Abstract
Bipolar disorder (BD) is a genetically and phenotypically complex psychiatric disease. Although previous studies have suggested that the relatives of BD patients have an increased risk of experiencing affective disturbances, most relatives who have similar genotypes may not manifest the disorder. We aim to identify the neuroimaging alterations—specifically, the cortical folding structures of the anterior limbic network (ALN)—in BD patients and their siblings, compared to healthy controls. The shared alterations in patients and their siblings may indicate the hereditary predisposition of BD, and the altered cortical structures unique to BD patients may be a probe of BD expression. High-resolution, T1-weighted magnetic resonance images for 17 euthymic patients with BD, 17 unaffected siblings of BD patients, and 22 healthy controls were acquired. We categorized the cortical regions within the ALN into sulcal and gyral areas, based on the shape index, followed by the measurement of the folding degree, using the curvedness. Our results revealed that the changes in cortical folding in the orbitofrontal and temporal regions were associated with a hereditary predisposition to BD. Cortical folding structures in multiple regions of the ALN, particularly in the striatal–thalamic circuit and anterior cingulate cortex, could be used to differentiate BD patients from healthy controls and unaffected siblings. We concluded that the cortical folding structures of ALN can provide potential biomarkers for clinical diagnosis of BD and differentiation from the unaffected siblings.
Highlights
Bipolar disorder (BD) is a genetically and phenotypically complex psychiatric disease [1,2].Previous studies have suggested that the unaffected relatives of patients with BD have an increased riskBrain Sci. 2019, 9, 240; doi:10.3390/brainsci9090240 www.mdpi.com/journal/brainsciBrain Sci. 2019, 9, 240 of experiencing affective disturbances than relatives of healthy controls [2,3,4]
The purpose of this study was to determine the following: (1) the brain regions associated with hereditary predisposition to BD, based on the changes in cortical folding structures occurring in patients with BD and their unaffected relatives, but not in healthy controls; (2) the brain regions associated with disease expression of BD, based on the changes in cortical folding structures occurring in patients with BD, but not in unaffected relatives or healthy controls; and (3) the brain regions associated with an absence of BD diagnosis, based on the changes in cortical folding structures occurring in unaffected relatives, but not in patients with BD or healthy controls
This study investigated the differences in cortical folding structures for BD patients and their unaffected siblings, compared with healthy controls, by using combined shape index (SI) and CVD analysis
Summary
Bipolar disorder (BD) is a genetically and phenotypically complex psychiatric disease [1,2].Previous studies have suggested that the unaffected relatives of patients with BD have an increased riskBrain Sci. 2019, 9, 240; doi:10.3390/brainsci9090240 www.mdpi.com/journal/brainsciBrain Sci. 2019, 9, 240 of experiencing affective disturbances than relatives of healthy controls [2,3,4]. An alternative method of examining disease expression of BD is comparing the phenotypes unique to BD patients with those of unaffected relatives and healthy controls. The shared alterations present in both patients with BD and their unaffected relatives, but not present in healthy controls, could be associated with a hereditary predisposition to BD. Neuroimaging studies based on magnetic resonance imaging (MRI) have been widely used to reveal changes in brain structure associated with disease expression and hereditary predisposition to BD. Meta-analysis studies of structural MRI have demonstrated that reduced volumes of the prefrontal lobe, anterior cingulate cortex, insula, and corpus callosum, as well as increased volumes in the globus pallidus and the lateral ventricles were associated with BD disease expression [9,10,11,12]
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