuring to know that such constellations of symptoms are the rule rather than the exception. Further, given that both the pharmacologic and nonpharmacologic treatment strategies don’t change much among the various anxiety disorders, the lack of a definitive single diagnosis should not delay intervention. Be alert to the possibility that anxiety and anxiety disorders can be the engine that drives what on the surface appears to be more disruptive and oppositional behavior.
Although medications can be a useful part of treatment, they are not recommended as a stand-alone intervention. Nonpharmacologic treatments generally should be tried before medications are considered. Among the different types of psychotherapy, cognitive-behavioral therapy (CBT) has the most empirical support from research trials, although other modalities such as mindfulness-based treatments show some promise. As anxiety disorders often run in families, it also can be very useful to explore the possibility that one or more parents also struggle with an anxiety disorder, which, if untreated, might complicate the child’s course.
With regard to medications, it is being increasingly appreciated that, despite SSRIs being most popularly known as antidepressants, these medications actually may be as efficacious or even more efficacious in the management of anxiety disorders. This class remains the cornerstone of medication treatment, and a brief review of current options follows.
SSRIs and SNRIs
A 2015 meta-analysis that examined nine randomized controlled trials of SSRIs and serotonin and norepinephrine reuptake inhibitors (SNRIs) for pediatric anxiety disorders concluded that these agents provided a benefit of modest effect size. No significant increase in treatment-emergent suicidality was found, and the medications were generally well tolerated.2 This analysis also found some evidence that greater efficacy was related to a medication with more specific serotonergic properties, suggesting improved response with “true” SSRIs versus SNRIs such as venlafaxine and duloxetine. One major study using sertraline found that, at least in the short term, combined use of sertraline with CBT resulted in better efficacy than either treatment alone.3 Dosing of SSRIs should start low: A general rule is to begin at half of the smallest dosage made, depending on the age and size of the patient. One question that often comes up after a successful trial is how long to continue the medications. A recent meta-analysis in adults concluded that there was evidence that stopping medication prior to 1 year resulted in an increased risk of relapse with little to guide clinicians after that 1-year mark.4
Benzodiazepines
Even though benzodiazepines have been around for a long time, data supporting their efficacy and safety in pediatric populations remain extremely limited, and what has been reported has not been particularly positive. Thus, most experts do not suggest using benzodiazepines for anxiety disorders, with the exception of helping children through single or rare events, such as medical procedures or enabling an adolescent who has been fearful of attending school to get to the building on the first day back after a long absence.
Guanfacine
In a recent exploratory trial of guanfacine for children with mixed anxiety disorders,5 the medication was well tolerated overall but did not result in statistically significant improvement relative to placebo on primary anxiety rating scales. However, a higher number of children were rated as improved on a clinician-rated scale. This medication is usually started at 0.5 mg/day and increased as tolerated, while checking vital signs, to a maximum of 4 mg/day.
Atomoxetine
A randomized control trial of pediatric patients with both ADHD and an anxiety disorder showed reductions in both symptom domains with atomoxetine dosed at an average of 1.3 mg/kg per day.6 There is little evidence to suggest its use in primary anxiety disorders without comorbid ADHD.
Buspirone
This 5-hydroxytryptamine 1a agonist has Food and Drug Administration approval for generalized anxiety disorder in adults and is generally well tolerated. Unfortunately, two randomized controlled studies in children and adolescents did not find statistically significant improvement relative to placebo, although some methodological problems may have played a role.7
Antipsychotics
Although sometimes used to augment an SSRI in adult anxiety disorders, there are little data to support the use of antipsychotics in pediatric populations, especially given the antecedent risks of the drugs.
Summary
Pharmacotherapy for anxiety disorders often includes the advice that, if medications are indicated in conjunction with psychotherapy, to start with an SSRI; and if that is not effective to try a different one.7 An SNRI such as venlafaxine or duloxetine may then be a third-line alternative, although for youth with comorbid ADHD, consideration of either atomoxetine or guanfacine is also reasonable. Beyond that point, there unfortunately are little systematic data to guide pharmacologic decision making, and increased potential risks of other classes of medications suggest the need for caution and consultation.
Looking for more mental health training? Attend the 12th annual Child Psychiatry in Primary Care conference in Burlington, on May 4, 2018,organized by the University of Vermont with Dr. Rettew as course director. Go to http://www.med.uvm.edu/cme/conferences.
References
1. Merikangas KR et al. J Am Acad Child Adolesc Psychiatry. 2010 Oct;49(10):980-9.
2. Strawn JR et al. Depress Anxiety. 2015 Mar;32(3):149-57.
3. Walkup J et al. N Engl J Med. 2008 Dec 25;359(26):2753-66.
4. Batelaan N et al. BMJ. 2017 Sep 13;358:j3927.
5. Strawn JR et al. J Child Adolesc Psychopharm. 2017 Feb;27(1): 29-37..
6. Geller D et al. J Am Acad Child Adolesc Psychiatry. 2007 Sep;46(9):1119-27.
7. Strawn JR et al. J Child Adolesc Psychopharm. 2017 Feb;28(1): 2-9.
Anxiety disorders, including separation anxiety disorder, social anxiety disorder, and generalized anxiety disorder, are some of the most common psychiatric conditions of childhood and adolescence, affecting up to 20% of youth.1 Patients commonly present with a mix of symptoms that often span multiple anxiety disorder diagnoses. While this pattern can present somewhat of a diagnostic conundrum, it can be reassuring to know that such constellations of symptoms are the rule rather than the exception. Further, given that both the pharmacologic and nonpharmacologic treatment strategies don’t change much among the various anxiety disorders, the lack of a definitive single diagnosis should not delay intervention. Be alert to the possibility that anxiety and anxiety disorders can be the engine that drives what on the surface appears to be more disruptive and oppositional behavior.
Although medications can be a useful part of treatment, they are not recommended as a stand-alone intervention. Nonpharmacologic treatments generally should be tried before medications are considered. Among the different types of psychotherapy, cognitive-behavioral therapy (CBT) has the most empirical support from research trials, although other modalities such as mindfulness-based treatments show some promise. As anxiety disorders often run in families, it also can be very useful to explore the possibility that one or more parents also struggle with an anxiety disorder, which, if untreated, might complicate the child’s course.
With regard to medications, it is being increasingly appreciated that, despite SSRIs being most popularly known as antidepressants, these medications actually may be as efficacious or even more efficacious in the management of anxiety disorders. This class remains the cornerstone of medication treatment, and a brief review of current options follows.
SSRIs and SNRIs
A 2015 meta-analysis that examined nine randomized controlled trials of SSRIs and serotonin and norepinephrine reuptake inhibitors (SNRIs) for pediatric anxiety disorders concluded that these agents provided a benefit of modest effect size. No significant increase in treatment-emergent suicidality was found, and the medications were generally well tolerated.2 This analysis also found some evidence that greater efficacy was related to a medication with more specific serotonergic properties, suggesting improved response with “true” SSRIs versus SNRIs such as venlafaxine and duloxetine. One major study using sertraline found that, at least in the short term, combined use of sertraline with CBT resulted in better efficacy than either treatment alone.3 Dosing of SSRIs should start low: A general rule is to begin at half of the smallest dosage made, depending on the age and size of the patient. One question that often comes up after a successful trial is how long to continue the medications. A recent meta-analysis in adults concluded that there was evidence that stopping medication prior to 1 year resulted in an increased risk of relapse with little to guide clinicians after that 1-year mark.4
Benzodiazepines
Even though benzodiazepines have been around for a long time, data supporting their efficacy and safety in pediatric populations remain extremely limited, and what has been reported has not been particularly positive. Thus, most experts do not suggest using benzodiazepines for anxiety disorders, with the exception of helping children through single or rare events, such as medical procedures or enabling an adolescent who has been fearful of attending school to get to the building on the first day back after a long absence.
Guanfacine
In a recent exploratory trial of guanfacine for children with mixed anxiety disorders,5 the medication was well tolerated overall but did not result in statistically significant improvement relative to placebo on primary anxiety rating scales. However, a higher number of children were rated as improved on a clinician-rated scale. This medication is usually started at 0.5 mg/day and increased as tolerated, while checking vital signs, to a maximum of 4 mg/day.
Atomoxetine
A randomized control trial of pediatric patients with both ADHD and an anxiety disorder showed reductions in both symptom domains with atomoxetine dosed at an average of 1.3 mg/kg per day.6 There is little evidence to suggest its use in primary anxiety disorders without comorbid ADHD.
Buspirone
This 5-hydroxytryptamine 1a agonist has Food and Drug Administration approval for generalized anxiety disorder in adults and is generally well tolerated. Unfortunately, two randomized controlled studies in children and adolescents did not find statistically significant improvement relative to placebo, although some methodological problems may have played a role.7
Antipsychotics
Although sometimes used to augment an SSRI in adult anxiety disorders, there are little data to support the use of antipsychotics in pediatric populations, especially given the antecedent risks of the drugs.
Summary
Pharmacotherapy for anxiety disorders often includes the advice that, if medications are indicated in conjunction with psychotherapy, to start with an SSRI; and if that is not effective to try a different one.7 An SNRI such as venlafaxine or duloxetine may then be a third-line alternative, although for youth with comorbid ADHD, consideration of either atomoxetine or guanfacine is also reasonable. Beyond that point, there unfortunately are little systematic data to guide pharmacologic decision making, and increased potential risks of other classes of medications suggest the need for caution and consultation.
Looking for more mental health training? Attend the 12th annual Child Psychiatry in Primary Care conference in Burlington, on May 4, 2018,organized by the University of Vermont with Dr. Rettew as course director. Go to http://www.med.uvm.edu/cme/conferences.
References
1. Merikangas KR et al. J Am Acad Child Adolesc Psychiatry. 2010 Oct;49(10):980-9.
2. Strawn JR et al. Depress Anxiety. 2015 Mar;32(3):149-57.
3. Walkup J et al. N Engl J Med. 2008 Dec 25;359(26):2753-66.
4. Batelaan N et al. BMJ. 2017 Sep 13;358:j3927.
5. Strawn JR et al. J Child Adolesc Psychopharm. 2017 Feb;27(1): 29-37..
6. Geller D et al. J Am Acad Child Adolesc Psychiatry. 2007 Sep;46(9):1119-27.
7. Strawn JR et al. J Child Adolesc Psychopharm. 2017 Feb;28(1): 2-9.
Anxiety disorders, including separation anxiety disorder, social anxiety disorder, and generalized anxiety disorder, are some of the most common psychiatric conditions of childhood and adolescence, affecting up to 20% of youth.1 Patients commonly present with a mix of symptoms that often span multiple anxiety disorder diagnoses. While this pattern can present somewhat of a diagnostic conundrum, it can be reassuring to know that such constellations of symptoms are the rule rather than the exception. Further, given that both the pharmacologic and nonpharmacologic treatment strategies don’t change much among the various anxiety disorders, the lack of a definitive single diagnosis should not delay intervention. Be alert to the possibility that anxiety and anxiety disorders can be the engine that drives what on the surface appears to be more disruptive and oppositional behavior.
Although medications can be a useful part of treatment, they are not recommended as a stand-alone intervention. Nonpharmacologic treatments generally should be tried before medications are considered. Among the different types of psychotherapy, cognitive-behavioral therapy (CBT) has the most empirical support from research trials, although other modalities such as mindfulness-based treatments show some promise. As anxiety disorders often run in families, it also can be very useful to explore the possibility that one or more parents also struggle with an anxiety disorder, which, if untreated, might complicate the child’s course.
With regard to medications, it is being increasingly appreciated that, despite SSRIs being most popularly known as antidepressants, these medications actually may be as efficacious or even more efficacious in the management of anxiety disorders. This class remains the cornerstone of medication treatment, and a brief review of current options follows.
SSRIs and SNRIs
A 2015 meta-analysis that examined nine randomized controlled trials of SSRIs and serotonin and norepinephrine reuptake inhibitors (SNRIs) for pediatric anxiety disorders concluded that these agents provided a benefit of modest effect size. No significant increase in treatment-emergent suicidality was found, and the medications were generally well tolerated.2 This analysis also found some evidence that greater efficacy was related to a medication with more specific serotonergic properties, suggesting improved response with “true” SSRIs versus SNRIs such as venlafaxine and duloxetine. One major study using sertraline found that, at least in the short term, combined use of sertraline with CBT resulted in better efficacy than either treatment alone.3 Dosing of SSRIs should start low: A general rule is to begin at half of the smallest dosage made, depending on the age and size of the patient. One question that often comes up after a successful trial is how long to continue the medications. A recent meta-analysis in adults concluded that there was evidence that stopping medication prior to 1 year resulted in an increased risk of relapse with little to guide clinicians after that 1-year mark.4
Benzodiazepines
Even though benzodiazepines have been around for a long time, data supporting their efficacy and safety in pediatric populations remain extremely limited, and what has been reported has not been particularly positive. Thus, most experts do not suggest using benzodiazepines for anxiety disorders, with the exception of helping children through single or rare events, such as medical procedures or enabling an adolescent who has been fearful of attending school to get to the building on the first day back after a long absence.
Guanfacine
In a recent exploratory trial of guanfacine for children with mixed anxiety disorders,5 the medication was well tolerated overall but did not result in statistically significant improvement relative to placebo on primary anxiety rating scales. However, a higher number of children were rated as improved on a clinician-rated scale. This medication is usually started at 0.5 mg/day and increased as tolerated, while checking vital signs, to a maximum of 4 mg/day.
Atomoxetine
A randomized control trial of pediatric patients with both ADHD and an anxiety disorder showed reductions in both symptom domains with atomoxetine dosed at an average of 1.3 mg/kg per day.6 There is little evidence to suggest its use in primary anxiety disorders without comorbid ADHD.
Buspirone
This 5-hydroxytryptamine 1a agonist has Food and Drug Administration approval for generalized anxiety disorder in adults and is generally well tolerated. Unfortunately, two randomized controlled studies in children and adolescents did not find statistically significant improvement relative to placebo, although some methodological problems may have played a role.7
Antipsychotics
Although sometimes used to augment an SSRI in adult anxiety disorders, there are little data to support the use of antipsychotics in pediatric populations, especially given the antecedent risks of the drugs.
Summary
Pharmacotherapy for anxiety disorders often includes the advice that, if medications are indicated in conjunction with psychotherapy, to start with an SSRI; and if that is not effective to try a different one.7 An SNRI such as venlafaxine or duloxetine may then be a third-line alternative, although for youth with comorbid ADHD, consideration of either atomoxetine or guanfacine is also reasonable. Beyond that point, there unfortunately are little systematic data to guide pharmacologic decision making, and increased potential risks of other classes of medications suggest the need for caution and consultation.
Looking for more mental health training? Attend the 12th annual Child Psychiatry in Primary Care conference in Burlington, on May 4, 2018,organized by the University of Vermont with Dr. Rettew as course director. Go to http://www.med.uvm.edu/cme/conferences.
References
1. Merikangas KR et al. J Am Acad Child Adolesc Psychiatry. 2010 Oct;49(10):980-9.
2. Strawn JR et al. Depress Anxiety. 2015 Mar;32(3):149-57.
3. Walkup J et al. N Engl J Med. 2008 Dec 25;359(26):2753-66.
4. Batelaan N et al. BMJ. 2017 Sep 13;358:j3927.
5. Strawn JR et al. J Child Adolesc Psychopharm. 2017 Feb;27(1): 29-37..
6. Geller D et al. J Am Acad Child Adolesc Psychiatry. 2007 Sep;46(9):1119-27.
7. Strawn JR et al. J Child Adolesc Psychopharm. 2017 Feb;28(1): 2-9.
When cannabis use becomes another disorder
Despite the justified concern about rising opiate use in the United States, cannabis remains the most commonly used substance in the 12- to 17-year-old population.1 Cannabis use is widespread, particularly in states in which it has been decriminalized or legalized. While use of alcohol and nicotine has fallen among high school students from the years 2010 to 2015, marijuana use has remained relatively constant.2 In addition, the potency of cannabis with regard to tetrahydrocannabinol (THC) content has increased over the years. Despite the common belief among the public that cannabis use is benign, accumulating research is revealing a number of concerning consequences, especially in vulnerable populations and those who use cannabis regularly.
Case summary
Case discussion
Treatment for these adverse effects of cannabis is cessation of the drug. This can be accomplished through hard work with a counselor, who may recommend any of a number of treatments, including contingency management, cognitive behavioral therapy, systematic multidimensional family therapy, and motivational enhancement therapy, among others.5 While common lore is that it is impossible to stop cannabis use, the effect sizes of these treatments is in the moderate to large range. There are viable options to stop cannabis use, especially when it becomes problematic.
Dr. Althoff is associate professor of psychiatry, psychology, and pediatrics at the University of Vermont, Burlington. He is director of the division of behavioral genetics and conducts research on the development of self-regulation in children. Email him at [email protected].
References
1. “Results from the 2013 National Survey on Drug Use and Health: Summary of National Findings,” Substance Abuse and Mental Health Services Administration Center for Behavioral Health Statistics and Quality, 2013.
2. “Monitoring the Future Survey, 2015,” National Institute on Drug Abuse.
3. Pharmaceuticals (Basel). 2012 Jul;5(7):719-26.
4. Nat Rev Neurosci. 2007 Nov;8(11):885-95.
5. Dtsch Arztebl Int. 2016 Sep;113(39): 653-9.
Despite the justified concern about rising opiate use in the United States, cannabis remains the most commonly used substance in the 12- to 17-year-old population.1 Cannabis use is widespread, particularly in states in which it has been decriminalized or legalized. While use of alcohol and nicotine has fallen among high school students from the years 2010 to 2015, marijuana use has remained relatively constant.2 In addition, the potency of cannabis with regard to tetrahydrocannabinol (THC) content has increased over the years. Despite the common belief among the public that cannabis use is benign, accumulating research is revealing a number of concerning consequences, especially in vulnerable populations and those who use cannabis regularly.
Case summary
Case discussion
Treatment for these adverse effects of cannabis is cessation of the drug. This can be accomplished through hard work with a counselor, who may recommend any of a number of treatments, including contingency management, cognitive behavioral therapy, systematic multidimensional family therapy, and motivational enhancement therapy, among others.5 While common lore is that it is impossible to stop cannabis use, the effect sizes of these treatments is in the moderate to large range. There are viable options to stop cannabis use, especially when it becomes problematic.
Dr. Althoff is associate professor of psychiatry, psychology, and pediatrics at the University of Vermont, Burlington. He is director of the division of behavioral genetics and conducts research on the development of self-regulation in children. Email him at [email protected].
References
1. “Results from the 2013 National Survey on Drug Use and Health: Summary of National Findings,” Substance Abuse and Mental Health Services Administration Center for Behavioral Health Statistics and Quality, 2013.
2. “Monitoring the Future Survey, 2015,” National Institute on Drug Abuse.
3. Pharmaceuticals (Basel). 2012 Jul;5(7):719-26.
4. Nat Rev Neurosci. 2007 Nov;8(11):885-95.
5. Dtsch Arztebl Int. 2016 Sep;113(39): 653-9.
Despite the justified concern about rising opiate use in the United States, cannabis remains the most commonly used substance in the 12- to 17-year-old population.1 Cannabis use is widespread, particularly in states in which it has been decriminalized or legalized. While use of alcohol and nicotine has fallen among high school students from the years 2010 to 2015, marijuana use has remained relatively constant.2 In addition, the potency of cannabis with regard to tetrahydrocannabinol (THC) content has increased over the years. Despite the common belief among the public that cannabis use is benign, accumulating research is revealing a number of concerning consequences, especially in vulnerable populations and those who use cannabis regularly.
Case summary
Case discussion
Treatment for these adverse effects of cannabis is cessation of the drug. This can be accomplished through hard work with a counselor, who may recommend any of a number of treatments, including contingency management, cognitive behavioral therapy, systematic multidimensional family therapy, and motivational enhancement therapy, among others.5 While common lore is that it is impossible to stop cannabis use, the effect sizes of these treatments is in the moderate to large range. There are viable options to stop cannabis use, especially when it becomes problematic.
Dr. Althoff is associate professor of psychiatry, psychology, and pediatrics at the University of Vermont, Burlington. He is director of the division of behavioral genetics and conducts research on the development of self-regulation in children. Email him at [email protected].
References
1. “Results from the 2013 National Survey on Drug Use and Health: Summary of National Findings,” Substance Abuse and Mental Health Services Administration Center for Behavioral Health Statistics and Quality, 2013.
2. “Monitoring the Future Survey, 2015,” National Institute on Drug Abuse.
3. Pharmaceuticals (Basel). 2012 Jul;5(7):719-26.
4. Nat Rev Neurosci. 2007 Nov;8(11):885-95.
5. Dtsch Arztebl Int. 2016 Sep;113(39): 653-9.
ADHD and the role of wellness
ADHD is a very common disorder with several medication treatment options. There also are wellness and parenting strategies that can address aspects of the challenges of ADHD that are not perfectly covered by medication, such as excess symptoms, times of day that are not covered, or oppositional behavior that often develops secondarily.
Case summary
James is a 6-year-old boy who has been an active, high-energy child since preschool. He has had difficulty with wiggling around in kindergarten and preschool, talking excessively, and being unable to follow directions and pay attention. He is impulsive, disruptive, and frequently doesn’t listen to what his parents tell him to do. Parents and teachers rank him in the clinical range for hyperactivity, impulsivity, and attention problems on standardized rating scales.
Discussion
When we first discuss a new diagnosis with a family, we have the opportunity to shape the family’s expectations about that diagnosis and how it should be addressed. When I discuss ADHD with a new family, I want them to understand the symptoms of inattention, hyperactivity, and impulsiveness, and that these symptoms are not the child’s fault, but rather related to the way his brain is connected. At the same time, I also emphasize that these connections are not entirely fixed, that they mature over time, and that they are affected by experiences in life. In particular, I stress that positive experiences and wellness activities can influence the brain in a positive way. While, of course, I discuss the range of medications that can address these issues, I also deal with wellness in the treatment plan.
Exercise
Studies in humans and animals have provided background evidence that exercise increases the release of neurotransmitters such as dopamine and norepinephrine that are important in the pathophysiology of ADHD. Cerillo-Urbina et al. did a meta-analysis in 2015 of randomized controlled trials and found medium to large effect sizes for a variety of physical activity programs with respect to attention, hyperactivity, and impulsivity, although the study quality was generally low.1 Clearly we need additional more rigorous studies, but given the positive direction of outcomes, the lack of side effects, and the many other positive effects of exercise, it does not seem too soon to add exercise as a prescription for our patients with ADHD. I review this evidence with families, ask them about physical activity they like, and ask if they are willing to work toward an hour of exercise a day.
Sleep
Many children with ADHD have problems with sleep even before they start on stimulant medications, which can further affect sleep. Addressing sleep early on can improve ADHD symptoms, as well as help parents change or avoid patterns like having children fall asleep to the sound of a television. Brief sleep hygiene and cognitive-behavioral therapy interventions over three visits were demonstrated in a randomized controlled trial by Hisock et al. to improve ADHD symptoms and behavioral function.2 These psychosocial interventions clearly are the first line in addressing sleep problems in ADHD, and can benefit even sleep problems connected to medication.
Parent training
Treatment plan
1. Have the child exercise 1 hour every day. Have fun!
2. Establish a nightly bedtime routine, with a bath at 7:30 p.m., brushing of teeth, a story, and lights out at 8 with no TV in the room.
3. Check out the CHADD website for Parent to Parent.
4. Start a trial of stimulant medication.
5. Return in 2 weeks to monitor these interventions, adjust goals, and adjust medications.
When to refer
Many parents will be able to put such a plan in motion with your support and that of other parents. If they are struggling, therapists, psychologists, and psychiatrists trained in motivational and behavioral methods can provide more individualized parent training. Also consider whether the parents themselves may have ADHD and could use referral and treatment.
Dr. Hall is assistant professor of psychiatry and pediatrics at the University of Vermont, Burlington. She said she had no relevant financial disclosures.
References
1. Child Care Health Dev. 2015 Nov;41(6):779-88.
2. BMJ. 2015. doi: 10.1136/bmj.h68.
ADHD is a very common disorder with several medication treatment options. There also are wellness and parenting strategies that can address aspects of the challenges of ADHD that are not perfectly covered by medication, such as excess symptoms, times of day that are not covered, or oppositional behavior that often develops secondarily.
Case summary
James is a 6-year-old boy who has been an active, high-energy child since preschool. He has had difficulty with wiggling around in kindergarten and preschool, talking excessively, and being unable to follow directions and pay attention. He is impulsive, disruptive, and frequently doesn’t listen to what his parents tell him to do. Parents and teachers rank him in the clinical range for hyperactivity, impulsivity, and attention problems on standardized rating scales.
Discussion
When we first discuss a new diagnosis with a family, we have the opportunity to shape the family’s expectations about that diagnosis and how it should be addressed. When I discuss ADHD with a new family, I want them to understand the symptoms of inattention, hyperactivity, and impulsiveness, and that these symptoms are not the child’s fault, but rather related to the way his brain is connected. At the same time, I also emphasize that these connections are not entirely fixed, that they mature over time, and that they are affected by experiences in life. In particular, I stress that positive experiences and wellness activities can influence the brain in a positive way. While, of course, I discuss the range of medications that can address these issues, I also deal with wellness in the treatment plan.
Exercise
Studies in humans and animals have provided background evidence that exercise increases the release of neurotransmitters such as dopamine and norepinephrine that are important in the pathophysiology of ADHD. Cerillo-Urbina et al. did a meta-analysis in 2015 of randomized controlled trials and found medium to large effect sizes for a variety of physical activity programs with respect to attention, hyperactivity, and impulsivity, although the study quality was generally low.1 Clearly we need additional more rigorous studies, but given the positive direction of outcomes, the lack of side effects, and the many other positive effects of exercise, it does not seem too soon to add exercise as a prescription for our patients with ADHD. I review this evidence with families, ask them about physical activity they like, and ask if they are willing to work toward an hour of exercise a day.
Sleep
Many children with ADHD have problems with sleep even before they start on stimulant medications, which can further affect sleep. Addressing sleep early on can improve ADHD symptoms, as well as help parents change or avoid patterns like having children fall asleep to the sound of a television. Brief sleep hygiene and cognitive-behavioral therapy interventions over three visits were demonstrated in a randomized controlled trial by Hisock et al. to improve ADHD symptoms and behavioral function.2 These psychosocial interventions clearly are the first line in addressing sleep problems in ADHD, and can benefit even sleep problems connected to medication.
Parent training
Treatment plan
1. Have the child exercise 1 hour every day. Have fun!
2. Establish a nightly bedtime routine, with a bath at 7:30 p.m., brushing of teeth, a story, and lights out at 8 with no TV in the room.
3. Check out the CHADD website for Parent to Parent.
4. Start a trial of stimulant medication.
5. Return in 2 weeks to monitor these interventions, adjust goals, and adjust medications.
When to refer
Many parents will be able to put such a plan in motion with your support and that of other parents. If they are struggling, therapists, psychologists, and psychiatrists trained in motivational and behavioral methods can provide more individualized parent training. Also consider whether the parents themselves may have ADHD and could use referral and treatment.
Dr. Hall is assistant professor of psychiatry and pediatrics at the University of Vermont, Burlington. She said she had no relevant financial disclosures.
References
1. Child Care Health Dev. 2015 Nov;41(6):779-88.
2. BMJ. 2015. doi: 10.1136/bmj.h68.
ADHD is a very common disorder with several medication treatment options. There also are wellness and parenting strategies that can address aspects of the challenges of ADHD that are not perfectly covered by medication, such as excess symptoms, times of day that are not covered, or oppositional behavior that often develops secondarily.
Case summary
James is a 6-year-old boy who has been an active, high-energy child since preschool. He has had difficulty with wiggling around in kindergarten and preschool, talking excessively, and being unable to follow directions and pay attention. He is impulsive, disruptive, and frequently doesn’t listen to what his parents tell him to do. Parents and teachers rank him in the clinical range for hyperactivity, impulsivity, and attention problems on standardized rating scales.
Discussion
When we first discuss a new diagnosis with a family, we have the opportunity to shape the family’s expectations about that diagnosis and how it should be addressed. When I discuss ADHD with a new family, I want them to understand the symptoms of inattention, hyperactivity, and impulsiveness, and that these symptoms are not the child’s fault, but rather related to the way his brain is connected. At the same time, I also emphasize that these connections are not entirely fixed, that they mature over time, and that they are affected by experiences in life. In particular, I stress that positive experiences and wellness activities can influence the brain in a positive way. While, of course, I discuss the range of medications that can address these issues, I also deal with wellness in the treatment plan.
Exercise
Studies in humans and animals have provided background evidence that exercise increases the release of neurotransmitters such as dopamine and norepinephrine that are important in the pathophysiology of ADHD. Cerillo-Urbina et al. did a meta-analysis in 2015 of randomized controlled trials and found medium to large effect sizes for a variety of physical activity programs with respect to attention, hyperactivity, and impulsivity, although the study quality was generally low.1 Clearly we need additional more rigorous studies, but given the positive direction of outcomes, the lack of side effects, and the many other positive effects of exercise, it does not seem too soon to add exercise as a prescription for our patients with ADHD. I review this evidence with families, ask them about physical activity they like, and ask if they are willing to work toward an hour of exercise a day.
Sleep
Many children with ADHD have problems with sleep even before they start on stimulant medications, which can further affect sleep. Addressing sleep early on can improve ADHD symptoms, as well as help parents change or avoid patterns like having children fall asleep to the sound of a television. Brief sleep hygiene and cognitive-behavioral therapy interventions over three visits were demonstrated in a randomized controlled trial by Hisock et al. to improve ADHD symptoms and behavioral function.2 These psychosocial interventions clearly are the first line in addressing sleep problems in ADHD, and can benefit even sleep problems connected to medication.
Parent training
Treatment plan
1. Have the child exercise 1 hour every day. Have fun!
2. Establish a nightly bedtime routine, with a bath at 7:30 p.m., brushing of teeth, a story, and lights out at 8 with no TV in the room.
3. Check out the CHADD website for Parent to Parent.
4. Start a trial of stimulant medication.
5. Return in 2 weeks to monitor these interventions, adjust goals, and adjust medications.
When to refer
Many parents will be able to put such a plan in motion with your support and that of other parents. If they are struggling, therapists, psychologists, and psychiatrists trained in motivational and behavioral methods can provide more individualized parent training. Also consider whether the parents themselves may have ADHD and could use referral and treatment.
Dr. Hall is assistant professor of psychiatry and pediatrics at the University of Vermont, Burlington. She said she had no relevant financial disclosures.
References
1. Child Care Health Dev. 2015 Nov;41(6):779-88.
2. BMJ. 2015. doi: 10.1136/bmj.h68.
Consider the siblings
Robert is a 5-year-old boy who presents for an autism diagnostic evaluation accompanied by his parents, who report longstanding concerns about their son’s communication difficulties. Robert has an older brother who has been diagnosed with an autism spectrum disorder (ASD). Robert’s caregivers have noticed his tendency to “copy cat” others and often repeat phrases from television or movies. Robert and his family provided additional history and, after a multidisciplinary evaluation, he was diagnosed as fitting the criteria for ASD. Our team spoke with Robert’s parents about their impressions and recommendations and further explored the family history and ways in which the family functions. Robert lives with his parents and four siblings (one older and three younger, including a set of fraternal twins), most of whom display language impairments and difficulties with emotional regulation, as well. Robert’s mother also discloses that she is pregnant again. “Where do we go from here?” Robert’s mother wonders. “Our family is already so affected by autism, should I be worried about the other children?”
Discussion
It’s well established that genetic factors play a significant role in the etiology of autism spectrum disorders, other neurodevelopmental disorders, and a vast array of mental health problems. Although quite complicated and multifactorial, heritability estimates garnered from twin studies for autism range up to well above 50%1, and although finding specific genetic causes of nonsyndromic autism is the exception to the rule, chromosomal microarray analysis (CMA) is recommended as a first-line genetic test for those with autism. Recent literature has shown that molecular diagnoses of ASD are found in about 9% of the population studied2, and families should be aware that genetic testing can potentially help make decisions about clinical management and can inform discussions about recurrence risk.
Families should be made aware that sibling recurrence rates of autism have been found to be around 20 times higher than the prevalence within the general population3. Certainly having one child with autism can afford a significant risk for parents having another child with the same disorder, and researchers are learning more about the influence of gender on such risk4. Curiously, siblings born after an older sister with autism seem to have a higher risk of ASD than if they were born after an older brother with autism. The authors of this study note, however, that even for those with the highest risk (younger brothers with an older sister with autism had about a 17% probability of recurrence), odds are they will be unaffected by autism. Complicating matters is the notion of the broad autism phenotype (BAP – denoting those who may have features of autism but do not reach diagnostic threshold) with literature indicating at least one BAP trait was found in about 50% of family members of those with ASD5.
In addition, autism also may share genetic vulnerabilities with other conditions – parental psychiatric diagnoses have been found to increase the risk for ASD in their children, and ASD frequently co-occurs with a constellation of other disorders – including anxiety disorders, intellectual disabilities, ADHD, and learning problems. This information can be helpful to clinicians when they speak with parents about the complicated nature of psychiatric and developmental disorders, and how such disorders can affect the family not only biologically, but through dynamic environmental means, as well. , including parents and siblings6. Data clearly indicate that, if a child carries an autism diagnosis, engaging family in family-based treatment, prevention, surveillance/screening, and general supportive interventions are critical in promoting positive outcomes.
Children and adolescents with ASD are a remarkably heterogeneous group with variable family dynamics; clinically, it’s not uncommon to meet parents from all backgrounds who speak eloquently about the stress they face raising a child with any neurodevelopmental disorder. This stress has been well documented in several scientific articles over the past decade (for mothers more so than fathers) but other family members (for example, typically developing siblings) undoubtedly experience similar stress, but this has been less robustly researched. Literature has, in fact, revealed that children who develop typically and who reside with a sibling who has a disability are more likely (compared with siblings living with other typically developing siblings) to have problems related to interpersonal relationships, school functioning, and use of leisure time7. Undeniably, complicated interactions with one’s functional profile, the quality of a sibling’s symptoms, parental stress, and other variables (parental marital status, birth order, presence of parental depression, available sources of support, etc.) are noted, and clearly, autism’s effects can extend far beyond the “identified patient.”
It’s important to note, however, that not all effects are negative. Siblings can demonstrate positive adjustments when growing up with a brother or sister who has autism. While siblings encounter unique demands (missing out on certain outings, feeling embarrassed by a brother’s social behaviors, having to “take care” of their brother, “why can’t we be a normal family?”), these demands can produce benefits, and parents should be aware that negative effects on siblings are far from inevitable. Siblings actually may show increased empathy, more sophisticated coping skills, and an advanced appreciation for those with developmental challenges, compared with most of their peers. Typically developing siblings can serve not only as a social and play partner for their family member with ASD (fostering social competencies), but also the individual with ASD can serve a positive role in influencing the development of those without ASD8.
All things considered, talking with families about the impact of autism on parents and siblings can be complicated but should focus on the positives while being realistic about potential challenges. It is important to inform families about the risk of recurrence and about the stress that autism can create on siblings while you are assessing a family’s functioning and care-giving burdens. Ultimately, this can help you determine how to offer them the most appropriate, evidence-based, and family-focused care.
Dr. Dickerson, a child and adolescent psychiatrist, is an assistant professor of psychiatry at the University of Vermont, Burlington, where he is director of the autism diagnostic clinic. Email him at [email protected].
References
1. J Child Psychol Psychiatry. 2016 May;57(5):585-95.
2. JAMA. 2015;314(9):895-903.
3. Child Adolesc Psychiatr Clin N Am. 2017 Jul;26(3):555-70.
4. (JAMA Pediatr. 2017 Sep 25. doi: 10.1001/jamapediatrics.2017.2832).
5. J Autism Dev Disord. 2007 Mar; 37(3):523-36.
6. JAMA Psychiatry. 2016;73(6):622-9.
7. Pediatrics. 2013. doi: 10.1542/peds.2013-0644.
Robert is a 5-year-old boy who presents for an autism diagnostic evaluation accompanied by his parents, who report longstanding concerns about their son’s communication difficulties. Robert has an older brother who has been diagnosed with an autism spectrum disorder (ASD). Robert’s caregivers have noticed his tendency to “copy cat” others and often repeat phrases from television or movies. Robert and his family provided additional history and, after a multidisciplinary evaluation, he was diagnosed as fitting the criteria for ASD. Our team spoke with Robert’s parents about their impressions and recommendations and further explored the family history and ways in which the family functions. Robert lives with his parents and four siblings (one older and three younger, including a set of fraternal twins), most of whom display language impairments and difficulties with emotional regulation, as well. Robert’s mother also discloses that she is pregnant again. “Where do we go from here?” Robert’s mother wonders. “Our family is already so affected by autism, should I be worried about the other children?”
Discussion
It’s well established that genetic factors play a significant role in the etiology of autism spectrum disorders, other neurodevelopmental disorders, and a vast array of mental health problems. Although quite complicated and multifactorial, heritability estimates garnered from twin studies for autism range up to well above 50%1, and although finding specific genetic causes of nonsyndromic autism is the exception to the rule, chromosomal microarray analysis (CMA) is recommended as a first-line genetic test for those with autism. Recent literature has shown that molecular diagnoses of ASD are found in about 9% of the population studied2, and families should be aware that genetic testing can potentially help make decisions about clinical management and can inform discussions about recurrence risk.
Families should be made aware that sibling recurrence rates of autism have been found to be around 20 times higher than the prevalence within the general population3. Certainly having one child with autism can afford a significant risk for parents having another child with the same disorder, and researchers are learning more about the influence of gender on such risk4. Curiously, siblings born after an older sister with autism seem to have a higher risk of ASD than if they were born after an older brother with autism. The authors of this study note, however, that even for those with the highest risk (younger brothers with an older sister with autism had about a 17% probability of recurrence), odds are they will be unaffected by autism. Complicating matters is the notion of the broad autism phenotype (BAP – denoting those who may have features of autism but do not reach diagnostic threshold) with literature indicating at least one BAP trait was found in about 50% of family members of those with ASD5.
In addition, autism also may share genetic vulnerabilities with other conditions – parental psychiatric diagnoses have been found to increase the risk for ASD in their children, and ASD frequently co-occurs with a constellation of other disorders – including anxiety disorders, intellectual disabilities, ADHD, and learning problems. This information can be helpful to clinicians when they speak with parents about the complicated nature of psychiatric and developmental disorders, and how such disorders can affect the family not only biologically, but through dynamic environmental means, as well. , including parents and siblings6. Data clearly indicate that, if a child carries an autism diagnosis, engaging family in family-based treatment, prevention, surveillance/screening, and general supportive interventions are critical in promoting positive outcomes.
Children and adolescents with ASD are a remarkably heterogeneous group with variable family dynamics; clinically, it’s not uncommon to meet parents from all backgrounds who speak eloquently about the stress they face raising a child with any neurodevelopmental disorder. This stress has been well documented in several scientific articles over the past decade (for mothers more so than fathers) but other family members (for example, typically developing siblings) undoubtedly experience similar stress, but this has been less robustly researched. Literature has, in fact, revealed that children who develop typically and who reside with a sibling who has a disability are more likely (compared with siblings living with other typically developing siblings) to have problems related to interpersonal relationships, school functioning, and use of leisure time7. Undeniably, complicated interactions with one’s functional profile, the quality of a sibling’s symptoms, parental stress, and other variables (parental marital status, birth order, presence of parental depression, available sources of support, etc.) are noted, and clearly, autism’s effects can extend far beyond the “identified patient.”
It’s important to note, however, that not all effects are negative. Siblings can demonstrate positive adjustments when growing up with a brother or sister who has autism. While siblings encounter unique demands (missing out on certain outings, feeling embarrassed by a brother’s social behaviors, having to “take care” of their brother, “why can’t we be a normal family?”), these demands can produce benefits, and parents should be aware that negative effects on siblings are far from inevitable. Siblings actually may show increased empathy, more sophisticated coping skills, and an advanced appreciation for those with developmental challenges, compared with most of their peers. Typically developing siblings can serve not only as a social and play partner for their family member with ASD (fostering social competencies), but also the individual with ASD can serve a positive role in influencing the development of those without ASD8.
All things considered, talking with families about the impact of autism on parents and siblings can be complicated but should focus on the positives while being realistic about potential challenges. It is important to inform families about the risk of recurrence and about the stress that autism can create on siblings while you are assessing a family’s functioning and care-giving burdens. Ultimately, this can help you determine how to offer them the most appropriate, evidence-based, and family-focused care.
Dr. Dickerson, a child and adolescent psychiatrist, is an assistant professor of psychiatry at the University of Vermont, Burlington, where he is director of the autism diagnostic clinic. Email him at [email protected].
References
1. J Child Psychol Psychiatry. 2016 May;57(5):585-95.
2. JAMA. 2015;314(9):895-903.
3. Child Adolesc Psychiatr Clin N Am. 2017 Jul;26(3):555-70.
4. (JAMA Pediatr. 2017 Sep 25. doi: 10.1001/jamapediatrics.2017.2832).
5. J Autism Dev Disord. 2007 Mar; 37(3):523-36.
6. JAMA Psychiatry. 2016;73(6):622-9.
7. Pediatrics. 2013. doi: 10.1542/peds.2013-0644.
Robert is a 5-year-old boy who presents for an autism diagnostic evaluation accompanied by his parents, who report longstanding concerns about their son’s communication difficulties. Robert has an older brother who has been diagnosed with an autism spectrum disorder (ASD). Robert’s caregivers have noticed his tendency to “copy cat” others and often repeat phrases from television or movies. Robert and his family provided additional history and, after a multidisciplinary evaluation, he was diagnosed as fitting the criteria for ASD. Our team spoke with Robert’s parents about their impressions and recommendations and further explored the family history and ways in which the family functions. Robert lives with his parents and four siblings (one older and three younger, including a set of fraternal twins), most of whom display language impairments and difficulties with emotional regulation, as well. Robert’s mother also discloses that she is pregnant again. “Where do we go from here?” Robert’s mother wonders. “Our family is already so affected by autism, should I be worried about the other children?”
Discussion
It’s well established that genetic factors play a significant role in the etiology of autism spectrum disorders, other neurodevelopmental disorders, and a vast array of mental health problems. Although quite complicated and multifactorial, heritability estimates garnered from twin studies for autism range up to well above 50%1, and although finding specific genetic causes of nonsyndromic autism is the exception to the rule, chromosomal microarray analysis (CMA) is recommended as a first-line genetic test for those with autism. Recent literature has shown that molecular diagnoses of ASD are found in about 9% of the population studied2, and families should be aware that genetic testing can potentially help make decisions about clinical management and can inform discussions about recurrence risk.
Families should be made aware that sibling recurrence rates of autism have been found to be around 20 times higher than the prevalence within the general population3. Certainly having one child with autism can afford a significant risk for parents having another child with the same disorder, and researchers are learning more about the influence of gender on such risk4. Curiously, siblings born after an older sister with autism seem to have a higher risk of ASD than if they were born after an older brother with autism. The authors of this study note, however, that even for those with the highest risk (younger brothers with an older sister with autism had about a 17% probability of recurrence), odds are they will be unaffected by autism. Complicating matters is the notion of the broad autism phenotype (BAP – denoting those who may have features of autism but do not reach diagnostic threshold) with literature indicating at least one BAP trait was found in about 50% of family members of those with ASD5.
In addition, autism also may share genetic vulnerabilities with other conditions – parental psychiatric diagnoses have been found to increase the risk for ASD in their children, and ASD frequently co-occurs with a constellation of other disorders – including anxiety disorders, intellectual disabilities, ADHD, and learning problems. This information can be helpful to clinicians when they speak with parents about the complicated nature of psychiatric and developmental disorders, and how such disorders can affect the family not only biologically, but through dynamic environmental means, as well. , including parents and siblings6. Data clearly indicate that, if a child carries an autism diagnosis, engaging family in family-based treatment, prevention, surveillance/screening, and general supportive interventions are critical in promoting positive outcomes.
Children and adolescents with ASD are a remarkably heterogeneous group with variable family dynamics; clinically, it’s not uncommon to meet parents from all backgrounds who speak eloquently about the stress they face raising a child with any neurodevelopmental disorder. This stress has been well documented in several scientific articles over the past decade (for mothers more so than fathers) but other family members (for example, typically developing siblings) undoubtedly experience similar stress, but this has been less robustly researched. Literature has, in fact, revealed that children who develop typically and who reside with a sibling who has a disability are more likely (compared with siblings living with other typically developing siblings) to have problems related to interpersonal relationships, school functioning, and use of leisure time7. Undeniably, complicated interactions with one’s functional profile, the quality of a sibling’s symptoms, parental stress, and other variables (parental marital status, birth order, presence of parental depression, available sources of support, etc.) are noted, and clearly, autism’s effects can extend far beyond the “identified patient.”
It’s important to note, however, that not all effects are negative. Siblings can demonstrate positive adjustments when growing up with a brother or sister who has autism. While siblings encounter unique demands (missing out on certain outings, feeling embarrassed by a brother’s social behaviors, having to “take care” of their brother, “why can’t we be a normal family?”), these demands can produce benefits, and parents should be aware that negative effects on siblings are far from inevitable. Siblings actually may show increased empathy, more sophisticated coping skills, and an advanced appreciation for those with developmental challenges, compared with most of their peers. Typically developing siblings can serve not only as a social and play partner for their family member with ASD (fostering social competencies), but also the individual with ASD can serve a positive role in influencing the development of those without ASD8.
All things considered, talking with families about the impact of autism on parents and siblings can be complicated but should focus on the positives while being realistic about potential challenges. It is important to inform families about the risk of recurrence and about the stress that autism can create on siblings while you are assessing a family’s functioning and care-giving burdens. Ultimately, this can help you determine how to offer them the most appropriate, evidence-based, and family-focused care.
Dr. Dickerson, a child and adolescent psychiatrist, is an assistant professor of psychiatry at the University of Vermont, Burlington, where he is director of the autism diagnostic clinic. Email him at [email protected].
References
1. J Child Psychol Psychiatry. 2016 May;57(5):585-95.
2. JAMA. 2015;314(9):895-903.
3. Child Adolesc Psychiatr Clin N Am. 2017 Jul;26(3):555-70.
4. (JAMA Pediatr. 2017 Sep 25. doi: 10.1001/jamapediatrics.2017.2832).
5. J Autism Dev Disord. 2007 Mar; 37(3):523-36.
6. JAMA Psychiatry. 2016;73(6):622-9.
7. Pediatrics. 2013. doi: 10.1542/peds.2013-0644.
Nature versus nurture: 50 years of a popular debate
This basic question has been debated at settings ranging from scientific conferences to dinner tables for many decades. The media also has covered it in forms ranging from documentaries to the popular comedy movie “Trading Places” (1983). Yet, despite so much attention and so much research devoted to resolving this timeless debate, the arguments continue to this day.
A lack of a clear answer, however, by no means implies that we have not made major advances in our understanding. This short review takes a look at the progression of this seemingly eternal question by categorizing the development of the nature versus nurture question into three main stages. While such a partitioning is somewhat oversimplified with regard to what the various positions on this issue have been at different times, it does illustrate the way that the debate has gradually evolved.
Part 1: Nature versus nurture
The origins of the nature versus nurture debate date back far beyond the past 50 years. The ancient Greek philosopher Galen postulated that personality traits were driven by the relative concentrations of four bodily fluids or “humours.” In 1874, Sir Francis Galton published “English Men of Science: Their Nature and Nurture,” in which he advanced his ideas about the dominance of hereditary factors in intelligence and character at the beginning of the eugenics movement.1 These ideas were in stark opposition to the perspective of earlier scholars, such as the philosopher John Locke, who popularized the theory that children are born a “blank slate” and from there develop their traits and intellectual abilities through their environment and experiences.
The other primary school of thought in the mid-1960s was psychoanalysis, which was based on the ideas of Sigmund Freud, MD. Psychoanalysis maintains that the way that unconscious sexual and aggressive drives were channeled through various defense mechanisms was of primary importance to the understanding of both psychopathology and typical human behavior.
While these two perspectives were often very much in opposition to each other, they shared in common the view that the environment and a person’s individual experiences, i.e. nurture, were the prevailing forces in development. In the background, more biologically oriented research and clinical work was slowly beginning to work its way into the field, especially at certain institutions, such as Washington University in St. Louis. Several medications of various types were then available, including chlorpromazine, imipramine, and diazepam.
Overall, however, it is probably fair to say that, 50 years ago, it was the nurture perspective that held the most sway since psychodynamic treatment and behaviorist research dominated, while the emerging fields of genetics and neuroscience were only beginning to take hold.
Part 2: Nature and nurture
From the 1970s to the end of the 20th century, a noticeable shift occurred as knowledge of the brain and genetics – supported by remarkable advances in research techniques – began to swing the pendulum back toward an increased appreciation of nature as a critical influence on a person’s thoughts, feelings, and behavior.
Researchers Stella Chess, MD, and Alexander Thomas, MD, for example, conducted the New York Longitudinal Study, in which they closely observed a group of young children over many years. Their studies compelled them to argue for the significance of more innate temperament traits as critical aspects of a youth’s overall adjustment.2 The Human Genome Project was launched in 1990, and the entire decade was designated as the “Decade of the Brain.” During this time, neuroscience research exploded as techniques, such as MRI and PET, allowed scientists to view the living brain like never before.
The type of research investigation that perhaps was most directly relevant to the nature-nurture debate and that became quite popular during this time was the twin study. By comparing the relative similarities among monozygotic and dizygotic twins raised in the same household, it became possible to calculate directly the degree to which a variable of interest (intelligence, height, aggressive behavior) could be attributed to genetic versus environmental factors. When it came to behavioral variables, a repeated finding that emerged was that both genetic and environmental influences are important, often at close to a 50/50 split in terms of magnitude.3,4 These studies were complemented by molecular genetic studies, which were beginning to be able to identify specific genes that conveyed usually small amounts of risk for a wide range of psychiatric disorders.
Yet, while twin studies and many other lines of research made it increasingly difficult to argue for the overwhelming supremacy of either nature or nurture, the two domains generally were treated as being independent of each other. Specific traits or symptoms in an individual often were thought of as being the result of either psychological (nurture) or biological (nature) causes. Terms such as “endogenous depression,” for example, were used to distinguish those who had symptoms that were thought generally to be out of reach for “psychological” treatments, such as psychotherapy. Looking back, it might be fair to say that one of the principle flaws in this perspective was the commonly held belief that, if something was brain based or biological, then it therefore implied a kind of automatic “wiring” of the brain that was generally driven by genes and beyond the influence of environmental factors.
Part 3: Nature is nurture (and vice versa)
As the science progressed, it became increasingly clear that the nature and nurture domains were hopelessly intertwined with one another. From early PET-scan studies showing that both medications and psychotherapy not only changed the brain but also did so in ways similar to behavioral-genetic studies showing how genetically influenced behaviors actually cause certain environmental events to be more likely to occur, research continued to demonstrate the bidirectional influences of genetic and environmental factors on development.5,6 This appreciation rose to even greater heights with advances in the field of epigenetics, which was able to document some of the specific mechanisms through which environmental factors cause genes involved in regulating the plasticity of the brain to turn on and off.7
In thinking through some of this complexity, however, it is important to remember the hopeful message that is contained in this rich understanding. All of these complicated, interacting genetic and environmental factors give us many avenues for positive intervention. Now we understand that not only might a medication help strengthen some of the brain connections needed to reduce and cope with that child’s anxiety, but so could mindfulness, exercise, and addressing his parents’ symptoms. When the families ask me whether their child’s struggles are behavioral or psychological, the answer I tend to give them is “yes.”
Dr. Rettew is a child and adolescent psychiatrist and associate professor of psychiatry and pediatrics at the University of Vermont, Burlington.
Email him at [email protected]. Follow him on Twitter @pedipsych.
References
1. “English Men of Science: Their Nature and Nurture” (London: MacMillan & Co., 1874)
2. “Temperament: Theory and Practice” (New York: Brunner/Mazel, 1996)
3. “Nature and Nurture during Infancy and Early Childhood” (New York: Cambridge University Press, 1988)
4. Nat Genet. 2015;47(7):702-9.
5. Arch Gen Psychiatry. 1992;49(9):681-9.
6. Dev Psychopathol. 1997 Spring;9(2):335-64.
7. JAMA Psychiatry. 2017;74(6):551-2.
This basic question has been debated at settings ranging from scientific conferences to dinner tables for many decades. The media also has covered it in forms ranging from documentaries to the popular comedy movie “Trading Places” (1983). Yet, despite so much attention and so much research devoted to resolving this timeless debate, the arguments continue to this day.
A lack of a clear answer, however, by no means implies that we have not made major advances in our understanding. This short review takes a look at the progression of this seemingly eternal question by categorizing the development of the nature versus nurture question into three main stages. While such a partitioning is somewhat oversimplified with regard to what the various positions on this issue have been at different times, it does illustrate the way that the debate has gradually evolved.
Part 1: Nature versus nurture
The origins of the nature versus nurture debate date back far beyond the past 50 years. The ancient Greek philosopher Galen postulated that personality traits were driven by the relative concentrations of four bodily fluids or “humours.” In 1874, Sir Francis Galton published “English Men of Science: Their Nature and Nurture,” in which he advanced his ideas about the dominance of hereditary factors in intelligence and character at the beginning of the eugenics movement.1 These ideas were in stark opposition to the perspective of earlier scholars, such as the philosopher John Locke, who popularized the theory that children are born a “blank slate” and from there develop their traits and intellectual abilities through their environment and experiences.
The other primary school of thought in the mid-1960s was psychoanalysis, which was based on the ideas of Sigmund Freud, MD. Psychoanalysis maintains that the way that unconscious sexual and aggressive drives were channeled through various defense mechanisms was of primary importance to the understanding of both psychopathology and typical human behavior.
While these two perspectives were often very much in opposition to each other, they shared in common the view that the environment and a person’s individual experiences, i.e. nurture, were the prevailing forces in development. In the background, more biologically oriented research and clinical work was slowly beginning to work its way into the field, especially at certain institutions, such as Washington University in St. Louis. Several medications of various types were then available, including chlorpromazine, imipramine, and diazepam.
Overall, however, it is probably fair to say that, 50 years ago, it was the nurture perspective that held the most sway since psychodynamic treatment and behaviorist research dominated, while the emerging fields of genetics and neuroscience were only beginning to take hold.
Part 2: Nature and nurture
From the 1970s to the end of the 20th century, a noticeable shift occurred as knowledge of the brain and genetics – supported by remarkable advances in research techniques – began to swing the pendulum back toward an increased appreciation of nature as a critical influence on a person’s thoughts, feelings, and behavior.
Researchers Stella Chess, MD, and Alexander Thomas, MD, for example, conducted the New York Longitudinal Study, in which they closely observed a group of young children over many years. Their studies compelled them to argue for the significance of more innate temperament traits as critical aspects of a youth’s overall adjustment.2 The Human Genome Project was launched in 1990, and the entire decade was designated as the “Decade of the Brain.” During this time, neuroscience research exploded as techniques, such as MRI and PET, allowed scientists to view the living brain like never before.
The type of research investigation that perhaps was most directly relevant to the nature-nurture debate and that became quite popular during this time was the twin study. By comparing the relative similarities among monozygotic and dizygotic twins raised in the same household, it became possible to calculate directly the degree to which a variable of interest (intelligence, height, aggressive behavior) could be attributed to genetic versus environmental factors. When it came to behavioral variables, a repeated finding that emerged was that both genetic and environmental influences are important, often at close to a 50/50 split in terms of magnitude.3,4 These studies were complemented by molecular genetic studies, which were beginning to be able to identify specific genes that conveyed usually small amounts of risk for a wide range of psychiatric disorders.
Yet, while twin studies and many other lines of research made it increasingly difficult to argue for the overwhelming supremacy of either nature or nurture, the two domains generally were treated as being independent of each other. Specific traits or symptoms in an individual often were thought of as being the result of either psychological (nurture) or biological (nature) causes. Terms such as “endogenous depression,” for example, were used to distinguish those who had symptoms that were thought generally to be out of reach for “psychological” treatments, such as psychotherapy. Looking back, it might be fair to say that one of the principle flaws in this perspective was the commonly held belief that, if something was brain based or biological, then it therefore implied a kind of automatic “wiring” of the brain that was generally driven by genes and beyond the influence of environmental factors.
Part 3: Nature is nurture (and vice versa)
As the science progressed, it became increasingly clear that the nature and nurture domains were hopelessly intertwined with one another. From early PET-scan studies showing that both medications and psychotherapy not only changed the brain but also did so in ways similar to behavioral-genetic studies showing how genetically influenced behaviors actually cause certain environmental events to be more likely to occur, research continued to demonstrate the bidirectional influences of genetic and environmental factors on development.5,6 This appreciation rose to even greater heights with advances in the field of epigenetics, which was able to document some of the specific mechanisms through which environmental factors cause genes involved in regulating the plasticity of the brain to turn on and off.7
In thinking through some of this complexity, however, it is important to remember the hopeful message that is contained in this rich understanding. All of these complicated, interacting genetic and environmental factors give us many avenues for positive intervention. Now we understand that not only might a medication help strengthen some of the brain connections needed to reduce and cope with that child’s anxiety, but so could mindfulness, exercise, and addressing his parents’ symptoms. When the families ask me whether their child’s struggles are behavioral or psychological, the answer I tend to give them is “yes.”
Dr. Rettew is a child and adolescent psychiatrist and associate professor of psychiatry and pediatrics at the University of Vermont, Burlington.
Email him at [email protected]. Follow him on Twitter @pedipsych.
References
1. “English Men of Science: Their Nature and Nurture” (London: MacMillan & Co., 1874)
2. “Temperament: Theory and Practice” (New York: Brunner/Mazel, 1996)
3. “Nature and Nurture during Infancy and Early Childhood” (New York: Cambridge University Press, 1988)
4. Nat Genet. 2015;47(7):702-9.
5. Arch Gen Psychiatry. 1992;49(9):681-9.
6. Dev Psychopathol. 1997 Spring;9(2):335-64.
7. JAMA Psychiatry. 2017;74(6):551-2.
This basic question has been debated at settings ranging from scientific conferences to dinner tables for many decades. The media also has covered it in forms ranging from documentaries to the popular comedy movie “Trading Places” (1983). Yet, despite so much attention and so much research devoted to resolving this timeless debate, the arguments continue to this day.
A lack of a clear answer, however, by no means implies that we have not made major advances in our understanding. This short review takes a look at the progression of this seemingly eternal question by categorizing the development of the nature versus nurture question into three main stages. While such a partitioning is somewhat oversimplified with regard to what the various positions on this issue have been at different times, it does illustrate the way that the debate has gradually evolved.
Part 1: Nature versus nurture
The origins of the nature versus nurture debate date back far beyond the past 50 years. The ancient Greek philosopher Galen postulated that personality traits were driven by the relative concentrations of four bodily fluids or “humours.” In 1874, Sir Francis Galton published “English Men of Science: Their Nature and Nurture,” in which he advanced his ideas about the dominance of hereditary factors in intelligence and character at the beginning of the eugenics movement.1 These ideas were in stark opposition to the perspective of earlier scholars, such as the philosopher John Locke, who popularized the theory that children are born a “blank slate” and from there develop their traits and intellectual abilities through their environment and experiences.
The other primary school of thought in the mid-1960s was psychoanalysis, which was based on the ideas of Sigmund Freud, MD. Psychoanalysis maintains that the way that unconscious sexual and aggressive drives were channeled through various defense mechanisms was of primary importance to the understanding of both psychopathology and typical human behavior.
While these two perspectives were often very much in opposition to each other, they shared in common the view that the environment and a person’s individual experiences, i.e. nurture, were the prevailing forces in development. In the background, more biologically oriented research and clinical work was slowly beginning to work its way into the field, especially at certain institutions, such as Washington University in St. Louis. Several medications of various types were then available, including chlorpromazine, imipramine, and diazepam.
Overall, however, it is probably fair to say that, 50 years ago, it was the nurture perspective that held the most sway since psychodynamic treatment and behaviorist research dominated, while the emerging fields of genetics and neuroscience were only beginning to take hold.
Part 2: Nature and nurture
From the 1970s to the end of the 20th century, a noticeable shift occurred as knowledge of the brain and genetics – supported by remarkable advances in research techniques – began to swing the pendulum back toward an increased appreciation of nature as a critical influence on a person’s thoughts, feelings, and behavior.
Researchers Stella Chess, MD, and Alexander Thomas, MD, for example, conducted the New York Longitudinal Study, in which they closely observed a group of young children over many years. Their studies compelled them to argue for the significance of more innate temperament traits as critical aspects of a youth’s overall adjustment.2 The Human Genome Project was launched in 1990, and the entire decade was designated as the “Decade of the Brain.” During this time, neuroscience research exploded as techniques, such as MRI and PET, allowed scientists to view the living brain like never before.
The type of research investigation that perhaps was most directly relevant to the nature-nurture debate and that became quite popular during this time was the twin study. By comparing the relative similarities among monozygotic and dizygotic twins raised in the same household, it became possible to calculate directly the degree to which a variable of interest (intelligence, height, aggressive behavior) could be attributed to genetic versus environmental factors. When it came to behavioral variables, a repeated finding that emerged was that both genetic and environmental influences are important, often at close to a 50/50 split in terms of magnitude.3,4 These studies were complemented by molecular genetic studies, which were beginning to be able to identify specific genes that conveyed usually small amounts of risk for a wide range of psychiatric disorders.
Yet, while twin studies and many other lines of research made it increasingly difficult to argue for the overwhelming supremacy of either nature or nurture, the two domains generally were treated as being independent of each other. Specific traits or symptoms in an individual often were thought of as being the result of either psychological (nurture) or biological (nature) causes. Terms such as “endogenous depression,” for example, were used to distinguish those who had symptoms that were thought generally to be out of reach for “psychological” treatments, such as psychotherapy. Looking back, it might be fair to say that one of the principle flaws in this perspective was the commonly held belief that, if something was brain based or biological, then it therefore implied a kind of automatic “wiring” of the brain that was generally driven by genes and beyond the influence of environmental factors.
Part 3: Nature is nurture (and vice versa)
As the science progressed, it became increasingly clear that the nature and nurture domains were hopelessly intertwined with one another. From early PET-scan studies showing that both medications and psychotherapy not only changed the brain but also did so in ways similar to behavioral-genetic studies showing how genetically influenced behaviors actually cause certain environmental events to be more likely to occur, research continued to demonstrate the bidirectional influences of genetic and environmental factors on development.5,6 This appreciation rose to even greater heights with advances in the field of epigenetics, which was able to document some of the specific mechanisms through which environmental factors cause genes involved in regulating the plasticity of the brain to turn on and off.7
In thinking through some of this complexity, however, it is important to remember the hopeful message that is contained in this rich understanding. All of these complicated, interacting genetic and environmental factors give us many avenues for positive intervention. Now we understand that not only might a medication help strengthen some of the brain connections needed to reduce and cope with that child’s anxiety, but so could mindfulness, exercise, and addressing his parents’ symptoms. When the families ask me whether their child’s struggles are behavioral or psychological, the answer I tend to give them is “yes.”
Dr. Rettew is a child and adolescent psychiatrist and associate professor of psychiatry and pediatrics at the University of Vermont, Burlington.
Email him at [email protected]. Follow him on Twitter @pedipsych.
References
1. “English Men of Science: Their Nature and Nurture” (London: MacMillan & Co., 1874)
2. “Temperament: Theory and Practice” (New York: Brunner/Mazel, 1996)
3. “Nature and Nurture during Infancy and Early Childhood” (New York: Cambridge University Press, 1988)
4. Nat Genet. 2015;47(7):702-9.
5. Arch Gen Psychiatry. 1992;49(9):681-9.
6. Dev Psychopathol. 1997 Spring;9(2):335-64.
7. JAMA Psychiatry. 2017;74(6):551-2.
Potential pitfalls of social media
Cassandra presents to the office anxious because of social media posts her peers have made regarding current events that she feels are inflammatory.
Jenna expresses suicidal thoughts in response to comments made by peers from several schools in the area about the nature of her friendship with a boy.
Social media was developed to increase connections between people, even despite geographic distances. It has helped create communities of people with similar interests or beliefs, as well as to help reconnect us with people. It can provide educational opportunities and enhance technical skills. These are all potential benefits, but risks exist as well.
Cyberbullying and harassment
Cyberbullying is defined as “willful and repeated harm inflicted through the use of computers, cell phones, or other electronic devices,” and can include sending denigrating messages or images.3 Studies have shown varying rates of victimization from cyberbullying, ranging from 6% to 72%, and perpetration ranging from 3% to 44%.4 Bullying in general has been associated with increased school drop-out rates, suicidal ideation, bringing weapons to school, and aggression. The sizable audience that social media can reach can amplify bullying’s impact.
Privacy concerns
Determining the appropriate amount of information to share and knowing that it is truly being shared with the person identified on the other end also can be a challenge. In addition, the digital footprint left by navigating different social media sites may have unforeseen effects on youth regarding inappropriate posts. They also may be particularly vulnerable to other predatory individuals. Other privacy concerns involve what information parents, guardians, or other family members may share online.
Addiction
While social media has the possible benefit of creating a broader social network, particularly for someone who may be anxious in more traditional settings, it also can reinforce isolation from “real-world” experiences and the sense that no one else “gets” him or her. Without knowing who is on the other end of the keyboard, tablet, or smartphone, it can be difficult to ascertain if others in the community are reinforcing maladaptive behaviors and further withdrawal.
Self esteem
Images promulgated online often are highly idealized and edited, and are meant to exhibit a specific point of view. Exposure to these images can have a negative impact on self-esteem.
Another study of preteen girls (10- to 12-year-olds) indicated that increased time spent on social media sites such as MySpace and Facebook led to greater internalization of a thin ideal, increased body image concerns, and decreased self-esteem.5 Further data suggest that youth who are in need of more mental health support may engage in increased amounts of social media use. In a Canadian study, daily use of more than 2 hours per day was associated with increased reports of emotional distress as well as suicidal ideation.6
So, given all of this information, how to address this in an appointment?
Dr. Strange is an assistant professor in the department of psychiatry at the University of Vermont Medical Center and University of Vermont Robert Larner College of Medicine, both in Burlington. She works with children and adolescents. She has no relevant financial disclosures.
Resources:
1. The Kaiser Family Foundation: Generation M2: Media in the Lives of 8- to 18-Year-Olds
2. The Pew Research Center: Internet & Technology, “Teens, Social Media and Technology Overview 2015.”
3. The Cyberbullying Research Center. Cyberbullying Fact Sheet 2009.
4. Cyberbullying: An Update and Synthesis of the Research, in “Cyberbullying Prevention and Response: Expert Perspectives,” (New York: Routledge, 2012, pp. 13-35).
5. J. Early Adolesc. 2014. Vol 34(5) 606-20.
6. Cyberpsychol Behav Soc Netw. 2015 Jul;18(7):380-5.
Cassandra presents to the office anxious because of social media posts her peers have made regarding current events that she feels are inflammatory.
Jenna expresses suicidal thoughts in response to comments made by peers from several schools in the area about the nature of her friendship with a boy.
Social media was developed to increase connections between people, even despite geographic distances. It has helped create communities of people with similar interests or beliefs, as well as to help reconnect us with people. It can provide educational opportunities and enhance technical skills. These are all potential benefits, but risks exist as well.
Cyberbullying and harassment
Cyberbullying is defined as “willful and repeated harm inflicted through the use of computers, cell phones, or other electronic devices,” and can include sending denigrating messages or images.3 Studies have shown varying rates of victimization from cyberbullying, ranging from 6% to 72%, and perpetration ranging from 3% to 44%.4 Bullying in general has been associated with increased school drop-out rates, suicidal ideation, bringing weapons to school, and aggression. The sizable audience that social media can reach can amplify bullying’s impact.
Privacy concerns
Determining the appropriate amount of information to share and knowing that it is truly being shared with the person identified on the other end also can be a challenge. In addition, the digital footprint left by navigating different social media sites may have unforeseen effects on youth regarding inappropriate posts. They also may be particularly vulnerable to other predatory individuals. Other privacy concerns involve what information parents, guardians, or other family members may share online.
Addiction
While social media has the possible benefit of creating a broader social network, particularly for someone who may be anxious in more traditional settings, it also can reinforce isolation from “real-world” experiences and the sense that no one else “gets” him or her. Without knowing who is on the other end of the keyboard, tablet, or smartphone, it can be difficult to ascertain if others in the community are reinforcing maladaptive behaviors and further withdrawal.
Self esteem
Images promulgated online often are highly idealized and edited, and are meant to exhibit a specific point of view. Exposure to these images can have a negative impact on self-esteem.
Another study of preteen girls (10- to 12-year-olds) indicated that increased time spent on social media sites such as MySpace and Facebook led to greater internalization of a thin ideal, increased body image concerns, and decreased self-esteem.5 Further data suggest that youth who are in need of more mental health support may engage in increased amounts of social media use. In a Canadian study, daily use of more than 2 hours per day was associated with increased reports of emotional distress as well as suicidal ideation.6
So, given all of this information, how to address this in an appointment?
Dr. Strange is an assistant professor in the department of psychiatry at the University of Vermont Medical Center and University of Vermont Robert Larner College of Medicine, both in Burlington. She works with children and adolescents. She has no relevant financial disclosures.
Resources:
1. The Kaiser Family Foundation: Generation M2: Media in the Lives of 8- to 18-Year-Olds
2. The Pew Research Center: Internet & Technology, “Teens, Social Media and Technology Overview 2015.”
3. The Cyberbullying Research Center. Cyberbullying Fact Sheet 2009.
4. Cyberbullying: An Update and Synthesis of the Research, in “Cyberbullying Prevention and Response: Expert Perspectives,” (New York: Routledge, 2012, pp. 13-35).
5. J. Early Adolesc. 2014. Vol 34(5) 606-20.
6. Cyberpsychol Behav Soc Netw. 2015 Jul;18(7):380-5.
Cassandra presents to the office anxious because of social media posts her peers have made regarding current events that she feels are inflammatory.
Jenna expresses suicidal thoughts in response to comments made by peers from several schools in the area about the nature of her friendship with a boy.
Social media was developed to increase connections between people, even despite geographic distances. It has helped create communities of people with similar interests or beliefs, as well as to help reconnect us with people. It can provide educational opportunities and enhance technical skills. These are all potential benefits, but risks exist as well.
Cyberbullying and harassment
Cyberbullying is defined as “willful and repeated harm inflicted through the use of computers, cell phones, or other electronic devices,” and can include sending denigrating messages or images.3 Studies have shown varying rates of victimization from cyberbullying, ranging from 6% to 72%, and perpetration ranging from 3% to 44%.4 Bullying in general has been associated with increased school drop-out rates, suicidal ideation, bringing weapons to school, and aggression. The sizable audience that social media can reach can amplify bullying’s impact.
Privacy concerns
Determining the appropriate amount of information to share and knowing that it is truly being shared with the person identified on the other end also can be a challenge. In addition, the digital footprint left by navigating different social media sites may have unforeseen effects on youth regarding inappropriate posts. They also may be particularly vulnerable to other predatory individuals. Other privacy concerns involve what information parents, guardians, or other family members may share online.
Addiction
While social media has the possible benefit of creating a broader social network, particularly for someone who may be anxious in more traditional settings, it also can reinforce isolation from “real-world” experiences and the sense that no one else “gets” him or her. Without knowing who is on the other end of the keyboard, tablet, or smartphone, it can be difficult to ascertain if others in the community are reinforcing maladaptive behaviors and further withdrawal.
Self esteem
Images promulgated online often are highly idealized and edited, and are meant to exhibit a specific point of view. Exposure to these images can have a negative impact on self-esteem.
Another study of preteen girls (10- to 12-year-olds) indicated that increased time spent on social media sites such as MySpace and Facebook led to greater internalization of a thin ideal, increased body image concerns, and decreased self-esteem.5 Further data suggest that youth who are in need of more mental health support may engage in increased amounts of social media use. In a Canadian study, daily use of more than 2 hours per day was associated with increased reports of emotional distress as well as suicidal ideation.6
So, given all of this information, how to address this in an appointment?
Dr. Strange is an assistant professor in the department of psychiatry at the University of Vermont Medical Center and University of Vermont Robert Larner College of Medicine, both in Burlington. She works with children and adolescents. She has no relevant financial disclosures.
Resources:
1. The Kaiser Family Foundation: Generation M2: Media in the Lives of 8- to 18-Year-Olds
2. The Pew Research Center: Internet & Technology, “Teens, Social Media and Technology Overview 2015.”
3. The Cyberbullying Research Center. Cyberbullying Fact Sheet 2009.
4. Cyberbullying: An Update and Synthesis of the Research, in “Cyberbullying Prevention and Response: Expert Perspectives,” (New York: Routledge, 2012, pp. 13-35).
5. J. Early Adolesc. 2014. Vol 34(5) 606-20.
6. Cyberpsychol Behav Soc Netw. 2015 Jul;18(7):380-5.
Prenatal SSRI exposure’s effect on development
Unfortunately, the bottom line for most of these important questions is that we really don’t know as much as we probably should.
Just when we’ve read a convincing finding from a reputable journal that establishes a link between prenatal SSRI use and an untoward outcome, we see it disputed the next month. Why is this always happening, and why can’t we really know anything with certainty? Much of the confusion can be attributed to research methods and the obvious difficulty of using randomized, controlled trials to control for potential confounding factors. While statistical techniques have become increasingly sophisticated in addressing these confounding factors, they remain imperfect. For example, one of the most difficult challenges that remains is separating any effects of a medication from any effects caused by the condition it was designed to treat. Comparing women with the same underlying condition, some of whom are treated with a medication and some of whom are not, is a step forward, but there may be important reasons that one group decides to seek treatment and the other doesn’t. One clever research design that was employed to look at congenital anomalies in the offspring of women taking SSRIs accounted for siblings of these children who were born when their mother was not taking an SSRI. This study demonstrated that these women were more likely to have children with congenital malformations even when they weren’t taking the SSRIs.1 Other factors that render this literature difficult to interpret include small sample sizes when looking at specific SSRIs (many studies cluster them all), dose effects, timing (which trimester), duration of treatment, and method of recording compliance.
The potential link between SSRIs and autism has received a fair amount of attention lately, especially after a very well-designed study in 2016 suggested a significantly increased risk.10 However, as with many of the findings, this study was quickly disputed by other high-quality, well-powered research that found no increased risk after controlling for maternal illness.11,12
ADHD generally has not been found to be related to maternal SSRI use, although one study did find a link between ADHD and tricyclic antidepressants.12,13
In terms of other neurodevelopmental outcomes, there have been many negative studies examining IQ, nonverbal communication, as well as speech and motor skills.14,15,16 However, as with so many other outcomes, some other studies contradict these negative results. According to a recent, large cohort study, there may be some concern regarding SSRI exposure prenatally and an increase in speech disorders by age 14 years, as well as lower language competence at age 3 years.17,18 Likewise, mild motor abnormalities have been observed, with maternal depression severity as an independent but contributing factor.19
Several studies demonstrate a connection between prenatal SSRI exposure and childhood internalizing symptoms, such as depression and anxiety, independent of maternal depression.12,20 These findings must be balanced with our knowledge of the serious mental health conditions in offspring that are associated with untreated maternal illness, including both internalizing and externalizing disorders.21,22
How does one come to any firm conclusions to guide a primary care clinician’s practice and recommendations? Hopefully, the evidence will become clearer over time as we adopt more sophisticated designs and accumulate observations. A larger number of observations would allow us to decrease heterogeneity by studying subgroups according to type of SSRI and duration of exposure. Enhanced understanding of the role of genetic factors also may shed some light on individual variation as the serotonin transporter gene has been suggested as a potential moderator of sensitivity.23
Dr. Guth is an assistant professor in the department of psychiatry at the University of Vermont Medical Center and the University of Vermont Robert Larner College of Medicine, both in Burlington. She works with children and adolescents as well as women in the perinatal period. She has no relevant financial disclosures.
References
1. BMJ. 2015 Apr 17;350:h1798.
2. Can J Clin Pharmacol. 2009 Winter;16(1):e66-7.
3. J Matern Fetal Neonatal Med. 2008 Oct;21(10):745-51.
4. PLoS ONE. 2014 Nov; 9(11): e111327.
5. Pediatr Res. 2017 Jun 30. doi: 10.1038/pr.2017.156. [Epub ahead of print].
6. J Clin Psychiatry. 2017 May;78(5):605-11.
7. Acta Psychiatr Scand. 2010 Jun;121(6):471-9.
8. Am J Psychiatry. 2016 Feb 1;173(2):147-57.
9. J Perinatol. 2011 Sep;31(9):615-20.
10. JAMA Pediatr. 2016 Feb;170(2):117-24.
11. JAMA. 2017 Apr 18;317(15):1544-52.
12. J Am Acad Child Adolesc Psychiatry. 2016 May;55(5):359-66.
13. Paediatr Perinat Epidemiol. 2017 Jul;31(4):363-73.
14. Acta Obstet Gynecol Scand. 2015 May;94(5):501-7.
15. J Psychopharmacol. 2017 Mar;31(3):346-55.
16. CNS Drugs. 2005;19(7):623-33.
17. JAMA Psychiatry. 2016 Nov 1;73(11):1163-70.
18. BJOG. 2014. doi: 10.1111/1471-0528.12821.
19. BJOG. 2016 Nov;123(12):1908-17.
20. Pediatr Res. 2015 Aug;78(2):174-80.
21. Neuroscience. 2017 Feb 7;342:154-66.
22. Depress Anxiety. 2014 Jan;31(1):9-18.
23. Neuroscience. 2017 Feb 7;342:212-31.
Unfortunately, the bottom line for most of these important questions is that we really don’t know as much as we probably should.
Just when we’ve read a convincing finding from a reputable journal that establishes a link between prenatal SSRI use and an untoward outcome, we see it disputed the next month. Why is this always happening, and why can’t we really know anything with certainty? Much of the confusion can be attributed to research methods and the obvious difficulty of using randomized, controlled trials to control for potential confounding factors. While statistical techniques have become increasingly sophisticated in addressing these confounding factors, they remain imperfect. For example, one of the most difficult challenges that remains is separating any effects of a medication from any effects caused by the condition it was designed to treat. Comparing women with the same underlying condition, some of whom are treated with a medication and some of whom are not, is a step forward, but there may be important reasons that one group decides to seek treatment and the other doesn’t. One clever research design that was employed to look at congenital anomalies in the offspring of women taking SSRIs accounted for siblings of these children who were born when their mother was not taking an SSRI. This study demonstrated that these women were more likely to have children with congenital malformations even when they weren’t taking the SSRIs.1 Other factors that render this literature difficult to interpret include small sample sizes when looking at specific SSRIs (many studies cluster them all), dose effects, timing (which trimester), duration of treatment, and method of recording compliance.
The potential link between SSRIs and autism has received a fair amount of attention lately, especially after a very well-designed study in 2016 suggested a significantly increased risk.10 However, as with many of the findings, this study was quickly disputed by other high-quality, well-powered research that found no increased risk after controlling for maternal illness.11,12
ADHD generally has not been found to be related to maternal SSRI use, although one study did find a link between ADHD and tricyclic antidepressants.12,13
In terms of other neurodevelopmental outcomes, there have been many negative studies examining IQ, nonverbal communication, as well as speech and motor skills.14,15,16 However, as with so many other outcomes, some other studies contradict these negative results. According to a recent, large cohort study, there may be some concern regarding SSRI exposure prenatally and an increase in speech disorders by age 14 years, as well as lower language competence at age 3 years.17,18 Likewise, mild motor abnormalities have been observed, with maternal depression severity as an independent but contributing factor.19
Several studies demonstrate a connection between prenatal SSRI exposure and childhood internalizing symptoms, such as depression and anxiety, independent of maternal depression.12,20 These findings must be balanced with our knowledge of the serious mental health conditions in offspring that are associated with untreated maternal illness, including both internalizing and externalizing disorders.21,22
How does one come to any firm conclusions to guide a primary care clinician’s practice and recommendations? Hopefully, the evidence will become clearer over time as we adopt more sophisticated designs and accumulate observations. A larger number of observations would allow us to decrease heterogeneity by studying subgroups according to type of SSRI and duration of exposure. Enhanced understanding of the role of genetic factors also may shed some light on individual variation as the serotonin transporter gene has been suggested as a potential moderator of sensitivity.23
Dr. Guth is an assistant professor in the department of psychiatry at the University of Vermont Medical Center and the University of Vermont Robert Larner College of Medicine, both in Burlington. She works with children and adolescents as well as women in the perinatal period. She has no relevant financial disclosures.
References
1. BMJ. 2015 Apr 17;350:h1798.
2. Can J Clin Pharmacol. 2009 Winter;16(1):e66-7.
3. J Matern Fetal Neonatal Med. 2008 Oct;21(10):745-51.
4. PLoS ONE. 2014 Nov; 9(11): e111327.
5. Pediatr Res. 2017 Jun 30. doi: 10.1038/pr.2017.156. [Epub ahead of print].
6. J Clin Psychiatry. 2017 May;78(5):605-11.
7. Acta Psychiatr Scand. 2010 Jun;121(6):471-9.
8. Am J Psychiatry. 2016 Feb 1;173(2):147-57.
9. J Perinatol. 2011 Sep;31(9):615-20.
10. JAMA Pediatr. 2016 Feb;170(2):117-24.
11. JAMA. 2017 Apr 18;317(15):1544-52.
12. J Am Acad Child Adolesc Psychiatry. 2016 May;55(5):359-66.
13. Paediatr Perinat Epidemiol. 2017 Jul;31(4):363-73.
14. Acta Obstet Gynecol Scand. 2015 May;94(5):501-7.
15. J Psychopharmacol. 2017 Mar;31(3):346-55.
16. CNS Drugs. 2005;19(7):623-33.
17. JAMA Psychiatry. 2016 Nov 1;73(11):1163-70.
18. BJOG. 2014. doi: 10.1111/1471-0528.12821.
19. BJOG. 2016 Nov;123(12):1908-17.
20. Pediatr Res. 2015 Aug;78(2):174-80.
21. Neuroscience. 2017 Feb 7;342:154-66.
22. Depress Anxiety. 2014 Jan;31(1):9-18.
23. Neuroscience. 2017 Feb 7;342:212-31.
Unfortunately, the bottom line for most of these important questions is that we really don’t know as much as we probably should.
Just when we’ve read a convincing finding from a reputable journal that establishes a link between prenatal SSRI use and an untoward outcome, we see it disputed the next month. Why is this always happening, and why can’t we really know anything with certainty? Much of the confusion can be attributed to research methods and the obvious difficulty of using randomized, controlled trials to control for potential confounding factors. While statistical techniques have become increasingly sophisticated in addressing these confounding factors, they remain imperfect. For example, one of the most difficult challenges that remains is separating any effects of a medication from any effects caused by the condition it was designed to treat. Comparing women with the same underlying condition, some of whom are treated with a medication and some of whom are not, is a step forward, but there may be important reasons that one group decides to seek treatment and the other doesn’t. One clever research design that was employed to look at congenital anomalies in the offspring of women taking SSRIs accounted for siblings of these children who were born when their mother was not taking an SSRI. This study demonstrated that these women were more likely to have children with congenital malformations even when they weren’t taking the SSRIs.1 Other factors that render this literature difficult to interpret include small sample sizes when looking at specific SSRIs (many studies cluster them all), dose effects, timing (which trimester), duration of treatment, and method of recording compliance.
The potential link between SSRIs and autism has received a fair amount of attention lately, especially after a very well-designed study in 2016 suggested a significantly increased risk.10 However, as with many of the findings, this study was quickly disputed by other high-quality, well-powered research that found no increased risk after controlling for maternal illness.11,12
ADHD generally has not been found to be related to maternal SSRI use, although one study did find a link between ADHD and tricyclic antidepressants.12,13
In terms of other neurodevelopmental outcomes, there have been many negative studies examining IQ, nonverbal communication, as well as speech and motor skills.14,15,16 However, as with so many other outcomes, some other studies contradict these negative results. According to a recent, large cohort study, there may be some concern regarding SSRI exposure prenatally and an increase in speech disorders by age 14 years, as well as lower language competence at age 3 years.17,18 Likewise, mild motor abnormalities have been observed, with maternal depression severity as an independent but contributing factor.19
Several studies demonstrate a connection between prenatal SSRI exposure and childhood internalizing symptoms, such as depression and anxiety, independent of maternal depression.12,20 These findings must be balanced with our knowledge of the serious mental health conditions in offspring that are associated with untreated maternal illness, including both internalizing and externalizing disorders.21,22
How does one come to any firm conclusions to guide a primary care clinician’s practice and recommendations? Hopefully, the evidence will become clearer over time as we adopt more sophisticated designs and accumulate observations. A larger number of observations would allow us to decrease heterogeneity by studying subgroups according to type of SSRI and duration of exposure. Enhanced understanding of the role of genetic factors also may shed some light on individual variation as the serotonin transporter gene has been suggested as a potential moderator of sensitivity.23
Dr. Guth is an assistant professor in the department of psychiatry at the University of Vermont Medical Center and the University of Vermont Robert Larner College of Medicine, both in Burlington. She works with children and adolescents as well as women in the perinatal period. She has no relevant financial disclosures.
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