Structural imaging studies of individuals at risk for bipolar disorder: imaging results
| Study | Year | Areas analyzed | Tesla | Antip | HR versus controls | HR versus BD |
|---|---|---|---|---|---|---|
| Noga et al.1 | 2001 | Striatum (bilateral caudate nuclei, putamen, globus pallidus), amygdala– hippocampus (bilateral), cerebral hemispheric volumes | 1.5 | N | ↑ bilateral caudate (HR > C and BD > C) no differences in hemispheric volumes | ↑ right hippocampus (HR > BD) no differences in hemispheric volumes |
| Kieseppä et al.27 | 2003 | Bilateral ventricles, frontal and temporal lobes | 1 | N | ↓ left hemispheric white matter (HR < C) no changes in grey matter or ventricular volumes | No white or grey matter differences between HR and BD. |
| Ahearn et al.28 | 2002 | Whole brain | 1.5 | ? | White matter hyperintensities in 60% of HR | White matter hyperintensities in 100% of BD |
| Connor et al.29 | 2004 | Hippocampus | 1.5 | N | No significant differences | No significant differences |
| McDonald et al.30 | 2004 | Whole brain | 1.5 | N | Vulnerability to bipolar disorder is associated with: ↓ grey matter in right anterior cingulate gyrus and ventral striatum and ↓ white matter in the left prefrontal, left temporoparietal, right frontal and parietal regions and in the anterior corpus callosum | |
| McIntosh et al.31 | 2004 | Whole brain (SVC: amygdala- hippocampus, thalamus) | 1.5 | N | ↓ bilateral thalamus and caudate (HR < C) | No significant differences |
| McIntosh et al.32 | 2005 | Whole brain (SVC: frontal white matter and anterior limb of the internal capsule) | 1.5 | N | No significant white matter differences (HR = C) | Not tested |
| Gulseren et al.33 | 2006 | Frontal, parietal, temporal, occipital lobe, internal capsule | 0.5 | N | Hyperintensities in the right cerebral hemisphere of HR | BD have more hyperintensity than HR in the right cerebral hemisphere |
| Mc Donald et al.34 | 2006 | Brain volume, lateral ventricular volume, third ventricular volume, bilateral hippocampus | 1.5 | N | No differences in ventricular or hippocampal volumes. Trend toward larger cerebral volume (HR > C) | No significant differences |
| McIntosh et al.35 | 2006 | Whole brain (SVC: prefrontal cortex, temporal lobe, amygdala– hippocampal complex, thalamus) | 1.5 | N | No significant structural alterations related with an increased liability to bipolar disorder | |
| Frazier et al.36 | 2007 | Superior longitudinal fasciculus and cingulate-paracingulate white matter | 1.5 | N | ↓ FA in bilateral superior longitudinal fasciculus | — |
| Hajek et al.37 | 2008 | Pituitary | 1.5 | N | No difference in pituitary volume (HR = C) | No significant differences (HR = BD) |
| Hajek et al.38 | 2008 | Subgenual cingulate | 1.5 | N | No significant differences (HR = C) | No significant differences (HR = BD) |
| Ladouceur et al.5 | 2008 | Whole brain (SVC: amygdala– orbitomedial prefrontal cortex volumes) | 3 | N | ↑ left parahippocampal gyrus extending into left hippocampus | — |
| Mondelli et al.39 | 2008 | Pituitary | 1.5 | N | No significant difference in pituitary volumes (HR = C) | No significant differences (HR = BD) |
| Singh et al.40 | 2008 | Striatum, amygdala, prefrontal cortex, thalamus | 1.5 | Y | No significant differences in the selected ROIs | — |
| Chaddock et al.41 | 2009 | whole brain | 1.5 | N | No significant differences in fractional anisotropy (HR = C); the HR showed intermediate alterations to C and BD | Genetic liability is correlated with lower FA in several major white matter tracts of the brain |
| Kempton et al.42 | 2009 | Whole brain (ROI: amygdala, anterior and posterior cingulate, prefrontal cortex, hippocampus) | 1.5 | N | ↑ left insula (HR > C), ↑ left cerebellum (HR > C) | ↑ left cerebellum (HR > BD) |
| Hajek et al.43 | 2009 | Caudate and putamen | 1.5 | N | ↑ caudate volume (HR > C) | No significant differences in caudate and putamen (HR = BD) |
| Hajek et al.44 | 2010 | Subgenual cingulate | 1.5 | N | No significant differences (HR = C) | No significant differences (HR = BD) |
| Hajek et al.45 | 2009 | Hippocampus, amygdala | 1.5 | N | No significant differences (HR = C) | No significant differences (HR = BD) |
| van der Schot et al.46 | 2009 | Cerebellum, frontal, temporal, parietal, occipital lobe, ventricles | 1.5 | N | Genetic risk to bipolar disorder is associated with decreased white matter volume | |
| Walterfang et al.47 | 2009 | Corpus callosum | 1.5 | N | No significant differences (HR = C) | Callosal area smaller in BD (BD < HR) |
| Gunde et al.48 | 2010 | Subcortical, deep, periventricular white matter hyperintensity | 1.5 | N | No significant differences in white matter hyperintensities (HR = C) | No significant differences in white matter hyperintensities (HR = BD) |
| Takahashi et al.49 | 2010 | Pituitary | 1.5 | N | No difference in pituitary volume | Significant ↑ pituitary volume (BD > HR) |
| Forcada et al.50 | 2010 | Whole brain | 1.5 | N | — | No significant differences in white or grey matter volumes (HR = BD) |
| van der Schot et al.51 | 2010 | Whole brain | 1.5 | N | The genetic risk to develop bipolar disorder was related to decreased grey matter density in the right medial frontal gyrus, precentral gyrus and insula and with decreased white matter density in the superior longitudinal fasciculi bilaterally. | |
| Versace et al.52 | 2010 | Whole brain | 3 | N | ↑ fractional anisotropy (HR > C) and ↓ radial diffusivity (HR < C) in left corpus callosum and in right inferior longitudinal fasciculus | — |
Antip = antipsychotic exposure; BD = bipolar disorder; C = controls; HR = high risk for bipolar disorder; N = no; ROI = region of interest; SVC = small volume correction;Y = yes.