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Moderated Poster Session 2 (44Ц52).

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monoamine transporter type 2, VMAT-2), and vesicular
docking and release proteins (VAMP-2, synaptotagmin,
SNAP-25, syntaxin, synaptophysin). Data from each TS
sample was calculated as a percentage of its control.
A dopaminergic abnormality was identified in all three TS
subjects with increases (greater than 130% of its matched
control) in DAT, D1DR, and D2DR. ␣-2A protein density
was also increased in several frontal regions.
Dopaminergic fibers arise from the ventral tegmentum
and innervate the frontal cortex, exciting pyramidal neurons
and inhibiting interneurons. Our data support the hypothesis
of a dopaminergic dysfunction in the frontal lobe and a
likely role in the pathophysiology of TS.
42. Use of fMRI to Identify Regional Activation of
Cerebral Cortex Involved in Successful Performance of
an Incidental Verbal Memory Task by Children
Maril A, Davis PE, Saygin ZM, Koo J, Mulkern RV,
Waber DP, Rivkin MJ (Boston, MA)
Functional magnetic resonance imaging (fMRI) has been used
effectively to study long term memory in adults. Little investigation has been conducted in children. We employed a subsequent memory fMRI experimental design to study 18 children (ages 7-18 years;2 males; all right-handed) who
performed an incidental verbal memory encoding task. While
in the scanner, children were simultaneously presented pairs of
concrete nouns auditorally with pictures depicting them. For
each noun pair, subjects were to replace the first phoneme of
the second word with the first phoneme of the first word to
yield a specific target concrete noun. After the scan, a surprise
recognition test was given in which target words presented one
at a time were intermixed with foils. Subjects rated each word
as “remembered” or “new”. fMRI data were analyzed for simple task performance and for words remembered using
SPM99. Task performance compared to rest generated increased blood oxygenation level dependent (BOLD) signal in
left prefrontal cortex, supplementary motor cortex, insula, left
parietal lobe, and bilateral occipital cortex. The fMRI map for
target words remembered compared to words forgotten consisted of a left lateralized network of BOLD activation in left
pallidum, left hippocampus/parahippocampus and left parietal
lobe. These data demonstrate a left hemisphere dominant neural network associated with incidental verbal memory encoding in children. While structures associated with verbal encoding in adults, such as left hippocampus and parahippocampus
are also activated in children, children appear to recruit other
loci, such as left subcortical gray matter, for successful incidental verbal encoding.
43. Functional Neuroimaging of Irony Comprehension
in Children with Autism: Role of Medial Frontal Gyrus
Williams DL, Kana RK, Keller TA, Minshew NJ, Just MA
(Pittsburgh, PA)
Background: Comprehension of irony requires common
ground between speaker and addressee in shared beliefs and
knowledge. For example, in the story, Tom and Mike planned
to go on a picnic. In the morning it was raining very hard. Tom
said, “Great weather for a picnic,” the reader must recognize
that the speaker’s mental state differs from the literal interpretation of the statement he makes, a process that may rely on
‘theory of mind’. Several neuroimaging studies have suggested
the role of medial frontal regions in processing theory of
mind, and the hypoactivation of these regions in autism. Objective: Compare activation of brain areas involved in dis-
course processing and theory of mind in individuals with autism and matched controls. Methods: 12 high functioning
children with autism and 12 age and IQ matched control participants read brief stories that concluded with either a literal
or ironic statement made by one of the characters in the story
during fMRI. Results: Behavioral data showed that the participants with autism performed more poorly than controls on
the ironic sentences, but not on the literal sentences. In the
fMRI data, when the processing of ironic utterances was compared to processing of literal utterances, the participants with
autism showed reliably lower activation than the controls in
left medial frontal cortex, right insula and left supramarginal
gyrus. Conclusion: The autism group had less activation in
areas involved in integrative aspects of sentence processing and
in areas involved in ‘theory of mind’.
Source of Funding: NICHD/NIDCD
DOI: 10.1002/ana.11480
MODERATED POSTER
SESSION 2: CLINICAL
MANAGEMENT
Friday, October 20, 2006
3:30 – 5:30 pm
44. Clinical and Radiographic Features of Thrombosis
Propagation in Neonatal and Childhood Cerebral
Sinovenous Thrombosis
Moharir M, Shroff M, MacGregor D, Adams M,
Bharucha P, deVeber G (Toronto, Ontario, Canada)
Background: Cerebral sinovenous thrombosis (CSVT) is increasingly encountered in neonates and children. Adults with
CSVT are treated with anti-coagulants (ACTs) to prevent
thrombus propagation and improve outcome. ACTs are not
offered to most neonates and many children due to lack of
clinical trials. The effects of no treatment on the acute thrombotic process are unknown. Aim: To study the clinical and
radiographic features of thrombus propagation in neonatal and
childhood CSVT. Methods: We conducted a consecutive cohort study of neonates (0-28days) and non-neonates (29 days18years) with CSVT diagnosed by CT venography
(CTV)/MR venography (MRV) from 1992-2005. Patients
without contraindications received standardised anticoagulation based on published institutional protocols. Monitoring
CTV/MRV was performed in untreated patients at 5days. A
study neuroradiologist assessed extent of thrombosis on initial
& each follow-up neuroimaging study and documented propagation or recanalization. Results: CSVT propagation occurred in 10/40 (25%) neonates and 7/22 (32%) nonneonates who were initially untreated, compared to only 1/28
(3%) neonates (p⫽0.04) and 3/55 (5%) non-neonates
(p⫽0.006) who were initially treated. Mean duration from
CSVT diagnosis to propagation was 4days in neonates and
7days in non-neonates. The commonest site of propagation
was superior sagittal sinus (70%). Propagation was asymptomatic in 11/11(100%) neonates and symptomatic in 5/10
(50%) non-neonates. Propagation was associated with new venous infarction in 1/11 (9%) neonates and 4/10 (40%) nonneonates. Conclusions: If untreated, 25% neonates and 32%
older children with CSVT propagate their initial thrombus.
Program and Abstracts, Child Neurology Society
S141
Therefore, untreated patients should be closely monitored
clinically and radiographically to detect CSVT propagation.
45. The Value of Positron Emission Tomography
(PET) and Proliferative Index (PI) in Predicting
Invasive LGA
Kaplan A, Kruer MC, Carpenteri D, Etzl MM, Bandy DJ,
Dickman PA (Phoenix, AZ)
Introduction: Primary CNS astrocytomas are the most common brain tumors of childhood. Low-grade astrocytoma
(LGA), in general, have favorable prognosis, but recurrence
or progressive disease (PD) with dissemination, malignant
transformation, and death may occur in some cases. Current
clinical and pathological measures including age, imaging
characteristics, location, histopathology, and degree of resection cannot predict with certainty which tumors will demonstrate invasive behavior. Objective: Determine the predictive value of PET and PI in identifying high risk/invasive
LGA. Patients and Methods: We reviewed 30 children, ages
5 months to 17 years, with low-grade (WHO I or II) astrocytomas. The patients had PET scans utilizing [18F] fluorodeoxyglucose (FDG) and/or proliferative index (PI) measurements (Ki67/MIB-1 immunohistochemistry). Results:
Review of our cases confirmed PD in 11 of 30 (37%) of
cases, with 7 (23%) deaths. Tumors characterized by increased FDG uptake showed PD in 58% of cases, with 42%
progressing to death. In comparison, 28% of those with low
metabolic activity showed clinical progression, and only 11%
progressed to death. Proliferative indicies between 2 - 5%
were associated with PD in 38% cases, whereas PI ⱖ 5%
was associated with progression in 67% of cases. Considered
together, 82% of invasive LGA exhibited high-grade FDG
uptake and/or had PI ⱖ 5%. Conclusion: Results demonstrate that PET and PI are useful measures in the identification and stratification of high risk LGA. The ability to predict a subset of invasive LGA suggests the need for second
surgical procedures or more intensified adjuvant treatment
which may improve outcome.
46. Co-expression and Interaction of Class III BetaTubulin and Gamma -Tubulin in Primary Astrocytic
Gliomas
Katsetos CD, Draberova E, Reddy G, Smejkalova B,
Bertrand L, Del Valle L, Nissanov J, Legido A, Baas PW,
Draber P (Philadelphia, PA and Prague, Czech Republic)
Alterations in the distribution of tubulin isotypes are pivotal
in tumor progression and response to chemotherapy. We
have previously shown that the class III b-tubulin isotype is
aberrantly expressed in gliomas according to an ascending
scale of malignancy (Cell Motil Cytoskeleton 2003; 55:7796) and that altered expression of g-tubulin supports centrosome protein amplification in astrocytomas (J Neuropathol
Exp Neurol in press). g-Tubulin is the major cytoskeletal
constituent of centrosomes, the cell’s microtubule organizing
centers. We have hypothesized that aberrant expression of
bIII-tubulin is linked to abnormal centrosomes and altered
g-tubulin expression. The aim of this study was to determine
the distribution and interaction of bIII-tubulin and g-tubulin
in adult (n⫽10) and pediatric (n⫽5) astrocytic gliomas
(grades II-IV) and the p53 mutant human glioblastoma cell
line T98G using antibodies against g-tubulin and bIIItubulin. bIII- and g-tubulin labeling was more widespread in
grades III/IV as compared to grade II tumors. Punctate and
diffuse co-localizations were identified by confocal micros-
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Annals of Neurology
Vol 60 (suppl 3)
2006
copy in both primary tumors and the glioblastoma line.
Monoclonal and polyclonal anti-bIII-tubulin antibodies precipitated bIII-tubulin and co-precipitated g-tubulin. Our observations indicate that aberrant expression of bIII-tubulin in
astrocytic gliomas is associated with ectopic g-tubulin distribution as part of centrosome dysfunction. We suggest that
bIII-tubulin might interact with g-tubulin destined for recruitment in the context of mitosis and ectopic microtubule
nucleating activity contributing to cytoskeletal abnormalities
associated with malignant (anaplastic) tumor phenotypes.
(Supported by a grant from the St. Christopher’s Foundation
for Children to CDK).
47. The Importance of Arteriopathy in Arterial
Ischemic Stroke in Children
The International Paediatric Stroke Study Group
Objective: The International Paediatric Stroke Study (IPSS)
has been collecting data on children with stroke internationally
since 2003. Methods: Patients aged 1 month to 18 years with
acute neurologic deficit and radiographically confirmed arterial
ischemic stroke (AIS) from January 2003-February 2006 were
analysed. Standardized data were collected from centres in
Canada, the US, Malaysia, Australia, Germany and the UK,
and entered into the IPSS web-database. Results: Of 610 patients enrolled, 315 are non-neonates with AIS with 38% female and median age at presentation 5 years. Common risk
factors include arteriopathy (48% of 246 patients with vascular imaging), cardiac disease (23%), acute illness (22%), head
and neck infections and trauma (23%), and chronic disease
(38%, including prothrombotic state (47), sickle cell disease
(17), migraine (16), haematologic malignancy (8), iron deficiency anaemia (5)). Of 246 children with vascular imaging
(78%), 118 children had evidence of an arteriopathy. Arteriopathies classified by pre-defined criteria include moyamoya
(38; 6 with sickle cell), craniocervical dissection (24), postvaricella angiopathy (9), transient cerebral arteriopathy of
childhood (8), vasculitis (6), and nonspecific stenosis (33). An
additional 32 (20%) had abnormal findings including occlusion only (21), and other vascular abnormalities (11). Conclusions: Arteriopathy is the most common risk factor among
older children with AIS, affecting 48% of patients screened
with vascular imaging. Nonspecific stenosis accounts for 28%
of arteriopathies and requires more careful study. Prospective
studies using standardized vascular imaging protocols and assessing the relationship between risk factors and outcomes will
be important in developing aetiology-specific treatments for
childhood AIS.
48. Eligibility for Hyperacute Thrombolytic Therapy
with Tissue Plasminogen Activator (tPA) in Children
Rafay MF, Pontigon A, Chiang J, Jarvis A, Silver F,
MacGregor D, deVeber G (Toronto, Ontario, Canada)
Objectives: Tissue plasminogen activator (tPA), standard of
care for hyperacute thrombolytic therapy in adults, is currently being investigated in children. Initial pediatric stroke
studies will assess intra-venous (⬍ 3 hours from stroke onset)
and intra-arterial (⬍ 6 hours from stroke onset) tPA safety
based on inclusion and exclusion criteria shown to be safe in
adults. We sought to determine the proportion of children
with AIS who meet tPA criteria. Methods: Consecutive children (1 month to 18 years) with acute AIS admitted to our
hospital from January 1992-January 2005 were assessed for
tPA eligibility including age ⬎2 yrs, presentation ⬍5 hrs,
and PedNIHSS score ⬎5. Results: In 209 consecutive chil-
dren with AIS, 132(63%) had AIS as out-patients and
77(37%) as in-patients. In 189 children with available data,
median delay to diagnosis was 22.7 hours: 19(10%) ⬍3hours, 19(10%) 3 to ⬍6-hours, and 151(80%) ⬎6-hours. In
38 children diagnosed within 6-hours presentations were seizures (14), focal motor deficits (18) or non-focal deficits (6).
Among these 38 children tPA exclusions included: age ⬍2
years (14), PedNIHSSK ⬍5 (2), intracranial trauma (1), recent cardiac surgery (2), deficit on awakening with time last
normal ⬎6-hours (4) and diagnosis 5-6 hours (leaving insufficient time for angiographic tPA administration) (4). None
had hemorrhage on neuroimaging. Only 11(6%) children
met all inclusion criteria for a tPA trial. Conclusion: Our
results support the feasibility of tPA studies, but emphasize
the need for improved awareness and rapid diagnostic strategies for children with stroke to improve access to acute specialized stroke treatments.
49. Photomodulation of Cytochrome Oxidase
Whelan H, Amlie-Lefond C, Eells J, Wong-Riley M, Das R,
Jett M, VerHoeve J (Milwaukee, WI)
Objectives: Photobiomodulation by red to near infrared light
is believed to activate mitochondrial respiratory chain components promoting cytoprotecton. Our prior studies demonstrate
that the action spectrum for stimulation of cytochrome oxidase activity and cellular ATP parallels the near-infrared absorption spectrum of cytochome oxidase and that 660-680 nm
irradiation upregulates cytochrome oxidase activity in cultured
neurons. Methanol intoxication injures the retina and optic
nerve.via formic acid, a mitochondrial toxin of cytochrome oxidase. KCN (potassium cyanide) also poisons cytochrome oxidase, and has been used to assess the efficacy of 660-680 nm
irradiation for mitochondrial neuroprotection. Methods: We
hypothesized that exposure to monochromatic red radiation
from light-emitting diode (LED) arrays would protect the retina against formate toxicity, and improve mitchondrial function in a rodent model of methanol toxicity. Results: 670 nm
LED treatment significantly attenuated the retinotoxicity of
methanol-derived formate. Gene expression profiles in the retina of untreated rats compared with those from the retina of
methanol-intoxicated rats and LED-treated methanolintoxicated rats showed striking differences in genes from cytochrome oxidase family, peroxiredoxin family and genes involved in cell growth and maintenance which may play an
important signaling role in the activation of retinoprotective
processes following LED treatment. Mitochondrial membrane
potential and mitochondrial dehydrogenase activity were also
increased, and apoptosis was attenuated, by LED treatment of
neuronal cells exposed to the mitochondrial toxin KCN. Conclusions: Photobiomodulation with near infrared light augments cellular energy production and neuronal function following mitochondrial injury in vitro and is neuroprotective for
cell injury in vivo.
50. Regulation of c-fos, p53 and AIF in Neonatal
Hypoxia-Ischemia
Ness J, Harvey C, Meyn D, Washington J, Zhang J
(Birmingham, AL)
BACKGROUND: Neonatal hypoxic-ischemic (HI) injury is
mediated by both caspase-dependent and caspapseindependent pathways. Prior studies in our laboratory have
shown that deficiency of p53 decreases neonatal HI by 50%,
suggesting that p53 is involved in neuronal cell death following neonatal HI. However, the mechanism of p53 action in
neonatal HI is unknown. OBJECTIVE: To determine
whether neonatal HI results in changes in protein expression
of regulators of caspase-independent neuronal death including the early immediate gene c-fos, p53 or in apoptosisinducing factor (AIF). METHODS: Postnatal day 7 mice
underwent left carotid ligation followed by 45 min exposure
to 8% oxygen then were sacrificed 0, 1, 3, 6, 12, 24 and 48
hrs later. Frozen 15-micron thick coronal brain sections were
stained with cresyl violet or processed for immunohistochemistry using antibodies against c-fos, p53, AIF, cleaved “activated” caspase-3 and glial fibrillary acidic protein (GFAP).
Alternatively, nuclear and non-nuclear fractions were prepared from left and right cortex and hippocampal homogenates at the same time points. RESULTS: Robust increases
in c-fos, p53 and AIF immunostaining were observed within
the CA1 region of ischemic hippocampus 3-12 hrs following
neonatal HI in the same distribution as that observed for
cleaved caspase-3 immunoreactivity and nuclear pyknosis.
Sub-cellular fractionation experiments showed p53 immunoreactivity peaked 6-12 hrs in non-nuclear fractions of ipsilateral cortex and hippocampus, then decreased by 48 hrs.
CONCLUSION: These studies demonstrate increased c-fos,
p53 and AIF protein expression in ischemic hippocampus
and point to additional pathways which may regulate neuronal death following neonatal HI.
51. CINRG Pilot Trial of Oxatomide in Steroid-Naive
Duchenne Muscular Dystrophy
Vasconcelos MM, Nascimento OJM, Werner J Jr,
Domingues RC, Brito AR, Cruz LCH Jr., Esteves L,
Freitas MR, Azevedo PMC, Nazar BP, Pinto FNV
(Rio de Janeiro/RJ/Brazil)
OBJECTIVE: To test the hypothesis that oxatomide will
improve muscle strength or delay progression of muscle
weakness in Duchenne muscular dystrophy patients by
blocking the mast cell mediator cascade and inhibiting cytokine release by dendritic cells . MATERIALS AND METHODS: We designed a pilot open-label clinical trial for ambulant steroid-naive DMD boys aged 5 – 11 year. Patients
were used as their own control, with a 3 months medicationfree lead-in period, followed by a 6 months treatment phase
with oral oxatomide (30 mg/day). Drug efficacy was tested
monthly by measuring muscle strength quantitatively
(QMT) and manually (MMT), and by timed function tests.
Linear evolution (change per month, slope) of the oxatomide
treatment period was compared between the lead in ad the
treatement phase and to the linear evolution of an external
natural disease cohort published by the same authors. RESULTS: During the 6 months oxatomide treatment period,
there was no improvement or deterioration in muscle
strength (measured either by QMT or MMT). A statistically
significant difference was seen when compared to the external age-matched controls, that showed strength deterioration
during the same period of time. No serius adverse events
were reported. CONCLUSIONS: We conclude that 6
months oxatomide treatment did not improve muscle
strength or function in DMD patients. However, there was a
strong trend showing that patients treated for 6 months with
oxatomide showed less deterioration in QMT measured muscle strength (QMT total) than during the natural course of
this disease. A minor disease-modifying effect of oxatomide
in DMD can therefore not be excluded.
Program and Abstracts, Child Neurology Society
S143
52. Modeling of Injury Severity in Newborns with
Hypoxia-Ischemia Using Volumetric Magnetic
Resonance Imaging
Ashwal S, Obenaus A, Holshouser B, Tone B, Tian Hui R,
Bartnik B, Graupner G, Tong K, Wycliffe N
(Loma Linda, CA)
Magnetic resonance imaging (MRI) has improved our ability
to detect neonatal hypoxic ischemic injury (HII). Various
imaging approaches and rating scales have been used to estimate injury severity and to correlate these findings with
long-term outcome. In the current study we used 3D volumetric post-processing of MRI to develop a 3-tiered model
of injury severity (mild, moderate, severe) in a group of HII
newborns. All infants met criteria for HII as used in the neonatal hypothermia trials and MRI was performed 3-14 days
after birth. Volumetric analysis (total and regional) was performed using DWI and T2 weighted images (Amira, TGS
Computer Systems Inc). Outcome was determined using the
Pediatric Cerebral Performance Category Scale score and was
performed at 12 months after injury. We demonstrate that
greater volumes of ischemic injury (Figure: mild, 16%; mod
39%; severe 75%) were associated with outcome and that
this type of analysis could also be applied to neonates with
arterial ischemic stroke (AIS). We also observed that the distribution of injury after diffuse HII was different than that
seen with AIS. Our findings demonstrate that volumetric imaging analysis can be applied to neonates with HII and be
used to objectively stratify injury severity. Such methodologies may be helpful for evaluating the severity of injury, for
prognosis and for assessment of potential treatments used
within the first 1 to 2 weeks after an insult has occurred.
DOI: 10.1002/ana.11481
E-01. Vagus Nerve Stimulator (VNS) Therapy in
Pediatric Epilepsy Patients: Reductions in Seizures and
Hospitalizations
Paolicchi JM, Terry D, Karn M, Choi Y (Columbus, OH)
Background: VNS US approval is for intractable partial epilepsy in patients ⬎12yrs, but younger patients with other
seizure types have benefited. Objective: Examine pediatric
epilepsy patients’ demographics with VNS therapy, measure
its effect on seizures and epilepsy-related hospitalizations.
Design/Methods: Review clinical data for 78 VNS patients
(⬍18 years), followed in our Epilepsy Clinic for 5 years.
Hospitalizations/emergency room visits for epilepsy or
epilepsy-related conditions (i.e. falls) in patients with ⬎1year
of VNS therapy were calculated annually, pre and postimplantation (n⫽70). Results: Implantation age averaged
9.47yrs (range: 1.5-17yrs, 51% boys). Mean epilepsy duration pre-implantation was 6.8yrs (range: 0.5-16.5yrs). VNS
therapy averaged 3.14yrs (range: 0.17-7.25yrs). Epilepsy syndromes included: localization-related idiopathic 5 (6.4%),
symptomatic 27 (34.6%); generalized idiopathic 5 (6.4%),
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Annals of Neurology
Vol 60 (suppl 3)
2006
symptomatic 10 (12.8%), Lennox-Gastaut 20 (25.6%),
mixed 10 (12.8%), infantile spasms 1 (1.3%). 4 pts (5%)
discontinued VNS. At 6 months, seizures decreased ⬎50%
in 50% of patients; ⬎75% in 35%, and ⬎90% in 16.7%.
At 12 months, seizures decreased ⬎50%, ⬎75% ⬎, and
⬎90% in 52.8%, 41.6%, and 20.8% respectively. At 24
months reductions were ⬎50%, ⬎75% ⬎, and ⬎90% in
57.6%, 51.8%, and 30.3% respectively. Pre-implantation,
mean annual rate of hospitalizations was 1.34 (range: 0-16)
vs. post-implantation 0.55 (range⫽0-5) (p⫽.003). Preimplantation, 4 patients had no hospitalizations vs. 38 postimplantation, reducing hospitalization risk 1/25 (McNemars). Conclusions: VNS Patients’ age averaged ⬍10years;
59% did not have localization-related epilepsy. Postimplantation hospital utilization decreased 41%; 9.5 times
more patients were not hospitalized. Lowered hospital utilization impacts cost-effectiveness of VNS and decreases overall patient morbidity.
E-02. Polysomnographic Abnormalities in Children
with Epilepsy
Cruz M, Valencia II, Zihlif M, Adams R, Khurana DS,
Melvin J, Legido A, Kothare SV (Philadelphia, PA)
Sleep disorders in children with epilepsy are underrecognized. Inadequate sleep may worsen seizure control,
and antiepileptic medications may alter sleep patterns. The
purpose of this retrospective study was to evaluate polysomnography (PSG) abnormalities in a cohort of children with
epilepsy. Forty patients with various sleep complaints were
studied. Analyzed variables included PSG data, body mass
index (BMI), concomitant developmental delay (DD), antiepileptic drug (AED) treatment, epilepsy-type, and seizure
control. PSG data were compared to14 age-matched controls from our sleep laboratory. Epilepsy patients included
19 females and 21 males, aged 9.9⫾4.9 years, and mean
BMI 22.5⫾7.7. Compared to controls, epilepsy patients
had a higher relative snoring index (49.6 vs. 1.36,
p⫽0.0001) and a higher arousal index (23.7 vs.14.8,
p⫽0.001). Thirty four epilepsy patients (85%) had sleep
disordered breathing: 17 (42.5%) snoring, 5 (12.5%) obstructive hypoventilation, 4 (20%) obstructive sleep apnea
and 3 (7.5%) upper airway resistance syndrome. Four
(10%) had periodic limb movements. No major sleep architectural abnormalities were observed when controlling
for DD, epilepsy type, or BMI (⬎25 or ⬍25). In addition,
REM sleep was decreased in patients with better seizure
control (r⫽-0.33, p⫽0.046), unrelated to AED use. One
patient had two brief generalized tonic seizures in nonREM sleep. Mean sleep time was increased by 30 minutes
in 36 patients taking AEDs. These findings suggest that
PSG abnormalities in children with epilepsy are independent of seizure treatment, presence of DD or BMI, suggesting that epilepsy may be an independent contributing factor to the sleep problems they may suffer.
E-03. Glucose Metabolism in Contralateral Cortex in
Children with Unilateral Sturge-Weber Syndrome
Batista CA, Juhasz C, Chugani HT (Detroit, MI)
Objective: To evaluate brain glucose metabolism ipsi- and
contralateral to the angioma in children with unilateral
Sturge-Weber syndrome (SWS) using 2-deoxy-2[18F]fluoroD-glucose (FDG) PET. Methods: FDG PET scans of 17
children with unilateral SWS (mean age 5.6 years) and epilepsy were analyzed. Regional glucose metabolism (normal-
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