Atrophic Corpus Callosum Associated with Altered Functional Asymmetry in Major Depressive Disorder

Impairments in intra- and inter-hemispheric information transfer circuits have been reported in patients with major depressive disorder (MDD). However, the specific anomalous connection (intra- and/or inter-hemispheric) and hemisphere (left and/or right) in which this connection plays a more dominant role in the pathogenic mechanism underlying MDD are still poorly understood.

Structural magnetic resonance imaging and resting-state functional magnetic resonance imaging were performed in 33 patients with MDD and 33 healthy controls. The intra- and inter-hemispheric functional connectivity (FC) strength in the default mode network areas and volume of the callosal subregions were computed using independent samples t-tests. The partial correlations between the volumes and FCs were also computed.

The patients with MDD had smaller volumes in the genu of the corpus callosum than the controls. The intrahemispheric FCs of the bilateral posterior cingulate gyrus, left precuneus, left medial superior frontal gyrus, left medial orbitofrontal gyrus, left angular gyrus and left middle temporal gyrus, and interhemispheric FCs of the bilateral posterior cingulate gyrus in the patients with MDD were lower than those in the controls. Moreover, the intrahemispheric FCs of the precuneus and interhemispheric FCs of middle frontal gyrus, orbital middle frontal gyrus, and anterior cingulate gyrus in the patients with MDD showed right-lateralized asymmetry, which were opposite from the asymmetry patterns observed in the controls. The functional asymmetry of the anterior cingulate gyrus was correlated with the volume of the genu of the corpus callosum and disease duration.

These findings provide robust evidence that intra- and inter-hemispheric disconnections are involved in MDD, and that functional disruptions in the left hemisphere may be more relevant to the pathophysiology of MDD. Furthermore, imbalanced interhemispheric exchanges may contribute to the anatomical deficits in the corpus callosum in patients with MDD.