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.
Katie is a 14-year-old girl diagnosed with morbid obesity, hypertension, ADHD, and binge-eating disorder. She is taking lisinopril, methylphenidate ER, and diphenhydramine. She has been in residential treatment to address overeating, and her parents report that, since she has returned home, they are very anxious about her eating behavior. Katie, however, presents less concern about eating, but rather identifies sleep difficulties, school performance, and family tension as priorities.
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 Given the general prevalence of mental health conditions, a psychiatric screening interview is prudent in any patient presenting with sleep difficulties.
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, .
Returning to Katie’s story, careful assessment revealed no evidence for active ADHD or binge eating, but instead, a significant predisposition to anxiety and high levels of intrafamilial hostility. In keeping with Katie’s own goals, we discussed ways to improve sleep and maintain school performance, while looking for opportunities to decrease family discord. Her methylphenidate ER was tapered to reduce early insomnia. The possibility of tolerance to diphenhydramine and its side effects, including increased appetite, led to a plan to taper this medication while titrating citalopram, one of the more soporific SSRIs, to reduce worry thoughts that might disrupt sleep onset. Education was provided about the circadian shift in adolescence that leads to later bedtimes and rising times with an ongoing need for about 8 hours of sleep nightly. Her behavior plan addressed increased daytime exercise, meditation as part of a pre-bedtime routine, and meeting with a nutritionist to regulate dietary variety and portion sizes without a focus on weight loss. Individual and family therapy were recommended, and Katie seemed to benefit from support and learning to talk back to her anxious automatic thoughts.
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
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.
