The Longitudinal Trajectory of Subclinical Manic Symptoms from Childhood to Adolescence and their Predictive Validity for Bipolar Disorder

Background<br/>Bipolar Disorder (BD) is one of the leading causes of disability worldwide. Much of the disability associated with BD is linked to the early onset of the disorder, typically between 16 and 30 years of age. The aim of the PhD was to examine whether subclinical manic symptoms are associated with subsequent onset BD and to identify the longitudinal trajectories associated with conversion to syndromal BD.<br/><br/>Methods<br/>I analyzed data from TRAILS (TRacking Adolescents’ Individuals Lives Survey), a<br/>prospective population based study of 2,230 Dutch adolescents. Participants were assessed with the Child Behaviour Checklist 6-18 (CBCL 6-18) at ages 11, 13 and 16 years and were administered the Composite International Diagnostic Interview (CIDI) at age 19. The prevalence rate for BD in TRAILS was 5.4%.<br/><br/>Results<br/>I developed and validated a new scale, the Child Behaviour Checklist-Mania Scale (CBCLMS) to capture subclinical manic symptoms. The CBCL-MS consists of 19 items of the CBCL 6-18 selected by an expert panel to map onto the DSM criteria for Mania. The CBCL-MS had a four factor structure that was interpretable and temporally stable, and presented with good reliability and discriminative ability for BD. Based on assessments with the CBCL-MS at age 11, a Latent Class Analysis extracted three classes, representing an asymptomatic class (n=862), a mildly symptomatic class (n=845) and a highly symptomatic class (n=199). Membership in the highly symptomatic class was associated with a 7-fold increase in the odds for subsequent BD. Non-conversion to BD for members of this class was characterised by a decreasing longitudinal trajectory of<br/>subclinical manic symptomatology.<br/><br/>Conclusions<br/>These results support the concept of “alarm symptoms” in BD, as highly deviant childhood manic symptoms were associated with a subsequently greatly elevated risk of BD, and for initiatives to identify underlying BD at an earlier and more amenable stage. However, there was little support for a detectable prodromal phase for BD.

Name dc:type.qualificationname

Doctor of Philosophy

Level dc:type.qualificationlevel

Doctoral Thesis

Grantor dc:publisher.institution

King's College London

Year dc:date.issued

2013

Author dc:creator

• Papachristou, Efstathios

Language dc:language

eng

Identifier

oai:kclpure.kcl.ac.uk:studenttheses/004176f1-b6c4-4321-8b4b-7f725cbdcfa8

OAI identifier oai:identifier

oai:kclpure.kcl.ac.uk:studenttheses/004176f1-b6c4-4321-8b4b-7f725cbdcfa8