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Transcript
Sleep in Children with Neurodevelopmental Disorders: What Can We Do in the Community Setting? SHHCC Sleep(y) Rounds October 22, 2009 Judith Owens MD MPH Alpert Medical School of Brown University Disclosures Grants: Shire, Boehringer-Ingleheim Speakers Bureau: Lilly, Shire Consultant/Advisory Board: Lilly, Shire, Isis Biopolymer, Sanofi-Aventis The material presented in this lecture has no relationship with any of these potential conflicts Off-label use of medications will be discussed Objectives Summarize common sleep issues in children with various neurodevelopmental disorders Attention Deficit Hyperactivity Disorder (ADHD)/Tourette Syndrome (TS) Autism Spectrum Disorders (ASD) Syndromes: Down, Prader-Willi, Angelman, Williams, Smith-Magenis Provide general clinical recommendations for managing sleep problems in these populations ADHD: Background Most common childhood psychiatric condition Affects 3-5% (8-10% school-aged; 3-6% adults) ADHD subtypes Predominantly hyperactive-impulsive (<15%) Predominantly inattentive (20-30%) Combined subtype (50-75%) M:F 4:1 (hyperactive/impulsive); 2:1 (Inattentive); 9:1 (clinical pop) 60% of patients diagnosed in childhood continue to exhibit symptoms into adulthood Sleep in ADHD: Subjective Measures Measure observations of sleep behavior in naturalistic settings (sleep quantity/quality, sleep problems, symptoms sleep disorders (ie, SDB, RLS) Parent surveys/interviews, sleep diaries, self-report Sleep problems in 25-50% Increase in wide variety sleep problems compared to healthy and psychiatric control groups; more night-to-night variability More problematic evening/bedtime behavior Increase snoring, bruxism, parasomnias, enuresis, PLMs Sleep in ADHD: Actigraphy Measures sleep patterns in naturalistic settings over time SOL, TIB, SE, NW (frequency, duration), MT, SD Actigraphy: No consistent differences in ADHD/controls sleep onset latency, duration Variable increased nocturnal activity, awakenings ADHD Increased night-to-night variability No differences by ADHD severity, subtype, ODD Inconsistent med-related differences Sleep Measures in ADHD What factors potentially account for the discrepancies between subjective and objective findings regarding sleep in children with ADHD? Parental perception of sleep problems may be heightened Evening behavior may be qualitatively different Clinicians may have decreased threshold for identifying sleep problems Parents may be primed to report sleep problems concomitant with ADHD medication PSG, actigraphy, parent report measure different sleep parameters Summary: PSG in ADHD Meta-analysis PLMs only significant effect size overall (d=0.26, p<.05) Many studies show modest REM differences; clinical significance? Summary: Sleep in ADHD 2009 meta-analysis 16 studies ADHD (exclusion meds/comorbidity) vs controls 10/13 ’87-05; 6/31 ’05-08; N=722 Subjective: increase BR, SOD, NW, DTS, symptoms SDB Objective: PSG: increase sleep stage shifts, AHI; decrease SE Actigraphy: increase SOL; decrease SD Sleep in ADHD: Intrinsic Impairments? Impaired sleep ADHD-related homeostatic dysregulation (altered sleep drive) Circadian dysfunction (phase delay) Studies suggest delayed endogenous circadian pacemaker in children with ADHD Sleep onset, morning wake time significantly later (actigraphy) Melatonin onset significantly later Positive response to bedtime dose exogenous melatonin Sleep-Alertness Studies in ADHD Increased daytime sleepiness (MSLT) No consistent group nocturnal sleep differences sleep architecture Decreased mean SOL, more likely to have SOL<10,<5min HI fall asleep more quickly Fall asleep in more naps Inattentive fall asleep on more naps Relative risk for falling asleep 1.57 ADHD vs controls Sleep Disordered Breathing (SDB) and ADHD Significant differences in observed sleepiness, mood, externalizing/internalizing behaviors, attention, learning difficulties Academic performance compromised Less consistent specific neurocognitive deficits At least partial resolution of deficits posttreatment (T&A) SDB and ADHD: Clinical Studies Percent of hyperactive/impulsive children with symptoms of SDB may be as high as 25% SDB more likely to resemble “mild” ADHD Primary snoring as well as OSA at risk for neurobehavioral deficits Compared to controls, children scheduled for T&A More likely to meet ADHD diagnostic criteria (22% vs 7%) T&A group significant improvement, no between-group differences 1-year post-op; 50% no longer met ADHD criteria PSG did not predict baseline neurobehavioral impairment nor correlate with improvement (except sleepiness) Case Study 1 10-year-old male with mild inattentive symptoms and declining school performance referred for ADHD evaluation Medical history significant for moderate tonsillar hypertrophy, seasonal allergies, GER, BMI 30 Snores “just like dad,” sweats during sleep Parents report difficulty in morning waking, occasional dozing off in school Case Study 1: Key Points Severity and onset of ADHD symptoms Multiple OSA risk factors OSA symptoms Presence of daytime sleepiness RLS/PLMD in Children RLS clinical diagnosis; PLMD PSG diagnosis Brief (0.5-10 sec) repetitive jerking movements of lower extremities at 20-40 sec intervals during Stage 1 and 2 sleep Early-onset high hereditability Iron deficiency (serum ferritin<50) risk factor Prevalence “definite” RLS 2% in 8-17yo Definition (International RLS Study Group 2003) Urge to move legs, usually accompanied by uncomfortable/unpleasant sensations Urge to move/unpleasant sensations beginning or worsening periods rest/inactivity Urge to move/ unpleasant sensations worse or only occur evening, night Urge to move/ unpleasant sensations partially/totally relieved by movement, at least as long as activity continues Pediatric definition includes child’s description, family history, PLMs on PSG A Child’s Eye View of RLS… “They (my legs) like feel weird, and they want to kick” 7 y.o. boy “OK, I'm in bed, and my legs really, really hurt. So I say, help, Mom, I need you.” 7 y.o. boy “It’s like my legs are wiggly” 8 y.o. boy “Well, sometimes it feels like little tiny nails are just lightly poking my legs at certain times, like whenever I get into the bed.” 11 y.o. boy RLS/PLMD and ADHD 44% children with PLMs on PSG with symptoms ADHD 8/32 RLS children with inattentive symptoms 26% adults with RLS have ADHD/symptoms In clinical samples (literature review) RLS/PLMs more prevalent in children with ADHD Up to 44% ADHD children/20% adults have RLS symptoms 26-64% children with ADHD have PLMI > 5 Treatment case studies suggest response to DA agents, iron RLS/PLMD and ADHD Potential mechanisms Sleep disruption→ADHD symptomatology Diurnal RLS manifestations mimic ADHD; nocturnal ADHD symptoms mimic RLS Common CNS pathology: dopaminergic dysfunction, iron deficiency Comorbid ADHD-RLS/PLMD Case Study 2 12-year-old girl with mostly inattentive symptoms Medical history of “growing pains,” iron deficiency anemia Maternal history of RLS Complains of difficulty falling asleep and “funny feelings” in her legs at night, relieved by movement Bedclothes “all over the place” in the morning; wakens unrefreshed Case Study: 2 Key Points Sleep-onset symptoms suggestive of RLS Sleep maintenance symptoms suggestive of PLMD Multiple risk factors for RLS/PLMD Medications and ADHD Medications used to treat ADHD or comorbid conditions may affect sleep and wakefulness Psychostimulants Subjective and parent reports inconsistent Objective effects on sleep architecture (PSG) and other sleep variables (actigraphy) duration variable; rebound effects Nonstimulants Other psychotropics (eg, SSRIs, mood stabilizers); may also affect REM sleep Comorbid Disorders Comorbid disorders may contribute to sleep problems Bedtime resistance/sleep onset delay related to ODD (60%)*, anxiety disorders (30%)*, OCD Insomnia, early morning awakening related to depression (10-30%)* Decreased need for sleep related to BPD (11-20%)* *Percent of ADHD patients with comorbid condition. Case Study 3 8-year-old male with ADHD, combined type and difficulty falling asleep; currently on Concerta 72 mg taken at 7:00AM Psychiatric: ODD, mild dyslexia Previous medications: mixed amphetamine salts (Adderall XR), dextroamphetamine, methylphenidate Sleep patterns Bedtime variable; typically falls asleep past midnight; “snacks” during the night; awakened with difficulty at 7:00AM for school Case Study: 3 Key Points Role of stimulant medication: type, dose, rebound Role of comorbid ODD Contribution of insufficient sleep to ADHD Role of inadequate sleep hygiene Tourette’s Syndrome (TS) Characterized by chronic motor/vocal tics Frequent comorbidities: ADHD in TS 40-60%; TS in ADHD 10-30% OCD, anxiety disorders Subjective increase sleep disturbances, especially sleep wake transition disorders, difficulties initiating/maintaining sleep; increased with comorbid ADHD PSG in TS Children/mixed samples: Decreased TST, SE; increase night wakings Variable effects architecture: PSG sleep parameter profiles vary with symptom complex (ADHD, OCD)? Variable differences REM parameters Variable MT; variable association with nocturnal tics Autism Spectrum Disorders (ASD) Autism, Pervasive Developmental Disorder NOS, Asperger Definition - neurodevopmental disorders characterized by: Impairments social interaction Communication deficits and severe language delays Restricted, repetitive, rigid, and stereotypic behaviors and routines Majority severe cognitive impairments Asperger syndrome (AS): Normal cognitive level No significant language delay but problems pragmatic language skills Sleep Disturbances in ASD: Subjective Estimates range from 34 to 89% Autism 44-89% past or concurrent Similar rates PDD NOS Parent/self-report increase sleep onset problems, short SD Rates largely independent of IQ High-IQ (> 55) children with autism have more sleep problems than normal controls Normal IQ ASD children have significantly more sleep problems (p < .002) than normal controls Sleep Disorders in Children with Severe Intellectual Disability (ID) Sleep problems in these children are common with prevalence rates ranging from 44% to 86% Majority persist over time Increased sleep problems with more severe ID and younger age More sleep problems in adolescents and young adults with severe ID with autism vs. severe ID without autism Sleep Disturbances in ASD: Subjective Most commonly include Highly irregular sleep-wake cycles Unusual, problematic sleep routines (often accompanied by repetitive behaviors) Difficulty settling, delayed sleep onset Frequent and prolonged nightwakings Short sleep duration Early morning wake times Possibly parasomnias (sleepwalking, bruxism, RBD) more common Sleep Disturbances in ASD: Subjective Association with severity daytime behavior problems, communication impairments Increased severity, chronicity, relapse rate Significant impact on caregivers Sleep Problems in ASD: Biological Etiology Circadian rhythm abnormalities Disturbance in melatonin production in autism Precursor (tryptophan, serotonin) levels altered Daytime elevation, decreased amplitude, nighttime decrease Anamolies in clock genes; ?motor planning/sleep Less entrainment by social/environmental cues Greater sensitivity changes in photoperiod; ?seasonal variations Sleep Problems in ASD: Biological Etiology Secretin hypothesis Endogenous GI polypeptide; ?role language, behavior, sleep Activation inflammatory response system Increased markers in autism; ?sleep effects Primary arousal dysfunction; ?altered homeostasis Dysfunction aminergic (DA, serotonin) pathways Decreased sleep duration Sleep Problems in ASD: Psychosocial Etiology Learned maladaptive sleep patterns Anxiety-related; high levels autistic children Inadequate parent limit-setting Parents may be more aware of difficulties than parents of typically developing children Many patients have more than one etiology Sleep Disturbances in ASD: Objective Discrepancy between parent report of sleep problems & actigraphy Adolescents and adults with high functioning autism Sleep Latency, Sleep Efficiency, Wake After Sleep Onset Down Syndrome Subjective difficulties with sleep onset (up to 70%) PSG: Increased AI, stage shifts Increased movement arousals, periodic limb movements Decreased TST, REM (negatively correlated IQ) Increased SDB OSA prevalence 30-80% Risk factors: Generalized hypotonia Obesity, central distribution of adipose tissue Midfacial hypoplasia, glossoptosis Adenotonsillar hypertrophy Hypothyroidism Central sleep apnea, Cheyne-Stokes Prader-Willi Syndrome Genetic disorder characterized by Paternal inherited abn chromo-15 (q11-q13) FTT, hypotonia (infants) Hypogonadism, short stature Hyperphagia/obesity, MR behavioral problems Increased prevalence sleep disordered breathing Rates SDB highly variable (0-100%) Hypoventilation, obstructive/central sleep apnea esp in REM Oxygen desaturation; correlated BMI Severity SDB may correlate with BMI; improvement with weight loss Delayed psychomotor development infants assoc with obstructive rather than central sleep apnea SDB in PWS High rates post-op complication T&A Possible increased risk sudden death GH therapy Occurs initial treatment period Linked OSA, concurrent URI Prader-Willi Syndrome: EDS Daytime sleepiness common Increase subjective complaints; correlated MSLT MSLT: severe EDS frequent (40% studies MSOL<5), SOREMPs, increased duration/depth (SWS) sleep May occur independently of obesity, SDB CPAP improves EDS Generally more severe adults vs children; increases adolescence Possible link hypothalamic dysfunction Angelman Syndrome Genetic disorder (abn maternal chromo 15 characterized by severe dev/exp language delays, motor impairments, seizures, behavioral phenotype (“happy puppet”) Subjective caregiver report sleep problems 20-80% Decreased sleep duration, frequent NW Irregular sleep-wake cycles Increased younger patients (2-6y); may improve in adolescence PSG: Increased SOL, WASO Decreased REM%, increased SWS Sleep fragmentation associated with seizures, esp REM ? Increase PLMs William Syndrome Deletion chromo 7q11.23, elastin/CNS development effect Characterized by MR, visual motor deficits, ADHD, alterations connective/vascular tissue Subjective sleep complaints inc DIMS, restless sleep PLMs 16/28 screened symptoms suggestive movement disorder PSG N=7 vs controls: PLMI 14.9 vs 1.9; increased PLMAI Increased WASO (2x), SWS No differences respiratory parameters; 1 with SDB Clinical response clonezapam Smith-Magenis Syndrome Genetic syndrome (deletion chromo 17p11.2) associated with severe developmental delay, behavioral difficulties including extreme hyperactivity and aggression Subjective significant sleep difficulties (60-100%) Caregivers report difficulty falling asleep, short sleep duration, frequent and prolonged night wakings, snoring, daytime sleepiness, nocturnal enuresis PSG studies Early sleep onset/offset with inversion circadian rhythm of melatonin Decreased TST, REM Clinical Issues Maintain high index of suspicion for sleep problems Systematically and regularly screen all children as part of routine care Recognize daytime sequelae (mood, behavior, cognition) Recognize impact on family functioning Clinical Issues Develop a systematic approach to evaluation Insomnia is a symptom, not a diagnosis; multiple potential causes Judicious use diagnostic tools (sleep logs, actigraphy, PSG) Consider comorbid sleep diagnoses (OSA and parasomnias, insomnia and PLMS) Consider underlying contributing factors (meds, sensory deficits, nocturnal seizures) Clinical Issues: Treatment Avoid the “inevitability/untreatable trap” Use empirically-supported behavioral management strategies Support parents – consider respite care Consider judicious use of medication in combination with behavioral therapies PAY ATTENTION TO SLEEP HYGIENE! Management of Sleep Problems Sleep hygiene1 Sleeping position: GER, immobility Sleep environment: Sensory issues: weighted blankets/vests, “white noise” machines Temperature dysregulation: absorbent bedding Safety concerns: fortified cribs Scheduling: bedtime/waketime, napping, daytime activities 1Jan et al Pediatrics 2008 Behavioral Insomnia of Childhood: ICSD-II Definition Sleep Onset Association subtype Falling asleep is an extended process that requires special conditions Sleep-onset associations are highly problematic or demanding In the absence of the associated conditions, sleep onset is significantly delayed or sleep is otherwise disrupted Nighttime awakenings require caregiver intervention for the child to return to sleep Behavioral Insomnia of Childhood: ICSD-II Definition Limit Setting subtype The child has difficulty initiating or maintaining sleep The child stalls or refuses to go to bed at an appropriate time or refuses to return to bed following a nighttime awakening The caregiver demonstrates insufficient or inappropriate limit setting to establish appropriate sleeping behavior in the child Management BIC: Sleep Onset Association Establishment of appropriate sleep onset associations that will be available to the child during the night Consistent, developmentally-appropriate bedtime routine, transitional objects Behavioral interventions Extinction Graduated extinction Scheduled awakenings Management BIC: Limit Setting Education and support of parents regarding developmentally appropriate limit setting Appropriate consistent bedtime, routine Clear, concise, and firm bedtime rules with limited choices Behavioral interventions Bedtime fading Positive reinforcement “Bedtime pass” Behavioral Interventions: Graduated Extinction Graduated extinction (“sleep training”, “checking” or “Ferber method”): variety of techniques in which parents are typically instructed to ignore bedtime crying and tantrums for specified periods of time Involve gradual shaping of appropriate behaviors and fading of interventions Behavioral Interventions: Graduated Extinction Put child to bed “drowsy but awake” Use fixed or progressively longer interval schedule tailored to the child’s age and temperament, parental tolerance Minimize interactions during check-ins that may reinforce child’s attention-seeking (reassuring, brief, boring) Checking method at bedtime only; generalization to night wakings Variations on Graduated Extinction Parent stays with child at sleep onset, gradually fades attention, assistance, and presence Parent sits in chair at sleep onset, gradually moves chair out of room Parent sleeps beside child’s bed, gradually moves bed out of room Child allowed to sleep on separate bed in parent’s room during night wakings Bedtime pass Other Treatment Issues Common for crying/protest to briefly intensify 2nd or 3rd night (“extinction burst”) Avoid intermittent reinforcement (the “lottery theory”) Avoid increasing reinforcement during checks Do not allow child to extend day sleep Improvement in one week if parents consistent Bedtime Fading Temporarily delay of bedtime to ensure rapid sleep initiation; bedtime then moved earlier by small increments (ie, 15 minutes) over successive nights (“fading”) until pre-established bedtime goal is achieved Management of Sleep Problems Circadian rhythm disruption Chronotherapy Bright light phototherapy Pharmacologic treatment Melatonin ASD, ADHD, blind, MR, Rett, Angelman Risperidone ASD Clonidine ADHD Percent of respondents prescribing Child Psychiatry Survey: Prescription Medications in MRDD 80 70 60 50 40 30 20 10 0 MRDD Owens, unpublished data Barbituate Chloral Hydrate Benzo Anticonvulsant Hypnotic TCA SSRI Antihistamine Antipsychotic Sedating Antidep Trazadone Alpha Agonist Sleeping Children Around the World (SCAW) What is SCAW? Registered Canadian charity based in Toronto founded in 1970 by Murray and Margaret Dryden Goal: “A world in which every child benefits from the comfort of a good night’s sleep.” Mission: Through free-will donations and in partnership with volunteers, to give bedkits to needy children in developing countries, thus helping them to face the challenges of the coming day. Scope* Bangladesh Chennai Honduras Kenya Kolkata Mumbai Togo Uganda Sri Lanka Philippines Tanzania SCAW has provided bedkits for more than one million children *Less than $2,000 U.S. average per capita income Bedkits Mat/mattress Pillow (pillowcase) Sheet, blanket/quilt Insecticide-treated mosquito netting Clothing: t-shirts, shorts, sweater, nightclothes, sandals, raincoat School supplies: workbooks, pencils, crayons, compass, bookbag, lunchbox Other: plastic bucket, pitcher, water bottle, umbrella, plates, cups Carrying bag How to Help Donate bedkits ($35 Canadian funds) Donate to Investment Account Purchase greeting cards Fund raise Volunteer Spread the word www.scaw.org “The comfort of a bed is a basic right for every child.” Murray Dryden, founder SCAW Thanks! ???????