SLEEP 2011 Abstract Supplement

B. Clinical Sleep Science XI. Pediatrics
Conclusion: These results are consistent with previous research on
drowsy driving showing increased eye-blinks in association with sleep
restriction/deprivation. We extend such findings to early childhood,
which support further development of the FACES using more challenging
experimental paradigms (e.g., late bedtimes), as well as with children
diagnosed with clinical sleep disorders.
Support (If Any): K01MH74643
0793
QUANTITATIVE ASSESSMENT OF EPILEPTIFORM
DISCHARGES IN CHILDREN WITH ATTENTION DEFICIT
HYPERACTIVITY DISORDER (ADHD)
Bondugula C 1 , Rao SC 1 , McCarthy V 2 , Thomas K 2
1
Neurology, University of Louisville School of Medicine, Louisville,
KY, USA, 2 Pediatrics/ Sleep Medicine, University of Louisville School
of Medicine, Louisville, KY, USA
Introduction: To identify and quantify the distribution of epileptiform
discharges in patients with Attention Deficit Hyperactivity Disorder
(ADHD) presenting to a pediatric sleep medicine center for nocturnal
video-polysomnography (PSG) because of a complaint of snoring, multiple
awakenings, witnessed apneas, daytime sleepiness or restless sleep.
Methods: The PSG of fifty- five children with ADHD (33 male, 22 female
and mean age= 6.8years) were identified retrospectively and evaluated
from January 2008 to June 2010 for epileptiform discharges using
scalp electroencephalography (EEG). Forty six patients were on stimulants.
Fifty- five non-ADHD patient controls were age, sex, Respiratory
Disturbance Index (RDI), and Periodic Limb Movement Index (PLMI)
matched. Polysomnographs were studied for epileptiform discharges using
the same montages.
Results: ADHD patients had a significant greater likelihood of EDs
compared to controls (p= 0.000) specifically, 32 (58.18%) ADHD patients
had epileptiform discharges (EDs) with a (range from 3- 984, and
mean= 71), and 23 (41.82%) were normal. Nine (16.34%) controls had
EDs with a (range from 4- 21 and mean= 10), and 46 (83.66%) were
normal. Of the 46 ADHD patients who were on stimulants, 28(60.9%)
had EDs with a (range from 3- 984, and mean= 77), and 18(41.86%) had
no EDs. Of the 9 ADHD patients who were not on stimulants, 4(44.4%)
had EDs with a (range from 8- 97 and mean= 32), and 5 (55.6%) had no
EDs, (p=0.46).
Conclusion: Children with ADHD had more epileptiform discharges
than age, sex, RDI, and PLMI matched controls. Our findings show that
ADHD is associated with epileptiform abnormalities on EEG.
0794
EFFECTS OF A STANDARDIZED PAMPHLET ON SLEEP
LATENCY IN CHILDREN WITH AUTISM
Malow BA 1 , Adkins K 1 , Clemons T 3 , Goldman SE 1 , Molloy C 2 ,
Wofford D 1 , Fawkes D 1 , Surdyka K 1
1
Neurology, Vanderbilt, Nashville, TN, USA, 2 Pediatrics, Cincinnati
Children’s Hospital Medical Center, Cincinnati, OH, USA, 3 EMMES
Corporation, Rockville, MD, USA
Introduction: Sleep difficulties, particularly sleep onset insomnia, are
common reasons why parents seek medical intervention in children with
autism spectrum disorders (ASD). We determined the efficacy of a sleep
education pamphlet on sleep latency (time to fall asleep) in children with
ASD.
Methods: Children ages 2-10 years, enrolled in the Autism Treatment
Network at Vanderbilt University Medical Center and Cincinnati Children’s
Hospital Medical Center, were eligible. All had a clinical diagnosis
of ASD, with confirmation by the Autism Diagnostic Observation
Schedule. Parents were randomly assigned to receive or not receive a
sleep education pamphlet containing information about daytime habits,
bedtime routine, and sleep environment. Children wore an actigraphy
device, which measures activity and rest to estimate sleep parameters,
prior to receiving the pamphlet (baseline) and two weeks after randomization
(treatment). Sample size of 36 participants was predetermined to
detect a difference in time to fall asleep of at least 30 minutes in children
whose parents received the pamphlet. Independent t-tests were performed
to compare mean SL at baseline, as well as the mean change in
SL by treatment.
Results: The group receiving the pamphlet showed improvement in SL
[from 56.7 minutes ± 27.1 at baseline; mean ± standard deviation) to
49.5 minutes ± 26.7 with treatment]. The group randomized to not receive
the pamphlet showed worsening in SL [from 52.1 minutes ± 25.1
at baseline to 61.3 minutes ± 47 with treatment). However, statistical
significance was not reached in either group (p > 0.10).
Conclusion: Providing a sleep education pamphlet to parents of children
with ASD did not significantly improve sleep latency. We are currently
conducting studies to determine if more intensive education improves
sleep patterns in this population.
Support (If Any): The authors acknowledge the members of the Autism
Treatment Network (ATN) for use of the data. The data for the study
was collected as part of the ATN, a program of Autism Speaks. Further
support came from a cooperative agreement (UA3 MC 11054) from the
U.S. Department of Health and Human Services, Health Resources and
Services Administration, Maternal and Child Health Research Program,
to the Massachusetts General Hospital.
0795
SLEEP HOMEOSTASIS IN ADOLESCENT DEPRESSION
Armitage R, Lopez J, Bertram H, Hoffmann RF
Psychiatry, University of Michigan, Ann Arbor, MI, USA
Introduction: Slow-wave activity (SWA) and sleep homeostasis show
significant sex differences in adults with major depressive disorders
(MDD). Men with MDD show a blunted SWA response to sleep challenge
compared to healthy control men whereas women with MDD
over-respond to a mild sleep challenge. The present study was undertaken
to determine if sleep homeostasis was impaired in early onset MDD
and if sex differences were also evident.
Methods: 50 physically mature (Tanner Stage 5) adolescents, 12-18years
of age were recruited, including 30 symptomatic, un-medicated MDD
(10 M, 20 F), and 20 healthy controls (HCs) with no personal or family
history of MDD (HC: 7 M and 13 F). Participants maintained a regular
sleep-wake schedule for 5 days, followed by 2 nights of PSG in the laboratory
on the same schedule. On the sleep homeostatic challenge night,
bedtime was delayed by 3 hrs, followed by recovery sleep. Power spectral
analysis quantified SWA in NREM sleep (excluding Stage 1) on the
baseline and sleep delay nights. SWA response to delay was compared
across groups.
Results: Sleep latency was shorter after sleep delay in all groups, roughly
half of baseline values and supported by a significant main effect
(p