Neuroanatomical characterization of child offspring of bipolar parents.
OBJECTIVE
To examine structural differences in selected anterior limbic brain regions between at-risk children of parents with bipolar I disorder and children with healthy parents. We hypothesized that at-risk (AR) children would exhibit abnormalities in brain regions that are involved in mood regulation.


METHODS
Children (8-12 years old) of parents with bipolar I disorder (AR children, n = 21) and of parents without any DSM-IV Axis I disorder (healthy controls, n = 24) were evaluated using diagnostic assessments and brain magnetic resonance imaging. Morphometric analyses were used to examine group differences in the prefrontal cortical, thalamic, striatal, and amygdalar volumes.


RESULTS
Nine (43%) of the AR children met DSM-IV-TR criteria for a nonbipolar mood disorder at the time of assessment. AR and healthy control children did not demonstrate statistically significant differences across regions of interest (Wilks lambda =.86, F4,39 = 1.64, p = .18; effect size, f = 0.19). Post hoc analyses of covariance showed the largest relative effect size was contributed by the prefrontal cortex (f = 0.26).


CONCLUSIONS
Eight- to 12-year-old children with a familial risk for mania do not exhibit any statistically significant volumetric differences in the prefrontal cortex, thalamus, striatum, or amygdala as compared with age-matched children of parents without any psychopathology. Longitudinal studies examining whether structural changes over time may be associated with vulnerability for developing subsequent bipolar disorder are needed to clarify the underlying pathophysiology of this disorder.
Singh
Manpreet K
MK
All of the authors are with the Department of Psychiatry, Division of Bipolar Disorders Research, University of Cincinnati.
Delbello
Melissa P
MP
All of the authors are with the Department of Psychiatry, Division of Bipolar Disorders Research, University of Cincinnati.. Electronic address: delbelmp@email.uc.edu.
Adler
Caleb M
CM
All of the authors are with the Department of Psychiatry, Division of Bipolar Disorders Research, University of Cincinnati.
Stanford
Kevin E
KE
All of the authors are with the Department of Psychiatry, Division of Bipolar Disorders Research, University of Cincinnati.
Strakowski
Stephen M
SM
All of the authors are with the Department of Psychiatry, Division of Bipolar Disorders Research, University of Cincinnati.
D000679:Amygdala / Q000473:pathology; D001714:Bipolar Disorder / Q000175:diagnosis / Q000235:genetics* / Q000503:physiopathology; D002648:Child; D016241:Child of Impaired Parents / Q000523:psychology*; D015897:Comorbidity; D003342:Corpus Striatum / Q000473:pathology; D004292:Dominance, Cerebral / Q000502:physiology; D004644:Emotions; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics / Q000523:psychology; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008032:Limbic System / Q000473:pathology*; D008279:Magnetic Resonance Imaging; D008297:Male; D001523:Mental Disorders / Q000175:diagnosis / Q000235:genetics; D009415:Nerve Net / Q000473:pathology; D017397:Prefrontal Cortex / Q000473:pathology; D013788:Thalamus / Q000473:pathology