8 In a retro-spective analysis, rates of treatment-emergent mania were approximately twice as high when children who met the modified DSM-IV diagnostic criteria for PBD received antidepressants (44%) compared with those who received stimulants (18%).9 When stimulants and their potential effects on treatment-emergent manic symptoms were analyzed, adolescents with a history of treatment exposure prior to

the onset of PBD had an earlier age of onset than children without prior stimulant exposure.10 Furthermore, Inhibitors,research,lifescience,medical DelBello and coworkers, who carried out this study, showed that PBD-diagnoscd adolescents who had been receiving Inhibitors,research,lifescience,medical at least two different stimulant medications were younger at onset compared with patients who had received monotherapy stimulant treatment. This suggests a possible cumulative effect of stimulant-emergent manic states as a contextual risk factor for later-onset BD.10 This finding is PXD101 supported by other researchers, whose studies

indicate that prior treatment with antidepressants and/or stimulants was associated with earlier bipolar diagnosis and who compare these results to those of children Inhibitors,research,lifescience,medical who were never exposed to these medications.11 However, in view of the limited sample sizes and methodological limitations of these studies, these findings must be regarded as far from definite. Furthermore, the diagnosis of juvenile mania is often complicated by the clinical overlap of PBD symptoms and ADHD symptoms.12 However, there is also evidence not supporting this hypothesis.13,14 In view Inhibitors,research,lifescience,medical of the limited number of studies available, particularly on developmental aspects, it is essential to tackle the diagnostic challenges posed. If a patient with initial ADHD symptoms and later hypomanic PBD-related characteristics was not seen by his or her child and adolescent

psychiatrist during this hypomanic episode, Inhibitors,research,lifescience,medical the patient could be classified as an “ADHD only” or “pure ADHD” patient, because the comorbidity of PBD or the shift from ADHD to PBD symptoms would not be observed. Such cases could Carfilzomib not only lead to distorted diagnostic prevalence rates for PBD in clinical samples, but also to a camouflage of the ADHD/PBD comorbidity relationship. Further diagnostic factors such as biased symptom reporting by parents and carers, which dilute the observed effects, complicate matters further. In spite of the methodological hurdles hindering the feasibility of studies investigating the ADHD/PBD relationship, future longitudinal research is vital to clarify the complex diagnostic relationship between PBD and ADHD.