Premium
Evidence for disruption in prefrontal cortical functions in juvenile bipolar disorder
Author(s) -
Bearden Carrie E,
Glahn David C,
Caetano Sheila,
Olvera Rene L,
Fonseca Manoela,
Najt Pablo,
Hunter Kristina,
Pliszka Steve R,
Soares Jair C
Publication year - 2007
Publication title -
bipolar disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.285
H-Index - 129
eISSN - 1399-5618
pISSN - 1398-5647
DOI - 10.1111/j.1399-5618.2007.00453.x
Subject(s) - working memory , psychology , neurocognitive , prefrontal cortex , bipolar disorder , spatial memory , verbal fluency test , executive functions , cambridge neuropsychological test automated battery , cognition , audiology , neuropsychology , neuroscience , medicine
Objectives: Systematic parsing of executive function processes is critical for the development of more specific models of neurobiological processes mediating disturbed cognition in youth with bipolar disorder (BPD). Methods: A sample of 33 children and adolescents with bipolar I disorder (BPD I) (mean age 12.1 ± 3.0 years, 39% female) and 44 demographically matched healthy participants (mean age 12.9 ± 2.8 years, 50% female) completed a neurocognitive battery including measures aimed at detection of disruption in prefrontal cortical circuitry (i.e., working memory, set shifting, and rule attainment). Results: Compared to healthy controls, BPD I children exhibited significant deficits in spatial working memory, visual sequencing and scanning, verbal fluency and abstract problem solving, particularly when a memory component was involved. In our spatial delayed response task, memory set size was parametrically varied; the performance pattern in BPD I children suggested deficits in short‐term memory encoding and/or storage, rather than capacity limitations in spatial working memory. Earlier age at onset of illness and antipsychotic medication usage were associated with poorer performance on speeded information‐processing tasks; however, severity of mood symptomatology and comorbidity with disruptive behavior disorders were not associated with task performance. Conclusions: These results suggest impairment in measures of prefrontal cortical function in juvenile BPD I that are similar to those seen in the adult form of the illness, and implicate both the ventral and dorsolateral prefrontal cortex as loci of pathology in juvenile BPD. As these deficits were not associated with clinical state or comorbidity with other disorders, they may reflect trait‐related impairments, a hypothesis that will be pursued further in longitudinal studies.