Prevalence and Correlates of Disruptive Mood Dysregulation Disorder Among Adolescents with Bipolar Disorder.

OBJECTIVE

The purpose of this study was to examine the prevalence and correlates of disruptive mood dysregulation disorder phenotype (DMDDP) in a clinical population of adolescents with bipolar disorder (BD).

METHODS

DMDD criteria were modified and applied to a sample of 116 adolescents with BD-I (n = 30), BD-II (n = 46) or BD-not otherwise specified (NOS) (n = 40) from a tertiary teaching hospital. Diagnoses were determined via the Kiddie Schedule for Affective Disorders and Schizophrenia for School-Aged Children, Present and Lifetime version (KSADS-PL). Diagnostic and Statistical Manual of Mental Disorders (DSM-5) DMDD Criteria A-G were derived from the KSADS oppositional defiant disorder (ODD) screening interview and supplement, as well as narrative summaries. Chi-square analyses or t tests (p < 0.05) were conducted as appropriate, followed by logistic regression. P values were adjusted using the false discovery rate (FDR) approach.

RESULTS

DMDDP criteria could not be determined for 8 adolescents because of missing data from the ODD supplement. Twenty-five percent of the remainder (27/108) met criteria for DMDDP. DMDDP was not associated with BD subtype or with family history of BD. In univariate analyses, after controlling for age, sex, and race, DMDDP was associated with lower functioning, increased family conflict, assault history, and attention deficit and/or hyperactivity disorder (ADHD) (FDR adjusted p values: <0.0001, < 0.0001, 0.007, and 0.007, respectively). Lifetime substance use disorder and medication use approached significance (adjusted p = 0.05). In logistic regression, DMDDP was independently associated with greater parent-reported family conflict (odds ratio [OR] 1.17; confidence interval [CI- 1.06-1.30; p = 0.001) and greater functional impairment (OR 0.89; CI 0.82-0.97; p = 0.006). DMDDP was also associated with a threefold increase in ADHD, although ADHD was only marginally significant (OR 3.3; CI 0.98-10.94; p = 0.05).

CONCLUSIONS

Despite the positioning of DMDD as phenotypically and biologically distinct from BD, these phenotypes commonly overlap in clinical settings. This overlap is not explained by BD-NOS or by nonfamilial BD. The association of ADHD with DMDDP in this sample draws into question whether arousal symptoms should have been retained as originally elaborated in the severe mood dysregulation phenotype. Strategies to mitigate the excessive functional impairment of this comorbidity are warranted.