CBCL pediatric bipolar disorder profile and ADHD: comorbidity and quantitative trait loci analysis
James J McGough1, Sandra K Loo, James T McCracken
1Division of Child and Adolescent Psychiatry, UCLA Semel Institute for Neuroscience and Human Behavior and David Geffen School of Medicine, USA.jmcgough@mednet.ucla.edu
Objective:
The pediatric bipolar disorder profile of the Child Behavior Checklist (CBCL-PBD), a parent-completed measure that avoids clinician ideological bias, has proven useful in differentiating patients with attention-deficit/hyperactivity disorder (ADHD). We used CBCL-PBD profiles to distinguish patterns of comorbidity and to search for quantitative trait loci in a genomewide scan in a sample of multiple affected ADHD sibling pairs.
Method:
A total of 540 ADHD subjects ages 5 to 18 years were assessed with the Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime version and CBCL. Parents were assessed with the Schedule for Affective Disorders and Schizophrenia-Lifetime version supplemented by the Schedule for Affective Disorders and Schizophrenia for School-Age Children for disruptive behavioral disorders. Patterns of psychiatric comorbidity were contrasted based on the CBCL-PBD profile. A quantitative trait loci variance component analysis was used to identify potential genomic regions that may harbor susceptibility genes for the CBCL-PBD quantitative phenotype.
Results:
Bipolar spectrum disorders represented less than 2% of the overall sample. The CBCL-PBD classification was associated with increased generalized anxiety disorder (p =.001), oppositional defiant disorder (p =.008), conduct disorder (p =.003), and parental substance abuse (p =.005). A moderately significant linkage signal (multipoint maximum lod score = 2.5) was found on chromosome 2q.
Conclusions:
The CBCL-PBD profile distinguishes a subset of ADHD patients with significant comorbidity. Linkage analysis of the CBCL-PBD phenotype suggests certain genomic regions that merit further investigation for genes predisposing to severe psychopathology.
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