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Journal of Autism and Developmental Disorders

Gepubliceerd in:

01-10-2008 | Original Paper

Food-related Neural Circuitry in Prader-Willi Syndrome: Response to High- Versus Low-calorie Foods

Auteurs: Anastasia Dimitropoulos, Robert T. Schultz

Gepubliceerd in: Journal of Autism and Developmental Disorders | Uitgave 9/2008

Abstract

Prader-Willi syndrome (PWS) is a neurodevelopmental disorder characterized by hyperphagia and food preoccupations. Although dysfunction of the hypothalamus likely has a critical role in hyperphagia, it is only one of several regions involved in the regulation of eating. The purpose of this research was to examine food-related neural circuitry using functional magnetic resonance imaging in individuals with PWS and matched controls. Individuals with PWS showed increased activation in neural circuitry known to mediate hunger and motivation (hypothalamus, OFC) in response to high- versus low-calorie foods and in comparison to controls. This suggests neural circuitry for PWS is abnormally activated during hunger, particularly for high-calorie foods, and may mediate abnormally strong hunger states, therefore playing a significant role in PWS-induced hyperphagia.

vorige artikel Social Behavior and Autism Traits in a Sex Chromosomal Disorder: Klinefelter (47XXY) Syndrome

volgende artikel Quality of Life of Adults with Pervasive Developmental Disorders and Intellectual Disabilities

This research was approved by the Human Investigations Committee of the Yale University School of Medicine. In order to prepare our participants for the MRI procedure, we conducted a mock scanning session using a replica of the actual MRI scanner, equipped with audio equipment to simulate the MRI noise level.

Prior to scanning this sample, a pilot study of six healthy-weight adults was conducted to solidify the study design and replicate previous findings with healthy-weight participants. No attempt was made to match the pilot sample to the PWS sample. Pilot data indicated food-related activation in areas consistent with previous research in normal-weight individuals, including the insula, thalamus, FG, and OFC (Dimitropoulos and Schultz 2004).

In PWS: (1) paroxetine, (2) paroxetine, risperidone, (3) fluoxetine. In MR/DD: (1) escitalopram, topiramate, (2) methylphenidate hydrochloride, (3) risperidone, (4) atomoxetine, zonisamide, sertraline, (5) methylphenidate hydrochloride , (6) divalproex sodium, olanzapine, (7) divalproex sodium, risperidone, (8) bupropion.

Our first three PWS participants received these stimuli presented over three runs instead of two (Stimulus duration = 3,000 ms, ISI = 1,500 ms) but short response times and high accuracy on the task led us to shorten the protocol to two runs. A direct comparison between data from those who received three runs versus two runs did not reveal any differences in activation level in our primary ROIs (p > .20).

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Titel: Food-related Neural Circuitry in Prader-Willi Syndrome: Response to High- Versus Low-calorie Foods
Auteurs: Anastasia Dimitropoulos
Robert T. Schultz
Publicatiedatum: 01-10-2008
Uitgeverij: Springer US
Gepubliceerd in: Journal of Autism and Developmental Disorders / Uitgave 9/2008
Print ISSN: 0162-3257
Elektronisch ISSN: 1573-3432
DOI: https://doi.org/10.1007/s10803-008-0546-x

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