SLEEP 2011 Abstract Supplement

B. Clinical Sleep Science XI. Pediatrics
0775
FEWER SPONTANEOUS AROUSALS IN INFANTS WITH
APPARENT LIFE THREATENING EVENT
Franco P 1 , Montemitro E 2 , Scaillet S 3 , Groswasser J 3 , Kato I 4 , Lin J 1 ,
Villa M 2
1
Pediatric Sleep Unit, HFME & INSERM U628, University Lyon
1, Lyon, France, 2 Department of Pediatrics, Sleep Disease Center,
University of rome “la Sapienza” S Andrea Hospital, Rome, Italy,
3
Pediatric Sleep Unit, Children’s Hospital Reine Fabiola, Free
University of Brussels, Brussels, Belgium, 4 Department of Pediatrics
and Neonatology, Graduate school of Medical Sciences, Nagoya
University, Nagoya, Japan
Introduction: A deficit in arousal process has been implicated as a
mechanism of Sudden Infant Death Syndrome (SIDS). Compared with
control infants, SIDS victims showed significantly more subcortical activations
and fewer cortical arousals than matched control infants. Apparent
life threatening event (ALTE) is often considered as an aborted
SIDS event. The aim of this study was to study the arousal characteristics
of ALTE infants during the first months of life.
Methods: 35 ALTE infants were studied with nighttime polysomnography
at 2-3, 5-6 and 8-9 months of age. 18 of the infants had mothers who
smoked. The infants were born full-term and were usually supine sleepers.
Sleep-state and cardiorespiratory parameters were scored according
to recommended criteria. Arousals were differentiated into subcortical
activations or cortical arousals, according to the presence of autonomic
and/or electroencephalographic changes. The results were compared
with those of 19 healthy infants with non-smoking mothers.
Results: During NREM sleep, the ALTE infants had fewer total arousals,
cortical arousals and subcortical activations at 2-3 and 5-6 months
(p < 0.001) than control infants. ALTE infants with smoking mothers
had more obstructive apnea (p = 0.009) and more subcortical activations
during REM sleep at 2-3 months of age (p < 0.001) than ALTE infants
with non-smoking mothers.
Conclusion: Spontaneous arousals were differently altered in ALTE infants
than in SIDS infants, suggesting an entity different from SIDS.
ALTE infants with smoking mothers had arousal and respiratory characteristics
that were similar to future SIDS victims, suggesting some common
abnormalities in brainstem dysfunction.
0776
SUPPLEMENTAL MELATONIN DECREASES SLEEP
LATENCY IN CHILDREN WITH AUTISM
Malow BA 1 , Adkins K 1 , Goldman SE 1 , McGrew SG 2 , Burnette C 2 ,
Wofford D 1 , Surdyka K 1 , Fawkes D 1 , Wang L 3
1
Neurology, Vanderbilt, Nashville, TN, USA, 2 Pediatrics, Vanderbilt,
Nashville, TN, USA, 3 Biostatistics, Vanderbilt, Nashville, TN, USA
Introduction: Retrospective and small prospective studies have shown
that supplemental melatonin promotes sleep in children with autism
spectrum disorders (ASD). However, most studies have not used objective
measures of sleep.
Methods: Children were ages 3-10 years, with a clinical diagnosis of
ASD based on DSM-IV-TR criteria. Diagnosis was confirmed by the
Autism Diagnostic Observation Schedule and by either clinical interview
or the Autism Diagnostic Interview-Revised. All children had
sleep delay, defined as inability to fall asleep within 30 minutes at least 3
nights a week. Medical causes of insomnia and primary sleep disorders
were addressed prior to enrollment. Children on medications which affect
melatonin pharmacokinetics were excluded. Parents were instructed
in optimizing sleep habits prior to treatment. Objective measures of
sleep were measured over 17 weeks with actigraphy (Phillips/Respironics/Mini
Mitter) in conjunction with sleep diaries. All children received
two weeks of an inert flavored liquid 30 minutes before bedtime and
then began 1 mg of supplemental melatonin (Natrol ®). The child’s response
to melatonin was reevaluated every three weeks based on mean
sleep latency (SL) Dose was increased every three weeks (from 1 mg,
to 3 mg, to 6 mg, to 9 mg) until the child reached a satisfactory response
(SAT-R), defined as SL within 30 minutes on 5 or more nights in the
week. Once a SAT-R was achieved, the child remained on that melatonin
dose for the remainder of the 17 weeks.
Results: Twenty-one children were included, two girls and 19 boys,
with a mean age of 6 years [standard deviation (SD) = 2.2]. A SAT-R was
reached in five children at 1 mg, 14 children at 3 mg, and two children at
6 mg. Mean sleep latency (minutes) improved with treatment compared
to baseline [41 (SD 33.9) to 24.8 (SD 21.6); p 1.5), and the mean AHI was 7.5. We found trends
for an association between OSA severity and chronological age, and an
association between age and performance on the ACTB. In order to assess
effects of OSA on cognition, we divided our sample into 14 chronological
age-matched pairs, in which one member of each pair had a
higher AHI (M = 14.5, SD = 16.66) and the other member had a clinically
less insignificant AHI (M = 1.8, SD = 1.41). Groups were equivalent
on gender, IQ, and surgical status. Participants in the high AHI group
performed worse on the CANTAB Intra-Extra Dimensional Set Shift
task stages completed (t (10) = -2.354, p = 0.04; d = -0.93), and showed
a trend toward worse performance on the CANTAB Paired Associates
Learning task mean trials to success (t(13) = 1.937, p = 0.07; d = 0.59).
Conclusion: This study is the first demonstration of a relationship between
OSA and neurocognitive morbidity in children with DS, emphasizing
the importance of early detection and treatment of sleep apnea in
this syndrome.
Support (If Any): Down Syndrome Research and Treatment Foundation,
Arizona Alzheimer’s Research Consortium, University of Arizona
Foundation, The Lejeune Foundation, and the Thrasher Research Fund.
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SLEEP, Volume 34, Abstract Supplement, 2011