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Updated: Jul 6, 2026

Measurement of Fronto-limbic Activity Using an Emotional Oddball Task in Children with Familial High Risk for Schizophrenia
Published on: December 2, 2015
Neuroanatomical characterization of child offspring of bipolar parents
Manpreet K Singh1, Melissa P Delbello2, Caleb M Adler1
1All of the authors are with the Department of Psychiatry, Division of Bipolar Disorders Research, University of Cincinnati.
Insights
Children at risk for bipolar disorder showed no significant brain structure differences compared to healthy peers. Further longitudinal studies are needed to understand the development of bipolar disorder in at-risk youth.
Area of Science:
- Neuroscience
- Child Psychiatry
- Genetics
Background:
- Bipolar I disorder has a strong genetic component, suggesting familial risk.
- Early identification of neurobiological markers in at-risk children is crucial for understanding disease development.
- Anterior limbic brain regions are implicated in mood regulation and are potential targets for investigation.
Purpose of the Study:
- To investigate structural brain differences in anterior limbic regions between children at familial risk for bipolar disorder and healthy controls.
- To test the hypothesis that at-risk children exhibit altered brain volumes in mood-regulating areas.
Main Methods:
- Magnetic resonance imaging (MRI) was used to assess brain structure in children aged 8-12.
- Morphometric analyses compared volumes of the prefrontal cortex, thalamus, striatum, and amygdala.
- Participants included children of parents with bipolar I disorder (at-risk group) and children of parents without psychiatric disorders (healthy controls).
Main Results:
- No statistically significant volumetric differences were found in the examined brain regions between at-risk and control children.
- The prefrontal cortex showed the largest, though not statistically significant, effect size.
- A significant proportion of at-risk children (43%) met criteria for a nonbipolar mood disorder at assessment.
Conclusions:
- Familial risk for bipolar disorder in children (8-12 years) is not associated with significant volumetric differences in key limbic brain regions.
- Longitudinal research is necessary to track potential structural brain changes over time that may indicate vulnerability to bipolar disorder.
- Clarifying the pathophysiology of bipolar disorder requires further investigation into developmental trajectories and genetic influences.
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.
Method:
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.
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