Regional Brain Perfusion before and after Treatment with Methylphenidate According to the MspI Polymorphism of the Alpha-2A Adrenergic Receptor Gene in Children with Attention-Deficit Hyperactivity Disorder.
- Author:
Subin PARK
1
;
Jeong Hoon BAE
;
Jae Won KIM
;
Young Hui YANG
;
Seungmin OH
;
Soon Beom HONG
;
Min Heyon PARK
;
Boong Nyun KIM
;
Min Sup SHIN
;
Hee Jeong YOO
;
Soo Churl CHO
Author Information
1. Division of Child and Adolescent Psychiatry, Department of Psychiatry, Seoul National University College of Medicine, Seoul, Korea. soochurl@snu.ac.kr
- Publication Type:Original Article
- Keywords:
Attention-Deficit Hyperactivity Disorder;
ADRA2A;
Single-Photon Emission Computed Tomography;
Pharmacogenetics
- MeSH:
Brain;
Child;
Corpus Striatum;
Genotype;
Gyrus Cinguli;
Humans;
Methylphenidate;
Perfusion;
Pharmacogenetics;
Receptors, Adrenergic, alpha-2;
Tomography, Emission-Computed;
Tomography, Emission-Computed, Single-Photon
- From:Journal of the Korean Academy of Child and Adolescent Psychiatry
2013;24(1):21-27
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVES: Dysregulation of the central noradrenergic system may be involved in the pathophysiology of attention-deficit hyperactivity disorder (ADHD). The aim of this study was to examine the differences in pre- and post-treatment cerebral perfusion according to the MspI polymorphisms of the alpha-2A-adrenergic receptor gene (ADRA2A) in children with ADHD. METHODS: Thirty seven drug-naive ADHD children (8.9+1.8 years old, M=32, F=5) were genotyped. Baseline single-photon emission computed tomography (SPECT) and clinical assessments were performed for ADHD children. After treatment with methylphenidate for eight weeks, SPECT and clinical assessment were repeated. RESULTS: No differences in baseline clinical assessments or cerebral perfusion were observed according to the MspI genotype. However, after treatment, ADHD children with the G/G genotype at the MspI polymorphism showed hyperperfusion in the right cerebellar declive (p=.001, uncorrected) and hypoperfusion in the left lentiform nucleus and left cingulate gyrus (p<.001 and p=.001, uncorrected), compared to children without the G/G genotype. CONCLUSION: Although the results of this study should be interpreted cautiously, they suggest a possible role of the MspI polymorphisms of the ADRA2A gene in methylphenidate-induced changes in cerebral perfusion.
